Dr. Alaa Mosbah, Professor of obstetrics and gynecology

Faculty of Medicine, Mansoura University,Egypt.

Professor Alaa Mosbah with Medical Graduates

Professor: Alaa Mosbah , Mansoura Manchester programme- sixth batch

Thursday, November 14, 2019

Prof. Alaa Mosbah YouTube channel

Dear Colleagues,
This is my YouTube channel ......You can watch some of my lectures via this link :

https://www.youtube.com/channel/UCZiadOpwdZPyAqQRwmL6ofw?view_as=subscriberhttps://www.youtube.com/channel/UCZiadOpwdZPyAqQRwmL6ofw?view_as=subscriber

Posted by Dr. Alaa Mosbah at 8:08 PM

Email This BlogThis!Share to Twitter Share to Facebook Share to Pinterest

No comments:

Featured Post

Huge multiple uterine fibroid, Broadligament fibroid & round ligament fibroid...Hysterectomy & BSO done by Dr. Alaa Mosbah

https://youtu.be/QDxnzQ5BTpU

Total Pageviews

Professor: Alaa Mosbah

Mansoura Faculty of Medicine

Huge cervical fibroid - TAH and BSO done by Dr. Alaa Mosbah

Mansoura University Hospital

Left solid ovarian tumor(dysgerminoma) in adolescent girl

Left salpingo-oophrectomy was done by Dr. Alaa Mosbah

Broad ligament fibroid - TAH and BSO done by Dr. Alaa Mosbah

Mansoura University Hospital- 5-1-2019

Right cystic ovarian tumor

TAH and BSO done by Dr. Alaa Mosbah

Myomectomy- for uterine fibroid- done by Dr Alaa Mosbah

Mansoura University Hospital

Endometrial hyperplasia -TAH done by Dr. Alaa Mosbah

Mansoura University Hospital- 30-3-2019

Endometrial carcinoma ,TAH & BSO &Omentectomy

Done by Dr.Alaa Mosbah,2-12-2013

Endometrioma- Laparoscopy ,done by Dr.Alaa Mosbah

Mansoura University Hospital

Endometrioma (Chocolate cyst) by laparoscopy -done by Dr. Alaa Mosbah

Mansoura University Hospital

Endometrioma (chocolate cyst)-TVS done by Dr. Alaa Mosbah

Mansoura University Hospital

Adolescent endometriosis,vesicle and red implants

Laparoscopy ,done by Dr.Alaa Mosbah

Multiple uterine fibroid - TAH and BSO -Done by Dr. Alaa Mosbah- 6-7-2019

Mansoura University Hospital

Left para ovarian cyst -TAH and BSO done by Dr. Alaa Mosbah

Mansoura University Hospital

Submucus Fibroid - TAH done by Dr. Alaa Mosbah

Mansoura University Hospital. 13-4-2019

Submucus fibroid and adenomyosis - TAH and BSO done by Dr. Alaa Mosbah

Mansoura University Hospital- 9-3-2019

Lt.ovarian mucinous cystadenoma

TAH&BSO ,done by Dr.Alaaa Mosbah 2013

Right ovarian tumor

TAH and BSO done by Dr. Alaa Mosbah

TAH &BSO for case (atypical endometrial hyperplasia

Done by Dr. Alaa Mosbah

Rt malignant ovarian tumor .TAH & BSO& Omentectomy

Done by Dr Alaa Mosbah 7-2-2015 in MUH

Lt.ovarian cystic teratoma discovered during cesarean section

Dr.Alaa Mosbah,2013

Hysterectomy for submucus fibroid. Done by Dr. Alaa Mosbah

Mansoura University Hospital, Egypt

Lt. Ovarian Tumor

TAH&BSO ,Done by DR. Alaa Mosbah

Right round ligament fibroid

Dr. Alaa Mosbah

Uterine sarcoma on top of fibroid

TAH&BSO done by Dr.alaa mosbah

Professor Alaa Mosbah

Mansoura University Hospital

Professor: Alaa Mosbah

Mansoura Manchester Programme

Cervical ectopic pregnancy diagnosed by TVS.

TVS was done by Dr. Alaa Mosbah

Laparoscopy

Dr. Alaa Mosbah

laparoscopy for a girl 7 years old with ovarian tumor

Excision of tumor was done by Dr. Alaa Mosbah

Laparoscopy

Dr. Alaa Mosbah

We not me event- a very special team of medical students with Dr. Alaa Mosbah

Mansoura Faculty of Medicine

Golden Jubilee of Mansoura Medical College

Dr. Alaa Mosbah

About Me

Dr. Alaa Mosbah: Mansoura, Egypt; Dr. Alaa Mosbah, professor of obstetrics and gynecology. I started my career as a House Officer (Intern) at Mansoura University Hospitals. This is one of the largest Teaching Hospitals in Egypt. This was followed by 12 month training at the Egyptian military air force hospital. My experience in Obstetrics and Gynecology started as a Resident Doctor (Registrar) and Assistant Lecturer (Senior Registrar) at the Department of Obstetrics and Gynecology, Mansoura University Hospitals with more than 8000 annual delivery rate. At 2007, Lecturer of Obstetrics and; Gynecology in Mansoura University Teaching Hospitals. Deputy director for Mansoura Manchester program from 2012 till 2019. I am Professor of Obstetrics and Gynecology at Faculty of Medicine, Mansoura University since 30 April 2017 till now.

View my complete profile

Professor: Alaa Mosbah

Dr. Alaa Mosbah with sixth year medical students

Mansoura Faculty of Medicine -2019

Miscarriage of 11 weeks pregnancy

Mansoura University Hospital

TAH and BSO for case with multiple uterine fibroid

Done by Dr. Alaa Mosbah

Adenomyosis (posterior wall) by TVS done by DR. Alaa Mosbah

Mansoura University Hospital

Guidelines

http://www.rcog.org.uk/guidelines
https://www.facebook.com/groups/878444208845457/

Dr. Alaa Mosbah

Mansoura Manchester programme, Egypt

Certificate of excellence to Professor Alaa Mosbah from IRB

Mansoura Faculty of Medicine

Visit of minister of higher education

Mansoura Manchester Programme

Visit of minister of higher education

Mansoura Faculty of Medicine

Certificate of Appreciation to Dr. Alaa Mosbah

Visit of the Malaysian Minister to Mansoura Manchester Programme - Mansoura Faculty of Medicine

Dr. Alaa Mosbah

Certificate of Appreciation to Professor Alaa Mosbah

Mansoura Manchester Programme, Egypt

Certificate of Appreciation to Dr. Alaa Mosbah

Honoring Dr. Alaa Mosbah in a celebration at the Faculty of Medicine

The sixth batch of Mansoura Manchester Programme

Professor: Alaa Mosbah

The 1 st International Meeting of the Egyptian Representative Committee (ERC) and Royal College of

Dr. Alaa Mosbah

Oncology conference in El-Hawar Hall, Mansoura, Egypt, 2016

Dr. Alaa Mosbah

Certificate of excellence as a reviewer

Dr. Alaa Mosbah

Mansoura Faculty of Medicine

Certificate of publication

Dr. Alaa Mosbah

Clinical Perspectives in Obstetrics and Gynecology (ACOG)

Dr. Alaa Mosbah - Received this program, 2015

Certidicate of excellence for Dr. Alaa Mosbah

IRB , Mansoura Faculty of Medicine

My lecture about OSCE, 2015

Dr. Alaa Mosbah

Oncology conference in Mansoura, Egypt

Dr. Alaa Mosbah

Certificate of accreditation of Mansoura Manchester Programme

Dr. Alaa Mosbah

Certificate of accreditation of Mansoura Manchester Programme

My lecture about OSCE, 2015

Dr. Alaa Mosbah

Dr Alaa Mosbah

Dr. Alaa Mosbah with 6th year medical students

Oncology conference, 2017. Fairmont Hotel, Cairo, Egypt.

International OBS & GYN Conference in Alexandria,2016

Dr. Alaa Mosbah

Dr. Alaa Mosbah (PBL class) with semester 10 students (Mansoura Manchester Programme),2017

Dr. Mansoura Manchester Programme

Mansoura University - Graduation day of a new batch from Mansoura Manchester programme , Egypt.

Mansoura Manchester programme, 2016

Dr. Alaa Mosbah with semester 10 students (Mansoura Manchester Programme)

Oncology conference, 2017. Fairmont Hotel, Cairo, Egypt.

Dr. Alaa Mosbah

Alexandria Library

Dr. Alaa Mosbah

Sheraton El-Montazah

Egyptian Representative Committee (ERC) and Royal College of Obstetricians and Gynaecologists 2010

Dr. Alaa Mosbah

Egyptian Representative Committee (ERC) and Royal College of Obstetricians and Gynaecologists (RCOG

Fairmont tour hotel ,Cairo ,Egypt 2010

Dr Alaa Mosbah

Blog Archive

► 2007 (2)
- ► December (2)

► 2008 (2)
- ► January (2)

► 2010 (1)
- ► November (1)

► 2011 (2)
- ► March (1)
- ► April (1)

► 2013 (3)
- ► January (2)
- ► February (1)

► 2015 (13)
- ► February (4)
- ► March (1)
- ► July (3)
- ► September (1)
- ► November (4)

► 2016 (7)
- ► January (1)
- ► May (5)
- ► August (1)

► 2017 (5)
- ► July (2)
- ► August (3)

► 2018 (5)
- ► July (5)

▼ 2019 (14)
- ► July (6)
- ► August (3)
- ► September (2)
- ► October (2)
- ▼ November (1)
  - Prof. Alaa Mosbah YouTube channel

► 2022 (1)
- ► January (1)

► 2023 (1)
- ► March (1)

DR. Alaa Mosbah M.D OBS and GYN, Private clinic

Mansoura,Porsaid Street,Ghonim tour,2nd floor,e mail:alaamosbah@hotmail.com ,Tel. No 0502361072 , Mobile : 01227455978

Search This Blog

Translate

Dr. Alaa Mosbah

Egyptian fertility society conference,J W Marriott

Dr. Alaa Mosbah

Cesarean section

DR. Alaa Mosbah

Lecturer of OBS&GYN

Dr. Alaa Mosbah

DR. Alaa Mosbah

Laparoscopy

Placenta ....... (delivery by C.S)

Dr Alaa Mosbah

The 6 th batch of Mansoura Manchester Programme

The 4 th batch of Mansoura Manchester programme

Dr. Alaa Mosbah

Textbook of Gynecology. Available on Amazon.com

Prof. Alaa Mosbah

Textbook of Obstetrics. Available on Amazon.com

Prof. Alaa Mosbah

Biophysical profile

Prof. Alaa Mosbah

CTG

Prof. Alaa Mosbah

Hyperemesis Gravidarum

Hyperemesis Gravidarum

Alaa Mosbah

Professor of Obstetrics & Gynecology

Faculty of Medicine, Mansoura University

2020

Definition

• Hyperemesis gravidarum refers to intractable vomiting during pregnancy that leads to weight loss and volume depletion, resulting in ketonuria and/or ketonemia.

Etiology

• The etiology of hyperemesis gravidarum is largely unknown, but several theories exist.

• Risk factors:

q Increased placental mass (multiple gestations)

q Molar pregnancy

q Consumption of estrogen-containing medications

q History of migraines

q Mothers or sisters, also experienced hyperemesis gravidarum.

q Psychological factors (unwanted pregnancy)

q Motion sickness

q The incidence of hyperemesis gravidarum ranges from 0.3% to 3%

q More common in western countries.

Pathophysiology

• Hormone Changes:

v Levels of human chorionic gonadotropin (hCG) have been implicated. hCG levels peak during the first trimester, corresponding to the typical onset of hyperemesis symptoms. There is a correlation between higher hCG concentrations and hyperemesis.

v Estrogen is also thought to contribute to nausea and vomiting in pregnancy. Estradiol levels increase early in pregnancy and decrease later, mirroring the typical course of nausea and vomiting in pregnancy.

• Changes in the Gastrointestinal System:

v The lower esophageal sphincter relaxes during pregnancy due to the elevations in estrogen and progesterone. This leads to an increased incidence of gastroesophageal reflux disease (GERD) symptoms in pregnancy, and one symptom of GERD is nausea.

• Genetics

v An increased risk of hyperemesis gravidarum has been demonstrated among women with family members who also experienced hyperemesis gravidarum.

v Two genes, GDF15 and IGFBP7, have been potentially linked to the development of hyperemesis gravidarum.

Diagnosis

• The history of a patient should include their pregnancy status, estimated gestational age, history of complications during prior pregnancies, the frequency of nausea and vomiting, any interventions during which the patient has already tried to treat symptoms, and the outcomes of the attempted interventions. Presence of constipation and epigastric pain

• The average onset of symptoms happens approximately 5 to 6 weeks gestational age.

• The physical exam should include:

q A patient weight should be obtained for comparison to previous and future weights.

q Examination of fluid status, which should include an examination of blood pressure, heart rate (Low blood pressure, weak rapid pulse), slight rise of temp, dry tongue, sunken eyes, negative capillary refill test, and dry wrinkled skin.

q Abdominal examination, as well as pelvic examination, if indicated, should occur to determine the presence or absence of tenderness to palpation.

q Fetal heart rate (depending on gestational age)

• Obstetrical ultrasounds may be considered to rule out multiple gestations, ectopic pregnancy, and gestational trophoblastic disease depending on the patient’s history and prior obstetrical evaluations.

• Magnetic resonance imaging (MRI) may be used to assess alternative diagnoses, such as appendicitis.

• Urine analysis to check for ketonuria, albuminuria and specific gravity (increased). Decrease Chloride (Fantus test).

• A complete blood count and electrolyte evaluation. An elevation in hemoglobin or hematocrit may be due to hemoconcentration in the setting of dehydration.

• Significant dehydration may result in acute kidney injury as evidenced by an elevation in serum creatinine, blood urea nitrogen, and a reduced glomerular filtration.

• Potassium, calcium, magnesium, sodium, and bicarbonate may be affected by prolonged bouts of vomiting and reduced oral intake of fluids.

• Thyroid tests, lipase, and liver function testing

• Ophthalmoscopy examination: retinal hge and retinal detachment in severe cases

• ECG: when there is abnormal serum potassium level

Differential Diagnosis

• Gestational trophoblastic disease

• Multiple gestations

• Ectopic pregnancy

• Preeclampsia

• HELLP syndrome

• Gastroenteritis

• Gastroparesis

• Small bowel obstruction

• Cholecystitis

• Pyelonephritis

• Ovarian torsion

Maternal Complications

q Severe vitamin deficiency, dehydration, and malnutrition

q Wernicke’s encephalopathy, caused by vitamin-B1 deficiency, can lead to death and permanent disability if it goes untreated.

q Peripheral neuropathy, retinal hge & coma

q Stress ulcer in the stomach & jaundice (liver damage)

q Renal failure

q Esophageal rupture and pneumothorax secondary to forceful and frequent vomiting,

q Electrolyte abnormalities such as hypokalemia can also cause significant morbidity and mortality.

q Higher rates of depression and anxiety during pregnancy.

q Esophageal rupture and pneumothorax secondary to forceful and frequent vomiting,

q Electrolyte abnormalities such as hypokalemia can also cause significant morbidity and mortality.

q Higher rates of depression and anxiety during pregnancy.

Fetal Complications

q Studies report conflicting information regarding the incidence of low birth weight and premature infants in the setting of nausea and vomiting in pregnancy.

q Studies have not shown an association between hyperemesis and perinatal or neonatal mortality.

q The frequency of congenital anomalies does not appear to increase in patients with hyperemesis

Treatment: Guided by the American College of Obstetrics and Gynecology (ACOG) Nausea and Vomiting in Pregnancy guidelines.

• Initial treatment should begin with non-pharmacologic interventions such as switching the patient’s prenatal vitamins to folic acid supplementation only, using ginger supplementation (250 mg orally 4 times daily) as needed, and by applying acupressure wristbands

• The first-line pharmacologic therapy should include a combination of vitamin B6 (pyridoxine) and doxylamine.

• These first-line medications demonstrate efficacy in the treatment of nausea and vomiting, preserved good fetal and maternal safety profiles and are listed as one of the few FDA pregnancy category A medications

• Second-line medications include antihistamines and dopamine antagonists such as:

q dimenhydrinate 25 to 50 mg every 6 hours orally,

q diphenhydramine 25 to 50 mg every 6 hours orally,

q prochlorperazine 25 mg every 12 hours rectally, or

q promethazine 12.5 to 25 mg every 6 hours orally or rectally.

• If the patient continues to experience significant symptoms without exhibiting signs of dehydration, metoclopramide, ondansetron, or promethazine may be given orally.

• In the case of dehydration, give intravenous fluid boluses or continuous infusions of normal saline should be given in addition to intravenous metoclopramide, ondansetron, or promethazine. Electrolytes should be replaced as needed.

• Treatment with antacids, histamine 2 antagonists (Ranitidine 150 mg OD-BD) or proton-pump inhibitors (omeprazole 20 mg OD-BD) should be added in all women with severe NVP or HG

• Severe refractory cases of hyperemesis gravidarum may respond to intravenous or intramuscular chlorpromazine 25 to 50 mg or methylprednisolone 16 mg every 8 hours, orally or intravenously.

• Intravenous fluid and parental feeding

v Fluid balance (input and output) should be monitored for the duration of the treatment cycle. IV fluid resuscitation with or without electrolyte (potassium, magnesium and phosphate) replacement should be prescribed as required

v Consider early treatment with IV fluids for women with dehydration or uncontrolled vomiting, prior to the development of electrolyte deficiency.

v If dextrose based solutions are used, IV thiamine must be administered prior as Wernicke’s encephalopathy may be precipitated in women with thiamine deficiency

v IV fluids have been shown to reduce vomiting and are therefore valuable for both outpatient and inpatient management of the symptoms of HG and severe NVP as well as associated dehydration and electrolyte disorders.

v In severe cases, if antiemetic and steroid therapy has failed, nutritional support via enteral or parenteral routes may be required to adequately restore hydration, correct electrolyte imbalance and maintain nutrition.

• Intravenous fluid and parental feeding

q I.V Normal Saline (2 L/day)

q I.V Glucose 5 % (1 L/day) only after correction of thiamine deficiency and exclusion of hyponatremia.

q Extra amount of crystalloids equal to vomitus & urine output per day

q Give Na, Cl, Mg and K guided by serum electrolytes

q Give vitamin B1, B6

q Give sodium bicarbonate or Ringer’s lactate, if there is acidosis or low serum Na

• Psychosocial assessment:

v Women with HG or severe NVP should be screened for depression and associated mental distress at first presentation with a validated tool and this should be repeated as indicated, particularly if symptoms are severe and prolonged.

Signs of improvement:

q Subsidence of vomiting

q Feeling of hunger

q Disappearance of acetone from breath and urine

q Normalization of biochemistry

q Normal pulse and blood pressure

q Normal urine output

q Better look

Therapeutic abortion:

q Is seldom indicated in cases on pregnancy associated with renal ,hepatic or neurological complications (life threating condition not responding to treatment)

q Failure of therapy should be clearly documented prior to consideration of medically-indicated termination of pregnancy

Prognosis

• Nausea and vomiting in pregnancy are common. Symptoms usually begin prior to 9 weeks gestation and the majority of cases are resolved by week 20 of gestation.

• A minority of patients, approximately 3%, will continue to experience vomiting during the third trimester.

• Approximately 10% of patients with hyperemesis gravidarum will be affected throughout the pregnancy

Fertilization, implantation and development of embryo: Dr. Alaa Mosbah 2021

Pregnancy occurs when mature capacitated sperm in the ampulla of the fallopian tubes fertilizes the ovum. The zygote migrates towards the uterine cavity and implantation of the blastocyst occurs in the fundus. Sperm transport: • Three to five-hundred million sperm are placed in the posterior fornix of the vagina during intercourse, near the external os of the cervical canal. • The sperm pass through the cervical canal by movement of their tails, whereas passage through the uterus and uterine tubes is facilitated by the muscular contractions of the walls of these organs. • Transport time to the fertilization site is short and takes about an hour or more. • About 300 to 500 sperm reach the fertilization site. Ovarian follicle maturation, ovulation and oocyte transport: • Maturation of ovarian follicle takes place in the ovary from an oocyte to a graafian follicle. • The oocyte, at ovulation, is carried in a peritoneal fluid stream, produced by the movements of the fimbriae of the uterine tube, into the infundibulum of the tube. • The ovum is "captured" by the ampulla of the uterine tube whose fimbriae sweep over the ovary. The oocyte passes into the ampulla of the uterine tube due to action of the cilia of the epithelial cells and by muscular contraction of the tubal wall. • Ovulation coincides with the first maturation division and with the elimination of the first polar body. Fertilization: • Definition: Fertilization is the union of a sperm nucleus, of paternal origin, with oocyte nucleus, of maternal origin, to form the primary nucleus of an embryo. • Fertilization takes place in the distal third of the uterine tube. • Spermatozoa arrive to fallopian tubes after an hour or more of coitus. • The ovum must be fertilized within 24 hours after ovulation. • Fertilization is the union of the male sperm, (23 chromosomes) and female oocyte, (23 chromosomes) gametes to form a zygote (46 chromosomes) and marks the beginning of pregnancy. • Embryonic life begins with fertilization. • Fertilization process requires about 24 hours. Morphologic changes in fertilization: • Sperm is the male gamete: it is derived from the Greek word 'sperma' (meaning 'seed'). It consists of three parts, o Head (containing DNA and enzymes in order to penetrate the oocyte), o Midpiece (containing cellular elements, centrioles, microtubules and a number of mitochondria for energy production required to promote sperm) o Tail (enabling sperm movement). • The three stages of fertilization: o Sperm preparation: Capacitation and acrosome reaction o Sperm- oocyte binding and fusion o Meiosis resumption of oocyte and activation of the zygote • The sperm:  The sperm must undergo capacitation (maturation and activation) in the female’s reproductive tract which increases its motility and destabilizes its membrane.  By destabilizing the membrane, the sperm prepares for the acrosome reaction and the enzymatic penetration of the zona pellucida.  Sperm passes through the corona radiata  Dispersal of cells is the result of enzymatic action of tubal mucosa and semen.  Sperm tail movements also help penetration of corona and zona pellucida  Sperm penetrates the zona pellucida: by action of enzymes released from its acrosome  Only 1 sperm enters the oocyte and fertilizes it, even though several may penetrate the zona pellucida. Two sperm may take part in fertilization during an abnormal process called dispermy resulting in a triploid embryo (69 chromosomes), but it nearly always aborts or dies shortly after birth.  Sperm head attaches to surface of the oocyte, plasma membranes of oocyte and sperm fuse, and then break at contact point  Head and tail of sperm enter oocyte cytoplasm with sperm's plasma membrane being attached to oocyte's plasma membrane  Once inside the cytoplasm of the oocyte, the sperm tail degenerates. • Oocyte responds by: o Zonal reaction: change in zona pellucida inhibits entry of more sperm, due to substance of oocyte cytoplasm. o Secondary oocyte completes second meiotic division and its chromosomes (22 plus X) arrange themselves in a vesicular nucleus called the female pronucleus. The second polar body is extruded. • Sperm head enlarges and forms the male pronucleus • The male and female pronuclei approach each other in the oocyte center, meet, and lose their nuclear membranes. They resolve their chromatin into a complete single haploid set of chromosomes which become organized on a spindle. • After the maternal and paternal chromosomes intermingle, metaphase of the first cleavage mitosis takes place, and the normal chromosome number is reconstituted. • Anaphase of the first cleavage mitosis then occurs. • The first 2 blastomeres are next seen, following cell division, and they are surrounded by the zona pellucida Consequences of fertilization: • Activation of the ovum • Modification of the cytoplasm and of the membranes • Modification of the nucleus: o Reconstruction or restoration of the diploid number of chromosomes (46). o Determination of sex by the X and Y chromosomes of the sperm gamete o Initiation of cleavage, stimulating the zygote to undergo rapid cell division Ovulation to Implantation: • The unfertilized ovum reaches the ampulla of the uterine tube and is fertilized, in the distal third of the tube by 12-24 hours, to form a zygote. • During its passage through the uterine tube, until the end of its morula stage, the egg undergoes almost no change in volume. • It remains surrounded by the zona pellucida which it loses upon entering the uterine cavity. • The zygote has made its way under the influence of peristaltic movements of the uterine tube and of ciliary movements of the tube epithelium. • During its passage, the egg maintains itself on its own reserves, and on tubular secretions. • Survival of the egg and its transport down the tube, as well as implantation of the blastocyst, depends on hormonal secretions of the ovary and anterior pituitary gland. • Division of the zygote into 2 daughter cells, the blastomeres, takes place by 30 hours. • Further divisions follow rapidly upon one another, forming progressively smaller and smaller blastomeres: 4 are seen in 50 hours, 8 by 60 hours, and 12-16 by day 3 or 4. • The 12-16 blastomere stage is a solid ball resembling a mulberry and is called a morula which enters the uterine cavity from the tube. • About day 4, fluid enters the morula from the uterine cavity and occupies the intercellular spaces. The fluid-filled spaces fuse to form a single, large cavity, the blastocele, and the morula is now called a blastocyst. • As fluid increases, the cells separate into 2 major areas: o An outer cell layer, the trophoblast, which gives rise to the placenta o The inner cell mass or embryoblast, which gives rise to the embryo proper • Zona pellucida disappears rapidly.

Dr. Alaa Mosbah -Professor of obstetrics and gynecology-Mansoura Faculty of Medicine- Egypt

Timing of birth for preeclampsia (NICE Guidelines, 2019)

Timing of birth for preeclampsia (NICE Guidelines, 2019)

Record maternal and fetal thresholds

for planned early birth before 37weeks in women with pre-eclampsia. Thresholds for considering planned early birth could include (but are not limited to) any of the following known features of severe pre-eclampsia:

• inability to control maternal blood pressure despite using 3or more classes of antihypertensives in appropriate doses

• maternal pulse oximetry less than 90%

• progressive deterioration in liver function, renal function, haemolysis, or platelet count

• ongoing neurological features, such as severe intractable headache, repeated visual scotomata, or eclampsia

• placental abruption
• reversed end-diastolic flow in the umbilical artery doppler velocimetry, a non-reassuring cardiotocograph, or stillbirth.

Other features not listed above may also be considered in the decision to plan early birth.

Involve a senior obstetrician in any decisions on timing of birth for women with pre-eclampsia.

Discuss with the anaesthetic team if birth is planned in a woman with pre-eclampsia.

Discuss with the neonatal team if birth is planned in a woman with pre-eclampsia, and neonatal complications are anticipated

Offer intravenous magnesium sulfate and a course of antenatal corticosteroids if indicated, if early birth is planned for women with preterm pre-eclampsia

Before 34 weeks:

Continue surveillance unless there are indications for planned early birth. Offer intravenous magnesium sulfate and a course of antenatal corticosteroids

From 34 to 36+6 week:

Continue surveillance unless there are indications for planned early birth. When considering the option of planned early birth, take into account the woman's and baby's condition, risk factors (such as maternal comorbidities, multi-fetal pregnancy) and availability of neonatal unit beds.

37 weeks onwards:

Initiate birth within 24–48hours.

Prof. Alaa Mosbah

2020

Laparoscopy for a case with severe adhesions- Adhesolysis was done by Dr. Alaa Mosbah

Mansoura University Hospital, 16-11-2019

Adenomyosis and HMB- TAH AND BSO done by Dr. Alaa Mosbah 14-12-2019

Mansoura Univesrsity Hospital

Multiple uterine fibroid. TAH and BSO was done by Dr. Alaa Mosbah

Mansoura University Hospital 1-2-2020

The best time for nonmedically indicated deliveries

The American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal–Fetal Medicine (Feb 2019) make the following recommendations:

1) Nonmedically indicated delivery, including cesarean delivery, inductions of labor, and cervical ripening should not occur before 39 0/7 weeks of gestation.

2) Implementation of a policy to decrease the rate of nonmedically indicated deliveries before 39 0/7 weeks of gestation has been found to decrease the number of these deliveries and, as a result, improve overall neonatal outcomes.

3) Avoidance of a nonmedically indicated delivery before 39 0/7 weeks of gestation is distinct from, and should not result in, an increase in expectant management of patients with medical indications for delivery before 39 0/7 weeks of gestation.

4) Indications for delivery before 39 0/7 weeks of gestation should be documented clearly and discussed with the patient.

5) Because nonrespiratory morbidities also are increased in early-term deliveries, documentation of fetal pulmonary maturity does not justify an early nonmedically indicated delivery. Amniocentesis for the determination of fetal lung maturity should not be used to guide the timing of delivery, even in suboptimally dated pregnancies.

Recommendation for Diagnosis & care for case with PPROM

GreenTop Guideline No. 73, June 2019.

Renal Calculi with Pregnancy - Prof. Alaa Mosbah, 2019

Renal Calculi with Pregnancy - Prof. Alaa Mosbah, 2019

-Renal stones during pregnancy can lead to significant morbidity for the woman and may also increase the risk of obstetric complications. Management is challenging because the optimum diagnostic tests and treatments are also associated with increased risks for the fetus.

-Incidence:

--The incidence of renal stones in pregnancy is quoted to be 1 in 1500

--Patients are more likely to be Caucasian

-- History of renal disease and hypertension increase incidence.

--A quarter has a history of previous stone disease

--Stones appear to be more common in multiparous women,

-- 80–90% stones occurring in the second and third trimester.

--Ureteral stones are encountered twice as often as renal calculi

--Both the right and left side appear to be equally affected despite greater dilatation of the right renal tract

-Risk factors:

--Positive family history,

--Dietary factors such as low intake of water or increased intake of animal protein and sodium

--Environment factors such as hot climate

--Underlying medical conditions such as hyperparathyroidism

-Clinical presentation

---Flank pain is the most common presentation (89–100%), hematuria is seen in (75–95%) of cases.

---Frequency and dysuria are common, particularly when the stone has moved to the lower urinary tract or there is infection.

---Renal stones may also present as preterm labor or uterine contractions

-Impact of renal stones on pregnancy:

A significant increase in the risk of:

.Recurrent miscarriage,

.Mild pre-eclampsia,

.Chronic hypertension,

.Gestational diabetes mellitus,

.Cesarean deliveries,

.PROM and preterm delivery

-Diagnosis of Renal Calculi:

---Laboratory assessment:

Urine analysis, culture, CBC, kidney function tests, serum calcium and investigations for hyperparathyroidism.

---Radiological diagnosis:

---Ultrasound is the first line investigation used in pregnant women. However, sensitivities for stone detection vary considerably, ranging from 29 to 69%. TVS may be used to improve detection rate for distal ureteral stones. Sensitivity for stone detection may also be improved in pregnancy by using Doppler US to measure renal vascular resistance.

---Colour Doppler can also be used to detect ureteral jets, or passage of urine, at the ureterovesical junction. Absence of a ureteral jet on the symptomatic side suggests complete obstruction with a stone.

---Magnetic resonance urography (MRU): MRI uses electromagnetic radio waves rather than ionising radiation. No harmful effects to the fetus have been reported, however it should be avoided in the first trimester due to limited data on safety during fetal organogenesis.

---CT scanning: CT is generally not recommended in pregnancy because of higher ionising radiation exposure.

---Limited IVU) has been proposed (harmful)

-Management of Renal Calculi:

---Expectant management:

As the rate of spontaneous passage of stones is high, expectant management is first-line treatment in both the general population and during pregnancy. It includes analgesia, hydration, and antibiotics if infection is suspected. Opioids are generally prescribed to treat acute renal colic and may be used safely in pregnancy.

----Medical management:

No data are available on medical expulsive therapy use in pregnancy. However, nifedipine (20–30 mg) could be used safely in pregnancy.

----Active intervention:

-An estimated 25–40% of pregnant women require active intervention.

-When active intervention is needed during pregnancy, it is imperative to use a multidisciplinary team approach, with involvement of urologists, obstetricians, anesthetists, radiologists, and neonatologists.

-Indications for active intervention: Uncontrolled pain, persistent vomiting, sepsis, obstruction of a solitary or transplanted kidney, bilateral obstruction, impending renal failure or obstetric complications such as premature onset of labor.

-Active management of renal stones includes:

(1)Temporising measures to relieve obstruction through insertion of a ureteral stent or per-cutaneous nephrostomy (PCN)

(2)Definitive treatment of the stone by lithotripsy, percutaneous nepthrolithotomy, or ureteroscopic stone removal.

How to write essay?

Professor Alaa Mosbah

Submucus and intramural fibroids - TAH and RT. salpingo-oophorectomy done by Dr. Alaa Mosbah

Mansoura University Hospital 30-11-2019

Myomectomy for uterine fibroid- by Dr. Alaa Mosbah

Mansoura Universty Hospital, 2-11-2019

Polycystic ovary syndrome (PCOS)- Key points

Polycystic ovary syndrome (PCOS)- Key points

Prof. Alaa Mosbah

-Definition: Polycystic ovary syndrome (PCOS) is a complex condition characterized by elevated androgen levels, menstrual irregularities, and/or small antral follicles in one or both ovaries. It is the commonest endocrinological disorder leading to reproductive as well as metabolic dysfunction in women.

-Prevalence: Polycystic ovary syndrome (PCOS) is a common condition, present in 12–21% of women of reproductive age.

-Etiology: PCOS can be described as an oligogenic disorder in which the interaction of a number of genetic and environmental factors determine the heterogeneous, clinical, and biochemical phenotype.

- Pathophysiological features of PCOS: Hyperandrogenaemia and insulin resistance are pathophysiological features of PCOS. Women are at risk if they have a genetic predisposition, and the onset of symptoms can be triggered by environmental factors, particularly obesity. It is important to be aware that some population groups have a higher risk of PCOS such as Australian Indigenous women.

-Features of presentations:

Hirsutism and male pattern balding consistent with hyperandrogenism
Irregular or absent menstrual cycles
Subfertility or infertility
Psychological symptoms – anxiety, depression, psychosexual dysfunction, eating disorders
Metabolic features – obesity, dyslipidaemia, diabetes

-Diagnosis:

---Diagnosis can generally be accomplished with a careful history, physical examination, and basic laboratory testing. Hyperandrogenism can be diagnosed clinically by the presence of excessive acne, androgenic alopecia, or hirsutism (terminal hair in a male-pattern distribution); or chemically, by elevated serum levels of total, bioavailable, or free testosterone or dehydroepiandrosterone sulfate

---According to Rotterdam Criteria, women with PCOS must have two of the following: oligo/anovulation, clinical or lab evidence of hyperandrogenism or polycystic ovaries on ultrasound (12 or more follicles, measuring between 2 and 9 mm, and/or an ovarian volume (OV) >10 cm). And, each case has to classify into a specific phenotype as Phenotype A: hyperandrogenism + ovulatory dysfunction + PCOM; Phenotype B: hyperandrogenism + ovulatory dysfunction; Phenotype C: hyperandrogenism + PCOM; and Phenotype D: ovulatory dysfunction + PCOM. Other aetiologies must be excluded such as congenital adrenal hyperplasia, androgen secreting tumours, Cushing syndrome, thyroid dysfunction and hyperprolactinaemia. Diagnosis of PCOS is crucial at adolescence because hormonal and reproductive transition of normal puberty may mimic features of the syndrome (3 out of 3 should be used).

-Treatment: Will depend on age of patient and main complaint such as menstrual irregularities, hirsutism or desire for fertility.

. A lifestyle program that addresses a healthy diet with caloric restriction, behavior change support and exercise to aid in weight loss and prevention of future weight gain is the best first line treatment for PCOS in obese women. The national guideline emphasises that a team approach is often required for psychological, nutritional and behavioural support.

. The combined oral contraceptive pill (COCP) is effective in achieving menstrual cycle regularity and also provides contraception if this is required.

. Generalized hirsutism may benefit from a combined medical and cosmetic (eg. laser and electrolysis) approach. The COCP is first line medical therapy. Metformin may also provide some benefit.

. Treatment of infertility could be by using medications such as clomiphene citrate, metformin or a combination of both. If it was unsuccessful in achieving pregnancy then gonadotrophins are the next pharmacological options.

. Laparoscopy with ovarian drilling is a suitable second line treatment if clomiphene citrate with metformin has failed and the pregnancy rate is as effective as 3–6 cycles of gonadotrophin ovulation induction.

Asymptomatic bacteriuria - Prof. Alaa Mosbah

Asymptomatic bacteriuria

-Is defined as the presence of a positive urine culture in an asymptomatic person and occurs in 2 to 7 percent of all pregnancies (Patterson and Andriole, 1997).

-Presence of pathogens more than 100,000 colonies of the same species/ml of urine in freshly voided midstream specimens.

-Asymptomatic bacteriuria is associated with an increased risk of adverse fetal outcomes. In particular, an increased risk of preterm birth and an increased risk of delivering a low birth weight infant (Millar and Cox, 1997) .

-Screening for asymptomatic bacteriuria should be performed ideally at 12 to 16 weeks gestation on all women.

-The diagnosis of asymptomatic bacteriuria is made following isolation of a significant growth of one bacterial species in a “clean catch” specimen of urine. -Urine microscopy and culture remain the gold standard in detection of asymptomatic bacteriuria. However, it can take 48 hours to obtain a result.

-A clean catch specimen involves collection of a mid-stream specimen of urine after cleaning of the perineum in order to minimise contamination by skin flora.

-Treatment:

-Co-amoxiclav 625mg TDS for 5 or for 7 days

-Cefuroxime axetil 500mg BD for 5

-Cefaclor 500mg for 5-7 days

-Fosfomycin 3g stat dose

-Nitrofurantoin 100mg BD PO for 7 days

Rules for writing MCQ - Prof. Alaa Mosbah

Mansoura Faculty of Medicine

Huge left ovarian tumor - TAH and BSO done by DR. Alaa Mosbah

Prof. Alaa Mosbah

Abnormal uterine bleeding – Key Points – Prof. Alaa Mosbah

Abnormal uterine bleeding – Key Points – Prof. Alaa Mosbah, 2019

- A normal menstrual cycle has a frequency of 24 to 38 days, lasts 4 to 8 days, with 5 to 80 milliliters of blood loss and variation of menstrual cycle length measured over 12 months less than 20 days (FIGO, 2011).

-Definition: Abnormal uterine bleeding (AUB) is a broad term that describes irregularities in the menstrual cycle involving frequency, regularity, duration, and volume of flow outside of pregnancy. Inter-menstrual bleeding (IMB) is the bleeding that occurs between otherwise normal menstrual periods. Abnormal bleeding is considered chronic when it has occurred for most of the previous six months, or acute when an episode of heavy bleeding warrants immediate intervention.

-Prevalence: Abnormal uterine bleeding is a common symptom in women with a prevalence of 10% to 30% among women of reproductive age with a higher incidence occurring around menarche and perimenopause.

-Classification: The PALM-COEIN classification, with PALM referring to structural etiologies (polyp, adenomyosis, leiomyoma, malignancy and hyperplasia), and COEIN referring to nonstructural etiologies (coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not otherwise classified).

-Diagnosis: Involves a detailed history (personal, menstrual, obstetric, past and family history), general, abdominal and pelvic examination (PV, bimanual and speculum) for cervical, uterine or adnexal masses. Laboratory testing that includes a pregnancy test and complete blood count, coagulation profile, Liver function tests and thyroid function test. Endometrial sampling should be performed in patients 45 years and older, and in younger patients with a significant history of unopposed estrogen exposure. Transvaginal ultrasonography is the preferred imaging modality and is indicated if a structural etiology is suspected like fibroid, adenomyosis and ovarian tumors. MRI may be needed in some cases.

-Treatment: Medical and surgical treatment options are available.

.Emergency interventions for severe bleeding that causes hemodynamic instability include uterine tamponade, intravenous estrogen, dilation and curettage, and uterine artery embolization.

.Patients with severe bleeding can be treated initially with oral estrogen, high-dose estrogen-progestin oral contraceptives, oral progestins, or intravenous tranexamic acid.

.Hemodynamically stable patients

---medical management is the preferred initial approach. Oral tranexamic acid and nonsteroidal anti-inflammatory drugs. The most effective long-term medical treatment for heavy menstrual bleeding is the levonorgestrel-releasing intrauterine system (Mirena). Other long-term medical treatment options include estrogen-progestin oral contraceptives, oral progestins, and depot medroxyprogesterone.

---Surgical treatment according to the cause of bleeding or after failure medical treatment like myomectomy, polypectomy, uterine artery embolization, endometrial ablation and hysterectomy.

Visit of the Malaysian Minister to Mansoura Manchester Programme - Mansoura Faculty of Medicine

Prof. Alaa Mosbah

Fetal Monitoring – Key points

Fetal Monitoring – Key points

-Fetal status must be monitored during labor. The main parameters are baseline fetal heart rate (HR) and fetal HR variability, particularly how they change in response to uterine contractions and fetal movement.

-Several patterns are recognized; they are classified into 3 categories:

Category I: Normal

Category II: Indeterminate

Category III: Abnormal

-A normal pattern

Strongly predicts normal fetal acid-base status at the time of observation. This pattern has all of the following characteristics:

-HR 110 to 160 beats/min at baseline

-Moderate HR variability (by 6 to 25 beats) at baseline and with movement or contractions

-No late or variable decelerations during contractions

-Early decelerations and age-appropriate accelerations may be present or absent in a normal pattern.

-An indeterminate pattern

Is any pattern not clearly categorized as normal or abnormal. Many patterns qualify as indeterminate. Whether the fetus is acidotic cannot be determined from the pattern. Indeterminate patterns require close fetal monitoring so that any deterioration can be recognized as soon as possible.

-An abnormal pattern

Usually indicates fetal metabolic acidosis at the time of observation. This pattern is characterized by one of the following:

.Absent baseline HR variability plus recurrent late decelerations

.Absent baseline HR variability plus recurrent variable decelerations

.Absent baseline HR variability plus bradycardia (HR < 110 beats/min without variability or < 100 beats/min)

.Sinusoidal pattern (fixed variability of about 5 to 40 beats/min at about 3 to 5 cycles/min, resembling a sine wave)

-Abnormal patterns require prompt actions to correct them (e.g., supplemental oxygen, repositioning, treatment of maternal hypotension, discontinuation of oxytocin) or preparation for an expedited delivery.

-Monitoring can be manual and intermittent, using a fetoscope for auscultation of fetal HR. However, in the US, electronic fetal HR monitoring (external or internal) has become standard of care for high-risk pregnancies, and many clinicians use it for all pregnancies. The value of routine use of electronic monitoring in low-risk deliveries is often debated. However, electronic fetal monitoring has not been shown to reduce overall mortality rates in large clinical trials and has been shown to increase rates of cesarean delivery, probably because many apparent abnormalities are false positives. Rate of cesarean delivery is higher among women monitored electronically than among those monitored by auscultation.

Fetal pulse oximetry has been studied as a way to confirm abnormal or equivocal results of electronic monitoring; status of fetal oxygenation may help determine whether cesarean delivery is needed.

Fetal ST-segment and T-wave analysis in labor (STAN) can be used to check the fetal ECG for ST-segment elevation or depression; either finding presumably indicates fetal hypoxemia and has a high sensitivity and specificity for fetal acidosis. For STAN, an electrode must be attached to the fetal scalp; then changes in the T wave and ST segment of the fetal ECG are automatically identified and analyzed.

-If manual auscultation of fetal HR is used, it must be done throughout labor according to specific guidelines, and one-on-one nursing care is needed.

For low-risk pregnancies with normal labor, fetal HR must be checked after each contraction or at least every 30 min during the 1st stage of labor and every 15 min during the 2nd stage.

For high-risk pregnancies, fetal HR must be checked every 15 min during the 1st stage and every 3 to 5 min during the 2nd stage.

-Listening for at least 1 to 2 min beginning at a contraction’s peak is recommended to check for late deceleration. Periodic auscultation has a lower false-positive rate for abnormalities and incidence of intervention than continuous electronic monitoring, and it provides opportunities for more personal contact with women during labor. However, following the standard guidelines for auscultation is often difficult and may not be cost-effective. Also, unless done accurately, auscultation may not detect abnormalities.

Electronic fetal HR monitoring may be

External: Devices are applied to the maternal abdomen to record fetal heart sounds and uterine contractions.

Internal: Amniotic membranes must be ruptured. Then, leads are inserted through the cervix; an electrode is attached to the fetal scalp to monitor HR, and a catheter is placed in the uterine cavity to measure intrauterine pressure.

-Usually, external and internal monitoring are similarly reliable. External devices are used for women in normal labor; internal methods are used when external monitoring does not supply enough information about fetal well-being or uterine contraction intensity (eg, if the external device is not functioning correctly).

-External electronic fetal monitoring can be used during labor or electively to continuously record fetal HR and correlate it with fetal movements (called a nonstress test).

-A nonstress test is typically done for 20 min (occasionally for 40 min). Results are considered reactive (reassuring) if there are 2 accelerations of 15 beats/min over 20 min. Absence of accelerations is considered nonreactive (non-reassuring). Presence of late decelerations suggests hypoxemia, potential for fetal acidosis, and the need for intervention.

-A nonreassuring nonstress test

Is usually followed by a biophysical profile (adding assessment of amniotic fluid volume and sometimes assessment of fetal movement, tone, breathing, and heart rate, to the nonstress test). A nonstress test and biophysical profile are frequently used to monitor complicated or high-risk pregnancies (e.g., complicated by maternal diabetes or hypertension or by stillbirth or fetal growth restriction in a previous pregnancy).

-External monitoring can be used with a contraction stress test as well as a nonstress test;

Fetal movements and HR are monitored during contractions induced by oxytocin ( oxytocin challenge test). However, contraction stress testing is now rarely done and, when done, must be done in a hospital.

If a problem (fetal HR decelerations, lack of normal HR variability) is detected during labor:

Intrauterine fetal resuscitation is tried; women may be given oxygen by a tight nonrebreather face mask or rapid IV fluid infusion or may be positioned laterally. If fetal heart pattern does not improve in a reasonable period and delivery is not imminent, urgent delivery by cesarean is needed.

Prof. Alaa Mosbah

2019

Large broad ligament fibroid - TAH and BSO done by Dr. Alaa Mosbah

Prof. Alaa Mosbah

Urinary tract infections during pregnancy – Key points

Urinary tract infections during pregnancy – Key points

-Incidence: Urinary tract infections are common during pregnancy, the incidence of UTI during pregnancy nearly 8 percent.

-The most common causative organism is Escherichia coli.

-Asymptomatic bacteriuria (10%) can lead to the development of cystitis or pyelonephritis. Significant bacteriuria has been historically defined as finding more than 10⁵ colony-forming units per mL of urine.

-Screening: All pregnant women should be screened for bacteriuria (urine culture be obtained at the first prenatal visit and again in third trimester) and subsequently treated with antibiotics such as nitrofurantoin, sulfisoxazole or cephalexin. Ampicillin should no longer be used in the treatment of asymptomatic bacteriuria because of high rates of resistance.

-Complications: Thirty percent of patients with untreated asymptomatic bacteriuria develop symptomatic cystitis and up to 50 percent develop pyelonephritis. Asymptomatic bacteriuria is also associated with IUGR and low-birth-weight infants. UTI may cause premature labor, hypertensive disorders of pregnancy, anemia and amnionitis.

-Pyelonephritis can be a life-threatening illness, with increased risk of perinatal and neonatal morbidity. Acute pyelonephritis during pregnancy is a serious systemic illness that can progress to maternal sepsis, preterm labor and premature delivery.

-Recurrent infections are common during pregnancy and require prophylactic treatment.

-Pregnant women with urinary group B streptococcal infection: GBS is found to be the causative organism in UTIs in approximately 5 percent of patients and should be treated and should receive intrapartum prophylactic therapy.

Prof. Alaa Mosbah

2019

I spent my life in wonderful places, Mansoura, Egypt

Faculty of Medicine, Mansoura University Hospital, Mansoura University and Mansoura city

Postpartum hemorrhage - Key points

Postpartum hemorrhage - Key points

1-Postpartum hemorrhage is common problem in obstetrics (approximately 3% to 5% of obstetric patients) and can occur in patients without risk factors for hemorrhage (20% of cases).

2-Active management of the third stage of labor should be used routinely to reduce its incidence. Use of oxytocin after delivery of the anterior shoulder is the most important and effective component of this practice.

3-Oxytocin is more effective than misoprostol for prevention and treatment of uterine atony and has fewer adverse effects.

4-Routine episiotomy should be avoided to decrease blood loss and the risk of anal laceration.

5-Appropriate management of postpartum hemorrhage requires prompt diagnosis and treatment.

6-The Four T's mnemonic can be used to identify and address the four most common causes of postpartum hemorrhage:

a- Tone: uterine atony

b- Trauma: laceration, hematoma, inversion, rupture

c- Tissue: retained tissue or invasive placenta

d- Thrombin: coagulopathy

7-Rapid team-based care minimizes morbidity and mortality associated with postpartum hemorrhage.

8- Massive transfusion protocols allow for rapid and appropriate response to hemorrhages more than 1,500 mL of blood loss.

Prof. Alaa Mosbah

2019

Mansoura is a city in Egypt, It is the capital of the Dakahlia Governorate

Mansoura is about 120 km northeast of Cairo.

Laparoscopy - Dr. Alaa Mosbah

Prof. Alaa Mosbah

Laparoscopy in pelvic surgery - Dr. Alaa Mosbah

Laparoscopy in pelvic surgery – Prof. Alaa Mosbah

Definition:

Laparoscopy is a minimally invasive surgery, a modern surgical technique in which operations are performed far from their location through small incisions (usually 0.5–1.0 cm) elsewhere in the body. Laparoscopic surgery includes operations within the abdominal or pelvic cavities.

Laparoscopes:

Laparoscopes are telescopes that vary in size from 2 to 10 mm. Zero-degree, 30-degree, 45-degree, and 70-degree viewing angles are available.

Advantages

There are a number of advantages to the patient with laparoscopic surgery versus an open procedure. These include:

Reduced hemorrhaging, smaller incision, which reduces pain and shortens recovery time, as well as resulting in less post-operative scarring, Less pain, leading to less pain medication needed. Although procedure times are usually slightly longer, hospital stay is less. Reduced risk of acquiring infections.

Patient Positioning

Proper patient positioning is paramount. The surgeon should position the patient so as to prevent any excessive pressure on the lower extremities. Nerve injuries can result from improper placement of the lower extremities in stirrups. Lithotomy position with access to steep Trendelenburg is appropriate. The physician should discuss with anesthesia personnel decisions regarding whether the arms should be extended or “tucked” along the sides of the patient. The latter requires particular attention to prevent any trauma to the hands and fingers when the table is maneuvered.

With the patient in the low lithotomy position and the legs supported in stirrups, the buttocks should protrude slightly from the lower edge of the table. The lateral aspect of the knee should be protected with padding in the stirrup to prevent peroneal nerve injury. The knees should be kept in slight flexion to minimize stretching of the sciatic nerves and to provide increased stability in the Trendelenburg position. With respect to positioning of the arms, care should be taken not to stretch or traumatize the brachial plexus.

It has been advocated that an angle of 145 degrees between the abdomen and the lower extremity (thigh) is ideal, providing the surgeon with adequate space for instrumentation.

Equipment

An array of instruments designed to facilitate operative laparoscopic procedures continues to evolve.

Viewing System

The video equipment should include a three-chip camera, a processor, a 300-watt xenon light source with fiberoptic cable, a high-resolution monitor, and a video recorder.

An operating room table that allows 30 degrees of flexion (Trendelenburg position) is ideal for visualization of the deep pelvis. Shoulder braces (Stierlen-Maquet Shoulder Braces, Siemens Medical Systems, Englewood, CO) placed at the acromioclavicular joints and the arms placed at the patient's sides will minimize nerve injuries.

Insufflator

For most procedures, the pneumoperitoneum may be maintained with an insufflator that flows at a rate of 2 to 7 L/min. High-flow insufflators that achieve up to 30 L/min are available and will maintain the pneumoperitoneum during procedures that allow escape of large amounts of CO₂, such as during tissue morcellation.

Carbon Dioxide Warmer

There is evidence that warmed CO₂ is less irritating to the peritoneal surface and, therefore, may cause less adhesion formation. CO₂ warmers are commercially available.

Electrosurgery

Unipolar electrosurgical

Instruments are used to cut and coagulate tissue. Cutting occurs when there is sufficient voltage (at least 200 volts) between the electrode and the tissue to produce an electric arc. This arc concentrates the current to points along the tissue, resulting in a cutting effect. In contrast to cutting current, coagulation is produced through instrument contact with the tissue. Contact allows heating of the tissue followed by irreversible cellular damage, evaporation of intracellular water, and contraction of blood vessels and surrounding tissue. Electrosurgical burns may occur due to insulation failure, direct coupling (activated electrode makes unintended contact with another metal object in the area of the surgical field), or capacitive coupling (induction of stray current to a surrounding conductor through the intact insulation of an active electrode).

Bipolar electrosurgical

Instruments contain the electrical current between an active and return electrode, usually the two blades of forceps. The flow of alternating current is passed between the two electrodes rather than passing through the patient to a grounding pad. This eliminates the risk of capacitive coupling and stray current.

Obtaining Intra-abdominal Access

Insufflation of CO₂ through a Veress needle is the most common method of entry, although some would argue the open technique should become the method of choice. One technique of access using a Veress needle is performed in the following manner:

· A vertical incision through the skin corresponding to the size of the trocar is made at the base of the umbilicus. Note that this incision ideally is made at the base of the umbilicus and not infraumbilically as is classically taught. This is because the distance between skin and peritoneum on the anterior abdominal wall is shortest at the base of the umbilicus. In addition, the peritoneum is firmly attached, which will prevent tracking through the subcutaneous tissue and subsequent retroperitoneal insufflation.

· The Veress needle is inspected for sharpness and a functioning spring mechanism to extend the protective sheath in the absence of pressure.

· The anterior abdominal wall inferior to the umbilicus is grasped with the nondominant hand and the umbilicus is moved in the caudad direction, further displacing it below the bifurcation of the aorta. Alternatively, the incision may be elevated by grasping the edges of the umbilical incision with two Alice clamps and lifting.

· The tip of the Veress needle is held in the dominant hand between the thumb and forefinger while the ulnar palm rests on the patient's abdomen. The needle is inserted carefully at a 90-degree angle, through the base of the umbilicus, millimeter by millimeter, until a click is heard and resistance is no longer felt, identifying intraabdominal placement.

· A saline-filled 10-cc syringe is attached to the Veress needle and aspirated, inspecting for blood or bowel contents. If only bubbles are visible, saline is injected and observed to fall from the trough on the needle into the peritoneal cavity.

· The syringe is removed, the insufflation tubing (with CO₂ turned on low flow) is attached, and the initial IAP is observed. If the pressure is greater than 10 mm Hg, the needle should be removed quickly to avoid retroperitoneal insufflation, which further displaces the peritoneum from its attachment to the anterior abdominal wall. A second needle placement attempt is then made.

· Once intraperitoneal placement is confirmed, CO₂ pneumoperitoneum is obtained. Insufflation up to an IAP of 20 to 25 mm Hg, as initially described by Reich and others, remains one accepted method. This temporary increase in IAP increases the distance between abdominal viscera and the anterior abdominal wall (in the absence of adhesions) during primary sharp trocar placement through the umbilicus. It is also extremely beneficial for surgeons with small hands, who may find it difficult to grasp and further elevate the abdominal wall if the initial pressure is less than 20 mm Hg.

· The end of the sharp trocar is held in the palm of the dominant hand, with the forefinger extended along the shaft as close to the sharp tip as possible. The tip is inserted through the umbilical incision until the fascia at the base of the umbilicus is felt. Insertion is carried through at a near-90-degree angle until the tip is felt to pass through the peritoneum. The trocar is then directed toward the pelvis to minimize risk of vascular or bowel injury.

· After placement of the primary trocar, the intraabdominal placement is confirmed visually and the IAP is reduced to 12 to 15 mm Hg.

Complications of laparoscopy:

-The anesthetic complications

-The induction of pneumoperitoneum (emphysema and Pneumothorax )

-Insertion of primary and secondary trocars (injury to vessel or hollow viscous)

- Thermal Instruments injury

-Mechanical Instruments causing trauma to organs

-Other associated conditions

Endometriosis of uterosacral ligament diagnosed by laparoscopy- done by Dr. Alaa Mosbah

Mansoura University Hospital

Endomtriosis of pelvic peritoneum-Laparoscopy done by Dr. Alaa Mosbah

Mansoura University Hospital

Bilateral ovarian endometrioma (kissing ovaries)- diagnosed by TVS -done by Dr. Alaa Mosbah

Mansoura University Hospital

Left ovarian endometrioma- Laparoscopy done by Dr. Alaa Mosbah

Mansoura University Hospital

Left ovarian endometrioma- TVS done by Dr. Alaa Mosbah

Cyst with low level homogenous echogenecity and thick wall charachterestics of endometrioma

Endometriosis vesicles- Laparoscopy done by Dr. Alaa Mosbah

Mansoura University Hospital

Endometriosis – Key points, Prof. Alaa Mosbah

Endometriosis – Key points

–Definition:

It is the presence of endometrial tissue outside of the uterine cavity.

-Incidence:

Endometriosis affects up to 10 percent of reproductive-aged women. It is more common in women with pelvic pain or infertility 70 to 90 percent and 21 to 40 percent, respectively.

-Risk Factors for endometriosis:

Early menarche ,First-degree relative with endometriosis ,Late menopause ,Low body mass index, Müllerian anomalies , Nulliparity ,Prolonged menstruation (> five days) ,Shorter lactation intervals ,Shorter menstrual cycles (< 28 days) and White race (compared with black race)

-Sites of occurrence of endometriosis:

The common sites of endometriosis are the ovaries, fallopian tubes, pelvic peritoneum, D.P, uterovesical pouch and uterosacral ligaments (alternatively called the "pelvic" site), whereas the atypical sites of endometriosis include the gastrointestinal tract, urinary tract, soft tissues, and chest (alternatively called the "extra-pelvic".

-Causes of endometriosis: no cause discovered yet

Theories of What Causes Endometriosis:

.The retrograde menstruation theory (transtubal migration theory) suggests that during menstruation some of the menstrual tissue backs up through the fallopian tubes, implants in the abdomen, and grows.

.One theory suggests that endometrial tissue is distributed from the uterus to other parts of the body through the lymph or blood systems.

.A genetic theory suggests that certain families have predisposing factors for the disease.

.Surgical transplantation has also been cited in many cases where endometriosis is found in abdominal scars, although it has also been found in such scars when accidental implantation seems unlikely.

.Another theory suggests that remnants of tissue from when the woman was an embryo may later develop into endo or that some adult tissues retain the ability they had in the embryo stage to transform under certain circumstances.

. Environmental toxins such as dioxin and PCBs, which act like hormones in the body and damage the immune system, can cause endometriosis. Dioxins are highly toxic chemicals which come from the production and use of pesticides and herbicides.

-Diagnosis:

Some women with endometriosis are asymptomatic, whereas others present with symptoms such as chronic pelvic pain, dysmenorrhea, dyspareunia, and decreased fertility. Hematuria and dysuria with bladder affection. Dyskasia with rectal lesions. Chest pain and hemoptysis with lung affection. Ultrasonography and MRI can diagnose edometrioma and other deep pelvic lesions. Laparoscopy is the gold standard for diagnosis. The cancer antigen 125 (CA125) level is often elevated in women with endometriosis, but its specificity for the disease is low.

- Biologic mechanisms that might Link endometriosis and infertility:

• Distorted pelvic anatomy

• Altered peritoneal function

• Altered hormonal & cell-mediated function

• Endocrine and ovulatory abnormalities

• Abnormal uterotubal transport

• Impaired implantation

• Oocyte and embryo quality

-Staging of endometriosis:

According to the American Society for Reproductive Medicine (ASRM),

.Minimal endometriosis also called stage 1, (1-5 points) endometriosis, and is characterized by isolated implants and no significant adhesions.

.Mild endometriosis ,stage 2, (6-15 points) is characterized by superficial implants that measure less than 5 cm in diameter without significant adhesions.

.Moderate endometriosis ,stage 3, (16-40 points) involves multiple deep implants, small cysts on one or both ovaries, and the presence of flimsy adhesions.

.Severe endometriosis ,stage 4 , (>40 points) consists of multiple deep implants, large cysts on one or both ovaries, and thick adhesions.

-Treatment:

.Treatment depend on the age of patient , desire for fertility , presence of sufficient number of children and stage of endometriosis.

.Treatment may be medical or surgical and includes nonsteroidal anti-inflammatory drugs, gestagen, dienogest, combination estrogen/progestin contraceptives, progestin-only contraceptives. Other treatments include gonadotropin-releasing hormone analogues, danazol and letrozole drugs and levonorgestrel-releasing intrauterine system (Mirena). Laparoscopy is used to confirm the diagnosis and to treat many cases such as cystectomy for ovarian endometrioma and electric diathermy coagulation for endometriosis implants and adhesolysis for pelvic adhesions. Hysterectomy and BSO for severe cases not desiring fertility.

Prof. Alaa Mosbah

2019

Dieonogest for treatment of endometriosis.

Dieonogest for treatment of endometriosis.

Structure:

Dienogest (DNG) is an oral progestin. It is a C-19-nortestosterone progestogen derivative.

Mechanism of action:

Dienogest is bound to albumin and does not accumulate in oral doses of 2 mg/day. It has the following mechanisms of action:

1-Antiandrogenic effect

2-Moderate inhibition of gonadotropin secretion leading to a moderate reduction in the endogenous production of estradiol .

3-It enables the suppression of the endometrium in low doses, When given continuously, dienogest induces a hypoestrogenic, hypergestagenic local endocrine environment, causing a decidualization of endometrial tissue followed by atrophy of the endometriotic lesions.

4- Dienogest may also reduce plasma estradiol levels directly, through inducing apoptosis of granulosa cells in the ovary.

5- Dienogest also demonstrates antiproliferative, anti-inflammatory, and antiangiogenic effects.

Dose:

It is effective with good tolerability with doses 2 mg daily in continuous administration for 3–24 months in patients with endometriosis.

Efficacy and safety:

-It has been found to be effective to control endometriosis-related pelvic pain.

-The main side effects were the bleeding problems that were observed in some of patients within the first 3 months of treatment, which later on were reduced.

-It has a good safety and efficacy profile, with a progressive decrease in adverse effects and bleeding irregularities.

-Decrease in pain of endometriosis for at least 6 months after cessation of the treatment.

- A rapid return to ovulation after cessation of dienogest administration.

Prof. Alaa Mosbah

2019

Progestins in resolving endometriosis-related pain

The suggested mechanisms of progestins in resolving endometriosis-related pain:

• Ovarian suppression

• Effects on endometrial morphology (desidualization, atrophy and alteration in steroid receptor ligand binding)

• Local modulation of immune response (suppression of IL-8 production, increase of nitric oxide production, reduction of TNF)

• Effects on angiogenesis (suppression of transcription of bFGF, suppression of VEGF and cysteine rich angiogenic inducer

• Progesterone receptor expression and progesterone resistance

• Direct effect on nerve fiber intensity

Adenomyosis - Laparoscopy done by Dr. Alaa Mosbah

Mansoura University Hospital

Endometrial Polyps

Endometrial Polyps

-They are common and estimated to be present in around 10–20% of women with AUB and 10% of women with subfertility.

-Endometrial polyps are focal endometrial outgrowths containing a variable amount of glands, stroma and blood vessels, which influence their macroscopic appearance. -Endometrial polyps may be asymptomatic but can cause abnormal uterine bleeding (AUB) (heavy menstrual bleeding [HMB], IMB and postmenopausal bleeding [PMB]) and adversely impact on fertility.

• Risk factors include obesity, late menopause, the use of the tamoxifen and hormone replacement therapy (HRT).

• They are relatively insensitive to cyclical hormonal changes, leading them to persist and cause unscheduled vaginal bleeding.

• Endometrial polyps may be pedunculated or sessile, single or multiple and vary in size (0.5–4 cm).

• Prognosis: Endometrial polyps contain hyperplastic foci in 10–25% of symptomatic cases and 1% is frankly malignant. The risk of polyps harboring serious endometrial disease is increased after the menopause and with the use of tamoxifen.

• Diagnosis:

-History: irregular vaginal bleeding

-Investigations: by transvaginal ultrasound scan (TVUSS) but because they are focal, intracavity pathologies the most accurate tests are outpatient hysteroscopy (OPH) and saline infusion sonography (SIS).

• Treatment:

-Smaller endometrial polyps can spontaneously resolve but most persist such that once diagnosed, removal is indicated (polypectomy) in order to alleviate AUB symptoms, optimize fertility and exclude hyperplasia or cancer. Polypectomy is a simple procedure that can be performed as a day-case under general anaesthesia, but is now increasingly performed as an outpatient with or without local anaesthesia.

-A hysteroscope is used to visualize the polyp(s) and to remove the polyp with scissors, electrodes or morcellators.

Hysterectomy for a case with endometrial polyps, adenomyosis and uterine fibroids by Dr.Alaa Mosbah

Prof. Alaa Mosbah

Hormone replacement therapy

Hormone replacement therapy: Key Points by

Dr. Alaa Mosbah

Research Continues, Recommendations May Change

1-Decisions regarding HRT therapy must be made between the woman and her physician on an individual basis.

2-HRT must be used for as short a time as possible with lowest effective dose .

3-HRT has long-term risks including breast cancer and venous thromboembolism.

4-HRT has not been proven to be beneficial in primary and secondary prevention of coronary heart disease in fact may result in a small increased rate of CHD.

5- The low dose hormone replacement therapy is as effective as the standard dose HRT, and may have a favorable side effect profile

6- HRT is the most effective treatment of menopausal symptoms .

7-For patients at risk of osteoporosis, other preventive therapies such as bisphosphonates and SERM are available. However, for women at risk of osteoporosis who also have vasomotor menopausal symptoms, HRT can be of benefit .

8-The decision to prescribe HRT should be based on a thorough evaluation of the potential benefits and potential risks of treatment

9-Evidence for the risks of HRT in women who had premature menopause is limited and the balance of benefits and risks may be more favourable than in older women .

Classifications of study designs- Prof. Alaa Mosbah

Prof. Alaa Mosbah- Mansoura Faculty of Medicine

Uterine rupture

Uterine rupture

Definitions

Uterine rupture Refers to a full thickness tear through the myometrium and serosa and may occur in a previously intact uterus or in one with a previous caesarean or myomectomy scar. By definition, it is associated with the following:

Clinically significant uterine bleeding

Fetal compromise

Protrusion or expulsion of the fetus and/or placenta into the abdominal cavity

Need for prompt caesarean delivery

Uterine repair or hysterectomy

Different terms may be used to describe partial separation (dehiscence) or healing defects (windows) of uterine scarsUterine scar dehiscenceA separation of a pre-existing scar that does not disrupt the overlying visceral peritoneum (uterine serosa) and that does not significantly bleed from its edges. In addition, the fetus, placenta, and umbilical cord must be contained within the uterine cavity

Incidence

Uterine rupture occurs in 0.05 % to 0.086 % of all pregnancies

Dehiscence of a caesarean section scar is the most common cause of uterine rupture and the incidence varies according to type and location of the uterine incision (previous classicalcaesareanuterineincision risk is 1 to 12 %)

Uterine rupture is rarely seen in developed countries in the absence of previous surgery, but is more commonly seen with the use of oxytocics in the presence of a uterine scar

Uterine rupture is more frequent in obstructed labour

Uterine scar dehiscence is a more common event seldom results in major maternal or fetal complications

Risk factors:

Grand multipara

Previous uterine scar

Obstructed labor

Obstetric trauma

Misuse of uterine stimulants ( PG & oxytocin)

Severe concealed accidental hemorrhage

Anterior sacculation or posterior sacculation

External trauma

Diagnosis

Rupture at the site of a previous uterine scar may occur with few warning signs because the scar is relatively avascular

Studies on vaginal birth after caesarean (VBAC) report that prolonged fetal bradycardia is the first sign in over 70 % of cases of uterine rupture. In these series, only 8 % presented with pain and 3 % with bleeding

If there is an atypical pattern of pain, or pain previously controlled by analgesia (epidural or otherwise) which becomes more severe, complete clinical reassessment by an experienced obstetrician is required. Shoulder tip pain may indicate peritoneal irritation and suprapubic pain may reflect local, including bladder, irritation

Presentation

Sudden, severe abdominal pain (may decrease after rupture)

Bleeding –intra-abdominal and / or vaginal unless the fetal head blocks the pelvis (blood may be retained within the broad ligament)

Tender abdomen

Easily palpable fetal parts

No fetal presentation on vaginal examination

Cessation of uterine contractions

Abdominal distension / free fluid

Abnormal uterine contour

Rapid maternal pulse

Absent fetal heart activity

Haematuria suggests bladder involvement Hypovolaemic shock if rupture involves major blood loss

Management

(A) Prophylactic treatment:

1- Hospitalization of high risk cases

2-Early recognition & treatment of obstructed labour .

3- Proper use of oxytocin.

4-Careful obstetric manipulation under anesthesia.

5-Proper management of cases with previous C.S.

(B) Active treatment:

Early involvement of senior experienced staff, including obstetrician, anaesthetist, midwife(s), paediatrician, and haematologist and intensivist as required (if available)

Resuscitate while arranging urgent laparotomy / caesarean section

The most senior person should take charge and assign roles and responsibilities to all other individuals

If major blood loss, recruit as many people as possible to assist during resuscitation e.g. to record events, drugs given, someone to make urgent phone calls, to organise transport of laboratory samples, to bring blood (products) to the site of resuscitation, and additional staff to support family members and significant others

Repair of the uterus is preferable, but in some cases hysterectomy may be required

Provide standard post-operative and post-natal care

Provide adequate counselling as soon as possible and arrange further followup

Counselling for future pregnancies

If tubal ligation was not performed at the time of laparotomy, explain the increased risk of rupture with subsequent pregnancies, and discuss the option of permanent contraception

If the defect is confined to the lower segment the risk of rupture in a subsequent pregnancy is similar to that of someone with a previous caesarean section

If there are extensive tears involving the upper segment, future pregnancy may be contraindicated

Women with a history of uterine rupture should have a planned elective caesarean section (37 to 38 weeks’ gestation) in their next pregnancy

Prof. Alaa Mosbah - Mansoura Faculty of Medicine

Mansoura University

Polyhydramnios- Key Points- Dr. Alaa Mosbah

Polyhydramnios- Key Points

Definition: Polyhydramnios is excessive amniotic fluid. Amniotic fluid index by US more than 25 cm.
Causes: Polyhydramnios can be caused by fetal malformations (GIT and neural tube defect) multiple gestation and maternal diabetes, fetal disorders (eg, infections) or genetic abnormalities or idiopathic.
Symptoms and signs: Polyhydramnios is often asymptomatic. However, some women, especially when polyhydramnios is severe, have difficulty breathing, and painful preterm contractions. The uterus is larger than expected for dates and malpresentation is common.
Complications: It is associated with increased risk of preterm labor, premature rupture of membranes, maternal respiratory compromise, cord prolapse, fetal malposition or death, and many complications during delivery like atonic postpartum hemorrhage.
Management: If polyhydramnios is suspected, US determine amniotic fluid index and test for possible causes (including a comprehensive fetal evaluation).
Prenatal monitoring with weekly nonstress tests as early as 32 weeks in patients with an amniotic fluid index more than 25 cm. Regular follow up by US according to severity of the case.
If no complications developed, delivery at nearly 39 weeks should be planned. Mode of delivery should be based on the usual obstetrical indications.

With my lovely students

Mansoura Faculty of Medicine

Preterm Prelabour Rupture of Membranes from 24+0 Weeks of Gestation, 2019

Care of Women Presenting with Suspected Preterm Prelabour Rupture of Membranes from 24+0 Weeks of Gestation.

Key recommendations

Green-top Guideline No. 73 June 2019.

i. The diagnosis of spontaneous rupture of the membranes is made by maternal history followed by a sterile speculum examination. [Grade D]

ii. If, on speculum examination, no amniotic fluid is observed, clinicians should consider performing an insulin-like growth factor-binding protein 1 (IGFBP-1) or placental alpha microglobulin-1 (PAMG-1) test of vaginal fluid to guide further management. (Grade B)

iii. Following the diagnosis of preterm prelabour rupture of the membranes, (PPROM) an antibiotic(preferably erythromycin) should be given for 10 days or until the woman is in established labour(whichever is sooner). [Grade A]

iv. Women who have PPROM between 24+0and 33+6weeks’ gestation should be offered corticosteroids; steroids can be considered up to 35+6weeks’ gestation. [Grade A]A combination of clinical assessment, maternal blood tests (C-reactive protein and white cell count) and fetal heart rate should be used to diagnose chorioamnionitis in women with PPROM; these parameters should not be used in isolation. [Grade D]

v. Women whose pregnancy is complicated by PPROM after 24+0weeks’ gestation and who have no contraindications to continuing the pregnancy should be offered expectant management until 37+0weeks;timing of birth should be discussed with each woman on an individual basis with careful consideration of patient preference and ongoing clinical assessment. [Grade A]

vi. In women who have PPROM and are in established labour or having a planned preterm birth within 24 hours, intravenous magnesium sulfate should be offered between 24+0and 29+6weeks of gestation. [Grade A]

Routine pelvic and paraaortic lymphadenectomy in advanced ovarian cancer ? (March 2019)

Routine pelvic and paraaortic lymphadenectomy does not extend overall survival in advanced ovarian cancer (March 2019)

A Randomized Trial of Lymphadenectomy in Patients with Advanced Ovarian Neoplasms.
The approach to lymphadenectomy (LND) in ovarian cancer varies between routine systematic pelvic and paraaortic LND versus selective resection of grossly suspicious nodes. In a randomized trial of women with advanced ovarian cancer who appeared to have normal lymph nodes and underwent complete cytoreduction, systematic LND did not result in higher overall or progression-free survival compared with no LND, but increased serious postoperative complications and 60-day mortality.
N Engl J Med. 2019;380(9):822.

Anemia during pregnancy – Key points

Anemia during pregnancy – Key points

A-Definition

-Anaemia is a condition in which the number of red blood cells or their oxygen-carrying capacity is insufficient to meet physiologic needs, which vary by age, sex, altitude, smoking, and pregnancy status.

-Global data shows that 56% of pregnant women in low and middle income countries (LMIC) have anemia

-Reduction of the total circulating hemoglobin (Hb) mass which is responsible for carrying O2 to different tissues in the body. Anemia is diagnosed if Hb is less than 11 gm/ dl (7.45 mmol/l) and a haematocrit value less than 0.33 (WHO definition) during pregnancy and puerperium

B-Types

1-Iron deficiency anemia.

2-Megaloblastic anemia

3-Anemia caused by infection.

4-Haemolytic anemia

5-Aplastic anemia (extremely rare)

C-Effects on pregnancy and labor

1- Increased incidence of abortion, premature labor and IUFD.

2- Uterine inertia.

3- P.P. hemorrhage & obstetric shock.

4- P.P. infection.

5- Inadequate breast feeding.

6- Hb and red cell volume of infant of anemic women are below normal.

Iron deficiency anemia

-The total iron need during pregnancy is between 1200-1350 mg ( 500mg is required for expanding blood volume, 300 mg is required for fetus, 100 for placenta and 75 for blood loss, in addition to 280 mg basal iron)

-The commonest type

-Etiology:

a) Inadequate intake: due to poor dietary habits and diet deficient in iron.

b) Decreased absorption: due to malabsorption syndrome,

c) Increased loss: due to bleeding during pregnancy

d) Increased demands: as in multiple pregnancy

Clinical picture:

May be no symptoms especially with mild and moderate anemia

Weakness, fatigability, headache

Dyspnea and palpitation.

Edema of ankle and pallor

Systolic murmur

Splenomegaly

Mild albuminuria

Investigations:

1- Peripheral blood smear: Hb below 11 gm/dl, Hct

2-Bone marrow: absence of stainable iron in B.M. (rarely indicated during pregnancy).

Severity of anemia:

Mild: HB 10-10.9 gm/dl

Moderate : HB 7.0-10.0 gm/dl

Severe: HB 7.0gm/dl

Decompensated: HB 4.0gm/dl

Management:

a) Prophylaxis:

- Diet: rich in iron, vitamins & protein.

- Oral iron supplements: Dose 60 mg elemental iron daily (300mg ferrous sulphate)

b) Therapeutic treatment:

-Diet: rich in iron

-Oral iron therapy: iron sulphate, iron gluconate

Dose 300 mg tablet tds

-Parenteral iron: Indicated in

Severe iron deficiency anemia when there is a need for a rapid response

-Blood transfusion: each blood unit raises the hemoglobin % by 0.5 gram

Megaloblastic anemia

The major cause is due to folic acid and vitamin B12 deficiency.

Pregnant women require 150-300 ug of folic acid tab./day ( for normal maturation of red cell in B.M essential for synthesis of nucleic acid).

Management:

A-Prophylaxis: Folic acid 100-300 ug/day orally, a dose which will not obscure the hematological abnormalities of B12 deficiency

B-Treatment:

- Diet. -Blood transfusion

- 1-5 mg folic acid orally daily for 4-5 weeks - Vitamin C 100 mg t.d.s.

Anemia caused by infection

The 3rd commonest cause of anemia during pregnancy. It is usually due to subclinical infection e.g. U.T infection that produce anemia through impairment of erythrocyte production and decreased erythrocyte survival. Treated by treatment of infection.

Haemolytic anemia

a) Sickle cell anemia:

Caused by inheritance gene for sickle cell hemoglobin without a gene for the normal B chain of adult hemoglobin. 2 types are known , sickle cell trait or sickle cell disease .

b) Thalassemia:

It is of 2 types: Thalassemia major and thalassemia minor

c) Hereditary spherocytosis:

Rare disease

d) Enzyme deficiency:

Sex linked glucose 6–phosphate dehydrogenase (G6PD) deficiency. When exposed to oxidant drugs or agents lead to hemolytic anemia.

Prof. Alaa Mosbah

2019

Histopathology Request form - done by Dr. Alaa Mosbah

Mansoura Faculty of Medicine

Evaluation and Treatment of Infertility – Key points

Evaluation and Treatment of Infertility – Key points

Prof. Alaa Mosbah

-Definition: Infertility is defined as the inability to achieve pregnancy after one year of regular, unprotected intercourse. Evaluation may be initiated sooner in patients who have risk factors for infertility or if the female partner is older than 35 years.

-Causes of infertility include male factors, ovulatory dysfunction, uterine abnormalities, tubal obstruction, peritoneal factors, and cervical factors or may be unexplained.

-Diagnosis: A history and physical examination can help direct the evaluation. Men should undergo evaluation with a semen analysis. Abnormalities of sperm may be treated with gonadotropin therapy, intrauterine insemination, or in vitro fertilization. Ovulation should be documented by serum progesterone level measurement at cycle day 21. Evaluation of the uterus and fallopian tubes can be performed by hysterosalpingography (HSG). For patients with a history of endometriosis, pelvic infections, or ectopic pregnancy, evaluation with hysteroscopy or laparoscopy is recommended.

-Treatment:

- Lifestyle Factors: All couples should be counseled to abstain from tobacco use, limit alcohol consumption, and aim for a body mass index less than 30 kg per m2 to improve their chances of natural conception or using assisted reproductive technology.

.Women with anovulation may be treated with clomiphene to induce ovulation. The initial dosage of clomiphene is 50 mg daily for five days starting on day 3 to 5 of the menstrual cycle. If this is unsuccessful, the dosage may be increased to 100 mg daily. There may be need in some cases for prescribing pulsatile administration of gonadotropin-releasing hormone or gonadotropins with luteinizing hormone activity to induce ovulation. Cases with PCOS may need the addition of 1,500 to 1,700 mg of metformin (Glucophage) daily which may increase ovulation and pregnancy rates.

.Treatment of tubal obstruction requires treatment of the cause such as adhesolysis for pelvic adhesions via laparoscopy or tubal canulation via hysteroscopy.

.Laparoscopy for treatment of endometriosis for example excision of endometrioma above 3 cm size.

.Unexplained infertility in women or men may be managed with another year of unprotected intercourse, or may proceed to assisted reproductive technologies, such as intrauterine insemination or in vitro fertilization.

Dr. Alaa Mosbah with lovely sixth year medical students

Mansoura Faculty of Medicine -2019

Australian Drug Categories with pregnancy

Australian Drug Categories with pregnancy

Pregnancy Category A - Have been taken by a large number of pregnant women and women of childbearing age without an increase in the frequency of malformations or other direct or indirect harmful effects on the fetus having been observed.

Pregnancy Category B1 - Drugs which have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed. Studies in animals have not shown evidence of an increased occurrence of fetal damage.

Pregnancy Category B2 - Have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed. Studies in animals are inadequate or may be lacking, but available data show no evidence of an increased occurrence of fetal damage.

Pregnancy Category B3 - Have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed. Studies in animals have shown evidence of an increased occurrence of fetal damage, the significance of which is considered uncertain in humans.

Pregnancy Category C - Have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible.

Pregnancy Category D - Have caused, are suspected to have caused or may be expected to cause, an increased incidence of human fetal malformations or irreversible damage. These drugs may also have adverse pharmacological effects.

Pregnancy Category X - Have such a high risk of causing permanent damage to the fetus that they should NOT be used in pregnancy or when there is a possibility of pregnancy.

Bedside teaching

Bedside teaching

Do you know that the best teacher for you is the patient himself !

Please practice bedside teaching.

During bedside teaching you are using many of your senses such as vision, hearing, smell and touch to learn more about patient or disease. You learn how to think and how to communicate with the patients.
Sir William Osler in 1903 stated that:

To study the phenomena of disease without books is to sail an uncharted sea, whilst to study books without patients is not to go to sea at all.

Prof. Alaa Mosbah

Lecture of Prof. Alaa Mosbah- How to do OSCE

Mansoura Faculty of Medicine

The development of the reproductive system

The development of the reproductive system

Development of Gonads

Endodermal cells, called primordial germ cells, migrate from the wall of the yolk sac near the allantois to the dorsal wall of the abdominal cavity during the third week. The primordial germ cells enter the gonadal ridges that parallel the mesonephros. Each ridge has a thick epithelium continuous with columns of cells called primary sex cords that extend into the center (medulla) of the ridge. At this gender indifferent stage, male embryos are indistinguishable from female embryos.

Development of the Ovaries

The primary sex cords in the female embryo degenerate and the primordial germ cells migrate into the outer region (cortex) of the genital ridge that will become the ovary.

Development of Ducts and Accessory Organs

A paramesonephric (Müllerian) duct develops anterior to each mesonephric duct in both sexes. The paramesonephric duct has no connection to the kidneys; instead it extends along the genital ridge and continues toward the cloaca. Thus, both genders have mesonephric and paramesonephric ducts during the indifferent stage of sexual development.

The embryo—regardless of its genetic sex—will develop into a female unless exposed to androgens. In a normal male embryo, cells in the medulla of the gonadal ridge begin to produce testosterone sometime after the sixth week. Testosterone triggers changes in the duct system and external genitalia shown in these figures.

Development of Genital Ducts in the Female

The mesonephric tubules and duct degenerate in the female embryo. The paramesonephric ducts develop a broad proximal opening into the peritoneal cavity; they fuse distally to form the uterus.

Development of External Genitalia

After four weeks of development, mesenchymal swellings called cloacal folds develop around the cloacal membrane. A genital tubercle develops that will form the glans of the penis in males and the clitoris in females. At six weeks, the cloaca has been subdivided, separating the cloacal membrane into a posterior anal membrane bounded by anal folds, and an anterior urogenital membrane bounded by the urethral folds. A prominent genital swelling develops lateral to each urethral fold.

Development of Female External Genitalia

In the female, the urethral folds do not fuse but develop into the labia minora. The genital swellings will become the labia majora. The genital tubercle develops into theclitoris, immediately posterior to which the urethra opens to the exterior. The hymen persists as an elaboration of the urogenital membrane.

Prof. Alaa Mosbah with Graduates

Mansoura University Hospital

Contracted pelvis and cephaopelvic disproportion

Contracted pelvis and cephalopelvic disproportion

Definition:

a contracted pelvis is a pelvis whose shape and size are sufficiently abnormal to cause difficulty in vaginal delivery of normal (average size body ) This may occurs when : 1- One or more of the pelvic diameters is reduced enough to cause dystochia (Obstetric definition) 2- One or more of the pelvic diameters is reduced below the average by on or more centimeters (antatomical definition)

-CPD: or fetopelvic disproportion in presentations other than cephalic) can arise from either :

1- Diminished pelvic capacity

2- Excessive fetal size or abnormal fetal development Or more usually a combination of both

-In contemporary obstetric practice dystochia literally means difficult labour and is characterized by abnormal progress by labour Generally this can occurs as a result of 3 distinct causes that may exist singly in combination

1- Abnormalities in the power: a. Uterine contractility (uterine dysfunction in significantly strong or inappropriately coordinated to affect the dilate the cervix = dysfunctional labour) b. Inadequately voluntary maternal expulsive effort during the 2nd stage of labour

2- Abnormalities in the passenger: a. Abnormal presentation and / or position b. Abnormal fetal development (congenitally malformed baby)

3- Abnormalities in the passage :

a. Abnormalities in size or shape of the bony pelvis (contracted pelvis)

b. Abnormalities of soft tissues of the reproduction tract and other pelvic organs (soft tissue obstruction)

Classification of contracted pelvis

A - Pelvic inlet contraction :

when the shortest onteroposterioer diameter of the inlet < 10cm or when the greatest transverse diameter is < 12cm or when the brim idea Anteroposterior diameter x 100) is < 85 Transverse diameter The Anteroposterior diameter of the pelvic inlet is commonly approximated by manually measuring the diagonal conjugate which is about 1.5cm greater therefore inlet contraction id dysnied as a diagonal conjugate < 11.5cm Contracted inlet can cause: 1- delayed desert of the fetal head or primigravida until after the onset of labour if at all. (usually the head is engaging or already engaged in the least 2 weeks of pregnancy in normal nullipara before the onset of labour 2- face and shoulder presentation (3 times more frequent) 3- cord prolpase (4-6 times more frequent) NB: contracted pelvis has no relation to breach presentation 4- in contracted pelvis, rupture of membranes the absnce of preserve of the head against the cervix and the lower uterine segment predisposes to less effective uterine contractions (inertia)

B- Midpelvic contraction:

1- More common that inlet contraction 2- It usually causes transverse arrest of the head resulting in difficulty or failed midforceps and increased CS rate 3- Average midpelvic measurements are: a. Transverse (interspinous) = 10.5cm b. Anteroposterior 9from the lower border of the symphysis pubis to the junction of 54- ) = 11.5cm posterioer sagittal (from midpoint of interspinous line namely the previous point of the sacrum to the junction of S4-S5= 5cm c. The definition of midpelvic contraction is not prescise as in inlet contraction d. Midpelvic is called contracted of the sum of interspinous and posterior sagittal < 13.5cm (normally 15.5cm) e. Although these is no precise manual method for measuring medpelvic diameters its suggested to be contracted if : i. The spines are prominent (under projection) ii. The pelvic side walls are convergent iii. The sacroscietic notch is narrow normally the sacrospinopus ligament should measure at least 2 fingers breath (if < 2 fingers the notch is suggested to be narrow) iv. The intertuberous diameter is narrow. Normally the relation between ineter spinous and inter tuberous diameter is constant. However a normal intertuberous interspinous diameter

C- Pelvic outlet contraction:

Usually defined as an interischil tuberous diameter < 8cm with consequent narrow subpubic angle Its incidence is usually about 1% Outlet contraction without concomitant midplane contraction is rare Diminution of the intertuberous diameter with consequent narrowing of the anterior saggital triangle of the outlet forces the fetal head posterioely resulting in increased incidence of perineal lacerations A contracted outlet may constitute dystocia not so much by itself as through the after associated midpelvic contraction

D- Combination of both inlet and outlet contractions generally contracted pelvis (just-minor pelvis)

Etiology of pelvic contraction

I-Congenital :

1- Naegel's pelvis = asymmetric or obliquely contracted pelvis due to absence of one of the sacrum 2- Robert's pelvis: transversly contracted pelvis due to absence of 2 sacral 3- High assimilation pelvis: the sacrum is made of 6 dused segments 4- Low assimilation pelvis: the sacrum is made of 4 fused segments 5- Split pelvis: absent pubic bone usually associated with extopia vesica 6- Dislocation of the hip joint

II- Acquired:

1- Metabolic disease : a. Rickets in which the following types of pelvis are found: i. Flat rachitic pelvis ii. Generally contracted rachitic pelvis iii. Generally contracted flat rachitic pelvis (rachitic stigmata on top of generally contracted pelvis) b. Osteomalcia : causing trirdiate or rosette shaped or peaked pelvis

2- Vertebral column disease : a. kyphasis b. scoliosis c. spondylolthesis

3- Lower limb disease : a. Resulting inmissing or shortening of one limb during childhood or adolescence before ossification of the pelvis b. This results in pelvis obliquity (coxolgic pelvis) froctuers (accidents inflammatory TB ostcomylitis)

4- Disease of the pelvic bones: a. Fractures b. Tumours of pelvic bones

MECHANISM OF LABOUR IN SOME COMMON TYPES OF CONTRACTED PELVIS

I- Generally contracted pelvic (justo minor) Features:

1- Commonest type of contracted pelvic usually in short women 2- It shows gynaecoid chometers but these is propotional dimination of all diameters with funneling in 20% of cases Mechanism of labour: 1- Delayed descent and engagement 2- Marked moulding and formation 3- Extreme felxsion of the head (roader obliquity) 4- Deep transverse arrest (failure of long anterior rotation ) in OP if associated with outlet contracted (20% of cases) NB: Cord proplase is rare due to narrow spaces and fitting of the presenting parts at the pelvic brim

II- Flat rachitic pelvis: Features :

1- Forward of the sacral promontory resulting in reduction of the true conjugate

2- Hyperplasia at the junction between sacral vertebra may result in false promontory

3- Divergence of the ischial tubersity and aceteabulum resulting in wide subpubic angle and increased bituveros diameter

4- Contractions occur only at the level of the inlet so if the head possed the inlet there will be more difficulty (single dimensionally contracted pelvis)

Mechanism of labour:

1- Head engagement in the transverse diameter 2- Asynclitism with anterioer porful bone presentment 3- Lateral displacement of the head to bring the short biterporal diameter in the short true conjugate 4- Deflection occurs with descent 5- With further descent both asynclitism and deflection are corrected 6- rotation (2/3 circles) interiorly because the outlet is wide

III- Simple flat pelvis: Features :

reduced AP diameter of the inlet cavirty and outlet without rachitic stigmata Mechanism of labour: 1- At the pelvis inlet: like flat rachitic pelvis 2- At the outlet there will be: a. Extreme flexsion and moulding (reduced AP diameter at the outlet) b. Increased incidence of perineal lacerations due to backwards dispalecment of the fetal head (narrow) subpubic angle ) c. In OP: deep transverse arrest or face to pubis (short posterior rotation)

IV – Funnel pelvis (contracted outlet)

Causes: 1- 20% if generally contracted pelvis 2- Android pelvis 3- High assimilation pelvis 4- Spreadylo lithesis: sublaxation of the 5the labour in front of the sacral promontory resulting in downwards and backward displacement of the sacrum deep, cavity and increased inclination of the plane of the inlet and some cases may show outlet contraction resulting in funneling 5- Lunbodacrel kyphasis 6- Obliquely contracted pelvis 7- Some cases of richets & asteomalacia Mechanism of labour : 1- Extreme flexion & moulding at the outlet 2- Backwards displacement of the head due to narrow subpubic angle resulting in increased incidence of perineal laceration 3- In OP: deep transverse arrest or face to pubis

Diagnosis of CP

I- History

1- post history of trauma or disease that cause pelvic contractions eg Rickets osteamalacia, poliomyelitis TB fractures or thopedic surgery 2- Bad obstetric history Malpresentation repeated fetal losses and operative deliveries

II- Examination:

1- General: a. Short stature b. Rachitic manifestation c. Abnormal gait (eg limbing waddling) 2- Abdominal (during pregnancy) a. Pendulous abdomen b. Scar of CS c. Malpresntation face brow shoulder presentation d. Non engaged head in last 2w of pregnancy in primigravida

III- Investigation:

1- Pelvimetry : a. Clinical pelvimetry b. MRI c. Radiographic pelvimetry (x-ray CT) d. Sonographic cephalometry

Cephalopelvic disproportion test Pelvimetry

I- Clinical Pelvimetry

1- External Pelvimetry of the inlet

2- External Pelvimetry of the outlet - Subpubic angle (normalley 90) - measured by fingers or morris disc - normally the angle can accommodate two fingers near the apex - Bituberous diameter (normally 11Cm) : - measured by pushing the knuckles of the 4 fingers or closed first between ischil tuberosities or by pelvimeter (Thom's crossing pelvimeter) - normally this diameter can accommodates the closed first or the knuckles of the 4 fingers easily

3- Anteroposterior diameter of the outlet normally 13cm - Measured by 2 fingers in the vagina by the same method used fordiagnal conjugate

4- Posterior and anterior sagittal diameter of the outlet (normalley 102 cm) measured by Thom's pelvimeter Thom's diction: for spontaneous vaginal delivery to occur the sum of the transverse and posterior diameter of the outlet must be > 15cm NB: pelvic outlet is accessible clinically so obstetrician must not be surprised by outlet contraction during labour outlet contraction must be diagnosed during pregnancy or very early in labour in the first exam. Internal pelvimetry : - Usually done after 36 weeks - Patient in lithotomy position without anesthesia by the gloved rt hand

1- Diagnosed conjugate (normally 12-15cm) - tip of rt middle finger reaching the sacral promontory mark the point that impringes on the lower border of the symphsis pubis on the radial border of the rt index - withdraw the rt 2 fingers and measure the distance between the tip of the middle finger and that point by a ruler NB: the same method is used to measure the anetroposteriorer diameter of the outlet but tip of middle finger touches the tip of sacrum 2- palpatic the shape of the sacrum normally it is broad with cancer or flat anterior surface 3- palpable the two ischial spines and approximate distance between them : normalley it is felt not prominent or undeuley projecting with the distance between them > 10.5cm

4- palpable the coccyx: normally is mobile and can recedes back wards easily

5- palpable the sacroscpinous ligaments normally it is 2 fingers breadth (3.5cm)

6- palpable side walls of the pelvis and sacroscietic notch - normalley parallel or divergent walls with wide notch

7- the anteroposterior diameter of the pelvic outlet - Measured by the same manner as diagonal conjugate

II- Radiological pelvimetry

A- Plain x-ray: - for borderline cases of pelvic contraction 1- lateral pelvimetry is the best to be done during labour look for the following an lateral fibm - Pelvic inclination (angle between the true conjugate and anterior surface of lunbar ureterbea ) - sacral promontory (jutting or not ) - length and shape of the sacrum - sacroscitic notch (wide or narrow) - level of the head in rotation to the ischial spine - true conjugate and posterior sagital measured by a ruller after putting a scale on the film 2- inlet and outlet radiological pelvimetry is of less importance x-ray pelvimetry is of little value in cephalic presentation (clinical cephalopelvic disproportion tests are more valuable )

-CT : Advantages : 1- reduced radiation exposure 2- greater accuracy and easier technique

-MRI : Advantages : 1- no ionizing radiation 2- accurate measurement 3- complete fetal and placental imaging 4- evaluation of soft tissue dystocia

-Disadvantages:

1- cost 2- time factor 3- equipments availability Cephalopelvic disproportion tests If the head is not engaged in the last 2 weeks of pregnancy

CPD is suspected and can be tested by the following maneuovers in which the fetal head is used as a pelvimeter

1- Pinard's maneuver: a. The women is examined in the seminstting position to coorect pelvic inclination (the oasis of the fetus and the uterus becomes perpendicular to the brim b. The head is grasped by the left head and pushed steadily in the pelvis c. The fingers of the rt hand is in front of the symphesis pubis to determine whether the head is engaged or not and degree overlap of the head on the symphsis pubis

2- Pinard's –Muller – Kerr's bimanual maneuver: a. The women on her back with the head and shoulder slightly abducted b. The left hand described in pinard's maneuver . the idea and middle fingers of the rt hand inside the vagina to note the degree of descent of the fetal head in relation to the ischial spine and the angle between the head and posterior surface of the symphesis pubis c. If the head is not engaged the throuth of the rt hand is placed on the sympysis pubis to note any overlap of the head over it d. Gentle fundle pressure by an assistant may be helpful e. If no CPD exists the head readily enters the pelvis and vaginal delivery can be predicted f. Inability to push the head into the pelvis doesn’t necessarily indicate that vaginal delivery is impossible g. if the head flexed head overrides the symphysis pubis this will be a presumptive widen of disproportion Degrees of CP and CPD CP CPD Minor degree Minor AP diameter 9-10cm No actual CPD because uterine contractions and pelvic reserve compensate this minor degree of contraction and vaginal delivery is the rule if no associated complication The a anterior surface of the head is in line with the posterior surface of the symphysis pubis flushing of the head with the S-pubis) with contraction during labour the head is engaged Moderate degree 1st degree CPD (moderate disproportion) - AP diameter 8-9cm - Resulting I CPD - Great majority of cases of CP - Difficult to predict its outcome so managed by trial labour and CS if failed - The anterior surface of the head is in line with the anterior surface of the symp pubis (overriding of the head with symphsysis pubis)

- During labour sufficient moulding and uterine contraction may allow vaginal delivery (trial of labour if failed CS)

-Major degree 2nd degree CPD (severe disproportion) - AP diameter 6-8cm - Results in 2nd degree CPD - With living fetus CS is absolutely indicated - With dead fetus craniotomy can be tried if experienced obstetrician is available Extreme degree - AP diameter

Graduation ceremony of the first batch of Mansoura Manchester Programme

Obstructed Labour

Obstructed Labour

Definition:

It is arrest of vaginal delivery of the foetus due to mechanical obstruction.

Aetiology:

(I) Maternal causes: 1-Bony obstruction : e.g. - Contracted pelvis. - Tumours of pelvic bones. 2-Soft tissue obstruction: i) Uterus: - Impacted subserous pedunculated fibroid. - Constriction ring opposite the neck of the foetus. ii) Cervix: cervical dystocia. iii) Vagina: - Septa. - Stenosis. - Tumours. iv) Ovaries : Impacted ovarian tumours. (II) Foetal causes: 1- Malpresentations and malpositions : e.g. - Persistent occipito- posterior and deep transverse arrest, - Persistent mento-posterior and transverse arrest of the face presentation. - Brow, - Shoulder, - Impacted frank breech. 2- Large sized foetus ( macrosomia). 3- Congenital anomalies : e.g. - Hydrocephalus. - Foetal ascitis. - Foetal tumours. 4- Locked and conjoined twins.

Diagnosis:

It is the clinical picture of obstructed labour with impending rupture uterus (excessive uterine contraction and retraction). (A) History: of - prolonged labour, - frequent and strong uterine contractions, - rupture membranes. (B) General examination : shows signs of maternal distress as: - exhaustion, - high temperature (³ 38oC), - rapid pulse, - signs of dehydration : dry tongue and cracked lips. (C) Abdominal examination: 1- The uterus : - is hard and tender, - frequent strong uterine contractions with no relaxation in between (tetanic contractions). - rising retraction ring is seen and felt as an oblique groove across the abdomen. 2- The foetus : - foetal parts cannot be felt easily. - FHS are absent or show foetal distress due to interference with the utero-placental blood flow. (D) Vaginal examination: 1- Vulva: is oedematous. 2- Vagina : is dry and hot. 3- Cervix: is fully or partially dilated, oedematous and hanging. 4- The membranes : are ruptured. 5- The presenting part: is high and not engaged or impacted in the pelvis. If it is the head it shows excessive moulding and large caput. 6- The cause of obstruction can be detected. (E) Differential diagnosis: 1- Constriction ring. 2- Full bladder. 3- Fundal myoma.

Complications:

(I) Maternal : 1- Maternal distress and ketoacidosis. 2- Rupture uterus. 3- Necrotic vesico -vaginal fistula. 4- Infections as chorioamnionitis and puerperal sepsis. 5- Postpartum haemorrhage due to injuries or uterine atony. (II) Foetal: 1- Asphyxia. 2- Intracranial haemorrhage from excessive moulding. 3- Birth injuries. 4- Infections.

Management:

(A) Preventive measures: Careful observation , proper assessment, early detection and management of the causes of obstruction. (B) Curative measures: Caesarean section is the safest method even if the baby is dead as labour must be immediately terminated and any manipulations may lead to rupture uterus.

Dr. Alaa Mosbah with medical students

Mabsoura Faculty of Medicine, Egypt

Dr. Alaa Mosbah with medical students from UK

Mansoura University Hospital, Egypt

With Graduates

Mansoura Manchester Programme

Prof. Alaa Mosbah with wonderful medical students doing event : we not me

Mansoura Faculty of Medicine

Some advices to medical students about how to manage MCQ exam

Professor Alaa Mosbah

Diagnosis of a case

Prof. Alaa Mosbah

Diagnosis of Pregnancy

Diagnosis of Pregnancy

(I) THE FIRST TRIMESTER (0-12 WEEKS)

(A) Symptoms:

1.Amenorrhoea :

Sudden cessation of a previously regular menstruation is the most common symptom denoting pregnancy. However, pregnancy may occur during lactational amenorrhoea. On the other hand, bleeding may occur early in pregnancy as in threatened abortion. Slight bleeding may occur also at the expected time of menstruation in the first 12 weeks of pregnancy but never afterwards due to separation of parts of the decidua vera.

2.Morning sickness: nausea with or without vomiting commences in the morning. It usually appears about 6 weeks after onset of the last menstrual period and usually disappears 6-12 weeks later.

3.Frequency of micturition: due to congestion and pressure on the bladder and disappear after the first trimester to reappear again near the end of pregnancy when the foetal head descends into the maternal pelvis.

4.Breast symptoms: as enlargement, sensation of fullness, tingling and tenderness.

5. Appetite changes and sleepiness.

(B) Signs:

(I)Breast signs:

1. Increase in size and vascularity. 2. Increase pigmentation of the nipple and primary areola. 3. Appearance of the secondary areola. 4. Montgomery’s follicles. 5. Expression of colostrum. 6. Breast signs are diagnostic only in primigravidae. In multigravidae , it may be due to the previous pregnancies .

(II) Uterine signs:

1. The uterus becomes enlarged, globular and soft. 2. Palmer's sign: uterine contractions felt during bimanual examination. 3. Hegar's sign: during bimanual examination, the two fingers in the anterior fornix can be approximated to fingers of the abdominal hand behind the uterus due to softening of the lower part of the uterus and its emptiness. This sign can be elicited between 6-10weeks but not after as the growing conception will fill the whole uterine cavity.

(III) Cervix : soft, hypertrophied and violet.

(IV) Vagina: violet, moist, warm with increased acidity.

(C) Investigations:

(I) Pregnancy tests:

These depend on presence of human chorionic gonadotrophin (hCG) in maternal serum and urine.

1- Urine pregnancy tests :

i- Agglutination Test: Latex particles, or sheep erythrocyte (tube) coated with anti-hCG.

ii- Agglutination Inhibition Tests

iii- Dip stick Rapid and simple tests based on enzyme-labelled monoclonal antibodies assay can detect low level of hCG in urine.

Causes of false positive results:

1. Proteinuria. 2. Haematuria. 3. At time of ovulation (cross reaction with LH). 4. HCG injection for infertility treatment within the previous 30 days. 5. Thyrotoxicosis (high TSH). 6. Premature menopause (high LH & FSH). 7. Early days after delivery or abortion. 8. Trophoblastic diseases. 9. hCG secreting tumours.

Causes of false negative results:

1. Missed abortion. 2. Ectopic pregnancy. 3. Too early pregnancy. 4. Urine stored too long in room temperature. 5. Interfering medications.

2- Serum pregnancy tests:

(i) Radioimmunoassay of B -subunit of hCG.

(ii) Radio receptor assay.

3- Enzyme- linked immunosorbent assay (ELISA).

Can be used for urine and serum.

The pregnancy test becomes negative about:

One week after labour, 2 weeks after abortion, and 4 weeks after evacuation of vesicular mole.

Uses of pregnancy test:

1. Diagnosis of pregnancy. 2. Diagnosis of foetal death. 3. Diagnosis of ectopic pregnancy. 4. Diagnosis and follow up of gestational trophoblastic diseases.

(II) Ultrasonography:

Gestational sac can be detected after 4-5 weeks of amenorrhoea. Foetal heart pulsation can be detected as early as 7 weeks.

(II) THE SECOND TRIMESTER (13-28 WEEKS)

(A) Symptoms:

1. Amenorrhoea. 2. Morning sickness and urinary symptoms decrease. 3.Quickening : The first sensation of the foetal movement by the mother, occurs at 18-20 weeks in primigravida and at 16-18 weeks in multiparas. 4. Abdominal enlargement.

(B) Signs:

1. Breast signs: become more manifested.

2. Skin signs : Cloasma, linea nigra and striae gravidarum appear.

3. Uterine signs:

i-The uterus is felt abdominally. ii-Braxton Hick's contractions: intermittent painless contractions can be felt by abdominal examination.

4-Foetal signs:

i- Internal ballottement: can be elicited at 16 weeks by a push to the foetal parts with the two fingers through the anterior fornix. ii- External ballottement: can be elicited at 20 weeks by a push to the foetal parts with one hand abdominally and the other hand receiving the impulse. iii- Palpation of foetal parts and movement: by the obstetrician at 20 weeks. iv- Foetal heart sound: can be auscultated at 20-24 weeks by the Pinard's stethoscope. v- Umbilical (funic) souffle: A murmur with the same rate of FHS due to rush of blood in the umbilical arteries. It is occasionally detected when a loop of the cord lies below the stethoscope.

(C) Investigations in doubtful cases.

1. Pregnancy tests.

2. Ultrasonography.

(III) THE THIRD TRIMESTER (29-40 WEEKS)

All signs of pregnancy become more evident. Pregnancy tests are positive and sonar is diagnostic.

Sure Signs of Pregnancy:

1. Palpation of foetal parts. 2. Palpation of foetal movements. 3. Auscultation of foetal heart sounds. 4. The occasional auscultation of the umbilical (funic) souffle. 5. Detection of foetal skeleton by X-ray. 6. Ultrasonographic detection of foetal parts, movements and /or heart movements.

Differential Diagnosis of Pregnancy:

(A) Early pregnancy:

(I) Causes of amenorrhoea.

(II) Causes of symmetrically enlarged uterus: 1- Myoma. 2- Adenomyosis. 3- Pyometra. 4- Haematometra. 5-Metropathia haemorrhagica.

(III) Pelvi-abdominal swellings: 1- Ovarian swellings. 2- Tubal swellings. 3- Pelvic haematocele. 4- Full bladder.

(B) Late pregnancy:

1- Myomas. 2- Ovarian neoplasm. 3- Ascitis. 4- Pseudocyesis. 5- Other causes of pelvi-abdominal mass.

Laparoscopic excision of left ovarian tumor for a girl 7 years old- done by Dr Alaa Mosbah

Mansoura University Hospital

Placenta Praevia

Placenta Praevia

Definition:

In placenta previa, the placenta is located over or very near the internal OS.

Four degrees have been recognized:

1. Total placenta previa: The internal cervical OS is covered completely by placenta.

2. Partial placenta previa: The internal OS is partially covered by placenta.

3. Marginal placenta previa: The edge of the placenta is at the margin of the internal OS.

4. Low lying placenta: The placenta is implanted in the lower uterine segment such that the placental edge actuallly does not reach the internal os but is in close proximity to it (within 30 mm from internal OS).

-In vasa previa, the fetal vessels course through membranes and present at the cervical os. This is an uncommon cause of antepartum hemorrhage and is associated with a high rate of fetal death.

Frequency

-In most cases, it does not become symptomatic until the late 2nd or 3rd trimester -It is about 1 in 200 deliveries, or 0.5 %

Etiology

-Multiparity and advancing age increase the risk of placenta previa, the incidence of previa in women over 35 is 1 in 100 and for those over 40 it was 1 in 50. Conversely, the incidence was 1 in 300 for women aged 20 to 29

-Prior cesarean delivery or induced abortion increases the placenta previa, it is about 3.9 % in women who had previously cesarean delivery.

-The incidence increased with the number of previous cesarean sections; it was 1.9 % with two prior cesarean and 4.1 % with three or more prior cesarean deliveries.

-Defective decidual vascularization, a possible result of inflammatory or atrophic changes, has been implicated in the development of placenta previa.

-The relative risk of placenta previa to be increased 2-fold related to smoking. The CO hypoxemia caused compensatory placental hypertrophy.

-A large placenta, which spreads over a larger area of the uterus, as seen with erythroblastosis and with multiple fetuses, predisposes to previa.

-It may be associated with placenta accreta or placenta increta or percreta. Such abnormally firm attachment of the placenta might be because of poorly developed decidua in the lower uterine segment. - 5 % of women with a placenta previa had a clinically significant placenta accreta. For women with a prior cesarean section, the incidence was almost 25 %.

Clinical Findings

-The most characteristic event is painless hemorrhage, which usually does not appear until near the end of the second trimester or after. -Some abortions, however, may result from such an abnormal location of the developing placenta. -Frequently, bleeding has onset without warning, presenting without pain. The initial bleeding is rarely profuse. Usually it ceases spontaneously, only to recur. -In some cases, particularly those with a placenta implanted near but not over the cervical os, bleeding does not appear until the onset of labor. -The cause of hemorrhage the placenta is located over the internal os, the formation of the lower uterine segment and the dilatation of the internal os result inevitably in tearing of placental attachments. The bleeding is increased by the inability of the myometrial fibers of the lower uterine segment to contract and constrict the torn vessels. -Coagulation Defects, coagulopathy is rare with placenta previa, even when extensive separation from the implantation site has occurred. Diagnosis 1-The diagnosis can seldom be established firmly by clinical examination unless a finger is passed through the cervix and the placenta is palpated. Such examination of the cervix is done in operating room .Today, a "double set up" examination is rarely necessary. 2-Sonography ,the simplest, most precise, and safest method of placental localization is provided by

(1) Transabdominal sonography, the average accuracy is about 95 %, false positive results are often a result of bladder distention. Therefore, ultrasonic scans in apparently positive cases should be repeated after emptying the bladder.

(2) The use of transvaginal ultrasonograpby improved diagnostic accuracy to visualize the internal os in all cases, in contrast to only 70 % using transabdominal equipment. 93 % positive predictive value and 98 % negative predictive value for TVS.

(3) Transperineal sonograrphy allow visualization of the internal os in all cases examined.

(4) Magnetic Resonance Imaging to visualize placental abnormalities including placenta previa

Placental "Migration"

- Placentas that lie close to the internal cervical os, but not over it, during the second trimester, or even early in the third trimester; are very unlikely to persist as previa. 1-Low lying placenta not covering the internal os, previa did not persist and hemorrhage was not encountered. 2-Of those placenta covering the os at midpregnancy, about 40 % persisted as a previa.

-The mechanism of placental movement is not completely understood. The term migration is clearly a misnomer -The apparent movement of the low lying placenta relative to the internal os probably results from inability to precisely define this relationship in a 3 -dimensional manner using 2 dimensional sonography in early pregnancy. This difficulty is coupled with differential growth of lower and upper myometrial segments.

Management

-Women with a placenta previa may be considered as follows: (1) Those in whom the fetus is preterm but there is no pressing need for delivery,

(2) Those in whom the fetus is reasonably mature,

(3) Those in labor, and

(4) Those in whom hemorrhage is so severe as to mandate delivery despite fetal immaturity.

(1) Management of the pregnancy complicated by placenta previa and a preterm fetus, but with no active bleeding, consists of hospitalization. The mother and her family must be prepared to transport her to the hospital immediately. Delivery - Cesarean section is the accepted method of delivery in all cases of placenta previa. In most cases a transverse uterine incision is made. Occasionally a vertical incision is recommended in some circumstances. -When placenta previa is complicated by degrees of placenta accreta, control bleeding from the placental bed by: 1 -Oversewing the implantation site with 0 chromic sutures. -Cho and colleagues (1991) described placing circular interrupted 0 chromic sutures around the lower segment, above and below the transverse incision. -Druzin (1989) described four cases in which the lower uterine segment was tightly packed with gauze that successfully arrested hemorrhage. The pack was removed transvaginally 12 hours later. 2 -In some cases, bilateral uterine artery ligation is helpful, 3 -In others, internal iliac artery ligation. 4- If these methods fail, hysterectomy is necessary. Prognosis -In 1927 Bill advocated adequate transfusion and cesarean section, this results in a marked reduction in maternal mortality from placenta previa -In1945, Macafee and Johnson independently suggested expectant therapy for patients remote from term, -Preterm delivery is a major cause of perinatal death. -The fetal growth retardation is increased with placenta previa.

Mansoura University Hospital

Pic was taken by Dr. Alaa Mosbah

Professor Alaa Mosbah with graduates

Ectopic Pregnancy

Ectopic pregnancy

Prof. Alaa Mosbah

Definitions:

Ectopic pregnancy is defined as implantation of a pregnancy outside the normal uterine cavity.

A hetero-tropic pregnancy is the simultaneous
development of 2 pregnancies: one within and one
outside the uterine cavity

Pregnancy of unknown location (PUL) is a working diagnosis defined as an empty uterus with no evidence of an adnexal mass on TVS in patients with positive pregnancy test.

Caesarean scar pregnancy (CSP) is a rare form of ectopic pregnancy whereby the gestational sac is fully or partially implanted within the scar caused by a previous caesarean section

Sites

-98 % in the fallopian tube:
80% in ampullary portion, 12%isthmus, 5 % fimbria and 3% cornual

-less common sites include:

intraabdominal, cervical and ovarian or rudimentary horn or in cesarean section scars

Fate of tubal pregnancy:
(I) Tubal mole
(II) Tubal abortion
III) Tubal rupture

Clinical Picture
General symptoms:
1- Short period of amenorrhoea:
2- Pain:
is present in almost every case and precedes vaginal bleeding. It may be:
a. Aching due to tubal distension.
b. Colicky in tubal abortion.
c. Stabbing in tubal rupture.
d. Shoulder pain if blood accumulates under the diaphragm.
e. Bladder and rectal irritability in pelvic haematocele.
3- Vaginal bleeding:
General signs:
General examination: general condition depends on twhether tubes has ruptured or not.
Breast signs of pregnancy.
Abdominal examination:
Lower abdominal tenderness and rigidity especially on one side may be present.
Vaginal examination:
- Bluish vagina and bluish soft cervix. - Uterus is slightly enlarged and soft.- Marked pain in one iliac fossa on moving the cervix from side to side.- Ill defined tender mass may be detected in one adnexa in which arterial pulsation may be felt.The other manifestations depend upon the clinical variety of the ectopic pregnancy:
(A) Undisturbed Tubal Pregnancy
It is the same general symptoms and signs mentioned before. The pain is aching in nature and there is no vaginal bleeding.
(B) Tubal Abortion
The more common so it is called the classical picture of ectopic pregnancy.
Symptoms:
1. The general symptoms and signs are present.
2. Fainting attacks due to pain and intraperitoneal haemorrhage.
3. Nausea and vomiting due to peritoneal irritation.
Signs:
General examination:
1. Anaemia of varying degree depending upon the blood loss.
2. Pulse is usually rapid.
3. Temperature slightly higher (up to 38oC ) due to absorption of blood from the peritoneal cavity.
4. Blood pressure: falls in proportion to the amount of internal haemorrhage.
Abdominal examination:
Cullen’s sign: a periumbilical bluish discoloration may be present due to absorption of the blood in the peritoneal cavity by lymphatics. It is a late sign.
Local examination:
Boggy swelling in the cul-de-sac if pelvic haematocele is present.
(C) Tubal Rupture
The most dramatic although not the most common.
Symptoms:
Short period of amenorrhoea (6-8 weeks) or even there is no missed period.
Signs
General examination:
- Rapidly developed shock, with pallor, sweating, air hunger, rapid thready pulse and hypotension.
- Shoulder tip pain and hiccoughs due to irritation of the phrenic nerve of the diaphragm by accumulated blood when the patient lying down
Abdominal examination:
- The abdomen is distended, rigid with generalised tenderness.
- Shifting dullness and periumbilical bluish discolouration due to intraperitoneal haemorrhage.
Local examination:
The same as in general signs of ectopic, although it is undesirable as it may induce more disruption and bleeding.
(D) Pelvic Haematocele
Symptoms:
1. Symptoms suggesting disturbed tubal pregnancy since a period of time.
2. Pressure symptoms due to accumulation of blood in the Douglas pouch as frequency of micturition, tenesmus and dyspareunia.
Signs:
1. A fixed tender swelling is felt in Douglas pouch.
2. The uterus is slightly enlarged, soft and pushed forwards and the external os is directed downwards.
3. Aspiration of Douglas pouch (culdocentesis) may reveal blood which does not clot on standing. If blood clots it means that needle has punctured a blood vessel.
4. Infection may be superadded and a pelvic abscess is formed.
Investigations of Ectopic Pregnancy
(1) Serum b -hCG:
Urine pregnancy tests are positive in only 50-60% of ectopic. Detection of b -hCG in the serum by ELISA or radioimmunoassay are more sensitive and can detect very early pregnancy about 10 days after fertilisation i.e. before the missed period.
· If the test is negative, normal and abnormal pregnancy including ectopic are excluded.
· If the test is positive, ultrasonography is indicated.
Doubling time:
· In normal pregnancy, the b -hCG level is doubling every 48 hours during the first 42 days of gestation.
· Ectopic pregnancy usually shows less than 66% increase in b -hCG level within 48 hours.
· Unfortunately, this is not specific to ectopic pregnancy. In 15% of normal pregnancies as well as in abortions there is also slow doubling time.

(2) Ultrasonography:
In general, a positive b -hCG test with empty uterus by sonar indicates ectopic pregnancy. This is true if the ß-hCG is at or above the threshold level in which an intrauterine gestational sac can be detected. This is called discriminatory zone.
Discriminatory hCG zones:
Diagnosis of ectopic pregnancy is made if there is:
1. An empty uterine cavity by abdominal sonography with b -hCG value above 6000 mIU/ml.
2. An empty uterine cavity by vaginal sonography with b -hCG value above 2000 mIU/ml.
(3) Culdocentesis:
If non-clotting blood is aspirated from the Douglas pouch through a wide pored needle, intraperitoneal haemorrhage is diagnosed. But if not, ectopic pregnancy cannot be excluded.
(4) Curettage:
· If microscopic examination of the products of curettage reveals decidua and chorionic villi, the condition is abortion of intrauterine pregnancy.
· If it reveals decidua only or Arias Stella reaction in the endometrium as well (cellular atypism, mitotic activity and glandular proliferation), ectopic pregnancy is diagnosed. The drawback is that in complete abortion also decidua only is curetted.
(5) Laparoscopy:
A good diagnostic aid particularly in undisturbed ectopic.
(6) Complete blood picture:
- Haemoglobin and haematocrit ---- to assess anaemia.
- Leucocytic count ---- exclude infections as appendicitis and salpingitis

Treatment of tubal ectopic pregnancy using an expectant, medical , or surgical approach depending on clinical presentation:

Expectant treatment:

-This option is suitable for patients who are hemodynamically
stable and asymptomatic.
-The patient requires serial hCG measurement until levels are undetectable.

Medical treatment of Ectopic
The use of Methotrexate become widely used to treat patients with ectopic pregnancy. Patient selection is important to avoid rupture of ectopic.
*patient must be haemodynamically stable
*No symptoms or signs of active bleeding or hemoperitoneum
*she must be reliable,compliant, and able to return for follow-up

Intramuscular mthotrexate (MTX) is a treatment option
for patients with: minimal symptoms, adnexal mass

• MTX is a folic acid antagonist that inhibits DNA synthesis, particularly affecting trophoblast .
• The dose is calculated based on patient’s surface area, and is 50 mg/m2 .
• After MTX treatment serum hCG is usually routinely measured on days 4,7 and 11 then weekly thereafter until undetectable (levels need to fall by 15% between day 4 and 7, and continue to to fall with treatment)

Surgical treatment:

. The standard surgical treatment approach is laparoscopy.
• Laparotomy is reserved for severely compromised
patients (also give antishock measures) or where there are no endoscopic
facilities.
• The operation of choice is removal of the fallopian tube (salpingectomy) , or in some cases a small opening is made over the site of ectopic pregnancy to be extracted via this opening (salpingostomy)

.All Rh-negative women should be offered anti-D
immunoglobulin at a dose of 50μg (=250 IU) as soon as
possible within 72 hours of the surgery.

.
Uncommon Sites of Ectopic Pregnancy:
(I) Cornual angular pregnancy:
- It is implantation in the interstitial portion of the tube.
- It is uncommon but dangerous because when rupture occurs bleeding is severe and disruption is extensive that it needs hysterectomy.
- In some cases, the pregnancy is expelled into the uterus and rupture does not occur.
(II) Pregnancy in a rudimentary horn:
- Pregnancy occurs in the blind rudimentary horn of a bicornuate uterus.
- As such a horn is capable of some hypertrophy and distension, rupture usually does not occur before 16-20 weeks.
- Treatment: Excision of the horn. During operation, pregnancy in a rudimentary horn can be differentiated from interstitial cornual tubal pregnancy by finding the attachment of the round ligament lateral to the first and medial to the later.
(III) Cervical pregnancy:
- Implantation in the substance of the cervix below the level of uterine vessels.
- May cause severe vaginal bleeding.
Treatment :
1. Evacuation and cervical packing with haemostatic agent as fibrin glue and gauze. Methotrexate IM injection. Uterine artery embolization. Cervical cerclage.
2. If bleeding continues or extensive rupture occurs hysterectomy is needed.
(IV) Ovarian pregnancy:
Aetiology:
1. Pelvic adhesions.
2. Favourable ovarian surface for implantation as in ovarian endometriosis.
Pathogenesis:
- Fertilisation of the ovum inside the ovary or ,
- implantation of the fertilised ovum in the ovary.
Spiegelberg criteria for diagnosis of ovarian pregnancy:
1. The gestational sac is located in the region of the ovary,
2. the ectopic pregnancy is attached to the uterus by the ovarian ligament,
3. ovarian tissue in the wall of the gestational sac is proved histollogically,
4. the tube on the involved side is intact.
Treatment:
Laparotomy and enucleation of the ectopic pregnancy and reconstruction of the ovary if possible. Otherwise, removal of the affected ovary is indicated.
V) Abdominal (peritoneal) pregnancy:
Types:
1. Primary: implantation occurs in the peritoneal cavity from the start.
2. Secondary: usually after tubal rupture or abortion. Intraligamentous pregnancy: is a type of abdominal but extraperitoneal pregnancy. It develops between the anterior and posterior leaves of the broad ligament after rupture of tubal pregnancy in the mesosalpingeal border or lateral rupture of intramural (in the myometrium) pregnancy.
Diagnosis:
(A) History:
of amenorrhoea followed by an attack of lower abdominal pain and slight vaginal bleeding which subsided spontaneously.
(B) Abdominal examination:
- Unusual transverse or oblique lie.
- Foetal parts are felt very superficial with no uterine muscle wall around.
(C) Vaginal examination:
- The uterus is soft, about 8 weeks and separate from the foetus.
- No presenting part in the pelvis.
(D) Special investigations:
1. Plain X-ray : shows abnormal lie. In lateral view, the foetus overshadows the maternal spines .
2. Ultrasound : shows no uterine wall around the foetus.
3. Magnetic resonance imaging (MRI): has a particular importance in preoperative detection of placental anatomic relationships.
Differential Diagnosis:
Rupture uterus.
Treatment:
The condition should be terminated surgically through laparotomy once diagnosed as the foetus is malformed in the majority of cases. In addition, there is risk of massive internal haemorrhage if separation of the placenta occurs.

At least 2000 ml of cross-matched blood should be on hand before proceeding to laparatomy. The foetus is removed and if the placenta is attached to an excisable structure as omentum, it is removed with it. If the placenta is attached to an important structure leave it for autolysis which may extend to few months or years. Any attempt to separate placenta will evoke uncontrollable bleeding. In this case, methotrexate 12.5 mg IM daily for 5 days will destroy trophoblastic tissue and accelerates the involution of the placenta.

VI) Caesarean scar pregnancy (CSP):

Caesarean scar pregnancy (CSP)

-Definition: Is a rare form of ectopic pregnancy whereby the gestational sac is fully or partially implanted within the scar caused by a previous caesarean section (CS).

-Diagnosis:

.Clinical presentation: CSP may present with slight vaginal bleeding and/or abdominal discomfort.11Incidental diagnosis later in the pregnancy is sometimes made in asymptomatic women. Rarely, women may present with acute pain and profuse vaginal bleeding. It is not uncommon to diagnose CSP during or after attempted surgical evacuation for missed miscarriage. Haemodynamic instability and collapse in a suspected CSP strongly indicates rupture with intra-abdominal bleeding.

.Ultrasound criteria for diagnosis of caesarean scar pregnancy:

1. Empty uterine cavity and closed and empty cervical canal

2. Placenta and/or a gestational sac embedded in the scar of a previous caesarean section

3. A triangular/round or oval-shaped gestational sac that fills the niche of the scar

4. A thin or absent myometrial layer between the gestational sac and the bladder

5. Yolk sac, embryo and cardiac activity may or may not be present

6. Evidence of functional trophoblastic/placental circulation on colour flow Doppler examination, characterised by high velocity and low impedance blood flow

7. Negative‘sliding organs’sign

-Treatment:

§ A primary preventive strategy is to focus on reducing the number of primary CS performed without medical indications.

§ Treatment options should be individualized:

Expectant management is generally not recommended except in very rare situations. Medical management should be considered for haemodynamically stable women with minimal or no symptoms. Methotrexate is the drug of choice for medical management and works best in pregnancies of less than 8 weeks of gestation and where hCG is less than 5000 IU/L. Intraregional injection of methotrexate (with sac aspiration) has a higher success rate and should be considered as an option for stable women. Surgical treatment should be considered for women with significant symptoms or for those who decline medical treatment (Surgical resection can be performed by laparotomy or laparoscopy, either as a primary procedure or as an interval after termination of pregnancy with methotrexate). For women with endogenous CSP, surgical evacuation or hysteroscopic resection carries less risk of perforation, whereas surgical resection with resuturing should be considered for women with exogenous CSP withthin myometrium.

Prof. Alaa Mosbah

Congratulations for Accreditation of the program

Golden Jubilee of Mansoura Medical College

Prof. Alaa Mosbah

Visit of Prof. Colin (UK) to Mansoura Faculty of Medicine

Prof. Alaa Mosbah

With lovely graduates

Professor Alaa Mosbah

Guidelines For First Trimester Ultrasound Examination

Guidelines For First Trimester Ultrasound Examination

1. INTRODUCTION

Recent advances in ultrasonographic technology enable detailed studies and evaluation of the rapidly developing embryo in vivo. It is at present the most accurate and reliable method for the evaluation of first trimester pregnancies and their complications. However, the precise role of ultrasound in the first trimester is still in evolution, mainly because of rapid development and availability of newer generations of ultrasonographic equipment, which enables better and earlier visualization of embryonic structures. The correct use and interpretation of first trimester ultrasound examination requires a good understanding of normal early embryonic developmental milestones and ultrasonographic landmarks.

2. AIMS

The use of ultrasound examination in the management of women with pregnancy complications in the first trimester, and the basic requirements of such an examination. The role of routine first trimester ultrasound examination and the safety of such examination will be examined in Part II of this guideline.

3. INDICATIONS

An ultrasound examination may provide valuable information to assist patient management in, but not limited to, the following clinical conditions in the first trimester of pregnancy:

3.1 Confirmation of the presence of normal intrauterine pregnancy

3.2 Estimation of gestational age

3.3 Confirmation of embryonic life or early pregnancy failure

3.4 Evaluation of the cause of vaginal bleeding

3.5 Evaluation of suspected ectopic pregnancy

3.6 Confirmation of multiple pregnancy

3.7 Evaluation of suspected pelvic, ovarian or uterine pathology.

4. NORMAL ULTRASONOGRAPHIC EMBRYONIC DEVELOPMENTAL MILESTONES

-The earliest detectable ultrasonogrraphic evidence of pregnancy is thickening of the decidua at approximately 3 to 4 weeks of menstrual age. This sign, however, is non-specific and therefore carries no significant value for clinical management of early pregnancy complications.

-Important transvaginal ultrasonographic milestones Gestational age (Menstrual day) CRL (mm) Signs3 to 4 week - Thickening of endometrium and decidua4 to 5 week - First appearance of gestational sac5 week 1-2 First appearance of yolk sac and embryonic pole5 to 6 week 5 Embryonic cardiac activity By about 4.5 week, a small 2-3 mm gestational sac, which represents the chorionic cavity, can be visualized by transvaginal sonography (TVS). This is the first reliable sonographic evidence of pregnancy. The gestational sac does not lie within the endometrial space but is intradecidual, and is sonographically surrounded by an echogenic ring of trophoblastic and decidual reaction. These features assist the differentiation between a small true gestation sac from collection of blood or fluid within the uterine cavity, although such distinction could sometimes be difficult.

-Visualization of the yolk sac/embryo complex is diagnostic of an intrauterine pregnancy and excludes blighted ovum. The yolk sac should always be seen with TVS when the gestational sac reaches a mean diameter of 8 mm at 5 to 6 week. With TVS, embryos as small as 1 to 2 mm may be identified at similar stage of pregnancy.

-Although embryonic cardiac activity may be demonstrable in some pregnancies as early as 35 days after onset of last menstrual period, or in embryos as small as 1 mm, the absence of cardiac activity at such early stage could be normal. Embryonic activity, however, should always be observed by TVS when the crown-rump length (CRL) is 5 mm or more1.

-It is important to realize that these milestones represent the average development of a normal pregnancy. The ability to demonstrate these sonographic milestones is not only affected by biological variations between individuals but also the quality of the ultrasound scanner, the frequency of the transducer, and the experience of the operator. In general, the same milestone is expected to be visualized 1 week later if transabodminal ultrasonography (TAS) is used. In case of uncertainty, one should always act on the safe side and request a repeat examination later.

-Average time of detection of Various Parameters in Early Pregnancy by Ultrasonography (Menstrual day)

Transabdominal Transvaginal Gestational sac Day 35-37 (5 mm f) Day 29-31 (2 mm f)Yolk sac Day 42-45 Day 35-37Embryo Day 45 - 46 (~ 5 mm) Day 35-40 (~ 2 mm)Heart motion Day 42 - 45 .

EARLY INTRA-UTERINE DEMISE or diagnostic purpose, the most important question is beyond what point, i.e. the discriminatory level, the absence of yolk sac or fetal cardiac activity can be considered definite signs of early pregnancy failure. Using TVS, visualization of a discrete embryo 5 mm without fetal cardiac activity can be considered diagnostic of embryonic demise. If the embryo is less than 5mm, the absence of cardiac activity could be normal and a repeat sonogram should be performed at least 1 week apart. If only TAS is performed, the discriminatory level should be at least 9 mm3. In the absence of an embryonic pole, the major sonographic diagnostic criterion of early pregnancy failure is a large gestational sac without a yolk sac (i.e. a condition also called blighted ovum or anembryonic pregnancy). Using TAS, and mean sac diameter (MSD)

Hirsutism: Evaluation and Treatment (JOGC, November 2017)

Hirsutism: Evaluation and Treatment (JOGC, November 2017)
Recommendations:

1.Women presenting with hirsutism should be evaluated with a focused history, physical examination, and appropriate investigations to differentiate among the possible etiologies (III-B).

2.Laboratory investigations for women with moderate to severe hirsutism should include total testosterone, although the benefit in mild hirsutism is questionable. Additional testing is indicated for women with irregular menses and/or signs of hyperandrogenism or other endocrinopathies (III-B).

3.Referral for evaluation by an endocrinologist or reproductive endocrinologist is indicated in the presence of the following: (1) virilisation, (2) serum testosterone or dehydroepiandrosterone sulfate levels more than twice the upper limit of normal, (3) signs or symptoms of Cushing's syndrome, or (4) early menstrual phase serum 17-hydroxyprogesterone levels >6 nmol/L (III-B).

4.All patients experiencing hirsutism who desire treatment should be offered combined hormonal contraceptive therapy as first-line therapy, provided they have no contraindications (I-A).

5.Mechanical hair removal and/or topical therapy can be offered as first-line therapy or as an adjuvant to medical therapy (I-A).

6.Depending on a woman's goals of treatment, anti-androgens should be considered for moderate to severe hirsutism or to ensure an optimal response in milder hirsutism (I-A).

7.Anti-androgens can be used in conjunction with combined hormonal contraceptive therapy to enhance treatment efficacy (I-A).

8.If a woman on anti-androgen therapy wishes to conceive, anti-androgen therapy should be stopped prior to discontinuing the use of contraception to prevent the potential feminization of a male fetus if pregnancy were to occur (III-B).

9.Health care providers assessing women with hirsutism should complete a comprehensive evaluation and, when applicable, explore the long-term health sequelae of hyperandrogenism and polycystic ovary syndrome, including abnormal uterine bleeding, infertility, and metabolic syndrome (III-B).

Physiology of Reproduction

Physiology of Reproduction

1-Hypothalamus

-It lies at the base of the brain just above the junction of optic nerves -It contains many nuclei including (Supraoptic, paraventricular & arcuate nuclei)

-It secrets both releasing & inhibiting hormones *Hypothalamic releasing factors

1-Gonadotrophin releasing hormone (LHRH or Gn RH), it consists of 10 amino acids

2-Thyrotophin releasing hormone (TRH), it consists of 3 amino acids

3-Corticotrophin releasing hormone (CRH), it consists of 41 amino acids

4-Growth hormone releasing hormone, it consists of 40 amino acids *Hypothalamic inhibiting factors 1-Growth hormone inhibiting hormone, it consists of 14 amino acids 2-Prolactin inhibiting factor (Dopamine) Functions of the hypothalamus 1-Regulation of the primitive functions needed for survival as (Appetite control, temperature control, salt & water retention, metabolism & growth)

2-Control of reproduction, it acts as a transducer to convert neuronal pulses into release of GnRH Gonadotrophin releasing hormone -It is a decapeptide (10 amino acids) -Secreted by the preoptic & arcuate nuclei in pulses every 60-90 minutes -Passes in the hypophyseal portal circulation to reach the anterior pituitary ----- secretion of FSH & LH -Half life ---- 2-4 minutes -Decreased GnRH pulse frequency is associated with oligomenorrhea or amenorrhea -Increased GnRH pulse frequency is associated with PCOD Control of GnRH Pulses 1-Dopamine ---- decrease the pulse frequency 2-Endogenous opioid ---- inhibit the pulse frequency 3-Neuropeptide Y ----- stimulate the pulse frequency 4-Noreoinephrine ------ stimulate the pulse frequency

II-Pitutary gland

-It consists of anterior lobe (adenohypophysis) & the posterior lobe (neurohypothesis)

-The adult pituitary measure 13 x 10 x 6 mm & weighs 0.5 gm -The anterior pituitary secretes: gonadotronhins (FSH & LH), & prolactin 1-Follicle stimulating hormone (FSH) -It is a water soluble glycoproteins, consists of α-subunit (92 amino acids) & β- subunit (118 amino acids) -Secreted by the basophilic cells -Begins to be secreted at the end of the previous cycle, reaching a peak at day 3 o the new cycle, then the level falls & again it rises to reach a second peak at the 13th day just before ovulation -Half life --- 3-4 hours -Actions of FSH 1-Stimulate growth, ripening & maturation of the ovarian follicles 2-Stimulate aromatase activity in the granulosa cells 3-In combination with LH, it results in ovulation 4-Stimulate the formation of LH receptors 2-Luteinizing hormone (LH) -It is a water soluble glycoprotein, consists of α- subunit (92 amino acids) & β- subunit (121 amino acids) -Secreted by the basophilic cells -LH level: It is fairly constant throughout the cycle & reaches a peak about the 13th day -Half life --- 20 minutes Actions of LH -In combination with FSH it promotes ripening of the follicles -The LH surge ----- rupture of the mature follicle & ovulation -Stimulate corpus luteum to secrete estrogen & progesterone 3-Prolactin -Polypeptide hormone (191 amino acids) -Secreted by the lactotrophs (acidophilic cells) -It is the only anterior anterior pitutary hormone controlled by hypothalamic inhibiting factor (Dopamine) Actions of prolactin 1-Lactation 2-High levels inhibit estrogen secretion by the ovary 3-Essential for corpus luteum function 4-Control of ovulation by preventing further ovulation after fertilization Hypothalamic-Pituitary-Ovarian Axis -Hypothalamus releases GnRH to & passes via the hypophyseal portal circulation & act on gonadotrophin receptors in the anterior pituitary cells resulting in cyclic release of FSH & LH -Secretions of the hypothalamic GnRH is influenced by negative feed- back effect of estrogen & progesterone -FSH stimulate the growth of primary follicles & only one predominate to form mature follicle & secrete increasing amounts of estrogen ----- estrogen peak----- stimulate the anterior pituitary to secrete LH (positive feed back) -LH surge will lead to ovulation & formation of corpus luteum that secretes estrogen & progesterone -This high estrogen level will lead to suppression of Gn.RH (negative feed back) ----- low LH levels & degeneration of corpus luteum resulting in menstruation

Types of feed back mechanisms

1-Long loop feed back (may be positive or negative)

-The effect of the target organ hormones (estrogens & progesterone) on the hypothalamus & pituitary

2-Short loop feed back

-The pituitary trophic hormones ---- suppression of the hypothalamic releasing factors

3-Ultra short loop feed back

-Autocrine & paracrine effects of GnRH on the gonadotropin secreting cells in the hypothalamic nuclei Ovaries The ovaries has two functions:

1-Production of ova (ovarian cycle)

2-Endocrine function ----- production of estrogens & progesterone -The length of the ovarian cycle range from 21-35 days -The ovarian cycle is composed of (follicular & luteal) separated by ovulation 1- Follicular phase -The phase of ripening of the ovum -Begins on the first day of menstruation & occupies the first 14 days -Under the effect of FSH, 50 or more follicles start to ripen, one of these ova outstrips the rest and matures, dominant follicle), while the others undergo atresia -During the process of ripening, the mature Graffian follicle makes its way towards the ovarian surface to bring the discus proligerus with the ovum under the peritoneum The mature Graffian follicle -Size ---- 12-24 mm -Structure ---- composed of: 1-Ovum 2-Perivitelline space surrounds the ovum 3-Zona pellucida surrounds the perivitelline space. 4-Corona radiata: granulosa cells arranged in rows surrounding the ovum and attached to the zona by fine cytoplasmic processes 5-Cumulus oophorus (discus proligerus): Group of granulosa cells that attach the corona radiata to the wall of the follicle 6-Granulosa cells that lines the inner wall of the follicle & surround the follicular space that is filled with liquor folliculi 7-Theca interna cells spindle shaped cells 8-Theca externa cells --- Stroma cells that are compressed & modified to from a false capsule Ovulation Definition ----- rupture of the mature Graffian follicle with escape of the ovum surrounded by corona radiata through a stigma in the follicular wall into the peritoneal cavity & is picked up by the fimbrae of the fallopian tube Mechanism of ovulation

Central mechanism due to LH surge

Peripheral mechanisms

1-Thinning & degeneration of the cyst wall due to the action of proteases 2-Contraction of micromuscle cells in the theca externa & the stroma (due to PG in the follicular fluid) 3-Increased intrafollicular tension due to increase in the fluid content 2- Luteal phase -The phase of formation, function & early degeneration of the corpus luteum -Duration of the luteal phase is more constant than the follicular phase -Duration is said to be 14 + 2 day

*Stages of corpus luteum formation

1- Stage of Proliferation 2-Vascularization: new blood vessels invade the follicle through the site of rupture 3-Maturity: the corpus luteum is functioning with maximum activity after 5 days for 3-4 days 4-Degeneration: occur 4-6 days before the next menstrual period ---- corpus albicans & results in low estrogen and progesterone levels & menstruation Corpus luteum of pregnancy The troplablast secrete human chorionic gonadotrophins within 7 days that prevents degeneration of corpus luteum & continues to produce estrogen & progesterone ---- suppression of anterior pituitary gland & the ovarian cycle Corpus fibrosum or atreticum The primary oocytes that do not mature will disappear at menopause or soon after 1-If the oocyte is blighted at an early stage the primordial follicle is obliterated & replaced by connective tissue 2-If there is some ripening -The oocyte will disintegrate by pyknosis & chromatolysis -A small cyst is formed lined with granulosa cells surrounded by theca lutein cells Causes of follicular atresia 1-Secretion of inhibitory peptide that impairs the binding of LH receptors 2-Inhibition of FSH by negative feed back from: (Estrogen & inhibin hormone) Ovarian Hormones I- Estrogens Sources --- produced by: 1-Ovary from (Graffian follicle & Corpus luteum) 2-Adrenal cortex (small amounts) 3-Placenta Metabolism: in the liver by conjugation with glucouronide or sulphate group, excreted in feces & urine Synthesis of estrogen (Two cell theory) 1-LH acts on the theca cells to produce androgens (androstendione & testosterone ) 2-Androgens diffuses from the theca cells to the granulosa cells 3-FSH stimulates aromatase enzyme to estrogens (estradiol E2 & estriol E3) Levels (2 peaks) -First peak before ovulation (about 300 pg/ml), then it falls -Second peak in the midluteal phase (about 200 pg/ml). then decrease when corpus luteum degenerates Biological actions of estrogen 1-General effects -Appearance of secondary sex characters at puberty -On the breast: it increase the duct system & vascularity -On bones stimulates osteoblastic activity & union of epiphysis -Salt & water retention 2-Central effects (On hypothalamus & pituitary), large dose inhibits FSH release 3-Actions on the genital tract @-On the uterus -Increased vascularity -Endometrium undergo proliferation & hyperplasia -Myometrium undergo hypertrophy & increased sensitivity to oxytocin @-On the cervix -Increase the volume of cervical mucus (water & salt content) -Positive spinabarkeit -Positive Fern test @-On the vagina -Epithelial lining: proliferation & increased glycogen deposition -Increased vaginal acidity due to conversion of glycogen into lactic acid 2-Progesterone Sources 1-Ovary ( corpus luteum), 2-Placenta Metabolism in the liver & 20% is excreted in urine as pregnanediol Levels -Progesterone level starts to rise just before ovulation -Reaches a peak in the mid luteal phase (15 ng/ml) & then drops gradually before menstruation

Biological effects of progesterone

1- General actions

1-Increases the basal body temperature (thermogenic)

2-Salt & water retention

3-Relaxes smooth muscles

4-On the breast: development of alveolar system

2- Central action

-Large doses inhibit LH secretion

3-On the genital tract

*On the uterus

1- Endometrium: induces secretory changes in an estrogen primed endometrium

2-Myometrium -- uterine contractions become frequent but of high amplitude

3-Isthmus ----- Constriction

*On the Cervix -The mucus becomes more viscid with negative sptinnbarkeit & negative fern test Menstrual Cycle 1-Menstrual phase Duration ----- 3-7 days -Scattered small areas of the endometrium are necrosed & are shed off at alternative times. then the whole endometrium is cast off except the deep compact layer -At the end of menstruation, the basal part of the glands start to grow and form new glands 2-Resting phase -Duration: 1-2 days following menstruation -Thickness of endometrium: 1-2 mm -Glands: simple tubular scattered widely in the stroma -Epithelium: cubical ciliated epithelium which dips down to from glands. -Stroma: small spindle shaped connective times cells with little cytoplasm 3-Proliferative phase -Duration: 9-10 days -Glands: tubular, increase in length & dilatation more numerous -Epithelium: more columnar with central nuclei. -Stroma cells are more globular & increase in size & vascularity

4-Secretory phase (Under the effects of progesterone & estrogens) -Duration: 12-14 day (from ovulation till menstruation) -Thickness: 5-7 mm -Glands: more tortous corkscrew, distended with secretions -Stroma: shows dense leucocytic infiltration 2-3 day before menstruation. The stroma cells become more polygonal & increase in size -Differentiated into 3 layers: (superficial compact zone, Middle spongy layer & Deep compact layer)

Medications in the Breast-Feeding Mother

Medications in the Breast-Feeding Mother

Prescribing medications for a breast-feeding mother requires weighing the benefits of medication use for the mother against the risk of not breast-feeding the infant or the potential risk of exposing the infant to medications. A drug that is safe for use during pregnancy may not be safe for the nursing infant.

The mammary tissue in the breast is composed of clusters of milk-producing alveolar cells surrounding a central lumen. The transfer of medication into breast milk is driven primarily by a concentration gradient that allows passive diffusion of nonionized and free (non-protein-bound) medication.

The drug concentration in breast milk is largely determined by the maternal serum drug concentration. This serum concentration tends to be lower with medications that have large volumes of distribution and fluctuates more with medications that have short half-lives.

Retrograde diffusion of the drug from breast milk to plasma may remove a medication from the milk even if the mother has not emptied her breasts. Medications that are highly protein bound, that have large molecular weights or that are poorly lipid-soluble tend not to enter the breast milk in clinically important quantities.

Specific Conditions

ALLERGIC RHINITIS

Pseudoephedrine (Sudafed) is excreted in breast milk in small amounts. According to the AAP, its use is compatible with breastfeeding although it may cause decreased milk production.

Diphenhydramine (Benadryl), which is frequently prescribed for children, is also excreted in breast milk in small quantities. Either of these medications can cause lethargy or irritability in infants. To reduce the risk to the infant, the mother can take these medications immediately after breastfeeding. The new, nonsedating antihistamines are not well-studied in breast-feeding and are not rated by the AAP. Because they have fewer effects on the central nervous system and are safe for use in children, these antihistamines are preferred for short-term use in breastfeeding women. For long-term treatment, nasal steroids or cromolyn (Intal) are safer alternatives.

ASTHMA

Inhaled steroids for the treatment of asthma achieve very low levels in maternal plasma and are of no concern for the breastfeeding mother.

Fluticasone (Flovent) has the lowest serum levels of the inhaled steroids. Oral steroids such as prednisone (Deltasone) and prednisolone (Delta-Cortef) penetrate into the breast milk poorly and are safe for short-term use. When daily dosages exceed 20 mg, prednisolone may be preferred over prednisone because it has only one peak in activity while prednisone has two peaks in activity—one for the pro-drug (prednisone) and the other for the drug (prednisolone). Infant exposure can be minimized by with holding nursing for four hours after taking the medication.

CARDIOVASCULAR

Diuretics and beta blockers, commonly preferred antihypertensives, are safe for use in lactating women, with some precautions. In general, it is preferable to avoid high dosages of any one medication by either changing medications or adding an additional agent.

Low dosages of thiazide diuretics (e.g., 25 mg per day or less of hydrochlorothiazide [Esidrix]) are excreted in small amounts into the breast milk but do not suppress lactation and, consequently, are compatible with nursing. Beta blockers vary widely in the amount excreted into breast milk. Propranolol (Inderal), metoprolol (Lopressor) and labetalol (Normodyne) are excreted in small quantities and are compatible with breastfeeding even in compromised infants. Atenolol (Tenormin), nadolol (Corgard) and sotalol (Betapace) are excreted in higher amounts, which can lead to hypotension, bradycardia and tachypnea in the infant.

Sustained-release nifedipine (Procardia XL) and verapamil (Calan SR) are excreted into breast milk in amounts that are less than the therapeutic dosage for children. Although diltiazem (Cardizem CD) is rated compatible with breast-feeding by the AAP, the levels found in breast milk are higher than the levels for other calcium channel blockers, so safer alternatives are preferred. Captopril (Capoten) and enalapril (Vasotec) are excreted into breast milk in small amounts. These medications are rated compatible with nursing by the AAP, although they have been studied less than other alternatives.Because neonates are highly sensitive to the effects of angiotensin-converting enzyme (ACE) inhibitors, their use by breast-feeding mothers in the first month of their infants' lives may be of concern.Hydralazine (Apresoline) is excreted in amounts far less than the pediatric dosage and is safe, especially for short-term use following delivery.

DIABETES

Insulin is not excreted into breast milk and is considered safe for use during breast-feeding. Based on studies of the distribution of first-generation sulfonylureas into breast milk, the AAP considers tolbutamide (Orinase) to be compatible with breast-feeding.Information on other diabetic agents is less complete. Glyburide (Micronase) and glipizide (Glucotrol) are highly protein-bound (92 to 99 percent), second-generation sulfonylureas. The nature of their protein binding is nonionic and, therefore, they are less likely to be displaced by other drugs and unlikely to pass into breast milk. If any of the sulfonylureas are used, it is important to monitor the nursing infant for signs of hypoglycemia, such as increased fussiness or somnolence.

The alpha-glucosidase inhibitors, such as acarbose (Precose), have low bioavailability, large molecular size and water solubility, so they are unlikely to be excreted into breast milk in clinically significant amounts.

Because of the potential for serious side effects (e.g., lactic acidosis, hepatotoxicity) in adults, it may be advisable to avoid the use of metformin (Glucophage) and thiazolidinediones (e.g., rosiglitazone [Avandia], pioglitazone [Actos]) until more information is available on their use in breast-feeding.

EPILEPSY

Although anticonvulsants are excreted into breast milk, most mothers who require the use of these drugs can safely breast-feed their infants. Determination of maternal serum drug levels may be a useful adjunct to clinical monitoring of the infant when evaluating the drug exposure of the infant.

Phenytoin (Dilantin) and carbamazepine (Tegretol) are compatible with breast-feeding. Although the AAP considers valproic acid and its derivatives (valproic sodium and divalproex sodium) to be compatible with breast-feeding, some experts recommend against their use during breast-feeding because of the potential for fatal hepatotoxicity in children younger than two years.

During breast-feeding, anticonvulsants other than phenobarbital and primidone (Mysoline) are preferred because the slow rate of barbiturate metabolism by the infant may cause sedation. Infant serum levels may be helpful in monitoring toxicity.

Specific Categories of Medications

ANTIBIOTICS

Penicillins and cephalosporins, which are excreted in milk in trace amounts, are compatible with breast-feeding. A remote possibility exists that the child will experience an allergic reaction to the antibiotic or develop diarrhea caused by changes in gut flora. Trimethoprim-sulfamethoxazole (Bactrim, Septra) is compatible with breast-feeding, but its use should be avoided when nursing infants are younger than two months because of its potential for causing increased bilirubin levels.

Tetracycline is excreted in small amounts in breast milk, but the calcium in breast milk limits its absorption. Although tetracycline is compatible with breast-feeding, other antibiotics are preferred, especially for long-term use.Newer derivatives such as doxycycline (Vibramycin) or minocycline (Minocin) should be avoided because of higher absorption by infants and toxicity in children (e.g., dental staining, decreased bone growth).Quinolones have not been well studied in breast milk and are not rated by the AAP. They should be used in the breast-feeding mother only when other, better-studied options cannot be used and after the risks and benefits have been assessed.

Metronidazole (Flagyl) is rated by the AAP as a drug whose effect on infants is unknown, but it may be of concern because older studies found its use in pregnancy to be associated with mutagenicity.Nevertheless, the amount transferred to the infant through breast milk is much lower than the therapeutic dosage for infants, and no adverse effects have been reported from exposure through breast milk. Following a 2-g dose, cessation of breastfeeding for 12 to 24 hours is recommended by the AAP. Topical preparations of metronidazole (MetroGel-Vaginal) produce very low serum concentrations in the mother and are not a concern.

Fluconazole (Diflucan) is commonly prescribed for yeast infections of the nipple in breast-feeding mothers. It is present in breast milk, but the nursing infant can only ingest 5 percent of the usual pediatric dosage. Although limited information is available, topical antifungal agents, such as clotrimazole (Gyne-Lotrimin) or miconazole (Monistat) produce very low maternal serum concentrations, and their use should pose little risk to the nursing infant.

ANTIDEPRESSANTS

Maternal depression is known to have an adverse effect on parenting and infant development. Tricyclic antidepressants have been shown to have little to no effect on the breastfeeding infant, although the AAP finds most tricyclic agents to be of possible concern.Taking a single daily dose at bedtime will limit the infant's exposure to the medication. The selective serotonin reuptake inhibitors (SSRIs) are generally the first choice of treatment for depression. Sertraline (Zoloft) is likely to be the safest choice among them because it has been studied extensively and because drug levels found in nursing infants are usually minimal.

Fluoxetine (Prozac) use during pregnancy has been well-studied, and many new mothers are already taking it at delivery. Its use during breast-feeding is controversial, however. Fluoxetine's long half-life and potential for accumulation in breast milk has prompted some recommendations to avoid its use in women who are breast-feeding young infants. Colic and fussiness have been attributed to elevated serum concentrations of fluoxetine and its metabolite in nursing infants. Results from a recent study showed a decrease in the level of fluoxetine and its metabolite in the early weeks of life in nursing infants whose mothers were maintained on fluoxetine throughout pregnancy and breast-feeding. This decrease implies an absence of accumulation of fluoxetine during exposure from breast milk. No long-term studies of neurologic outcomes of children with breast milk exposure to SSRIs are available. These children should be observed closely.

At this time, it seems prudent to choose an SSRI with the lowest plasma levels in infants, such as sertraline (Zoloft) or paroxetine (Paxil). Another option is to measure serum concentrations of the SSRI and major metabolites in the infant at two to six weeks postpartum to verify that the medication is not accumulating. If the mother has taken fluoxetine during pregnancy, an infant serum level of fluoxetine and norfluoxetine at about six weeks should reflect drug accumulation from the breast milk instead of continued presence of the prenatal medication

ANALGESICS

Of the nonsteroidal anti-inflammatory drugs (NSAIDs), ibuprofen (Motrin) is the preferred choice because it has poor transfer into milk and has been well-studied in children. Long half-life NSAIDs such as naproxen (Naprosyn), sulindac (Clinoril) and piroxicam (Feldene) can accumulate in the infant with prolonged use.

Epidural use of bupivacaine (Marcaine), lidocaine (Xylocaine), morphine, fentanyl (Sublimaze) and sufentanil (Sufenta) is generally safe in breast-feeding mothers. Morphine, codeine and hydrocodone are considered compatible with breast-feeding by the AAP.

Meperidine (Demerol) is not the preferred analgesic for use in breast-feeding women because of the long half-life of its metabolite in infants. Repeated exposure to analgesic agents, especially meperidine, may result in drug accumulation and toxic effects in young or compromised infants because of their underdeveloped hepatic conjugation.When possible, mothers should breast-feed their infants before taking the medication, and low to moderate dosages should be used.

CONTRACEPTIVE AGENTS

Hormones contained in combination oral contraceptive pills (OCPs) are not harmful to infants but, because estrogen diminishes the maternal milk supply, these products should be avoided in breast-feeding mothers whenever possible, especially during the first two months of breast-feeding. Progestin-only contraceptives are preferable, although these also may decrease milk supply. Delaying the use of OCPs, including the progestin-only mini-pill, until six weeks after starting breast-feeding and then using a progestin-only mini-pill (such as Micronor) will allow the mother to assess the drug's effect on her milk supply. If the medication is well-tolerated, repository medroxyprogesterone (Depo-Provera) can be used. When appropriate, the use of an intrauterine contraceptive device or other barrier method of birth control is ideal.

ANESTHETIC AGENTS

Although limited information is available regarding anesthetic agents and their compatibility with breast-feeding, use of propofol (Diprivan), thiopental sodium (Pentothal) and enflurane (Ethrane), should result in negligible amounts of drug exposure to the nursing infant. In general, the healthy term infant can safely nurse as soon after surgery as the mother is awake and alert.

Blood Transfusion in Obstetrics,Green-top Guideline, May 2015

Blood Transfusion in Obstetrics,Green-top Guideline, May 2015

- For normocytic or microcytic anaemia, a trial of oral iron should be considered as the first step and further tests should be undertaken if there is no demonstrable rise in Hb at 2 weeks and compliance has been checked.

- Pregnant women should be offered screening for anaemia at booking and at 28 weeks. Women with multiple pregnancies should have an additional full blood count done at 20–24 weeks.

-Treatment and management Oral iron should be the preferred first-line treatment for iron deficiency.

- Parenteral iron is indicated when oral iron is not tolerated or absorbed or patient compliance is in doubt or if the woman is approaching term and there is insufficient time for oral supplementation to be effective. Women should receive information on improvement of dietary iron intake and factors affecting absorption of dietary iron.

- The role of recombinant human erythropoietin (rHuEPO) for non-end-stage renal anaemia is still to be established and it should only be used in the context of a controlled clinical trial or on the expert advice of the haematologist. Active management of the third stage of labour is recommended to minimise blood loss. Women at high risk of haemorrhage should be advised to deliver in hospital. General principles of blood transfusion Consent for blood transfusion Valid consent should be obtained where possible prior to administering a blood transfusion. In an emergency, where it is not feasible to get consent, information on blood transfusion should be provided retrospectively.

- Requirements for group and screen samples and cross-matching All women should have their blood group and antibody status checked at booking and at 28 weeks of gestation. Group and screen samples used for provision of blood in pregnancy should be less than 3 days old. In a woman at high risk of emergency transfusion, e.g. placenta praevia, and with no clinically significant alloantibodies, group and screen samples should be sent once a week to exclude or identify any new antibody formation and to keep blood available if necessary.

-Close liaison with the hospital transfusion laboratory is essential. Women should have a group and screen sample taken in line with clear locally agreed protocols for provision of blood. Blood product specification in pregnancy and the puerperium ABO-, rhesus D- (RhD-) and K- (Kell-) compatible red cell units should be transfused. If clinically significant red cell antibodies are present, then blood negative for the relevant antigen should be cross-matched before transfusion; close liaison with the transfusion laboratory is essential to avoid delay in transfusion in life-threatening haemorrhage. Cytomegalovirus- (CMV-) seronegative red cell and platelet components should be provided for elective transfusions during pregnancy.

-What are the strategies to minimise the use of banked blood? Is there a role for preoperative/predelivery autologous blood deposit? Predelivery autologous blood deposit is not recommended.

-Is there a role for intraoperative cell salvage (IOCS)? Cell salvage is recommended for patients where the anticipated blood loss is great enough to induce anaemia or expected to exceed 20% of estimated blood volume. Consent should be obtained for IOCS where possible and its use in obstetric patients should be subject to audit and monitoring. Cell salvage should only be performed by multidisciplinary teams who develop regular experience of IOCS. Where IOCS is used during caesarean section in RhD-negative, previously nonsensitised women and where cord blood group is confirmed as RhD positive (or unknown), a minimum dose of 1500 iu anti-D immunoglobulin should be administered following the reinfusion of salvaged red cells.

- A maternal blood sample should be taken for estimation of fetomaternal haemorrhage 30–40 minutes after reinfusion in case more anti-D is indicated. Management of obstetric haemorrhage with blood components There should be a clear local protocol on how to manage major obstetric haemorrhage.

The protocol should be updated annually and practised in ‘skills drills’ to inform and train relevant personnel. Are there mechanical strategies that can be employed? Clinicians should familiarise themselves with mechanical strategies that can be employed to reduce postpartum blood loss. What blood components can be used for obstetric haemorrhage? When should red cells be used? There are no firm criteria for initiating red cell transfusion.

-The decision to provide blood transfusion should be made on clinical and haematological grounds. In an extreme situation and when the blood group is unknown, group O RhD-negative red cells should be given (although they may be incompatible for patients with irregular antibodies). Staff working in obstetric units should be aware of the location of the satellite blood fridge (where available) and should ensure that access is possible for blood collection. In what circumstances should fresh frozen plasma (FFP) and cryoprecipitate be used? FFP at a dose of 12–15 ml/kg should be administered for every 6 units of red cells during major obstetric haemorrhage.

-Subsequent FFP transfusion should be guided by the results of clotting tests if they are available in a timely manner, aiming to maintain prothrombin time (PT) and activated partial thromboplastin time (APTT) ratios at less than 1.5 x normal. It is essential that regular full blood counts and coagulation screens (PT, APTT and fibrinogen) are performed during the bleeding episode. Cryoprecipitate at a standard dose of two 5-unit pools should be administered early in major obstetric haemorrhage.

- Subsequent cryoprecipitate transfusion should be guided by fibrinogen results, aiming to keep levels above 1.5 g/l. The FFP and cryoprecipitate should ideally be of the same group as the recipient. If unavailable, FFP of a different ABO group is acceptable providing that it does not have a high titre of anti-A or anti-B activity. No anti-D prophylaxis is required if a RhD-negative woman receives RhD-positive FFP or cryoprecipitate. When should platelets be used? Aim to maintain the platelet count above 50 x 109 /l in the acutely bleeding patient. A platelet transfusion trigger of 75 x 109 /l is recommended to provide a margin of safety.

-The platelets should ideally be group compatible. RhD-negative women should also receive RhDnegative platelets. Is there a role for near patient testing of coagulation? Centres that are using thromboelastography or rotation thromboelastometry for guiding blood transfusion during major obstetric haemorrhage must ensure that their transfusion algorithm protocol has been validated and that quality assurance measures are followed.

-The use of rFVIIa may be considered as a treatment for life-threatening postpartum haemorrhage (PPH), but should not delay or be considered a substitute for a live-saving procedure such as embolisation or surgery, or transfer to a referral centre.

-Is there a role for fibrinogen concentrate therapy? Fibrinogen concentrate is not licensed in the UK for the management of acquired bleeding disorders. Thus, its use in PPH should be considered only in the context of clinical trials. Is there a role for antifibrinolytics? For those centres not participating in clinical trials, consideration should be given to using tranexamic acid during major obstetric haemorrhage.

-How should intrapartum anaemia be managed? In addition to major haemorrhage guidelines, obstetric units should have guidelines on criteria for red cell transfusion in anaemic women who are not actively bleeding. If the Hb is less than 70 g/l in labour or in the immediate postpartum period, the decision to transfuse should be made according to the individual’s medical history and symptoms. How should women with postpartum anaemia be managed in the postnatal period? If the Hb is less than 70 g/l in the postnatal period, where there is no ongoing or threat of bleeding, the decision to transfuse should be made on an informed individual basis.

-How should women who decline blood products be managed? Hb should be optimised prior to delivery to prevent avoidable anaemia. Consent/refusal of blood and components or other transfusion-sparing techniques should be discussed and documented during the antenatal period. Use of pharmacological, mechanical and surgical procedures to avert the use of banked blood and blood components should be considered early. IOCS has a role in the management of patients who refuse allogeneic blood transfusion.

DR. Alaa Mosbah

LAPAROSCOPY

DR. Alaa Mosbah

Professor of obstetrics and gynecology

Radiation exposure during pregnancy

Radiation exposure during pregnancy

The 5 types of radiation include:

(1) Ionizing rays (x-rays),
(2) Cosmic rays,
(3) Microwaves,
(4) Ultrasound, and

(5) Electromagnetic fields.

1- Ionizing rays
X-rays are the most frequent iatrogenic exposure besides prescription medications. During their careers, all obstetricians and gynecologists are asked about the effects of radiation exposure on a pregnancy, and they are expected to be able to judge the need for diagnostic or therapeutic radiation. The effects of radiation are well studied, but as cohort age and long-term effects become clear, information continues to evolve in this ever-changing field. Knowledge about exposures also changes rapidly.

The primary exposures are diagnostic x-rays, radio-pharmaceuticals, workplace exposures, and environmental exposures such as those that occurred after the Three Mile Island and Chernobyl nuclear reactor accidents,

II. Documented effects include

(1) intrauterine lethality,

(2)organ malformation,

(3)mental impairment, and later-onset

(4) leukemia and solid tumors.

X-rays are measured in several types of units,

the most important of which are

the radiation absorbed dose (rad), which is the measure in the United States, and

the gray (Gy), which is an international measure. Both rads and grays typically refer to single-time exposures (eg, diagnostic procedures).

The roentgen equivalent man (rem) unit of measure and

sievert (Sv) unit are used to quantify radiation exposure over time (eg, environmental releases).

Conversion factors for these measurements are 1 Gy equals 100 rad and 1 Sv equals 100 rem.

X-rays have both immediate effects and delayed effects:

A].Immediate effects:

Immediate (deterministic) effects are usually intrauterine, often post-conceptual, effects involving damage to growing and pattern-forming cell populations. If the exposure occurs when cell numbers are few, such as during the blastocyst or pre-implantation stage, very early abortion or implantation failure occurs. These effects demonstrate both a dose-response curve and a threshold below which no effects are observed.
As with other teratogens, the embryonic stage is crucial because windows exist for the appearance of effects. The fetal dose is also critical, and a simple application of a maternal calculated dose should not be substituted.

The damage threshold begins at 0.1-0.15 Gy, which causes abortion at pre-implantation, and extends to 1 Gy, which is associated with fetal death in utero at term. Organogenesis represents a window of sensitivity for the fetus during gestational weeks 3-7. The threshold is thought to be 0.05-0.5 Gy.

Skeletal defects have been noted in humans, most particularly reduced head circumference. Animal data point to more frequent defects of the genitourinary system and eye in addition to skeletal effects. Severe mental retardation is another human effect noted at this threshold (0.05-0.5 Gy). The window for these effects is gestational weeks 8-25. Mental retardation has been noted at maternal doses of 1.5 Gy. Fetuses exposed during weeks 8-25 also demonstrate an onset of effects secondary to radiation. These effects include mental retardation, a downward shift in intelligence quotient (IQ) of 30 IQ units/Gy, lower school performance, and unprovoked seizure. All effects are more severe if the exposure occurs during gestational weeks 8-15. Importantly, note that while infants of normal intelligence remain within 1 standard deviation of normal following exposure, borderline infants are rendered mentally retarded at relatively low exposures.

B].Delayed effects:
These effects do not show a threshold, and they occur in the later years of the exposed individual’s life. Fetal x-ray exposures are associated with later-onset childhood leukemia and solid tumors. The demonstrated relative risk in multiple case-control studies is 1.39 (95% confidence interval: 1.3-1.49). This increased risk was documented by the very large Oxford Survey of Childhood Cancers, and the finding was confirmed by multiple US and European studies. The increased risk is thought to occur following an exposure of 0.05 Gy.

Thyroid cancer in childhood is a special concern. Multiple studies have shown that direct external exposure of children’s thyroids results in an increased frequency of cancer. Such exposures occurred following the Chernobyl accident and during medical procedures. The lag time until detection of cancer is 5 years after exposure. In contrast, in utero exposure during the second and third trimester of pregnancy (eg, Chernobyl, maternal thyroid ablation) is associated with an onset of childhood thyroid cancer before the 5-year lag time; these cancers are associated with increased morbidity and aggressiveness.
Radiation is a dose-dependent teratogen. Below a certain threshold, radiation levels are similar in exposed populations and control populations who have received only background radiation.1 A fetus is most vulnerable to radiation-induced central nervous system damage 8 to 15 weeks after conception . Radiation from x-ray and CT scans is measured in rad, rem, gray, and sievert (1 rad = 1 rem = 0.01 Gy = 0.01 Sv).

Estimated fetal radiation doses during some common radiodiagnostic procedures
FETAL DOSE (MRAD)
X-RAY

Upper gastrointestinal series
100
Cholecystography
100
Lumbar spine radiography
400
Pelvic radiography
200
Hip and femur radiography
300
Retrograde pyelography
600
Abdominal (kidneys, uterus, bladder) radiography
250
Lumbar spine,

• Anteroposterior
750
• Lateral
91
• Oblique
100
Barium enema
1000
Intravenous pyelogram
480
COMPUTED TOMOGRAPHY

Head
0
Chest
16
Abdomen
3000
Intervention;

Clearly, preventing exposure during the first trimester is advisable. Clear counseling is needed for patients with conditions that require uptake scans or radio-nuclide therapy. Patients should be advised that no known safe dose exists in regard to later-onset childhood cancers. The balancing of risk to both patients (fetus and mother) must take into account the value that any given diagnostic test will have for decision-making. For occupational exposures, the limit is 1 mSv after pregnancy notification.
2- Cosmic rays:
Cosmic radiation is ionizing radiation by heavy particles, such as protons and helium nuclei that originate outside the earth. This form of ionizing radiation is most evident at very high altitudes. Primary exposure requires many in-air hours; therefore, airplane crewmembers and pilots, rather than passengers, are typically at risk.
Relatively few studies have been performed on human exposure to cosmic radiation. Risks are real, but the medical community and the general public have little awareness of them.

Two organizations, the US National Council on Radiation Protection and Measurement (NCRP) and the International Commission on Radiologic Protection (ICRP), provide the following recommendations on permissible doses:
General public - 1 mSv
Aircrews - 20 mSv/y averaged over 5 years (maximum 50 mSv/year)
Fetuses - 2 mSv (not to exceed 0.5 mSv/month)
Notably, aviators generally have a lower overall incidence of cancer compared to the general population. The risks of all other forms of transportation outweigh those of flight, although an association exists between frequent flying and certain specific cancers, most notably brain, colon, and hematopoietic cancers.
Also, ionizing radiation has the previously noted fetal effects of decreased head circumference, mental retardation, and childhood cancer.
Aviation workers can easily exceed the NCRP and ICRP limit recommendations. Charter jet crews and passengers fly at higher altitudes with more consequent exposure. Changes in intensity occur with changes in solar flare activity on the sun, and the intensity may exceed 10 mSv/h at 42,000 ft. The US Federal Aviation Administration and the US Occupational Safety and Health Administration recognize flight crews as individuals exposed to radiation. Computer systems are available to calculate exposures, but these systems are not mandatory.

Intervention;
Health care providers should obtain complete occupational histories and discuss risk of exposure with pregnant patients. Given the variability of exposure and that no easy monitoring is possible, any mandatory cut-off or exclusion of pregnant workers from their jobs would be potentially discriminatory and may lead to risks to the child due to altered socioeconomic status.

3- Microwaves:
Microwaves are a form of electromagnetic radiation with particularly long wavelengths. In contrast to ionizing radiation, which travels in extremely short, high-energy waves, energy in microwave radiation affects objects and cells by thermal action only. Microwaves raise the temperature within cells and are cytotoxic to individual cells only at high exposures. No specific DNA-damaging mechanism exists, and no stochastic effects are observed in exposed populations.

4- Ultrasound:Ultrasound involves the creation of very high-frequency sound, emission of this sound, and analysis of how the sound alters upon encountering objects of different densities when reflected back to the emitter. Physical effects, such as well-contained thermal effects, occur when the vibration at these very high speeds is used (e.g. between the paddles of a harmonic scalpel).The energy of ultrasound is carried by the physical particles of the media and objects affected. The energy does not reach an ionizing level, and no DNA-specific effects are observed.
5- Electromagnetic fields:
Despite multiple studies, including some very large studies, the low-energy electromagnetic fields generated by power lines, video displays, and other electric and electronic devices have no demonstrable effects. Some of these studies have been conducted in response to clusters of events, such as increased spontaneous abortion rates in a specific area.

High-risk pregnancy

High-risk pregnancy

Definition :

High-risk pregnancy is broadly defined as one in which the mother, fetus, or newborn is at or may possibly be at increased risk of morbidity or mortality before, during, or after delivery. Many factors are involved, including maternal health, obstetric history, and fetal disease.

PRECONCEPTIONAL EVALUATION
Preconceptional evaluation and counseling of women of reproductive age has gained increasing acceptance as an important component of women's health.

MATERNAL ASSESSMENT FOR POTENTIAL FETAL OR PERINATAL RISK

INITIAL SCREENING :

History

A. MATERNAL AGE
Extremes of maternal age increase risks of maternal or fetal morbidity and mortality. Adolescents are at increased risk for preeclampsia-eclampsia, intrauterine growth restriction (IUGR), and maternal malnutrition.
Women 35 years of age or older at the time of delivery are at higher risk of pregnancy-induced hypertension, diabetes, and obesity as well as other medical conditions. Chromosomal abnormalities are also more common in infants born to older women, as will be discussed in detail later. An increased risk of cesarean section, preeclampsia, and placenta previa is noted in women with advanced maternal age.
B. MODALITY OF CONCEPTION
It is important to differentiate spontaneous pregnancy from that resulting from assisted reproductive technologies (ART). Use of ART increases the risks of multiple gestation, pregnancy-induced hypertension, and preterm delivery.
C. PAST MEDICAL HISTORY
Specific disease states may adversely affect the outcome of pregnancy for the mother or infant. Pregnancy itself may aggravate certain medical disorders and alleviate others.
D. FAMILY HISTORY
A detailed family history is helpful in determining any increased risk of heritable disease states (eg, Tay-Sachs, cystic fibrosis, sickle cell disease) which may affect the mother or fetus during the pregnancy or the fetus following delivery.
E. ETHNIC BACKGROUND
Population screening for certain inheritable genetic diseases is not cost effective due to the relative rarity of the gene in the general population. However, many genetic diseases affect certain ethnicities in disproportionate amounts, allowing those groups to be screened in a cost-effective way.
F. PAST OBSTETRIC HISTORY
1. Habitual abortion
A diagnosis of habitual abortion can be made after 3 or more consecutive spontaneous losses of a previable fetus. Habitual abortion is best investigated before another pregnancy occurs. If the patient is currently pregnant, as much of the work-up as possible should be performed.
Karyotype of abortus specimen
Parental karyotype
Survey for cervical and uterine anomalies
Connective tissue disease work-up
Screening for hormonal abnormalities (ie, hypothyroidism)
Acquired and inherited thrombophilias
Infectious disease evaluation of the genital tract
2. Previous stillbirth or neonatal death
A history of previous stillbirth or neonatal death should trigger an immediate investigation as to the conditions or circumstances surrounding the event. If the demise was the result of a nonrecurring event such as cord prolapse or traumatic injury, then the present pregnancy has a risk approaching a background risk. However, stillbirth or neonatal death may also suggest a cytogenetic abnormality, structural malformation syndrome, fetomaternal hemorrhage or thrombophilia (fetal or maternal), requiring a similar investigation as above.
3. Previous preterm delivery
The greater the number of preterm deliveries, as well as the degree of prematurity, the higher the risk at present for preterm delivery in the index pregnancy. Despite intense investigation, the incidence of preterm delivery has remained unchanged. Two-thirds of preterm deliveries occur near term (34 to 37 weeks), and these carry minimal fetal or neonatal morbidity. The remaining one-third of preterm deliveries accounts for nearly all of the perinatal morbidity and mortality. Approximately 50% of newborns born under 1000 grams suffer from intracranial hemorrhage, retinopathy of prematurity, or bronchopulmonary dysplasia, all of which carry significant long-term consequences. Approximately 40% of preterm delivery is due to spontaneous preterm delivery, another 40% is due to preterm rupture of membranes, and the remaining 20% is due to iatrogenic preterm delivery (eg, delivery due to preeclampsia or deteriorating fetal status). Spontaneous preterm labor is a complex process, but discrete pathophysiological processes have been identified (but may coexist): maternal and/or fetal stress, ascending genital tract infection, abruption (decidual hemorrhage), and uterine distension. Risk factors for preterm labor include prior history of preterm labor, multifetal pregnancy, vaginal bleeding in more than one trimester, in utero exposure to diethylstilbestrol (DES), uterine anomalies, incompetent cervix, and preterm labor in the index pregnancy. Screening for preterm labor in high-risk patients may include cervical length measurements by transvaginal sonography, fetal fibronectin of cervicovaginal secretions, and salivary estriol.
4. Rh isoimmunization or ABO incompatibility
Blood typing of both parents and maternal antibody screening should be performed at the initial prenatal visit. Women at risk for Rh(D) isoimmunization should be screened for anti-Rh(D) antibody at presentation, at 28 weeks gestation, and at delivery.
5. Previous preeclampsia-eclampsia
Previous preeclampsia-eclampsia increases the risk for hypertension in the current pregnancy, especially if there is underlying chronic hypertension or renal disease.
6. Previous infant with genetic disorder or congenital anomaly
A woman with a previously affected infant should be offered genetic counseling. Screening or testing is available for some defects using maternal blood samples (eg, alpha-fetoprotein; AFP), ultrasonography, amniocentesis, chorionic villus sampling, and DNA analysis.
7. Teratogen exposure
A teratogen is any substance, agent, or environmental factor that has an adverse affect on the developing fetus. Whereas malformations caused by teratogen exposure are relatively rare, knowledge of exposure can aid in the diagnosis and management.
a. Drugs
Alcohol, anti-seizure medications (pheny-toin, valproic acid, etc), lithium, mercury, thalidomide, diethylstilbestrol (DES), coumadin, isotretinoin, etc.
b. Infectious agents
CMV, Listeria, rubella, toxo-plasmosis, varicella, Mycoplasma, etc.
c. Radiation
It is commonly believed that medical diagnostic radiation delivering less than 0.05 Gy to the fetus has no teratogenic risk.

ANTEPARTUM COURSE

Uniform Perinatal Record

A consistent method of recordkeeping which is easily understandable from doctor to doctor and location to location is ideal to manage the high-risk patient. In the event of a transfer of care during a pregnancy, or a review of a previous pregnancy, having a coherent, accessible prenatal record helps avoid duplication of tests and helps to expedite diagnostic confirmation and the onset of treatment. Preprinted records such as American College of Obstetricians and Gynecologists (ACOG) forms provide uniform data for each patient and are helpful in diagnosis as well as in management decision making.
Prenatal Visits

Every prenatal visit is an opportunity to not only screen for problems that may complicate the course of the pregnancy but also to anticipate any problems before they develop. Several factors should be evaluated at each visit.

Examination:
A. VITAL SIGNS
Fever (> 100.4° F), even without other subjective complaints may be due to a wide source of infectious etiologies. Urinary, pulmonary, and hematological sources of the fever should be considered. Signs or symptoms of chorioamnionitis should be assessed, and if chorioamnionitis is suspected, amniocentesis for microscopy and culture should be considered. Depending on clinical correlation, delivery may be necessary. Very high fevers (> 103° F) may trigger preterm labor and may also have an adverse effect on the early development of the fetal central nervous system. Antipyretics may be necessary to lower the temperature.

B. PULSE
Maternal tachycardia can be a sign of infection, anemia, or both. Isolated mild tachycardia (> 100 beats per minute [bpm]) should be evaluated and followed up. Moderate to severe tachycardia (> 120 bpm) needs immediate evaluation, including but not limited to a hemogram and an ECG.

C. BLOOD PRESSURE

The normal pattern of maternal blood pressure readings is for a decrease from baseline during the first trimester, reaching its nadir in the second trimester, and slightly rising in the third trimester, although not as high as the baseline levels. Repeated blood pressure readings of 140/90 mm Hg 6 hours apart or a rise of 30 mm Hg systolic pressure or 15 mm Hg diastolic pressure should be considered evidence of pregnancy-induced hypertension. Consideration of the patient's medical history, prepregnancy blood pressure, and gestational age should all be considered in forming a diagnosis and management strategy.
D. URINALYSIS

At the first prenatal visit, a clean-catch urine culture and sensitivity should be performed. Any growth should be treated with the appropriate antibiotics. At all subsequent visits, urine dipstick testing to screen for protein, glucose, leukocyte esterase, blood, or any combination of markers is useful in identifying patients with a change in their baseline urinary composition.

Screening Tests :
Screening tests are performed at the appropriate time during the pregnancy.
A. FASTER (FIRST AND SECOND TRIMESTER EVALUATION OF RISK FOR ANEUPLOIDY) TRIAL
Transvaginal sonography between 103/7 weeks and 136/7 weeks to visualize and measure nuchal translucency, along with serum measurements of PAPP-A and free β-hCG is currently being studied in several institutions throughout the United States as a screen for Down syndrome, as well as other aneuploidies and malformations.
B. MATERNAL SERUM ANALYTE TESTING
Frequently known as the “triple screen,” this test includes maternal serum alpha-fetoprotein (msAFP), β-hCG, and estriol. In some institutions, only the msAFP is used, while in other institutions a fourth test, inhibin, is included, making it a “quad test.” The usefulness of this screen is its ability to identify pregnancies at an increased risk for open neural tube defects, as well as for certain chromosomal abnormalities, especially trisomy 21 (75% sensitivity for Down syndrome detection). This test is effective at 15–19 weeks' gestation and can therefore identify an at-risk pregnancy in time to pursue more definitive diagnosis, if desired. It is important to note, however, that the triple screen is not a definitive test and that many positive screens have yielded normal fetuses and many abnormal fetuses have had normal screens.
C. DIABETES SCREEN
Routine screening consists of performing a glucose challenge test between 24 and 28 weeks. The test consists of a 50-g oral glucose load with a plasma glucose level drawn exactly 1 hour after. If the value is over 140 mg/dL, a more specific glucose tolerance test (GTT) should be performed. The GTT involves obtaining a fasting plasma glucose level, giving a 100-g oral glucose load, then drawing plasma levels at 1 hour, 2 hours, and 3 hours after the glucose load. A test is considered positive for gestational diabetes if two out of the four values are elevated.
D. ISOIMMUNIZATION
A patient who is Rh-negative with a pregnancy fathered by an Rh-positive man should be screened for antibodies at the first prenatal visit and again at 24–28 weeks. If there continues to be no antibodies, Rhogam should be administered at 28 weeks to prevent sensitization of the mother during the last trimester and delivery. In the event of a previously isoimmunized patient, the typing and screening performed at the initial visit would detect antibodies, which are reported as a numerical titer. These titers should be followed every 4 weeks to assess for worsening isoimmunization. In the presence of worsening titers, follow-up with amniocentesis may be appropriate. Peak systolic velocity of the fetal middle cerebral artery as determined by sonographic Doppler evaluation has been demonstrated to correlate with degree of fetal anemia, allowing for noninterventional diagnosis and management of fetal isoimmunization; however, the definitive treatment is intrauterine fetal transfusion.
E. BETA HEMOLYTIC STREPTOCOCCUS
This is also known as the group B Streptococcus (GBS) test, and between 10% and 30% of pregnant women are colonized with GBS in the vaginal or rectal areas. Whereas they are usually asymptomatic colonizations, perinatal transmission can result in a severe and potentially fatal neonatal infection. Any documented GBS bacteriuria needs to be treated at the time of diagnosis, as well as intrapartum. Intrapartum antibiotic prophylaxis has been shown to decrease the risk of perinatal GBS transmission. There are two approaches to screening: Screen patients at 35–37 weeks' gestation and treat positive cultures with intrapartum antibiotics, or treat patients based on risk factors with intrapartum antibiotic prophylaxis.

Fetal Assessment

Comprehensive fetal assessment begins in the first trimester with nuchal translucency and continues throughout the pregnancy into labor and delivery. Conceptually, antepartum testing in pregnancies at risk falls into one of two categories: assessment of prenatal diagnosis and assessment of fetal well-being.

A. ASSESSMENT OF PRENATAL DIAGNOSIS
Performed during all trimesters, the techniques used are diverse, and the information obtained varies according to the quality of imaging, depth of investigation, and gestational age of pregnancy.
1. Ultrasound
Ultrasound has had a continuous evolution over the last 20 years, with better equipment being produced each year. Real-time sonography allows a 2-D image to demonstrate fetal anatomy, as well as characteristics such as fetal weight, movement, volume of amniotic fluid, and structural anomalies such as myomas or placenta previa which may affect the pregnancy. 3-D sonography allows volume to be ascertained, creating a three-dimensional appearing image on the 2-D screen, which assists in identifying certain anatomical anomalies. Most recently, 4-D machines have been developed, which produce a 3-D image in real time. As the machines become more technically advanced and the computers that run them become faster, the images obtained will continue to improve and push the boundaries of sonographic prenatal diagnosis.
Diagnostic ultrasonography is widely used in the assessment of the pregnancy and the fetus. It is not, however, the standard of care, nor is it recommended by ACOG for every pregnancy. The indications for ultrasonography are multiple and diverse, and the type and timing of the examination varies depending on the information being sought.
A basic ultrasound examination should provide such information as fetal number, presentation, documentation of fetal viability, placental location, and assessment of gestational age. A limited ultrasound examination is a goal-directed search for a suspected problem or finding. A limited ultrasound may be used for guidance during procedures such as amniocentesis or external cephalic version, assessment of fetal well being, or documentation of presentation or placental location intrapartum. A comprehensive ultrasound examination provides information on fetal anatomy, growth, anomalies, and physiologic complications.
Ultrasound evaluation of fetal anatomy may detect some major structural anomalies. Gross malformations such as anencephaly and hydrocephaly are more commonly diagnosed and rarely missed; however, more subtle anomalies such as facial clefts, diaphragmatic hernias, and neural tube defects are more commonly reported to have been missed by ultrasound. The basic fetal anatomy survey should include visualization of the cerebral ventricles, four-chamber view of the heart, and examination of the spine, stomach, urinary bladder, umbilical cord insertion site, and renal region. Any indication of an anomaly should be followed by a more comprehensive sonogram. Typically, the fetal anatomic survey is performed at 17–20 weeks; however, there is controversy surrounding the potential benefits of an earlier sonogram at 14–16 weeks using the transvaginal probe. The earlier scan allows earlier detection of anomalies that are almost always present by the second trimester, as well as allowing greater detailed viewing of the fetal anatomy by using the higher-resolution vaginal transducers.
2. Aneuploidy screening
Multiple sonographic markers for aneuploidy have been identified. The presence of single or multiple markers adjusts the patient's age-related risk of aneuploidy based on the particular markers present. Such sonographic findings include, but are not limited to:
Echogenic intracardiac focus
Choroid plexus cysts
Pyelectasis
Echogenic bowel
Short femur
Hypomineralization of the fifth digit of the fetal hand
3. Amniocentesis
Amniocentesis is frequently performed under the guidance of ultrasonography. A needle is inserted transcutaneously through the abdominal wall into the amniotic cavity, and fluid is removed. There are many uses for this amniotic fluid, including cytology for detection of infection, alpha-fetoprotein evaluation for neural tube defect assessment, assessment of fetal lung maturity (which will be discussed later in the chapter), and the most common indication of cytogenetic analysis. In this case, amniocentesis is often performed between 15 and 20 weeks' gestation and fetal cells from the amniotic fluid are obtained. Risks associated with the procedure are considered to be very low, with the risk of abortion as a result of amniocentesis considered to be between 1 in 200 to 1 in 450 amniocenteses.
4. Chorionic villus sampling
Chorionic villus sampling (CVS) is an alternative to amniocentesis. It is performed between 10 and 12 weeks' gestation, and can be performed either transcervically or transabdominally. CVS is also performed under sonographic guidance, with the passing of a sterile catheter or needle into the placental site. Chorionic villi are aspirated and undergo cytogenetic analysis. The benefit of CVS over amniocentesis is its availability earlier in pregnancy; however, the rate of abortion is higher—as high as 1%. One disadvantage
of CVS is that unlike amniocentesis, it does not allow diagnosis of neural tube defects.
5. Fetal blood sampling
Also referred to as cordocentesis or percutaneous umbilical blood sampling (PUBS), this is an option for chromosomal or metabolic analysis of the fetus. Benefits of the procedure include a rapid result turnaround rate and the ability to perform the procedure in the second and third trimester. Intravascular access to the fetus is useful for the assessment and treatment of certain fetal conditions such as Rh sensitization and alloimmune thrombocytopenia. There is a higher risk of fetal death, however, when compared to the other methods. Fetal loss rates are approximately 2%, but can vary depending on the fetal condition involved.

B. ASSESSMENT OF FETAL WELL-BEING
1. Fetal monitoring techniques
Assessment of fetal status can be performed using a wide variety of techniques.
a. External fetal monitoring
The external measurement of the fetal heart rate is done by using a continuous beam of ultrasound waves focused on the fetal heart. This ultrasound monitor utilizes Doppler effects to sample the frequency of moving fetal heart valves and the atrial and the ventricular systole. The complex received signal wave is then peak detected and entered into the heart rate monitor. The computer averages several consecutive frequencies, which helps minimize artifact, before the signal is displayed and printed. This process of averaging is called autocorrelation, and produces a fetal heart rate pattern which closely resembles that derived from a fetal ECG, although there is more baseline variability inherent in this method.
b. Internal fetal monitoring
The internal measurement of the fetal heart rate is an invasive procedure, utilizing an electrode attached to the fetal scalp. A bipolar spiral electrode is placed transcervically and penetrates the fetal scalp. A reference electrode is placed on the maternal thigh to eliminate electrical interference. The fetal ECG is detected, and the R wave is the signal used for peak detection and for counting. This signal is very clear, and allows accurate beat-to-beat and baseline variability to be measured. Artifact is kept to a minimum, and there is little need for autocorrelation.
c. Sonographic fetal monitoring
There have been reports of a number of sonographically related surveillance techniques for fetal status published in the literature. Such testing techniques as biophysical profile and Doppler velocimetry have been extensively studied and widely used for antepartum evaluation. Doppler velocimetry is a noninvasive technique based on vascular impedance. Most often, the umbilical artery is utilized for this purpose. Both the peak values as well as the actual waveform can be utilized to identify abnormally growing fetuses, or fetuses at risk of cardiac failure or other adverse outcome. Most of the benefit is seen in growth-restricted pregnancies, and use for generalized surveillance is not recommended. Biophysical profile consists of fetal heart rate evaluation combined with sonographically assessed parameters of fetal well being, including fetal breathing movements, fine motor movement, gross fetal tone, and amniotic fluid volume.
2. Fetal heart rate interpretation
a. Antepartum fetal surveillance
In determining which patients should have antepartum fetal surveillance, a major factor to consider is the lack of evidence that any routine surveillance method results in a decreased risk of fetal death. Therefore, we generally begin monitoring in pregnancies in which the risks of fetal demise are known to be increased. These can include maternal conditions such as antiphospholipid syndrome, lupus, diabetes, or other maternal medical problems. They can also include pregnancy-related conditions such as preeclampsia, IUGR, multiple gestation, poor obstetrical history, or postterm pregnancy.
Antepartum surveillance should include a nonstress test (NST) as a minimum. The addition of sonographic monitoring is common, most often as some variant of the biophysical profile. The criteria for the NST are: baseline between 120 and 160 bpm, the presence of periodic accelerations (ie, two accelerations in 20 minutes) of fetal heart rate of 15 bpm over baseline for 15 seconds, the absence of decelerations of the fetal heart rate, and the subjective assessment of variability of the fetal heart rate. In the case of a nonreassuring NST, further evaluation or delivery depend on the clinical context. In a patient at term, delivery is warranted. Near term, determination of fetal lung maturity can be considered. Remote from term poses a more challenging dilemma to the clinician. If resuscitative efforts are not successful in restoring reactivity to the NST, ancillary tests or testing techniques may prove useful in avoiding a premature iatrogenic delivery for nonreassuring fetal heart rate patterns, since the false-positive rate may be as high as 50–60%.
C. ANCILLARY TESTS
1. Vibroacoustic stimulation
An auditory source, often an artificial larynx, is placed on the maternal abdomen. A short burst of sound is delivered to the fetus. This has proven successful in shortening the duration needed for the test to show reactivity, without compromising the predictive value of the absence of acidosis with a reactive NST.
2. Fetal scalp stimulation
The presence of an acceleration after a vaginal exam where the examiner stimulates
the fetal vertex with the examining finger confirms the absence of acidosis (pH > 7.2).
3. Oxytocin challenge test

This may be used to elicit a confirmatory abnormal fetal heart rate response, with one report showing a better correlation with adverse outcome than the NST alone. Other studies, however, have demonstrated no improvement in predicting morbidity over an NST. This is performed by intravenous infusion of dilute oxytocin until three contractions occur in 10 minutes. A positive test indicates decreased fetal reserve, with a 20–40% incidence of abnormal fetal heart rate (FHR) patterns in labor. A positive test is the presence of a late deceleration after each of the three contractions, a negative test shows no decelerations, and anything else is equivocal. Repetitive variable decelerations are termed “suspicious” and are associated with abnormal FHR patterns in labor, particularly in postterm gestations.

Fetal Maturity Tests
Indications for assessing fetal lung maturity—The American College of Obstetricians and Gynecologists has recommended that fetal pulmonary maturity should be confirmed before elective delivery at less than 39 weeks' gestation unless fetal maturity can be inferred from any of these criteria: Fetal heart tones have been documented for 20 weeks by nonelectronic fetoscope or for 30 weeks by Doppler; and 36 weeks have elapsed since a serum or urine hCG-based pregnancy test was reported to be positive.
A. LECITHIN:SPHINGOMYELIN RATIO
The lecithin:sphingomyelin (L:S) ratio for assessment of fetal pulmonary maturity was first introduced by Gluck and colleagues in 1971. The test depends upon outward flow of pulmonary secretions from the lungs into the amniotic fluid, thereby changing the phospholipid composition of the latter and permitting measurement of the ratio of lecithin to sphingomyelin in a sample of amniotic fluid. The concentrations of these two substances are approximately equal until 32–33 weeks of gestation, at which time the concentration of lecithin begins to increase significantly while the sphingomyelin concentration remains about the same. The measurement of sphingomyelin serves as a constant comparison for control of the relative increases in lecithin because the volume of amniotic fluid cannot be accurately measured clinically. Determination of the L:S ratio involves thin-layer chromatography after organic solvent extraction. It is a difficult test to perform and interpret; care at each step of sample handling is critical for consistent results. The sample should be kept on ice or refrigerated if transport to a laboratory is required. Improper storage conditions can change the L:S ratio since amniotic fluid contains enzymes that can be affected by temperature. The amniotic fluid samples must be mixed well. The presence of blood or meconium can interfere with test interpretation. Bloody samples give false information due to the presence of sphingomyelin in blood and decreased extraction of lecithin by cold acetone techniques in the presence of red blood cells. Therefore, if blood or other particulate matter is present in the amniotic fluid sample, a low-speed, short centrifugation can be used to remove the cellular component.
Interpretation of the results should be carried out with consideration of the individual clinical circumstances. For example, some physicians require a higher L:S ratio for confirmation of fetal pulmonary maturity in pregnancies complicated by isoimmunization or diabetes mellitus.
A threshold value for prediction of lung maturity should be calculated in individual centers by correlation with clinical outcome, because the variation within and between laboratories can be considerable. Empirically, the risk of respiratory distress syndrome (RDS) is exceedingly low when the L:S ratio is greater than 2.0.
B. PHOSPHATIDYLGLYCEROL
Phosphatidylglycerol (PG) is a minor constituent of surfactant. It begins to increase appreciably in amniotic fluid several weeks after the rise in lecithin. Its presence is more indicative of fetal lung maturity as PG enhances the spread of phospholipids on the alveoli; thus, its presence indicates a more advanced state of fetal lung development and function.
PG determination is not generally affected by blood, meconium, or other contaminants; its ability to predict pulmonary maturity is the same whether or not contam-ination is present. This is an advantage for assessing fetal lung maturity status since these substances are commonly found in amniotic fluid.
PG testing is performed by thin-layer chromatography (as for the L:S measurement), so it may be determined alone or in conjunction with L:S testing. It can be reported qualitatively as positive or negative, where positive represents an exceedingly low risk of RDS, or in a quantitative fashion, in which a value ≥ 0.3 is associated with a minimal rate of respiratory distress.
C. FOAM STABILITY INDEX
The foam stability index (FSI) is a rapid predictor of fetal lung maturity and is based upon the ability of surfactant to generate stable foam in the presence of ethanol. Ethanol is added to a sample of amniotic fluid to eliminate the effects of nonsurfactant factors on foam formation. The mixture is shaken and will demonstrate generation of a stable ring of foam if surfactant is present in the amniotic fluid. The FSI is calculated by utilizing serial dilutions of ethanol to quantitate the amount of surfactant present.

Amniotic fluid samples should not be collected in silicone tubes when this test is planned, as the silicone will produce “false foam.” The discriminating value indicative of lung maturity is usually set at ≥ 47. A positive result virtually excludes the risk of RDS; however, a negative test often occurs in the presence of mature lungs. The presence of blood or meconium interferes with results of the FSI.

D. FLUORESCENCE POLARIZATION
The fluorescence polarization test uses polarized light to quantitate the competitive binding of a probe to both albumin and surfactant in amniotic fluid; thus, it is a true direct measurement of surfactant concentration. It reflects the ratio of surfactant to albumin and is measured by an automatic analyzer, such as the TDx-FLM. An elevated ratio has been correlated with the presence of fetal lung maturity; the threshold for maturity is 55 mg of surfactant per gram of albumin.
Evaluation of the accuracy of TDx measurements has also been studied, specifically in diabetic patients. Despite initial evidence that higher cutoffs were required for diabetics, it is currently believed that the same cutoff for lung maturity can be used for both nondiabetic and diabetic patients.
The accuracy of this test compares favorably with the well-established L:S and PG tests. Blood and meconium contamination interfere with interpretation, although the degree or direction of the interference is unclear. There is insufficient evidence regarding the accuracy of this test for determination of fetal lung maturity in vaginally-collected specimens.
A disadvantage to the TDx-FLM method is the large quantification scale. Values greater than 55 are regarded as mature; however, values of 35–55 are considered borderline. In addition, there is controversy as to whether gestational age should be used in interpreting the TDx for determining the likelihood of RDS. In one report, higher threshold values were needed at earlier gestational ages to determine lung maturity and lower thresholds were required at later gestational ages.
Intrapartum Fetal Surveillance
Assessment of the fetus in labor is a challenging task. Certain techniques that were useful in the antepartum period are no longer accurate, and certain new techniques have become available. With the presence of contractions, fetal heart rate monitoring is no longer a nonstress test. Fetal heart rate assessment is still the initial test of choice. Continuous fetal monitoring and intermittent auscultation have been extensively reviewed, and the evidence does not support one over the other for routine obstetric care. Several reports suggest that continuous monitoring results in higher operative delivery rates without an associated neonatal benefit. For the present, the controversy over routine FHR monitoring remains, but the clinical practice is nearly universal for continuous electronic monitoring of the FHR in hospitals and many birthing centers.
In the intrapartum period, access to the fetus allows for further evaluation in the face of a nonreassuring FHR tracing. Direct measurement of the physiologic status of the fetus is possible after adequate cervical dilation and rupture of the membranes.

A. ANCILLARY TESTS

1. Fetal scalp blood sampling
Capillary blood collected from the fetal scalp typically has a pH lower than arterial blood. A pH of 7.20 was initially believed to be the critical value to identify serious fetal stress and an increase in the incidence of low Apgar scores. However, there is much debate over the accuracy of scalp pH in predicting fetal distress with subsequent neurologic sequelae. Continuous scalp pH during labor was highly successful in defining abnormal FHR patterns associated with acidosis, although the advanced technical skill and expense prohibited widespread use. In fact, despite the correlation with FHR, fetal scalp pH is no longer used in many institutions. The only proven benefits reported for scalp pH testing were demonstration of adverse neurologic outcome with pH < 7.1, and fewer cesarean sections for fetal distress.
2. Fetal lactate levels
Collected in the same fashion as scalp pH, lactate levels demonstrated a higher predictive value than pH as markers of neurologic disability.
3. Fetal pulse oximetry
This has been studied over the past 10 years. Controversy exists over its potential clinical value. There is debate about its accuracy in correlating with acidemia. Studies have demonstrated no benefit in relation to FHR patterns, or in detecting neurologically-compromised fetuses. A recent report demonstrating a reduction in the rate of cesarean section for a diagnosis of distress, without an actual decrease in the incidence of cesareans compared with the control group, raised questions about the usefulness of the test, since it was hoped that it could reduce the cesarean section rate in a manner similar to scalp pH and lactate assays. Clearly, more studies need to be initiated to demonstrate a clear benefit to this test.

B. FETAL HEART RATE PATTERNS

1. Reassuring fetal heart rate patterns
Slight deviations from the normal baseline of 120–160 bpm and some periodic changes are innocuous in the continuum of the fetal heart rate pattern. Early decelerations and bradycardia of 100–119 bpm are believed to be vagally mediated due to fetal head compression, and are not associated with fetal acidosis or poor neonatal outcome. Certain cardiac arrhythmias also pose no threat to the fetus while the fetal heart rate pattern deviates from what is considered “normal.” In fact, the majority of fetal arrhythmias are benign and spontaneously convert to normal sinus rhythm by 24 hours postpartum. Persistent tachyarrythmias are well tolerated, but may proceed to fetal hydrops if present for many hours to days. Persistent bradyarrhythmias are often associated with fetal heart disease, but are seldom associated with hypoxia or acidosis in fetal life or labor. Accelerations and variable decelerations of variable shape and timing are indicative of a normal autonomic nervous system.
2. Nonreassuring fetal heart rate patterns
This category is of more concern to the clinician, and while there is still evidence that the fetus is not acidotic, continuation or worsening of the clinical situation may result in fetal distress. Late deceleration is a smooth fall in the fetal heart rate beginning after the contraction has started, and ending after the contraction has ended. They are associated with a fall in fetal pH and a potential for perinatal morbidity and mortality. Another nonreassuring pattern is the sinusoidal heart rate. It is best defined as a pattern of regular variability resembling a sine wave with a fixed period of 3–5 cycles per minute and an amplitude of 5–40 bpm. The mechanism for the sinusoidal pattern is believed to be a response to moderate fetal hypoxemia, including secondary to fetal anemia. It was previously thought to carry a high perinatal mortality. However, follow-up with serial scalp pH has been successfully performed with no adverse outcome. The significance of sinusoidal heart rate patterns depends on the clinical setting. Variable decelerations may be divided into categories, with the deciding characteristic being the onset and the timing of the return to baseline. If a variable deceleration, no matter how deep, does not have a late component, then the pattern is benign and at most is mild cord compression not associated with acidosis or low Apgar scores. When there is a late recovery, the fetal pH falls progressively during the period of deceleration.
3. Fetal distress patterns
Fetal distress should be defined operationally as a pathological condition of the fetus that is likely to cause fetal or neonatal death or damage to the newborn if left uncorrected for a period of greater than 1 hour. It is often, but not always, associated with fetal acidemia and hypoxemia. These metabolic changes are highly correlated with a decompensated fetal homeostasis, but not necessarily with all nonreassuring .
FHR patterns. There are numerous causes and multiple factors associated with fetal distress; however, only a few fetal heart rate patterns are associated with true fetal distress, including:
a. Undulating baseline
Alternating tachycardia and bradycardia with wide swings, often with reduced variability in between.
b. Severe bradycardia
Fetal heart rate below 100 bpm for a prolonged period of time of at least 10 minutes.
c. Tachycardia with diminished variability unrelated to drugs
d. Tachycardia associated with additional nonreassuring periodic patterns such as late decelerations or variable decelerations with late recovery
With careful interpretation, FHR patterns can be a useful screening test for fetal acidemia and hypoxemia. The monitoring and interpretation of the fetal heart rate is ideally used as a screening tool. The presence of a reassuring FHR pattern is just that, reassuring that there is no fetal acidemia at that time. The absence of a reassuring tracing is not necessarily problematic, and ancillary testing can be performed to eliminate false positives. However, it must be remembered that a given segment of FHR monitoring is a single point in time. Pregnancy and labor are ongoing dynamic states. Maternal and fetal conditions and the processes of gestation, especially labor, are stresses which challenge fetal homeostasis. Fetal stress may be manifested in the FHR pattern, while the fetus remains compensated. The clinician must discriminate between stress and distress, using interpretation and ancillary testing. All monitoring techniques are to be ultimately used as supplements to clinical judgment, to obtain the best outcome of pregnancy.

Abdominal Incisions and Sutures in Gynecologic Surgery

Abdominal Incisions and Sutures in Gynecologic Surgery

Location and type :

-Abdominal incisions for gynecologic surgery requires consideration of several factors.

-These factors include the disease process, patient’s weight, operative exposure, simplicity, and speed of the procedure. -The most important factor is adequate exposure to the operative field.

-Complications during surgery can occur due to inadequate exposure, which often is due to the unwillingness of the surgeon to extend the incision. Incision location is particularly important when the patient has a gynecologic malignancy. These patients may need a colostomy, urinary diversion, or extraperitoneal lymph node dissection to satisfactorily treat their disease.

Anatomy :
A thorough understanding of abdominal wall anatomy is essential for choosing and making the proper surgical incision. The musculature of the abdominal wall is composed of 2 groups of muscles. One group, the flat muscles, consists of the external oblique, internal oblique, and the transversus abdominis. The second group is composed of 2 muscles that run vertically, the rectus abdominis and the pyramidalis.
The external oblique muscle is the largest and most superficial of the flat muscles of the abdominal wall. Arising from the lower 8 ribs, the external oblique courses transversely to insert upon the iliac crests. The aponeurosis is a strong tendinous sheath that ends medially in the linea alba. The internal oblique muscle arises from the upper surface of the inguinal ligament, the iliac crest, and the thoracolumbar fascia. This muscle courses at a right angle to the fibers of the external oblique muscle. The aponeurosis of the internal oblique splits at the edge of the rectus muscle to envelope the rectus. The anterior layer blends with the aponeurosis of the external oblique. Posterior to the rectus muscle, this aponeurosis blends with the aponeurosis of the transversus abdominis to form a portion of the posterior rectus sheath.
The innermost of the flat muscles is the transversus abdominis. This muscle arises from the inguinal ligament, the iliac crest, the thoracolumbar fascia, and the lower costal cartilages. Coursing transversely to the midline, the upper three fourths of the transversus aponeurosis lies behind the rectus muscle. The lower one fourth of the aponeurosis passes in front of the rectus muscle. The aponeurosis of each flat muscle joins medial to the rectus muscle to form the linea alba.
Originating from the pubic crest, the rectus muscle runs vertically to insert into the xiphoid process and the fifth, sixth, and seventh costal cartilages. The muscle fibers contain 3 fibrous insertions known as the linea transversae. The rectus is surrounded by the rectus sheath, which consists of the aponeuroses of the oblique muscles and the transversus abdominis. A small, vestigial, triangular-shaped muscle, the pyramidalis, arises from the symphysis and inserts upon the linea alba. This muscle marks the midline and assists in the identification of the medial borders of the rectus muscle.

Two important surgical landmarks are formed by the aponeuroses of the muscles of the abdominal wall. The linea alba is in the midline between the 2 rectus muscles. Formed by the fusion of the aponeuroses of the external oblique, internal oblique, and transversus abdominis, identifying this structure during a midline incision is important. A second surgical landmark is the arcuate line that is found below the rectus muscle, approximately halfway between the umbilicus and the symphysis pubis. Above the arcuate line, the aponeuroses of the internal oblique and transversus abdominis fuse to form the posterior rectus sheath. Below the arcuate line, the posterior rectus sheath is absent. This anatomic finding occurs as the aponeuroses of the oblique muscles and the transversus pass in front of the rectus muscle.

Blood supply
The primary blood supply to the abdominal wall is from the inferior and superior epigastric arteries, the deep circumflex arteries, and the musculophrenic arteries. The inferior epigastric artery originates from the external iliac artery and courses posterior to the lateral one third of the rectus muscle. Another branch of the external iliac is the deep circumflex artery, which courses cephalad lateral to the inferior epigastric artery. The superior epigastric artery is the terminal branch of the internal thoracic artery. This artery has multiple branches leading to the rectus muscle and has an anastomosis with the inferior epigastric artery. The internal thoracic artery is the source of the musculophrenic artery, which has an anastomosis with the deep circumflex artery. A larger network of vascular anastomoses exists in the abdominal wall and provides an excellent blood supply to all areas of the abdominal wall.
Nerve supply

Innervation of the abdominal wall is by the thoracoabdominal nerves, the ilioinguinal nerves, and the iliohypogastric nerves. The thoracoabdominal nerves travel caudad between the transversus abdominis and the internal oblique. These nerves innervate the flat muscles of the abdominal wall and the rectus muscle. Innervating the lower abdominal wall are the iliohypogastric nerves and the ilioinguinal nerves. Both of these nerves arise primarily from the first lumbar nerve root. Damage to these nerves results in sensory changes in the mons pubis and the labia majora.

Types of abdominal incisions :
Vertical incision
Several types of vertical abdominal incisions have been used in gynecologic surgery, including midline, paramedian, and wide paramedian incisions. A midline incision is almost exclusively the type of vertical incision used in gynecologic oncology surgery. The midline incision is the easiest and most versatile vertical incision for performing gynecologic cancer surgery. This incision allows quick entry into the abdominal cavity with little blood loss, and it easily can be extended in length to accommodate the operative findings. The disadvantages of this incision include an increase risk of wound dehiscence and hernia formation (compared to a transverse incision).
For a midline incision, the skin and subcutaneous fat is incised down to the level of the fascia. The scalpel or electrocautery can be used to incise this tissue. Some surgeons believe the infection rate is higher with the use of electrocautery, but randomized control trials comparing these 2 techniques are lacking. Using either instrument, the principle is to make long smooth strokes through the subcutaneous fat to the fascia. Do not dissect the subcutaneous fat from the fascia because this creates unnecessary dead space. Next, the fascia is incised and the rectus muscles separated vertically in the midline. The midline may not be evident in patients with previous abdominal surgery. Identifying where the rectus muscles diverge around the umbilicus or locating the pyramidalis muscles assists in identifying the midline. Once the rectus muscles are divided, the peritoneum is grasped between 2 hemostats, opened with a scalpel, and extended the length of the incision.
If the operative findings necessitate extending the incision above the umbilicus, avoid cutting through the umbilicus. Postoperative wound infections may be increased due to bacterial colonization of the umbilicus. Extension of the incision should pass to the left of the umbilicus to avoid cutting through the ligamentum teres.
Closure of the midline incision has evolved over the last 2 decades. Layered closure using interrupted sutures previously was the choice of many surgeons. Today, many surgeons prefer to close the abdominal wall using a continuous running suture. The use of a continuous suture to close the fascia is faster, with dehiscence rates comparable to interrupted closures. Two basic techniques are used to close the abdomen with continuous suture, the single-layer mass closure and the internal mass closure. The single-layer mass closure involves using a heavy monofilament delayed-absorbable or permanent suture. Fascial closure involves penetrating the fascia 1.5 cm from the edge with the suture. The suture also should include the underlying muscle and peritoneum.
Some surgeons close the wound using the internal mass closure technique advocated by Smead-Jones. This is a far-far, near-near suturing technique. The anterior fascia is included in the near-near bite. The initial stitch is similar to the single-layer mass closure. The second bite only includes the anterior rectus fascia, approximately 0.5 cm from the fascial edge. Either technique requires starting from each end of the incision. Securing the suture with 5 knots at each end is sufficient. In thin patients, burying the knot is helpful. Some surgeons place a small hemoclip above each knot to prevent unraveling.
Transverse incision
Several useful transverse abdominal incisions are available to the surgeon performing gynecologic cancer surgery. Historically, the obstetrician-gynecologist has preferred this type of incision. Reported advantages include better cosmetic results, less pain, and low incidence of hernia formation. Gynecologic oncologists have embraced certain types of transverse incisions for specific gynecologic cancer operations. However, several disadvantages to the transverse incision exist. These incisions limit exploration of the upper abdomen, are associated with greater blood loss, and are more prone to hematoma formation when compared to a midline incision. An increased risk of injury to nerves innervating the area also exists, thus leading to subsequent anesthesia of the overlying skin.
Pfannenstiel incision
The Pfannenstiel incision results in good exposure to the central pelvis but limits exposure to the lateral pelvis and upper abdomen. These factors limit the usefulness of this incision for gynecologic cancer surgery. If the patient is thin and has a gynecoid or platypelloid pelvis, this incision can be used for a radical hysterectomy and pelvic lymph node dissection.
The incision usually is made 1-2 fingerbreadths above the pubic crest. Use of a marking pen is helpful to keep the incision symmetric. An incision length of 10-14 cm is sufficient. Increasing the length of the skin incision usually does not improve exposure due to the rectus muscles. The incision is made through the subcutaneous fat to the fascia. The superficial epigastric vessels often are near the lateral edges of the incision.
The anterior fascia is incised in the midline with a scalpel. Using curved scissors or electrocautery, the fascia is incised in a curvilinear fashion 1-2 cm lateral to the rectus muscle. The upper edge of the fascia is grasped with 2 Kocher clamps on either side of the midline. Using electrocautery, the rectus muscle is dissected free from the fascia. Electrocautery allows coagulation of multiple small vessels that perforate the rectus muscle to the fascia. The rectus muscles are mobilized off the fascia to the level of the umbilicus. Next, the lower fascial edge is grasped with Kocher clamps. Electrocautery is used again to dissect the rectus muscles and the pyramidalis muscle from the fascia. The rectus muscles are separated. The peritoneum is opened and incised vertically to complete a Pfannenstiel incision.

Closure of the Pfannenstiel incision is straightforward. The peritoneum is closed with an absorbable suture. Some surgeons elect not to suture this layer, citing little information clearly indicating a benefit. Regardless of whether the peritoneum is closed, thoroughly irrigate the rectus muscles with water or saline, and cauterize or ligate any bleeding areas. Bleeding from small perforating vessels through the rectus muscle is the most common source of subfascial hematoma. The fascia is approximated with an absorbable suture. Usually, a separate suture is started at each end of the fascial incision, and they incorporate all layers of the anterior rectus sheath. Unless a large area of dead space exists between the fascia and skin, closure of the Scarpa fascia is not needed.

Maylard incision
In an effort to improve surgical exposure to the lateral pelvic sidewall with a transverse incision, Maylard proposed a transverse muscle-splitting incision. This incision usually refers to a subumbilical transverse incision. For gynecologic surgery, the incision is made 3-8 cm superior to the pubis symphysis. The anterior rectus sheath is cut transversely. The inferior epigastric vessels are identified under the lateral edge of each rectus muscle. After ligating these vessels, the rectus muscles are incised transversely with electrocautery. The peritoneum is opened and cut laterally.

To facilitate closure of a Maylard incision, flex the operating table. Close the peritoneum with an absorbable suture. Next, inspect the ties placed on each inferior epigastric vessel, and irrigate with water. Examine the cut edges of the rectus muscles for any bleeding areas. The fascia and underlying rectus muscle can be closed with a monofilament absorbable suture.

Cherney incision
Cherney described a transverse incision that allows excellent surgical exposure to the space of Retzius and the pelvic sidewall. The skin and fascia are cut in a manner similar to a Maylard incision. The rectus muscles are separated to the pubis symphysis and separated from the pyramidalis muscles. A plane is developed between the fibrous tendons of the rectus muscle and the underlying transversalis fascia. Using electrocautery, the rectus tendons are cut from the pubic bone. The rectus muscles are retracted and the peritoneum opened.
Closing a Cherney incision begins with closure of the peritoneum. Attach the cut ends of the rectus muscle to the distal end of the anterior rectus sheath with interrupted nonabsorbable sutures. Fixing the rectus muscle to the pubis symphysis can result in osteomyelitis. Next, the fascia is closed with 2, running, continuous, delayed-absorbable sutures.

Several types of incisions facilitate extraperitoneal paraaortic lymph node dissection. An upper abdominal transverse incision, which is a high Maylard incision, is made approximately 2 cm above the umbilicus. The incision is extended laterally and caudad to the anterior superior iliac spines. The fascia and rectus muscles are incised transversely, usually requiring ligation of the inferior and superior epigastric vessels. Next, the transversus abdominis muscle is cut, exposing the peritoneum. Using blunt dissection, the peritoneal sac is dissected caudad to cephalad to expose the psoas muscle, the aorta, and the common iliac vessels. Often, a drain needs to be placed in the area of the lymph node dissection.

Modified Gibson incision

Some gynecologic oncologists perform an extraperitoneal lymph node dissection using a modification of the Gibson incision. This incision can be made on each side of the midline, but often, the skin is cut only on the left. The incision is started 3 cm superior and parallel to the inguinal ligament. Extension is made vertically 3 cm medial to the anterior superior iliac spine to the level of the umbilicus. The fascia is cut and the peritoneum bluntly dissected, as described above. The round ligament and the inferior epigastric vessels are ligated to facilitate surgical exposure. Care is needed when exposing the lymph nodes using only a left-sided incision. Too much traction on the peritoneum can result in avulsion of the inferior mesenteric vessels.

Incisions in obese patients :
Surgery in patients who are obese and morbidly obese represents a challenge for every surgeon. Wound complication rates uniformly are higher in patients who are obese, regardless of the type of incision. Obtaining adequate surgical exposure requires patience, understanding of changes in anatomical landmarks, and proper surgical equipment.
The abdominal wall landmarks are distorted in patients who are obese, particularly if a large panniculus is present. The umbilicus is located caudad to its normal position. If a vertical incision is needed, first pull the panniculus downward. A periumbilical incision is made and the fascia incised to the symphysis. Care is needed not to buttonhole the skin under the panniculus. Use of a ring retractor, such as the Bookwalter, optimizes surgical exposure.

The site of a transverse incision in patients who are obese should never be made under the fold of the panniculus because wound infection rates are invariably higher. Make a transverse incision close to the umbilicus. However, in some patients, this incision may be too far from the pelvic organs. The surgeon may find the distance to the pelvic structures exceeds the length of the surgical instruments and the retractors. In this scenario, perform a panniculectomy. A panniculectomy allows the fascial incision to be within several centimeters of the pubis symphysis, allowing easier access to the pelvic organs. Place large suction drains above the fascial closure with a panniculectomy, and keep them in place until the drainage is less than 25 cc in 24 hours.

Sutures :
A suture is any strand of material used to approximate tissue or ligate vessels. Various materials have been used for sutures throughout history. Materials incorporated into sutures include horsehair, linen, silk, animal intestines, and wire. The ideal suture has yet to be created. Qualities important in a suture include uniform tensile strength, knot security, nonallergenic properties, and high tensile-strength retention during wound healing. Choosing the correct suture requires knowledge of the healing characteristics of tissues and understanding of the physical properties of various suture materials.
Absorbable sutures
Today, sutures are classified based on their absorptive properties. Absorbable sutures are prepared from the collagen of animals or synthetic polymers. These sutures are removed from the body by enzymatic action or hydrolysis. The ability of the suture to retain tensile strength dictates where the suture should be used in wound closure. Do not confuse the loss of tensile strength with the rate of absorption. Sutures can maintain adequate tensile strength until wound healing is complete, followed by rapid absorption. Conversely, some sutures may lose tensile strength rapidly and undergo slow absorption. All absorbable sutures eventually completely dissolve.

Absorbable sutures have some limitations. For patients with fever, infection, or poor nutritional status, absorption of absorbable suture may accelerate and lead to premature diminution of tensile strength. If these sutures are exposed to significant moisture, such as ascites, absorption rates are accelerated.

The common absorbable sutures used in gynecologic surgery are as follows:

Surgical gut
Plain
Chromic
Fast absorbing
Polyglactin 910 (Vicryl)
Uncoated
Coated
Polyglycolic acid (Dexon)
Poliglecaprone (Monocryl)
Polydioxanone (PDS)
Polyglyconate (Maxon)
Poly (L-lactide/glycolide)(Panacryl)
Surgical gut sutures can be used to reapproximate mucosal surfaces or peritoneal edges, but they lack the tensile strength for use in fascial closure.
Synthetic absorbable sutures are used extensively in most gynecologic surgeries. Polyglactin (Vicryl) and polyglycolic acid (Dexon) often are used during a hysterectomy. These 2 sutures retain enough tensile strength to be used in fascial closure. Poliglecaprone 25 (Monocryl) is a newer absorbable suture that retains 50% of its tensile strength after 2 weeks.
Two monofilament absorbable sutures useful in fascial closure are polyglyconate (Maxon) and polydioxanone (PDS). Both of these sutures invoke little tissue reaction and maintain 50% of their tensile strength at 4 weeks. These sutures often are used with midline incision closures, especially in patients with cancer or other major comorbidities. Poly (L-lactide/glycolide) (Panacryl) is a new absorbable suture that is useful in patients with delayed wound healing. At 40 weeks, these sutures retain 50% of their tensile strength.
Nonabsorbable sutures
Enzymatic activity or hydrolysis does not digest nonabsorbable sutures. These sutures are composed of multiple filaments of metal, synthetic fibers, and organic fibers fashioned into a strand by twisting, braiding, or spinning. The commonly used nonabsorbable sutures are as follows:
Natural
Silk
Cotton
Stainless-steel wire (Flexon)
Nylon (Dermalon, Surgilon)
Polypropylene (Prolene, Novofil)
Braided synthetics (Dacron, Tevdek)
Use of nonabsorbable sutures, polypropylene (Prolene) or polybutester (Novofil), is recommended to close the fascia in the presence of infection. Tie these sutures with at least 6 throws.

Conditions Associated With CPP With Available Level of Evidence

1. Gynecological causes of chronic pelvic pain

Ovaries

-Ovarian retention syndrome (residual ovary
syndrome) (A)
-Ovarian remnant syndrome (A)
-Adnexal tumors and cysts (C)
-Accessory and supernumerary ovaries (C)
-Tubo-ovarian abscess
-Ovarian ovulation pain (C)

Fallopian tubes

PID (A)
Chlamydial endometritis or salpingitis
Endosalpingiosis (C)
Endometriosis (A)
Subacute salpingo-oophoritis
Tuberculous salpingitis (A)
Hydrosalpinx
Peritubal adhesions (B)

Uterus

Leiomyoma (B)
Adenomyosis (C)
Intrauterine contraceptive device (C)
Endocervical and endometrial polyps (C)
Atypical dysmenorrhea (C)
Chronic endometritis (C)
Congenital anomalies (Cervical stenosis) (C)

Other gynecological

Extrauterine adhesions (A)
Endometriosis (A)
Pelvic varicosities and pelvic congestion
syndrome (A)
Gynecological malignancies (A)
Post-operative peritoneal cysts (B)
Benign cystic mesothelioma (B)
Pelvic support defects (pelvic ﬂoor relaxation genital
prolapse) (C)
Vulvodynia
Pelvic ﬂoor dysfunction (C)
Chronic pelvic infection (A)

2. Gastrointestinal

Chronic constipation (A)
Irritable bowel syndrome (A)
Inﬂammatory bowel disease (A)
Diverticular disease(C)
Diverticulitis (C)
Carcinoma of the colon (A)
Colitis (C)
Chronic intermittent bowel obstruction (C)
Lactose intolerance (C)
Gastric/duodenal ulcer
Proctalgia fugax (C)

3. GU-Urology

Bladder neoplasm (A)
Urolithiasis (A)
Urethral diverticula (C)
Chronic urethral syndrome (A)
Uninhibited bladder contractions (C)
(detrusor-sphincter dyssynergia) (B)
Urethral carbuncle (C)
Detrusor overactivity(B)
Interstitial cystitis (A)
Chronic urethral syndrome (A)
Chronic and recurrent urinary tract
infections (C)
Recurrent cystitis (C)
Recurrent urethritis (C)
Urethral diverticulum (B)
Radiation cystitis (A)

4. Neurological
Neuralgia/cutaneous nerve entrapment (C)
(surgical scar in the lower part of the
abdomen; usually iliohypogastric
ilioinguinal, genitofemoral, and lateral
femoral cutaneous nerves) (A)
Mononeuropathy and nerve entrapment (A)
Neurologic dysfunction (B)
Sympathetic dystrophy (C)

5. Medical

Heavy metal poisoning (lead, mercury)
Uremia
Porphyria (B)
Shingles (herpes zoster infection) (B)
Abdominal epilepsy (C)
Abdominal migraine (C)
Familial Mediterranean fever (C)

6. Musculoskeletal
Fibromyalgia (A)
Abdominal wall myofascial pain (trigger
points, fasciitis) (A)
Cutaneous nerve entrapment in abdominal
surgical scar (A)
Compression fracture of lumbar vertebrae
Muscular strains and sprains (C)
Chronic fatigue syndrome (A)
Pelvic ﬂoor myalgia (levator ani spasm,
Piriformis syndrome) (A)
Pelvic ﬂoor pain syndrome (A)
Coccydynia (A)
Chronic coccygeal pain (A)
Myofascial pain (trigger points, spasms)
Rectus tendon strain (A)
Low back pain (B)
Poor or faulty posture (A)
Hernias (e.g., obturator, sciatic, inguinal,
femoral, perineal, spigelian, umbilical, and
incisional) (C)
Mechanical low back pain (A)
Scoliosis/lordosis/kyphosis
Disk problems (A)
Degenerative joint disease (C)
Spondylosis (C)
Osteitis pubis (C)
Rectus abdominis tendon pain (C)
Neoplasia of sacral nerve or spinal cord (B)
Spinal injury (C)

7. Psychiatric
Depression (A)
Personality disorders (C)
Bipolar personality disorder (C)
Psychological disorders including
somatization (A)
Eating disorder
School avoidance (C)
Sleep disorders (B)

8. Others
Sexual and/or physical abuse, abuse (A)
(physical or sexual, prior or current)
psychosexual dysfunction
Substance abuse (A)
Psychosocial stress (marital discord, work stress) (A)

Level A: consistent good scientiﬁc evidence of causal relationship to CPP.
Level B: limited or inconsistent scientiﬁc evidence of causal relationship to CPP.
Level C: causal relationship to CPP based on expert opinions. (Adapted from ACOG)

Breast Awareness and Breast Diseases . Dr. Alaa Mosbah ,MD OBS and GYN

WHAT IS BREAST AWARENESS

-Breast awareness is a part of general body awareness. It is a process of getting to know your own breasts and becoming familiar with their appearance.

- Learning how your breasts feel at different times will help you to know what is normal for you. You can become familiar with your breast tissue by looking and feeling – in any way that is best for you(e.g. in the bath, shower, when dressing). Being breast aware and knowing what is normal for you will help you to be aware of any changes from normal .

THE NORMAL BREAST

Before the menopause

normal breasts feel different at different times of the month. The milk-producing tissue in the breast becomes active in the days before a period starts. In some women, the breast at this time feel tender and lumpy, especially near the armpits.

After a hysterectomy

the breasts usually show the same monthly differences until the time when your periods would have stopped.

After the menopause

activity in the milk-producing tissue stops. Normal breasts feel soft, less firm and not lumpy.

CHANGES TO LOOK OUT FOR

-Appearance

. Any change in the outline or shape of the breast, especially those caused by arm movements, or by lifting the breasts. Any puckering or dimpling of the skin.

-Feelings

. Discomfort or pain in one breast that is different from normal, particularly if new and persistent.

- Lumps. Any lumps, thickening or bumpy areas in one breast or armpit which seem to be different from the same part of the other breast and armpit. This is very important if new.

-Nipple change

. Nipple discharge, new for you and not milky

. Bleeding or moist reddish areas which don’t heal easily

. Any change in nipple position – pulled in or pointing differently

. A nipple rash on or around the nipple.

WHAT TO DO IF YOU FIND A CHANGE

-There can be many reasons for changes in the breast. Most of them are harmless but all of them need to be checked as there is a small chance they could be the first sign of cancer. If you are aware of any change in your breast from what is normal for you, tell your doctor without delay.
-Remember, you are not wasting anyone’s time. If there is a cancer present, the sooner it is reported, the more simple treatment is likely to be. This offers greater prospects of benefit in terms of quality of life.
-Breast cancer is very rare in women under the age of 40. The likelihood of developing breast cancer increases with age.

BREAST SCREENING

-If you are aged 50 and over it is strongly recommended that you take advantage of the National Health Service Breast Screening Programme which offers three-yearly mammography.
-This is an X-ray procedure which can detect breast changes at a very early stage. for more information about the Breast Screening Programme ask your doctor.
- Routine X-ray breast screening is not available for women under 50 as it has not been shown to be of benefit. If you have any cause for concern about your breasts tell your doctor.
BREAST AWARENESS
FIVE-POINT CODE

Know what is normal for you

• Look and feel

• Know what changes to look for

• Report any changes without delay

• Attend for breast screening if aged 50 or over

Anatomy of female breast:

-The breast lies between the 2nd and 6th ribs on the vertical axis and between the sternal edge and the midaxillary line on the horizontal axis. Breast tissue also projects into the lower axilla as the axillary tail.

-The breast is made up of the secretory glandular tissue and surrounding adipose tissue. The glandular tissue comprises between 15 and 20 lobes with varying numbers of ducts and lobules surrounded by connective tissue. Each lobe connects to a lactiferous duct, several of which converge to form a lactiferous sinus or milk chamber. These sinuses empty into the nipple where there are a number of duct openings. The nipple is surrounded by a pigmented area, the areola, which is lubricated by secretions from the sebaceous glands. Beneath the tissues of the breast lie the muscles of the chest wall and between the two is a layer of connective tissue known as the fascia.

Blood supply: the internal mammary artery, the axillary artery and the intercostal arteries

Lymph drainage:

is from superficial to deep

- The major drainage is then to the axilla and internal mammary chain.

- To lesser extent, lymph also drains by intercostal routes to nodes adjacent to vertebrae. The axillary nodes found below the level of the axillary vein are divided into 3 groups in relation to pectoralis minor muscle.

Level I lymph nodes: lateral to the lateral border of pectoralis minor .

Level II lymph nodes: behind pectoralis minor .

Level III lymph nodes: medial to the medial border of pectoralis minor Physiology of lactation: Lactation is inhibited during pregnancy by the action of estrogen on the hypoth. & pituitary. Inhibition is removed immediately after delivery ® PRL ® initiate lactation which is then maintained by suckling (nerve reflex via hypothalamus), PRL, GH & ACTH and ¯ Gonadotropins. Delivery of milk from the nipple is by contraction of myoepithelial cells around acini by the action of oxytocin secreted by neurohypophysis.

Breast diseases:

I- Bening breast problems:

A) Congenital abnormalities and development :

1- Supernumerary or accessory nipple

2- Supernumerary or accessory breast

3- Excessive breast enlargement

4- Hypoplasia or aplasia

5- Inversion of the nipples.

B) Breast pain (Mastalgia):

-Due to breast causes:

.Cyclic: premenstrual and relieved with the onset of menstruation. It may be unilateral or bilateral and radiate to axilla.
. Non cyclic: various causes as hormonal fluctuation, firm adenomas, duct ectasia, macrocysts and soreness in the pectoralis muscle from exertion or trauma

-Due to non – breast causes :

e.g. angioma, cholelithiasis, costochondritis, …..etc
Treatment:
1) Bromocriptine : Reduce PRL ® relief cyclic mastalgia, Dose: 2.5 mg twice daily
2) Danazol: Relief symptoms and reduce nodularity, Dose : 200 mg
3) Tamoxifen : Reduce breast pain, Dose 20 mg
4) Gammalenolenic acid ( GLA ): Dose 6- 8 capsules / day
5) Non medical measures: A well fitting brassier worn 24 hours / day, ¯ caffeine intake , regular exercise, phytoestrogen )

C)Nipple discharge:

Common, not all nipple discharge is pathologic

Types:

i) Physiologic:
. not associated with underlying breast disease, Bilateral, from multiple ducts and serous in character.
.Causes: exogenous estrogen and nipple stimulation Require no treatment.

ii) Galactorrhea: see hyperprolactinemia

iii) Pathologic discharge:
.Localized to a single duct and spontaneous. May be greenish , gray , serosangunous , serous or bloody
.Causes :Benign breast disease
.Investigation: mammography, biopsy from a mass

D) Duct ectasia:
. in women over 35 years.
.Presentation:
-Nipple discharge (from several ducts – cheesy in nature or with a palpable mass which may be hard or doughy)
-Nipple retraction
- Duct dilate & shorten (inspissated material )
Treatment: - formation - Antibiotics to avoid abscess Total duct excision with histological examination

E) Fibrocystic diseases:
-most common benign breast complaint in 10% of women < 21 years and more common in the premenopausal period. It produces bilateral pain and tenderness 7-10 days before menstruation
-General lines of Treatment: - Regular examination - OCS - NSI - Diuretic therapy - Avoid coffee, tea, chocolate and caffeinated soda
-Types:
.Fibroadenoma (breast mouse ):
It is the most common mass lesion < 25 years Palpable breast mass in upper outer quadrant, well circumscribed, firm, mobile discrete and may be multiple or bilateral Treatment: conservative or excision and biopsy. Needs careful follow up
.Breast cyst:
Common in perimenopausal age. Small discrete lump (fluctuant) Treatment: aspiration Galactocele: - During or after pregnancy or breast feeding - Contain breast milk Treatment: Aspiration (diagnostic and therapeutic)

II- Bening neoplastic lump:

1- Duct papilloma: rarely common. Treatment: may need excision of the duct

2- Lipoma: Treatment: excise only if suspicion of malignancy or if troublesome

III- Breast cancer:

What is the incidence of breast cancer?

-In 2006 there were 45,508 new registrations of breast cancer in women in the UK, and 314 in men.

-One in 9 women will develop breast cancer at some time in their life.

-The estimated risk of developing it for each of the other age groups has been calculated as:

Up to age 25, 1 in 15,000

Up to age 30, 1 in 1,900

Up to age 40, 1 in 200

Up to age 50, 1 in 50

Up to age 60, 1 in 23

Up to age 70, 1 in 15

Up to age 80, 1 in 11

Up to age 85, 1 in 10

-Age factors The incidence of breast cancer increases with age.
-Eighty per cent of cases occur in post-menopausal women. The risk of developing breast cancer continues to rise as women get older.
-Breast cancer is extremely rare in women in their teens or early twenties and uncommon in women under 35. After this age the risk begins to increase, rising sharply after the menopause.

-Breast cancer is the most common cancer in women worldwide.
-It accounts for about 25 per cent of all female malignancies and the proportion is higher in women in western, developed countries.

Incidence

-has been rising in many parts of the world, including the USA, Canada, Europe, the Nordic countries, Singapore and Japan.

-Over one million new cases occur each year worldwide.

-How many people die from breast cancer in the UK? 11,990 women and 92 men died from breast cancer in 2007

Survival

-The five-year survival rate for patients diagnosed 2001-2006 in England (period estimates) was 82 per cent.
-The stage at which a woman has breast cancer diagnosed greatly influences her survival chances.
-In general, the earlier the detection, the greater the chance of survival.

What are the causes of breast cancer?

- It is not clear exactly what causes breast cancer but it is thought that there are many risk factors, some already well established and some still being investigated.

-Age is strongly linked with breast cancer. The risk of breast cancer increases with age.

-Two breast cancer genes have been identified; BRCA1 and BRCA2. These genes have been found in approximately 85 per cent of families with four or more cases of breast cancer diagnosed under the age of 60. However, only about five per cent of all breast cancer cases (fewer than 2000 per year) are thought to be caused by breast cancer genes.

-There is a higher risk of breast cancer in the south of England and in Wales than in the north of the UK. The risk of breast cancer also appears to be higher in women from more affluent backgrounds. There is an increase in risk when people move from low risk to high risk countries. For example, Japanese immigrants to the USA increase their risk of breast cancer and acquire incidence rates similar to the American population within two generations. This suggests that risk may be linked to environmental and behavioural factors.

Risk Factors

Known risk factors for breast cancer are:

-being female

-increasing age

-previous history of breast cancer

-having proven benign breast disease in the past

-not breastfeeding long term

-current use of hormone replacement therapy or oral contraceptives

-having a family history of breast cancer

-having no children or few childrenhaving children at late ages (especially over 30)

-early puberty

-having a later menopause

-obesity (for post-menopausal women only)

-high consumption of alcohol

Breast cancer during or shortly after pregnancy :
- more worse than women with the same age and not pregnant which may be due to delay of the diagnosis and immunosuppressive effect of pregnancy.
-So, breast examination should be a part of prenatal examination, and mammography can be done if suspicion with the use of shield.
-Cancer breast diagnosed during pregnancy should be staged and treated in the same manner as in non pregnant.
Abnormal signs and symptoms:

1.Change in breast size, puckering , dimpling or retraction, thickening of skin or lump

2.Nipple discharge, retracted nipple, change in nipple position, Scaling around nipples

3.Pain or tenderness and redness

4.Sore on breast that does not heal

Screening of breast cancer:
-all women should be screened at the age 50 – 64 every 3 years with single oblique view mammography.
--In women with family history, mammography is routine before 50 years

Diagnosis:

1- Careful breast examination

2- Conventional mammography

3- Ultrasound

4- Fine needle aspiration or biopsy

5- Excision biopsy: the only definitive diagnosis Breast Cancer Screening : Two tests are commonly used by health care providers to screen for breast cancer:

-Mammogram
.A mammogram is an x-ray of the breast. This test may find tumors that are too small to feel. A mammogram may also find ductal carcinoma in situ, which may become invasive cancer in some women. .
.The ability of a mammogram to find breast cancer may depend on the size of the tumor, the density of the breast tissue, and the skill of the radiologist.
.Mammograms are less likely to find breast tumors in women younger than 50 years than in older women. This may be because younger women have denser breast tissue that appears white on a mammogram. A tumor also appears white on a mammogram, which makes it hard to find.

-Clinical breast exam (CBE)
A clinical breast exam is an exam of the breast by a doctor or other health professional. The doctor will carefully feel the breasts and under the arms for lumps or anything else that seems unusual.

Management:

·Breast surgery:

conservative lumpectomy with axillary dissection in combination with radiotherapy is as effective as mastectomy for local control in most cases.

· Tamoxifen:

prolongs disease – free interval.

· Chemotherapy:

has survival benefit in premenopausal women.

· Endocrine therapy:

-Aromatase inhibitors, LHRH analogues and ovarian ablation.
-Steroid receptor is best predictive

Follow up:

life long follow up is required

Subsequent contraception, pregnancy and HRT:
·Contraception: OCs is not recommended. Other alternative should be considered
· Pregnancy: subsequent pregnancy have no adverse effect. Patients are advised to wait 2 years before becoming pregnant.
·HRT: Tamoxifen is recommended if menopausal symptoms are severe.

EXAMPLE SCREENING ASSESSMENT PROTOCOL:

1. INTRODUCTION

1.1 Screening assessment is carried out to confirm (or otherwise) the presence of any significant breast abnormality identified at screening.
1.2 This is achieved by following the principles of triple assessment (imaging, clinical examination and needle biopsy) carried out by the screening assessment team.
1.3 All cases recalled are reviewed by the team immediately before the start of the assessment clinic to inform the team about what assessment procedures are required.
1.4 The reason for recall and the required diagnostic procedures should be discussed with each woman.
1.5 Whenever possible all of the necessary diagnostic procedures should be carried out at the first assessment clinic visit.
1.6 The imaging and clinical opinion should be recorded according to the following categories: • usually a 1–5 score (‘normal’ through to ‘definitely malignant’) • local categories vary but should be consistent and agreed by all the members of the clinical breast team.
Examples of categories are:
1. normal/definitely benign 1 normal
2. probably benign 2 benign
3. indeterminate 3 indeterminate
4. probably malignant 4 probably malignant
5. definitely malignant 5 definitely malignant.
1.7 All significant radiological and clinical abnormalities require needle biopsy.
1.8 Needle biopsy is reported according to the categories defined in Guidelines for Non-operative Diagnostic Procedures and Reporting in Breast Cancer Screening (NHSBSP Publication No 50, June 2001).
1.9 All women attending for assessment must be told of their assessment outcome and receive clear details of any further appointments and when and how they will receive their results before leaving the assessment clinic.
1.10 The results of all assessment investigations must be reviewed and a clear management decision made at the weekly multidisciplinary screening meeting held before the patient is seen again for results.
1.11 There should be only three possible outcomes after complete assessment: • no significant abnormality – return to normal screening • significant benign abnormality requiring surgery (eg Phyllodes tumour) • diagnosis of cancer.
1.12 All women attending for assessment and their GP must receive written confirmation of the outcome.
2. IMAGING
2.1 The majority of women recalled for assessment have a mammographic abnormality. Further mammography and/or ultrasound are performed to determine if this is significant.
2.2 The imaging assessment performed will depend on the type of lesion being assessed. See Clinical Guidelines for Breast Cancer Screening Assessment (NHSBSP Publication No 49, 2nd edition, January 2005). 2.3 The imaging opinion (based on both mammography and ultrasound findings) is classified according to the categories 1–5 defined in paragraph 1.6 above.
2.4 Abnormalities not visible on ultrasound should be managed on the basis of their mammographic and clinical features. Clinical abnormalities with no imaging correlate must be managed on the basis of their clinical features. Needle biopsy should be on the basis of the most suspicious imaging or clinical feature.
2.5 For suspicious microcalcifications, core biopsy must be performed and specimen radiography used to confirm satisfactory sampling.
2.6 Cysts should be aspirated if there is any doubt about their nature.
3. CLINICAL ASSESSMENT
3.1 Clinical examination is mandatory for all women recalled for assessment of significant symptoms and/or signs whether or not the screening mammogram is normal.
3.2 Clinical assessment must also be performed when a significant radiological lesion is confirmed and before any needle biopsy.
3.3 Clinical examination may not be necessary for women who are shown to be entirely normal after further imaging.
3.4 When a significant clinical abnormality has been found, the team should be certain that there is radiological clinical concordance.

Mammographic/ultrasound abnormality and clinical abnormality.
If there is a discordance in the site of the abnormality, review of mammogram and ultrasound of the clinical abnormality should be performed together by the radiologist and the clinician. Clinical needle biopsy in addition to imaging needle biopsy must be performed if the site of the significant clinical abnormality does not correspond with the imaging abnormality. Mammogram normal with clinical abnormality. Ultrasound of the abnormal clinical site may be useful particularly in the dense breast (eg cysts found on ultrasound may be aspirated). When imaging is normal in the presence of clinical abnormality, then a freehand needle biopsy of the abnormality should be considered.
4. TRIPLE ASSESSMENT
4.1 The clinical and radiological opinions are used independently to decide on the significance of any abnormality.
4.2 The clinical and radiological opinions are formally documented before any further intervention (eg needle biopsy).
4.3 The most suspicious opinion prevails. If the radiological opinion is that the abnormality is ‘probably malignant’ and the surgical opinion is that there is ‘no significant abnormality’ then the woman is managed on the basis of the radiological opinion. Similarly, if there is a clinically suspicious lesion and imaging is normal, the patient is managed on the basis of the clinical opinion.
4.4 The clinical opinion may not downgrade the imaging opinion or vice versa.
4.5 The need for needle biopsy is decided by the prevailing opinion: • needle biopsy is not required for lesions classified as normal or definitely benign • needle biopsy is mandatory for all abnormalities classified as probably benign or more suspicious.
4.6 All needle biopsy results must be discussed in the context of the imaging and clinical finding at the multidisciplinary screening assessment meetings. Needle biopsy result not consistent with the clinical/imaging opinion must be discussed fully and a clear management decision reached at this meeting to ensure that either false negative or false positive results are managed appropriately.
5. IMAGING/CLINICAL CATEGORIES
The categories listed may vary from unit to unit. For example, it is common for the ‘normal’ and ‘definitely benign’ categories to be listed separately.
Normal/definitely benign

5.1 The patient can be reassured and discharged (eg normal mammography, ultrasound and clinical examination). Needle biopsy is not required.
Probably benign

5.2 This category applies when there is normal imaging but with clinical abnormality that is almost certainly benign (eg a prominent area of ‘thickening’ that is normal on imaging).
5.3 Although the risk of malignancy is low (less than 5%), needle biopsy is required for all cases classified as ‘probably benign’.
5.4 A result of ‘inadequate/benign’ on fine needle aspiration (FNA) or ‘normal breast tissue/benign breast tissue’ on core biopsy is acceptable. 5.5 With any of these outcomes the woman can be advised that further procedures or surgical biopsy are not required.
5.6 With any other diagnosis (C3–C5; B3–B5), a repeat core biopsy should be performed before surgical biopsy.
5.7 For C5 or B5 results, definitive therapeutic surgery, especially mastectomy, should only take place after careful re-evaluation in light of the low clinical and imaging suspicions of malignancy. Indeterminate/probably benign
5.8 This classification applies to abnormalities that have benign features on either imaging or clinical assessment, but a definitive cytological or histological diagnosis of a benign lesion is required to avoid excision biopsy (eg a clinically smooth and mobile 1 cm lump with benign imaging features that is most likely to represent a fibroadenoma).
5.9 The risk of malignancy is 5 to 50%. FNA must show a good yield of unequivocally benign epithelial cells and core biopsy must provide a benign diagnosis consistent with the clinical and imaging findings – ‘normal breast tissue’ (B1) should not be accepted as representative when the patient has a discrete lump with a provisional diagnosis of a fibroadenoma.
5.10 An ‘inadequate’ FNA (C1) or ‘normal’ core biopsy (B1) is not acceptable and, along with an ‘equivocal’ (C3 or B3) and ‘suspicious’ (C4 or B4) result, requires repeat sampling. If FNA cytology was performed initially, the repeat procedure is usually performed as a core biopsy.
5.11 With a ‘malignant’ result (C5 or B5), definitive surgical excision can be planned. Repeat needle biopsy may be considered necessary before performing mastectomy. Probably malignant
5.12 This classification is used when there is a strong clinical or imaging suspicion of malignancy (50 to 90%) but the features are not sufficiently characteristic to classify as definitely malignant (eg an area of architectural distortion).
5.13 Therapeutic surgery can be performed if needle biopsy shows unequivocal evidence of malignancy (C5 or B5).
5.14 For all other needle biopsy results (C1–C4 or B1–B4), a diagnostic open surgical biopsy should be performed if repeat sampling fails to provide a definitive diagnosis of cancer (C5 or B5). If FNA cytology was performed initially, the repeat procedure is usually performed as a core biopsy.
Malignant

5.15 This classification is given when there are unequivocal clinical or imaging signs of malignancy.
5.16 Needle biopsy is performed to obtain a definitive non-operative diagnosis and allow for counselling for therapeutic surgery.
5.17 For all other needle biopsy results (C1–C4 or B1–B4), a diagnostic open surgical biopsy should be performed if repeat sampling fails to provide a definitive diagnosis of cancer (C5 or B5). If FNA cytology was performed initially, the repeat procedure is usually performed as a core biopsy.
6. SHORT-TERM RECALL
6.1 Properly applied, the assessment procedure should result in a definitive result from which either the woman is discharged back to normal screening or referred for treatment.
6.2 Short-term recall should only be recommended when needle biopsy is not possible and the risk of malignancy is low, or when the woman refuses to undergo either needle biopsy or diagnostic surgery.
6.3 This outcome should only be decided after attendance at an assessment clinic and/or full discussion at the multidisciplinary screening assessment meeting.
6.4 Women placed on short-term recall should have the reasons fully explained in the presence of the nurse specialist.
6.5 The short-term recall attendance should be to the assessment clinic. 6.6 No woman should be placed on short-term recall more than once in each screening round.
7. MANAGING THE NEEDLE BIOPSY RESULT
7.1 A pathological result of C1/B1 is acceptable when needle biopsy has been performed for a category 2 (probably benign) imaging/clinical opinion.
7.2 A result of C2/B2 is required for all category 3 (indeterminate) lesions before the woman can be discharged back to normal screening. 7.3 For microcalcifications, specimen radiography of the core specimens should be performed and must demonstrate representative microcalcification. In the absence of representative calcification, the presence of histological calcification should not be accepted as indicating that a representative sample has been obtained. In these circumstances, the core biopsy should be repeated or open surgical biopsy performed. 7.4 A diagnosis of atypical ductal hyperplasia (ADH) on needle biopsy necessitates surgical excision to definitively exclude ductal carcinoma in situ (DCIS) in the adjacent tissue.
7.5 A diagnosis of radial scar or complex sclerosing lesion with no evidence of epithelial atypia can be managed by offering the patient a choice of either wider sampling with vacuum assisted mammotomy or diagnostic surgical excision. The presence of epithelial atypia in association with a radial scar or complex sclerosing lesion necessitates surgical excision to definitively exclude associated malignant change.
7.6 A C5 or B5 result is required before definitive therapeutic surgery can take place. 7.7 C3, C4, B3 and B4 results should result in a repeat needle biopsy (preferably core biopsy or vacuum assisted mammotomy) or open surgical biopsy to obtain a definitive result.

Role of Caudal, Pudendal and Paracervical blocks

Role of Caudal, Pudendal and Paracervical blocks :

CAUDAL BLOCK

Caudal epidurals in labour have become less popular because better perineal analgesia can be achieved by the use of epidural infusions and primigravidae are more likely to receive an epidural block. Also, there have been recent concerns about the risks of inadvertent intravenous and fetal injection. A modified caudal epidural technique can provide rapid onset perineal anaesthesia without cardiovascular disturbance and with relatively little loss of expulsive power. If used for perineal anaesthesia only, caudal block is a useful, safe technique for experienced anaesthetists provided that the volume of local anaesthetic is limited to a maximum of 10 mls, injected slowly (with multiple aspirations). It should be noted that this dose is less than half that which is required to achieve full labour analgesia. The block should be inserted before the head is on the perineum . Since it has been shown that pencil point spinal needles have a low incidence of headache (0 to 0.66% with 27G and 25G whitecare needles) spinal anaesthesia is often more appropriate than lumbar or caudal epidural anaesthesia for rotational forceps, manual removal of placenta and, at times, low forceps delivery. INDICATIONS1. Unrelieved perineal pain.2. Premature urge to push.3. Low forceps delivery.4. When lumbar epidural analgesia is contraindicated. INCIDENCEIn most Australian hospitals, caudal blocks are being used less frequently in labour as the number of spinals has increased. The major indications for caudals are perineal pain, labour pain, forceps delivery, and manual removal of placenta. Less commonly, caudals can provide anaesthesia for artificial rupture of the membranes, suturing of episiotomies and repair of vaginal lacerations.

CAUDAL ANALGESIA IN COMBINATION WITH OTHER MAJOR REGIONAL BLOCKS

At the Royal Women's Hospital, of those women who had a caudal, at least 62% also had a lumbar epidural. The lumbar epidural was either already in situ or was inserted at the same time as the caudal. It has been shown that for the lumbar epidural route, increasing the volume of anaesthetic is more likely to secure good sacral blockade than injection in the sitting position. However, in our experience sacral blockade can occasionally only be achieved with a caudal or spinal block. COMPLICATIONSl. Vascular tap and intravascular injection of local anaesthetic .2. Failed block (8%) - the sacral hiatus is absent in 5% of adults. 3. Subarachnoid injection - the dural sac reaches S2 .4. Infection.5. Fetal injection . Modified caudal block is a safe technique with a limited specific place in modern obstetric anaesthesia.

PARACERVICAL BLOCK

The risk of complications, particularly fetal bradycardia, generally make this technique an unsuitable form of anaesthesia for obstetric patients. However, if used, it should be avoided in the presence of fetal distress or uteroplacental insufficiency and the fetal heart rate should be monitored continuously during and after insertion of the paracervical block . COMPLICATIONS1. Vaginal trauma.2. Systemic local anaesthetic toxicity due to excessive dosage or intravenous injection .3. Parametrial haematoma.4. Sacral plexus trauma.5. Infection and deep abscess formation.6. Fetal scalp injection of local anaesthetic.7. Fetal bradycardia probably caused by decreased uteroplacental perfusion.8. Needle stick injury.

PUDENDAL NERVE BLOCK

Pudendal nerve block provides anaesthesia for spontaneous vaginal delivery or low forceps delivery. The pudendal nerve (S2 - S4) is the major sensory innervation of the lower vagina, vulva and perineum and provides motor fibres to the external anal sphincter and the perineal muscles. Pudendal nerve block was first reported for vaginal delivery in 1916 . It is inadequate for rotational forceps delivery and manual removal of the placenta. Either a transvaginal or transperineal approach can be used. The bilateral success rate has been reported as 50% after the transvaginal approach and 25% after the transperineal approach. INDICATIONS.1. Low forceps delivery.2. Vaginal and perineal pain when lumbar or caudal epidural or spinal analgesia is unavailable, contraindicated or declined. COMPLICATIONS 1. Vaginal trauma.2. Systemic local anaesthetic toxicity due to excessive dosage or intravenous injection.3. Vaginal or ischio-rectal haematoma. 4. Infection and deep abscess formation.5. Fetal trauma or direct local anaesthetic injection.6. Needle stick injury.

Caudal Analgesia

Although the caudal route was the first widely used approach to the epidural space for continuous block in labour (Hingson and Edwards, 1942), and remained in frequent use in a few centres until the late 1970's (McCaul), its present role is very limited. Apart from providing good analgesia for low instrumental deliveries and perineal repair, the use of caudal block is usually restricted to a very few enthusiasts and to those cases in which a lumbar epidural is anatomically impossible or contraindicated by local infection . (However, local sepsis may also preclude the use of caudal block) . The patient should be prepared according to the guidelines shown in . Following the provision of secure venous access and preloading with crystalloid, the patient is either turned into the left lateral position with both knees flexed and forward tilt of the upper hip, or (occasionally) the knee-elbow position according to patient or operator preference. The skin of the lumbosacral area is prepared with a bactericidal solution and sterile drapes are applied. A bleb of local anaesthetic is raised in the skin overlying the sacral hiatus, between the sacral cornua, at a site deep to the proximal extremity of the natal cleft. A 21- gauge needle may then used to infiltrate the deeper tissues, but this is not essential. A variety of needles and cannulae may be used for the block itself, including a:1. 7.6 cm 19-gauge caudal needle,2. disposable 3.8 cm 19-23g hypodermic needle,3. 20-24-g intravenous catheter for a "single-shot" technique, or4. Tuohy needle (17 or 18g) and catheter for a continuous technique. Whichever needle is used, it is gently inserted at an angle of 70-80degrees to the skin and slowly advanced until the bony resistance of the sacrum is detected . The needle is withdrawn slightly, the entry angle reduced by about half, and then reinserted until the resistance of the sacrococcygeal ligament is felt at a depth of 1.5-3.8 cm. The ligament is then penetrated and the needle or catheter inserted to a depth of 2-3 cm, bearing in mind that the dural sac terminates at the S2 level, and that dural puncture should be avoided . Test aspiration for blood or CSF is performed. If the test is negative, this is followed by the injection of a 3ml test dose of local anaesthetic, with a hand positioned over the sacrum to detect any tissue swelling, resulting from malposition of the needle or catheter either subperiosteally or along the dorsal surface of the sacrum. Following a negative test dose and in the absence of pain on injection, the definitive dose may be injected slowly in small, repeated increments . If CSF is aspirated or if blood continues to be aspirated after repositioning of the needle or catheter the block should be abandoned. Single-shot needles or cannulae are withdrawn following injection. Catheters are affixed to their connectors and filters and strapped in position. Lignocaine is preferred to bupivacaine in view of the potential for large doses of bupivacaine to produce cardiovascular collapse and intractable ventricular dysrhythmias . should intravascular injection occur into one of the abundant epidural veins . The dose and concentration of lignocaine depends on the indication for the block. A recommended dose for outlet forceps delivery would be 15 to 20mls of 1.5% lignocaine with adrenaline. For perineal analgesia, a dose of 10 to 15mls of 1.0% lignocaine with adrenaline would suffice .

Pudendal Nerve Block

During the second stage of labour, pain largely results from distension of the lower vagina, vulva and perineum. In addition, the musculature of the anterior compartment of the pelvis must be negotiated by the descending presenting part. These structures obtain most of their sensory and motor innervation from the second to fourth sacral nerve roots via the pudendal nerve. Pudendal nerve blocks are of value in providing analgesia for the second stage when contraindications to neuraxial blockade exist and for the provision of pelvic floor relaxation when forceps delivery is required. They may also be used to provide anaesthesia of the perineum in order to create or repair an episiotomy. Pudendal nerve blocks have been utilized in the past as an alternative to epidurals in assisted twin and breech deliveries . Increasing evidence supporting the safety of epidurals in these situations has contributed to a diminished use of pudendal nerve blocks . The anatomy of the pudendal nerve should be considered when performing the block. The block is performed with the patient in the lithotomy position. Two approaches have been described: transvaginal and transcutaneous or perineal. The basis of both approaches is to block the nerve before it gives off its terminal branches. Its most reliable landmarks are exploited - the ischial spine in the transvaginal, and the ischial tuberosity, in the perineal approach. Transvaginal approach:In the transvaginal approach, the ischial spine can be palpated either transvaginally or per rectum. It is important to use a needle with a guide in order to limit the depth of submucosal penetration ("Huber" security point ). When a left sided block is performed, the ischial spine is palpated with the index finger of the left hand, the syringe is held in the right hand and the needle is guided between the index and middle fingers of the left hand towards the ischial spine. The sacrospinous ligament lies 1 cm medial and posterior to the spine. The needle is passed through the ligament for a distance of 1 cm until a loss of resistance is appreciated. The tip now lies in the area of the pudendal nerve. The pudendal vessels are closely associated. After aspiration, 10 mls of local anaesthetic solution are injected. The block is repeated on the other side. Perineal approach:The perineal approach is considered valuable when the engaged head makes vaginal palpation difficult. The ischial tuberosity is located by palpation . The needle is introduced slightly medial to this point, for a distance of 2.5 cm. The nerve is usually encountered without eliciting paraesthesia. Up to 8 mls of solution is infiltrated at this point. The needle is then withdrawn and directed into the deep and superficial tissue of the vulva along its anterior margin in order to block the the ilioinguinal and genitofemoral component . The block is repeated on the other side. The limitations of this block include:- Failure to provide adequate analgesia. It has been reported that up to half of all bilateral pudendal blocks are ineffective on one or both sides . A pudendal nerve block will not abolish sensation to the anterior part of the perineum because this region is supplied by branches of the ilioinguinal and genitofemoral nerves. Subcutaneous infiltration anteriorly along the vulva is therefore described as a component of this technique. Failure to wait sufficient time is a commonly cited reason for failure of a pudendal block. Pudendal nerve blocks do not abolish the pain of uterine contraction and cervical dilation which is transmitted via sympathetic nerve fibres derived from spinal levels T10 - L2 . It does not cause relaxation of the uterus. - Intravascular injection with subsequent local anaesthetic toxicity is a risk imposed by the close proximity of the pudendal vessels . - Fetal complications are uncommon. Exposure of the fetus to a high plasma level of local anaesthetic is a possibility that should be considered. Delivery usually occurs within a short period of time which may not allow for clearance of local anaesthetic from fetus via the placenta. 1% lignocaine is the most commonly used agent. Peak concentrations occur within 10 - 20 minutes. The maternal plasma concentrations which occur after this block are much lower than after either epidural or paracervical blocks. This block has been reported to prolong the second stage of labour as a result of loss of the bearing-down reflex. The addition of adrenaline may further prolong the second stage of labour .

Paracervical Block

Paracervical blockade may be used as a means of reducing pain during the first stage of labour. Pain associated with uterine contraction and cervical stretching and dilatation is transmitted from these structures on visceral afferents which accompany sympathetic fibres. These pass sequentially through the uterine, cervical, inferior hypogastric and superior hypogastric plexuses to the lumbar and lower thoracic sympathetic chains. During early labour, the bulk of these enter the spinal cord at the T11 - T12 segments. As pain becomes more severe, the two adjacent segments, T10 and L1 become involved . The block is performed bilaterally with the patient in the lithotomy position. The proximity of the broad ligaments just deep to the lateral fornices of the vagina is exploited with the aim of interrupting pain transmission at the level of the uterine and pelvic plexuses . An 18.5 cm needle with a security tip (Iowa trumpet, Kobak) is used to limit the injection to within 1.5 - 2 cm of the epithelium. The needle is connected to a 20 ml Luer-Lok syringe. Measures to avoid intravascular injection are vital. After careful aspiration non-adrenaline containing local anaesthetic solution is infiltrated. The specific injection sites have been variously described: 3 and 9 oclock; 4 and 8 oclock; or alternatively all sites . The distribution of radio-opaque dyes observed in X-ray studies is similar . An interval of 15 minutes should be observed between injections during which time signs of maternal and fetal toxicity should be excluded. Paracervical blockade can be used to provide analgesia during the first stage of labour when contraindications of epidural analgesia are present. The optimal time for institution of this block is the accelerated phase of the first stage when the severity of pain increases. The presenting part is typically engaged. The cervix is thin and effaced and has a tendency to be drawn up during uterine contractions . Paracervical blockade does not provide analgesia of the perineum during the second stage during which pain is transmitted primarily via the pudendal nerves to the S2 - 4 spinal cord segments . The technique has several limitations. The failure rate is reported to be as high as 18% . The proximity of uterine blood vessels in the vaginal fornices creates maternal and fetal risks. Fetal bradycardia occurs in 10-50% of cases . This is attributed to asphyxia which is believed to result from transient uterine artery vasospasm due to high concentrations of local anaesthetic in the paracervical region. The technique has a duration of action limited to 90 minutes with plain lignocaine. The use of adrenaline or bupivacaine in an attempt to increase the duration of the block should be avoided as both increase the incidence of fetal bradycardia .

Preparation and Monitoring for Regional Blockade

Adequate preparation of the obstetric patient is vital in order to minimise the complications of regional anaesthesia. This will be achieved by obtaining a history, performing a physical examination, and, if indicated, performing preliminary investigations. Of particular relevance in the history is the presence of cardiac disease, pre-eclampsia, coagulopathy, or any maternal condition which may present a relative contraindication to neuraxial blockade. The presence of any of these conditions may preclude the selection of the spinal and/or epidural route for analgesia or anaesthesia. Informed consent must be obtained. Fasting and acid-aspiration prophylaxis should be observed in patients undergoing caesarean section. The presence of a skilled assistant is essential. During the performance of the block and subsequently, careful attention to positioning will increase the likelihood of a succesful block. Large bore intravenous access and adequate prehydration will be required to minimise hypotension. Either reusable or disposable Tuohy needles and syringes may be used. Tuohy needles feature blunt cutting tips whose ends are curved. This assists in identification of the epidural space without dural puncture. The commonly used sizes for obstetric analgesia are 16g and 18g. These needles accept 18 and 20 gauge catheters respectively. Epidural catheters are typically made from PVC. The tip features either three helically-arranged lateral injection holes, or a single end hole . Three holed designs have been criticised for their potential to result in a malpositioned catheter such that individual holes may lie between different meningeal layers or in an epidural vein. This can result in a multi-compartment block or inadvertent intravascular injection of local anaesthetic . Single ended catheters have a higher incidence of false negative aspiration for blood and missed segments. Appropriate monitoring should be instituted. This should include monitoring of:1. The maternal circulation (pulse rate and blood pressure).Hypotension may complicate neuraxial blockade despite careful attention to prehydration and avoidance of aortocaval compression. A baseline pulse rate and blood pressure must be obtained before initiating the block. Blood pressure should be measured at intervals of not more than 5 minutes during establishment of the block and thereafter hourly whilst the block is being maintained. During caesarean section the blood pressure should be measured at 5 minute intervals. A qualified person should be responsible for hemodynamic monitoring. Appropriate management of hypotension should be instituted early. 2. The level of the block.The level of the block should be monitored 3. The fetus.

Methods of monitoring fetal wellbeing include:

a. Auscultation of heart rate with pinnards or doppler.b. Graphical display of the cardiotocograph .c. The use of scalp electrodes.d. Measurement of fetal scalp pH. The fetus should be monitored whenever an epidural is being utilised. In uncomplicated labours this is usually accomplished with a cardiotocograph. Scalp electrodes are used when the cardiotocograph fails to generate a reliable trace or when fetal distress is present. This requires a sufficiently dilated cervix. Scalp pH is used to gain more information on fetal wellbeing when other signs of fetal distress are present. 4. Bladder function.Painless bladder distension as the result of neural blockade may contribute to postpartum stress incontinence. This has been observed to occur in association with concentrations of bupivacaine of 0.5% .The bladder should be emptied intermittently. Prevention of local anaesthetic toxicity How do we Prevent the Development of Local Anaesthetic Toxicity? The use of local anesthetics (LA) may be accompanied by systemic and Iocalised adverse reactions, usually secondary to:1. accidental intravascular injection,2. inadvertent intrathecal injection, or3. administration of an excessive dose. Intravenous injection of 20-25 mg of bupivacaine has been reported to induce fatal cardiovascular collapse . Factors which can diminish the incidence of toxic reactions are:1. fractionation of the injected dose, 2. aspiration before injection, 3. selection of less toxic LAs . 4. reduction in the concentration of LA, and 5. test-dosing before injection of the main dose. The diagnosis of inadvertent intravascular placement of an epidural needle or catheter can be made by using either air or a sympathomimetic amine as the 'marker' agent. Unintended intrathecal placement can be diagnosed by the injection of an appropriately small dose of a rapid onset LA. Injection of 1 ml of air into an epidural catheter can be a highly specific and sensitive marker of intravascular catheter Iocalisation, but the safety of the doppler test has yet to be proven and, moreover, a precordial doppler and an extra person have to be available . Epinephrine, the catecholamine currently used in most test-doses, has several disadvantages. This mixed alpha- and beta-adrenergic agent does not consistently produce maternal tachycardia in laboring women. Cyclic maternal heart rate changes, due to painful uterine contractions, occur normally in unanesthetised parturients. The effect of epinephrine superimposed on these physiological changes in heart rate is not always discernible. Moreover, a major adverse effect of systemic epinephrine is its inhibition of uterine blood flow (UBF). This reduction of UBF has been demonstrated in gravid ewes and lasts for 2-5 minutes . Although the chronotropic response in term pregnant women is reduced, a test dose containing 5 mcg of isoproterenol (isoprenaline) might be a safer and more effective alternative .Isoproterenol produces a superior increase in maternal heart rate with minor effects on uterine blood flow in the chronic maternal fetal sheep preparation . In this animal model, incorporation of isoproterenol as a test dose does not produce neurotoxicty . These results suggest that isoproterenol may be safe for use as an epidural test dose in pregnant women. Some contradictory results exist concerning the increased sensitivity, during pregnancy, to the toxicity of local anesthetics. Santos et al. compared the systemic toxicity of ropivacaine and bupivacaine in non-pregnant and pregnant ewes and concluded that..."The systemic toxicity of ropivacaine or bupivacaine is not enhanced by gestation in sheep. This is in contrast to an earlier study in which cardiotoxicity of bupivacaine was enhanced during ovine pregnancy." A major concern in pregnancy is the trans-placental distribution of local anesthetics . Differences in the cord-to-maternal plasma drug concentration ratio essentially reflect trans-placental differences in the extent of plasma binding . When this ratio is high there should be a delay in the equilibration of drug in fetal tissues. Conversely, similar umbilical artery and umbilical vein concentration ratios observed for the various agents argue against large differences in their equilibration rates in the fetus. Thus, the impact, if any, of plasma binding on the risks of fetal toxicity is unclear . The prevention of toxicity of local anesthetics in the mother and the fetus is of utmost importance but, in this field, many questions remain to be answered. Regional techniques compared The use of subarachnoid local anaesthetic agents and narcotics for labour and delivery varies between institutions and individual anaesthetists. While practices may vary, the role of subarachnoid anaesthesia in comparison with other regional techniques can be defined in terms of the relative advantages and disadvantages of this method of anaesthesia. Efficacy and application of blockade:Local anaesthetics may be used intrathecally to accomplish sacral anaesthesia for instrumental vaginal deliveries and for other obstetric procedures. Subarachnoid blockade to a level above T7 may also be employed for cesarean section. Under these circumstances, subarachnoid blockade provides reliable, dense surgical anaesthesia. Epidural anaesthesia is also suitable for both labour and delivery but, sometimes, sacral segments may be difficult to block (with a lumbar epidural) and the blocks may occasionally be patchy or asymmetrical . In comparison to subarachnoid blockade, caudal blockade is only suitable for sacral anaesthesia . Opiates may also be administered by the subarachnoid route and provide good analgesia for labour but not for delivery . Furthermore, intrathecal opiates provide superior analgesia when compared to opiates administered via the epidural route . Side effects such as pruritus may be higher in patients receiving intrathecal opiates. Speed of onset:When compared to epidural or caudal anaesthesia, subarachnoid anaesthesia offers a rapid onset of action which is often of benefit to the patient, anaesthetist and surgeon. Unfortunately, an increased speed of onset of anaesthesia is only purchased at the price of a greater degree of hypotension . Postdural puncture headache:Postdural puncture headache may occur in up to 20% of patients when a 25-gauge spinal needle is used . This miserable complication occurs more frequently in young females and is responsible for the reluctance of many anaesthetists to use this technique in the parturient. Except in cases of inadvertent dural puncture with the needle, this problem is not seen with epidural or caudal anaesthesia. The use of 26-gauge spinal needles has been shown to lower the incidence of postdural puncture headache . The use of 29-gauge needles has been associated with little risk of postdural puncture headache, even in young patients . The low incidence of headache with these small needles increases the acceptability of subarachnoid blockade in obstetric anaesthesia . Titratable level of blockade and continuous infusions:The use of epidural catheters to provide a means by which the level of anaesthesia can titrated, topped up, or continuously infused for labour and delivery has been well established. The routine use of subarachnoid catheters for uncomplicated vaginal delivery has not gained wide acceptance in obstetric anaesthesia for several reasons. It has been stated that the large bore needles usually employed to introduce catheters would be associated with a high incidence of postdural puncture headache but this does not appear to occur in clinical practice . These catheters may increase the risk of infection, although again, there is very little supporting evidence for this concern. In an attempt to address these issues, microcatheters (32-gauge) which can be passed through a standard 25 or 26-gauge spinal needle have been used. Continuous spinal anaesthesia is obtained with negligible risk of local anaesthetic toxicity to the mother and fetus. Significant problems have been reported with these microcatheters and include cauda equina syndrome, kinking, difficulty in threading and catheter fracture. The more recent use of combined spinal epidural techniques allows for continuous and titratable anaesthesia with the advantage of a rapid and dense subarachnoid block. The potential disadvantages of an intrathecal catheter are avoided and, with a small spinal needle, the risk of postdural puncture is minimal . Overall, because of its advantages spinal anaesthesia (especially with the use of smaller spinal needles) continues to challenge the pre-eminent role of epidural anaesthesia in obstetrics.

CHARACTERISTICS OF LOCAL ANESTHETIC TOXICITY

(I) CNS toxicity:a) Excitation Phase: tinnitus, confusion, restlesness, perioral numbness or tingling, metallic taste, lightheadness, sense of dread and impending doom.b) Convulsive Phase: grand-mal clonic-tonic seizurec) Depression Phase: CNS depression with drowsiness and unconsciousness.d) Repiratory depression and apnea. (II) CVS Toxicity:a) Excitation Phase: - hypertension, tachycardia (with convulsions) b) Depression Phase:(i) Negative inotropic effect with decreased blood pressure, cardiac output and stroke volume.(ii) Peripheral vasodilation with further hypotension. c) Cardiovascular Collapse

KEY FEATURES OF BUPIVACAINE TOXICITY

(i) More likely to result in cardiovascular collapse (CV collapse dose / dose for convulsions = 3.7 for bupivacaine and 7.1 for lidocaine). (ii) Ventricular arrhythmias are more likely to accompany cardiac toxicity (use bretylium). (iii) Pregnant women are more sensitive to cardiac toxicity from bupivacaine. (iv) Resuscitation is usually legthy. (v) Toxicity is enhanced by acidosis and hypercarbia. PossibleEffects of Major Regional Blockade on Cardiotocographic Patterns. Uterine Contractions Mechanism Increased Frequency and intensity Analgesia decreases catechol amine leels Decreased Frequency and intensity Decreased blood supply to uterus. ?Inhibition of motor nerve supply to uterus?Direct effect of Local Anaesthetic on smooth muscle Fetal heart rate: beat to beat variability Increase Acute fetal hypoxia due to placental hypoperfusion Decrease Direct effect of local anaesthetic agents.Chronic hypoxia and acidosis from placental hypoperfusion Fetal heart rate:Long term deceleations Early Head compression from increased uterine tone. Late Placental insufficiency worsened by placental hypoperfusion Variable/td> Cord compression aggravated by maternal hypotension and increased intensityof uterine contractions.

RECOMMENDED MAXIMUM DOSES OF LOCAL ANAESTHETICS

-Illustrated in the case of a 60Kg woman Drug Dose Dose/ Kg AMIDES Lidocaine with epi 420 (7mg/kg) Lidocaine plain 300 (5mg/kg) Bupivacaine with epi 180 (3mg/kg) Bupivacaine plain 120 (2mg/kg) Etidocaine 240 (4mg/kg) Mepivacaine 420 (7mg/kg) Prilocaine 720 (12mg/kg) ESTERS Cocaine 180 (3mg/kg) Procaine 840 (14mg/kg) Chloroprocaine 840 (14mg/kg) Tetracaine 180 (3mg/kg)

Screening for Breast Cancer , November 2009

U.S. Preventive Services Task Force (USPSTF)
Rationale
Importance
-Breast cancer is the second-leading cause of cancer death among women in the United States.
-Widespread use of screening, along with treatment advances in recent years, have been credited with significant reductions in breast cancer mortality.
Detection
Mammography, as well as physical examination of the breasts (CBE and BSE), can detect presymptomatic breast cancer. Because of its demonstrated effectiveness in randomized, controlled trials of screening, film mammography is the standard for detecting breast cancer; in 2002, the USPSTF found convincing evidence of its adequate sensitivity and specificity.
Benefits of Detection and Early Intervention
-There is convincing evidence that screening with film mammography reduces breast cancer mortality, with a greater absolute reduction for women aged 50 to 74 years than for women aged 40 to 49 years. The strongest evidence for the greatest benefit is among women aged 60 to 69 years.
-Among women 75 years or older, evidence of benefits of mammography is lacking.
-Adequate evidence suggests that teaching BSE does not reduce breast cancer mortality.
-The evidence for additional effects of CBE beyond mammography on breast cancer mortality is inadequate.
-The evidence for benefits of digital mammography and MRI of the breast, as a substitute for film mammography, is also lacking.
Harms of Detection and Early Intervention
-The harms resulting from screening for breast cancer include psychological harms, unnecessary imaging tests and biopsies in women without cancer, and inconvenience due to false-positive screening results. Furthermore, one must also consider the harms associated with treatment of cancer that would not become clinically apparent during a woman's lifetime (overdiagnosis), as well as the harms of unnecessary earlier treatment of breast cancer that would have become clinically apparent but would not have shortened a woman's life. Radiation exposure (from radiologic tests), although a minor concern, is also a consideration.
-Adequate evidence suggests that the overall harms associated with mammography are moderate for every age group considered, although the main components of the harms shift over time. Although false-positive test results, overdiagnosis, and unnecessary earlier treatment are problems for all age groups, false-positive results are more common for women aged 40 to 49 years, whereas overdiagnosis is a greater concern for women in the older age groups.
-There is adequate evidence that teaching BSE is associated with harms that are at least small. There is inadequate evidence concerning harms of CBE.
USPSTF Assessment
The USPSTF has reached the following conclusions:
-For biennial screening mammography in women aged 40 to 49 years, there is moderate certainty that the net benefit is small. Although the USPSTF recognizes that the benefit of screening seems equivalent for women aged 40 to 49 years and 50 to 59 years, the incidence of breast cancer and the consequences differ. The USPSTF emphasizes the adverse consequences for most women—who will not develop breast cancer—and therefore use the number needed to screen to save 1 life as its metric. By this metric, the USPSTF concludes that there is moderate evidence that the net benefit is small for women aged 40 to 49 years.
-For biennial screening mammography in women aged 50 to 74 years, there is moderate certainty that the net benefit is moderate.
-For screening mammography in women 75 years or older, evidence is lacking and the balance of benefits and harms cannot be determined.
-For the teaching of BSE, there is moderate certainty that the harms outweigh the benefits.
-For CBE as a supplement to mammography, evidence is lacking and the balance of benefits and harms cannot be determined.
-For digital mammography and MRI as a replacement for mammography, the evidence is lacking and the balance of benefits and harms cannot be determined.

Clinical Considerations
Patient Population Under Consideration
This recommendation statement applies to women 40 years or older who are not at increased risk for breast cancer by virtue of a known underlying genetic mutation or a history of chest radiation.
Assessment of Risk
Increasing age is the most important risk factor for breast cancer for most women. Women without known deleterious genetic mutations (such as BRCA1 or BRCA2) may still have other demographic, physical, or historical risk factors for breast cancer, but none conveys a clinically important absolute increased risk for cancer.
Screening Tests
-In recent decades, the early detection of breast cancer has been accomplished by physical examination by a clinician (CBE), by a woman herself (BSE), or by mammography.
-Standardization of mammography practices enacted by the
Mammography Quality Standards Act have led to improved mammography quality.
Screening Intervals
In trials that demonstrated the effectiveness of mammography in decreasing breast cancer mortality, screening was performed every 12 to 33 months. The evidence reviewed by the USPSTF indicates that a large proportion of the benefit of screening mammography is maintained by biennial screening, and changing from annual to biennial screening is likely to reduce the harms of mammography screening by nearly half. At the same time, benefit may be reduced when extending the interval beyond 24 months; therefore the USPSTF recommends biennial screening.
Treatment
-Effective treatments, including radiation, chemotherapy (including hormonal treatment), and surgery, are available for invasive carcinoma.
-Although the standard treatments women receive for ductal carcinoma in situ (DCIS) include surgical approaches as well as radiation and hormonal therapy, considerable debate exists about the optimal treatment strategy for this condition.
Considerations for Practice Regarding I Statements
Clinical Breast Examination
-Potential Preventable Burden. The evidence for CBE, although indirect, suggests that CBE may detect a substantial proportion of cases of cancer if it is the only screening test available. In parts of the world where mammography is infeasible or unavailable (such as India), CBE is being investigated in this way.
-Potential Harms. The potential harms of CBE are thought to be small but include false-positive test results, which lead to anxiety and breast cancer worry, as well as repeated visits and unwarranted imaging and biopsies.
-Costs. The principal cost of CBE is the opportunity cost incurred by clinicians in the patient encounter.
-Current Practice. Surveys suggest that the CBE technique used in the United States currently lacks a standard approach and reporting standards. Clinicians who are committed to spending the time on CBE would benefit their patients by considering the evidence in favor of a structured, standardized examination .
Digital Mammography
-Potential Preventable Burden. Digital mammography detects some cases of cancer not identified by film mammography; film mammography detects some cases of cancer not identified by digital mammography. Overall detection is similar for many women. For women who are younger than 50 years or have dense breast tissue, overall detection is somewhat higher with digital mammography. It is not clear whether this additional detection would lead to reduced mortality from breast cancer.
-Potential Harms. The possibility of false-positive test results is similar for film and digital mammography. It is uncertain whether overdiagnosis occurs more with digital mammography than with film mammography.
-Costs. Digital mammography is more expensive than film mammography.
-Current Practice. Some clinical practices are now switching their mammography equipment from film to digital. This may curtail the availability of film mammography in some areas.
Magnetic Resonance Imaging
-Potential Preventable Burden. Studies of the use of contrast-enhanced MRI for breast cancer screening have been conducted only in very high-risk populations. In these studies, MRI detected more cases of cancer than did mammography. It is unknown whether detecting these additional cases of cancer would lead to reduced breast cancer mortality.
-Potential Harms. Contrast-enhanced MRI requires the injection of contrast material. Studies of MRI screening have shown that MRI yields many more false-positive results than does mammography. Magnetic resonance imaging has the potential to be associated with a greater degree of overdiagnosis than mammography.
-Costs. Magnetic resonance imaging is much more expensive than either film or digital mammography.
Current Practice. Magnetic resonance imaging is not currently used for screening women at average risk for breast cancer.
Screening Mammography in Women 75 Years or Older
-Potential Preventable Burden. No women 75 years or older have been included in the multiple randomized clinical trials of breast cancer screening. Breast cancer is a leading cause of death in older women, which might suggest that the benefits of screening could be important at this age. However, 3 facts suggest that benefits from screening would probably be smaller for this age group than for women aged 60 to 69 years and probably decrease with increasing age: 1) the benefits of screening occur only several years after the actual screening test, whereas the percentage of women who survive long enough to benefit decreases with age; 2) a higher percentage of the type of breast cancer detected in this age group is the more easily treated estrogen receptor-positive type; and 3) women of this age are at much greater risk for dying of other conditions that would not be affected by breast cancer screening.
-Potential Harms. Screening detects not only cancer that could lead to a woman's death but also cancer that will not shorten a woman's life. Women cannot benefit from—but can be harmed by—the discovery and treatment of this second type of cancer, which includes both cancer that might some day become clinically apparent and cancer that never will. Detection of cancer that would never have become clinically apparent is called overdiagnosis, and it is usually followed by overtreatment. Because of a shortened life span among women 75 years or older, the probability of overdiagnosis and unnecessary earlier treatment increases dramatically after about age 70 or 75 years. Overdiagnosis and unnecessary earlier treatment are important potential harms from screening women in this age group.
-Current Practice. Studies show that many women 75 years or older are currently being screened.
Useful Resources
Other USPSTF recommendations on screening for genetic susceptibility for breast cancer and chemoprevention of breast cancer are available on the Agency for Healthcare Research and Quality Web site(http://www.preventiveservices.ahrq.gov).
Other Considerations
Implementation
The Task Force on Community Preventive Services has reviewed the evidence on methods to increase breast cancer screening, including reminder systems and other interventions .
Explanation of Change in Recommendation
The 2002 USPSTF issued a B recommendation for screening mammography for women 40 years or older. However, it went on to say:
The precise age at which the benefits from screening mammography justify the potential harms is a subjective judgment and should take into account patient preferences. Clinicians should inform women about the potential benefits (reduced chance of dying from breast cancer), potential harms (for example, false-positive results, unnecessary biopsies), and limitations of the test that apply to women their age. Clinicians should tell women that the balance of benefits and potential harms of mammography improves with increasing age for women between the ages of 40 and 70 .
The updated USPSTF recommendation endorses this approach to deciding when to start screening. However, the current USPSTF is now further informed by a new systematic review ,which incorporates a new randomized, controlled trial that estimates the "number needed to invite for screening to extend one woman's life" as 1904 for women aged 40 to 49 years and 1339 for women aged 50 to 59 years. Although the relative risk reduction is nearly identical (15% and 14%) for these 2 age groups, the risk for breast cancer increases steeply with age starting at age 40 years. Thus, the absolute risk reduction from screening (as shown by the number needed to invite to screen) is greater for women aged 50 to 59 years than for those aged 40 to 49 years.
The current USPSTF statement is also informed by the Cancer Intervention and Surveillance Modeling Network (CISNET) modeling studies that accompany this recommendation. The Task Force considered both "mortality" and "life-years gained" outcomes. In this case, given that the age groups (40 to 49 years and 50 to 59 years) are adjacent, the Task Force elected to emphasize the mortality outcomes from the modeling studies. Of the 8 screening strategies found most efficient, 6 start at age 50 years rather than age 40 years. The frontier curves for the mortality outcome show only small gains but larger numbers of mammograms required when screening is started at age 40 years versus age 50 years.
In conclusion, the USPSTF reasoned that the additional benefit gained by starting screening at age 40 years rather than at age 50 years is small, and that moderate harms from screening remain at any age. This leads to the C recommendation. The USPSTF notes that a "C" grade is a recommendation against routine screening of women aged 40 to 49 years. The Task Force encourages individualized, informed decision making about when to start mammography screening

Summary of Recommendation and Evidence :
-The USPSTF recommends biennial screening mammography for women aged 50 to 74 years. Grade: B recommendation.
-The decision to start regular, biennial screening mammography before the age of 50 years should be an individual one and take patient context into account, including the patient's values regarding specific benefits and harms. Grade: C recommendation.
-The USPSTF concludes that the current evidence is insufficient to assess the additional benefits and harms of screening mammography in women 75 years or older. Grade: I Statement.
-The USPSTF recommends against teaching breast self-examination (BSE).Grade: D recommendation.
-The USPSTF concludes that the current evidence is insufficient to assess the additional benefits and harms of clinical breast examination (CBE) beyond screening mammography in women 40 years or older. Grade: I Statement.
-The USPSTF concludes that the current evidence is insufficient to assess the additional benefits and harms of either digital mammography or magnetic resonance imaging (MRI) instead of film mammography as screening modalities for breast cancer. Grade: I Statement.

Shoulder dystocia . Dr. Alaa Mosbah , M.D OBS & GYN

Definition:

-Shoulder dystocia is the inability to deliver the fetal shoulders after delivery of the head, without the aid of specific maneuvers .

-Prolonged head-to-body expulsion time , > 60 seconds .

Incidence:

Reported to occur in 0.2-2% of births

Risk factors:

A) Antepartum risk factors:

1- Fetal macrosomia 2- Maternal obesity

3- Diabetes mellitus 4- Post-term pregnancy

5- Male gender 6- Advanced maternal age

7- Excessive maternal weight gain

8- Prior shoulder dystocia

9- Prior macrosomic infant

10- Contracted pelvis and platypelloid pelvis

B) Intrapartum risk factors:

1- 1st stage of labour abnormalities as protraction disorders and arrest disorders

2- Prolonged 2nd stage of labour

3- Oxytocin administration

4- Mid-forceps and mid-vacuum extraction

Remember :

-Many cases of shoulder dystocia occur with no readily identified risk factors!!!!

-Shoulder dystocia with neonatal injury occurs in about 0.4 to 3 vaginal births per 1000

- Medical liability payouts for a baby with subsequent disability average around $500,000

Causes:

1. Large shoulders which may be due to :

- Maternal obesity.

- Diabetic mothers.

- Post-term pregnancy.

- Anencephaly.

2. Failure of shoulder rotation.

3. Contracted and platypelloid pelvis.

Degrees:

1- Severe (bilateral): both posterior & the anterior shoulders do not cross the pelvic brim.

2- Mild (unilateral): the posterior shoulder enters the pelvic cavity, while the anterior shoulder hooked behind the S. pubis

Diagnosis :

-Shoulder dystocia should be anticipated in women with risk factors

-Various sonographic parameters to evaluate a macrosomic fetus (fetal weight > 4 kg)

-During labour, protracted cervical dilatation, prolonged second stage or difficult midforceps.

- The head is delivered and the chin is applied firmly against the perineum.

- There is no further progress in spite of gentle traction on the head.

-Congestion of the face and difficult vaginal examination .

Complications:

A) Fetal complications:

increase mortality and morbidity

1) Brachial plexus injuries :

.Strain or stretch ,

.Partial disruption ,

.Complete avulsion

-Injury primarily to lateral trunk (C5,6, 7) leads to Erb’s palsy – adducted shoulder, extended elbow, and flexed wrist (“waiter’s tip”)

-Injury primarily to the medial trunk (C8, T1) leads to Klumpke’s palsy – paralyzed hand with good shoulder and elbow function

2) Fracture clavicle or humerus.

3) Asphyxia and death.

B) Maternal complications :

· Increase blood loss

· Uterine rupture

· Extensive vaginal lacerations and cervical tears

Management:

(A) Prophylaxis:

1. Proper antenatal care particularly for high risk mothers as diabetics.

2. Antepartum assessment of foetal weight---- macrosomic babies should be delivered by caesarean section.

(B) Management of shoulder dystocia:

Calling urgently an anaesthetist and paediatrician.

The following methods are used in a rapid succession when the previous one failed:

(1) Generous episiotomy + gentle downward traction + suprapubic pressure by an assistant obliquely to

flex the anterior shoulder against the foetal chest.

(2) Mc Roberts' manoeuvre: It is sharp flexion of the maternal thighs against her abdomen. This can free the shoulders by:

i- backward displacement of the sacral promontory.

ii- upward displacement of the symphysis pubis.

iii- Decrease the inclination of the pelvic inlet.

iv- Decrease in lumbar lordosis.

(3) Rotation of the anterior shoulder : by applying pressure on the posterior aspect of the impacted anterior shoulder to move it from the anteroposterior to the oblique diameter of the pelvic inlet.

(4) Woods screw manoeuvre:

Woods (1943) described this manoeuvre to rotate the foetus as a screw between the resisted promontory and symphysis.

-Two fingers of the right hand is pressing from the posterior aspect of the posterior shoulder to rotate it 180 anteriorly where it escapes from below the symphysis.

-The left hand is placed on the mother’s abdomen and assists this rotation by pressing on the foetal buttock in the same direction of rotation.

(5) Extraction of the posterior arm: by pressing with 2 fingers against the cubital fossa to sweep the

posterior arm in front of the chest and deliver it giving space for the anterior shoulder to escape from below the symphysis.This is aided by suprapubic pressure.

(6) Zavanelli manoeuvre (cephalic replacement):

1. Prepare for caesarean section.

2. Subcutaneous terbutaline (tocolytic) is given to relax the uterus.

3.Rotate the head manually to the antero-posterior diameter (pre-restitution position).

4. Flex the head and press on it firmly and constantly to replace it intravaginally where it is supported by an assistant.

5. Immediate caesarean section is performed.

(7) Clavicular fracture:

was described to reduce the diameter of the shoulders. It is done by upward pressure against its

midportion to avoid injury of the subclavian vessels.

(8) Cleidotomy:

It is cutting of the clavicle and usually reserved for a dead foetus.

(9) Symphysiotomy:

It is advocated by some authors to overcome contracted pelvis in women living in uncivilised areas.

(10)The all four maneuver .

-ACOG Guidelines 2002 :

1. Most cases of shoulder dystocia can not be predicted or prevented because there are no accurate methods for identifying which fetus will develop this complication.

2. Ultrasonic measurements to estimate macrosomia have limited accuracy

3. Planned cesarean section based on suspected macrosomia was not a reasonable strategy for most women

4. Planned cesarean section may be reasonable for the nondiabetic woman with an estimated fetal weight exceeding 5000 g or the diabetic whose fetus is estimated over 4500 g

Pelvic Inflammatory Disease( PID) , Dr. Alaa Mosbah ,MD OBS and GYN

Definition:
PID is defined as acute clinical syndrome associated with ascending spread of microorganism from the vagina or cx to the endometrium fallopian tube / or contiguous structures but not related to (pregnancy or surgery). By other mean, it refers to infection resulting from sexual activity and excludes that due to childbirth, surgery or T.B.
A more descriptive and accurate term is salpingitis or salpingoophritis

Epidimiology:
1- An accurate incidence is difficult to determine because there is no diagnostic test which is simple, safe and specific and also the patient may be a symptomatic or run a very benign clinical course.
2- The highest incidence is among sexually active women in their teenage years. So it is strongly correlated with prevalence of STD
3- The incidence in developing world is more difficult to assess and the high incidence of STD in many African countries can be attributed to
· High proportion of teenagers
· Early sexual practice and multiple sex. Partners
· Delay in ttt of STD
· Female circumcision
4- Chlamydia and N. gonorrhea are the most prevalent S.T. bacteria in western world (implicated in 60% of PID in young women)
5- In U.K., uncomplicated gonococcal infection is halved in frequency in last decade while chlamydia continued to rise

Risk factors:
[1]. Age:
with young age (15 – 20y.) due to :
· sexual activity in young age
· Col. Cell ectopy susceptible to chlamydial infection and gonococcal infection
the risk is unlikely after 30y.
[2]. Parity: with nulliparity
[3]. Race: pressure in black due to low socioeconomic status
[4]. Douching:pressure in the vagina forcing material up through the cx.
[5].Cigarette smoking: risk due to:
· Damage of immune system
· Alteration of bl. supply to f.t.
[6]. Previous episodes of acute acute salpingitis: previously damaged tube is susceptible to altered defense mechanism
[7]. Sexual intercourse: pressure gradient bet. lower and upper genital T. cervical barrier compromisation
[8].Multiple sexual partner
risk of meeting male with STD.
[9]. Use of IUD: highest risk in 20 days following menstruation ¯ thereafter. IUD strings facilitates access of vaginal bacteria

Contraception and PID
· IUD: risk
· Barrier contraception: ¯ STD and hence PID
· O.Cs : ¯ risk due to:
- thick cervical mucus
- atrophy of endomet.
- ¯ menstrual bl. loss
· Sterilisation: incidence is very rare and is confined to the stump of the tube that remain attached to the uterus

Microbiology of PID:
· Cervical culture do not reflect the microbiology tube infection
· Culture obtained by culdecentesis correlates with tube exudate culture
· Endometrial culture obtained by swab or biopsy correlate best with culture obtained by swab or biopsy correlate best with culture of tubal exudate
1- Sexually transmitted pathogens: (young women – recent infection)
N. gonorrhea is most common in 3rd world and north America chlamydia trachomatis is more likely to cause mild or subclinical infection serious tubal damage results from sites infection as from clinically apparent salpingitis
2- Aerobic and anaerobic organisms:
most commonly recovered from
- older women
- recurrent cases
- long standing cases
· Aerobes: gm –ve as E coli
gm +ve as streptococcus viridans, enterococci
· Anaerobes: peptococci, peptostreptococci and bacteroides
Anaerobes are present in very severe disease often as mixed with aerobes
3- Mycoplasma hominis and ureaplasma urealyticum:
cause parametritis rather than salpingitis
4- Actinomyces israeli:
- Common with IUD
- High rate of abscess formation
5- True viruses: Coxsachie virus, Echo, Herpes simplex virus type II

Pathogenesis:
Most cases fall into 2 groups;
1-Those due to sexually transmitted organisms: found in young adults & nulliparous women.
2-Those due to endogenous vaginal or large bowel organisms which are associated with B.V organisms. It occurs in older women & in parous women.

Any organism from lower genital tract has to pass the uterine cervix to gain access to the endometrium and fallopian tube.
In young nullipara, there is competent anatomical, physiological, biochemical and immunological barrier. With increasing age & trauma of childbirth or surgery, this barrier is less effective.

How pathogens pass this barrier in young nullipara?
1- Adherence to spermatozoa
2- In suck due to pressure gradient of coitus and subsequent uterine activity
3- Menstruation
4- Surgical intervention
5- IUD

· In gonococcal salpingitis:
Spread is direct canalicular from endocx along endomet. surface to the tubal mucosa leading to endosalpingitis
70% occur at the end or just after the menstrual period. This is attributed to:
- Loss of cervical mucus plug.
- Sloughing of endomet.
- Menstrual blood (good culture medium)
- Uterine contractions during menses
® retrograde menstruation

· In non – gonococcal salpingitis:
Usually polymicrobial and include
- aerobic
- anaerobic
- chlamydia
- mycoplasma
- possibly viral agents

· Chlamydia: spread as gonococcus
· Mycoplasma: reach the adnexa by lymphatic spread via the parametrial tissue and broad ligament ® parasalpingitis and parametritis
· Other organisms: a critical number of organisms in the cervix is needed to overcome local host defense mechanism in the cervix, so allowing infection to ascend.
B.V organisms are associated with high colony count of anaerobic bacteria.

· In IUD associated salpingitis
Most infection occur at time of insertion
- break sterile technique
- introduction of pathogenic org.
Infection 5 fold
After that infection is due to
- IUD strings act as wick for org.
- IUD act as f.t. that interfere with local host defense
There is of adnexal abscess which is usually unilateral
Pathology:
In mild PID;
· The pelvic organs are much affected
· The serosal surfaces of f.t. appear reddened and hyperemic
· The tubes are edematous but freely mobile with patent abdominal ostia
· The may be sticky, purulent exudate on the serosal surfaces of the pelvic organs and exuding from the fimbrial end of the tube

In moderate PID;
· Inflammation and oedema of f.t. is more pronounced
· Tubal mobility may be limited
· Patchy fibrin deposits are seen on the serosal surfaces and loose adhesions may from between the pelvic and abdominal viscera
· The distal end of f.t. often appear phimotic and the tubes may not be patent

In severe PID;
· Occlusion of tubal ostia as a result of the fimbria sticking together resulting in pyosalpinx
· Marked distortion of pelvic anatomy
· Pelvic peritoneum is severely damaged (congested) and the pelvic organs become adherent resulting in the formation of complex inflammatory mass
· If the infectious process has not been sealed off in the f.t., then a tuboovarian abscess, the most severe manifestation of PID may develop. it is likely that development of TOA is the natural progression when PID is not arrested by either host’s natural defense or by medical ttt

- The extent of damage of tubal function varies often an episode of PID
· At best: in mild disease, there will be complete resolution of tubal morphology with no effect on function
· At worst: distal tubal occlusion with hydrosalpinx formation, intrluminal fibrosis and damage to tubal mucosa and cilia ® irreversible impairment of function

- Fitz – Hugh Curtis syndrome (FHCS):
is an extrapelvic manifestation of PID and is composed of 2 phases
· Acute phase: perihepatitis and focal peritonitis that result from transport of inflammatory peritoneal fluid either directly or by lymphatic to the subphrenic and subdiaphragmatic space
Both N G and C. trachomatis are isolated from liver surface in FHCS
M/E: of liver parenchyma reveals on acute infl. of liver capsule without involvement of parenchyma
Liver function: are normal
· Chronic phase: is characterized by adhesions bet. the ant. surface of the liver and the ant. abdominal wall

- The organisms spectrum in PID:
· Chlamydia, mycoplasma ®mild or subclinical disease
· N. gonorrhea ® moderate disease
· Anaerobes ® severe disease with abscess formation

Chronic sequelae of PID:
1- Infertility: 15% after one attack
35% after 2 attack
65% after 3 attack
2- Ectopic preg. : 8%
3- Recurrent PID: 25%
4- Chronic pelvic pain

Diagnosis of PID:
(I) Clinical : diagnosis of acute salpingitis is accurate in only 65% the other diagnosis will be:
- normal findings: 25%
- acute appendicitis
10% - endometriosis
- ruptured cyst
- ectopic preg

Hager criteria : 1983
a) Major criteria: all must be present
1- Lower abdominal pain
2- Cervical mobility tenderness
3- Adnexal tenderness
4- Negative serum hCG by RIA
5- Pelvic ultrasound not suggestive of an alternate diagnosis

b) Minor criteria: one must be present
1- Oral temp. > 38°c
2- Leucocytosis > 10,000/mm3
3- Culdecentesis yielding WBCs / bacteria
4- ESR > 15mm/hr or CRP > 30mg/l
5- Presence of inflammatory mass noted on pelvic ex. or pelvic U/S gm stain or +ve culture from endocx suggestive of N.G or +ve culture or monoclonal antibody directed smear for chlamydia

(II) Laboratory investigations: to detect organisms or evidence of their presence (antibodies)
1- Gram stain and cervical culture for gonococci.
2- High vaginal swab for trichomonas vaginalis
3- gm stain for B.V.
4- ELISA or culture from the cx for chlamydia
5- Uretheral, rectal or oral cultures for gonococci
6- Serologic test for $, hepatitis B and C, HIV as the patient with one STD is at risk for other infection

(III) Laparoscopic diagnosis: gold standard as s & s are not specific
Jacobson and Westrom 1969
· Pronounced hyperemia of tubal surface
· Oedema of tubal wall
· A sticky exudate on tubal surface and from tubal ends when patent
Diagnostic accuracy is enhanced by (BHCG – U/S).

Modification of these criteria by Hager 1983 for assessment of severity
a- Mild disease: tubal erythema and oedema, expression of exudate from tube
b- Moderate disease: gross purulent material, tubes are patent
c- Severe disease: Tuboovarian abscess, pyosalpinx, pelvic abscess

Also, laparoscopy can assess the chronicity
a- Acute disease
· Normal fimbriae with no adhesions
· Purulent exudate from fimbrial end
b- Subacute disease
· Gelatinous adhesions with or without pyosalpinx or abscess
· Pelvic peritonitis with bowel adhesions and abundant purulent exudate
c- Chronic or recurrent disease: with dense fibrous adhesions presence of adhesions and hydrosalpinx ® difficult to determine if there is an acute infection. However, presence of exudate (purulent) does not indicate active infection
Oedema and hyperemia does not indicate active infection

Treatment of PID
Principles
· The goal of therapy in uncomplicated acute salpingitis is:
1- Prevention of infertility
2- Prevention of ectopic preg
3- Prevention of tubo-ovarian abscess
· The goal of the therapy in salpingitis complicated by abscess is
1- Preservation of life
2- Prevention of septic complications
· As PID is polymicrobial, antibiotic coverage should include:
1- Chlamydia
2- N.G
3- Anaerobes
4- gm +ve and gm –ve aerobes

Regimens: acc. to severity, it may be outpatient or inpatient regimens
(A) Outpatient regimen: if symptoms and signs are mild
Cefoxitin 2gm I.M
Or Amoxycillin 3gm oral
Or Ampicillin 3.5gm oral
Or Aqueous procaine penicillin G 4.8 million U I.M. + 1gm probencid
+
Doxycycline 100mg twice daily for 10 – 14 days
This regimen cover N.G, chlamydia and few anaerobes

Another regimen
Metronidazole + Tetracycline orally

(B) Inpatient regimen
Criteria for hospitalization
1- Diagnosis is uncertain (exclude appendicitis, ectopic)
2- Suspected pelvic abscess
3- Pregnancy
4- IUD
5- Temp. > 38°c
6- Adolescent
7- Nausea and vomiting
8- Failure to respond to oral antibiotics within 48hr

Regimens
1] Cefoxitin 2gm I.V. / 6hr
+ Doxycycline 100mg I.V. / 12hr
for at least 4 days or 2 days after patient is a febrile
then doxycycline 100mg orally to complete 2w
this regimen cover all pathogens

2] Clindamycin 600mg / 6hr
+
Gentamycin 2mg/kg 3 times / day followed by 1.5gm /kg 3 times / day for 4 days or 2 days after being a febrile
Then clindamycin 450mg p.o./6hr to complete 10 days
This regimen moderately cover chlamydia but no coverage for PPNG

3] Metronidazole
+ Doxycycline 100mg I.V. / 12hr
for 4 days or 2 days after being a febrile
then continue both drugs for 2 weeks orally
this regimen moderately cover gm –ve aerobes but no coverage for gm +ve aerobes or PPNG

4] Cefotaxime 1gm / 6hr
+
Metronidazole 1gm / 12hr. rectal supp.

Therapeutic failure: occur if:
1- No improvement for 48hr.
2- CT or U/S to reassess the possibility of T.O. abscess
3- Wrong diagnosis
4- Resistant pathogens
5- Pelvic thrombophelebitis

In this case, laparoscopy is indicated
If salpingitis is diagnosed (culdesac, tubal exudate cultured) ® give triple antibiotics
- Ampicllin + Gentamycin + Clindamycin
If no response, add heparin to cover the possibility of thrombophelebitis.
Pelvic Abscess

Aetiology : pelvic abscess can be divided acc. to mode of infection into:
1) Primary: due to ascending infection without predisposing factor i.e. without surgery, trauma or pregnancy
2) Secondary
a- Following pregnancy:
1- Postabortal infection
2- Purpeural infection
3- Injected chronic ectopic preg.

b- Direct extension
e.g. following appendicitis or diverticulitis

c- Following surgery
e.g. cuff abscess

The proportion of patients falling into the different etiologic groups will differ in different population will depend on certain factors
1- Abortion practice
2- Surgical technique
3- Resistance to infection

Microbiology
Any pathogenic or potentially pathogenic org. introduced into the upper genital tract can cause infection

· In primary and postpregnancy pelvic infection:
The route of entry is usually via the vagina and cx so, in such patients, the organisms isolated from the upper genital T. are the same as those which can normally be found lower genital tract
* In primary ascending infection
It is thought to be initiated by gonococcal infection of endocx and in those progressed to pelvic abscess, a mixed growth of organisms is nearly always found.
i.e. pelvic abscess in this care is polymicrobial
1- N. gonorrhea
2- Chlamydia T.
3- Anaerobes e.g. bacteroides
4- Mycoplasma hominis
5- Aerobes (gm +ve and gm –ve) e.g. E coli, enterobacter strept. gp. B., staphylococci. Klebsiella

* In postpergnancy infection: most authors stress the importance of anaerobic infection which results mainly from bacteroides species

In postsurgical injection
The organisms are those found in the lower genital tract of normal a symptomatic women

In isolated ovarian abscess: mixed flora of aerobes and anaerobes with actinomyces israeli

Pathogenesis
(A) Primary ascending infection:
It is suggested that gonococci become attached to spermatozoa to reach the f.t. following intercourse
The organism attaches to mucosal epith., penetrates it via phagocytosis ® destruction of epith. and cilia. Also, further destruction is caused by lipopolysaccharide endotoxin
This destruction ® production of purulent exudate which at early stages (when the tube is patent) exudes from the fimbrial and ® peritonitis
The area involved is walled off by bowel, omentum and surrounding structures ® pelvic abscess which is fed by purulent exudate from the f.t.
The abscess may remain localized to the tube and ovary or it may involve other structures during this stage, the ovary may be involved. It is suggested that ovulation site serves as portal of entry of organisms into the ovary ® tuboovarian abscess.
At any point of progression, rupture may occur and if the fimbrial end is blocked ® pyosalpinx.
Tuboovarian abscess is usually bilateral but unilateral tuboovarian abscess is reported especially with IUD

(B) Postsurgical infection:
Infection is initiated by direct contact of freshly traumatized tissue with pathogenic organisms
The tissue is traumatized or devitalized 2ry to crush clamp technique and due to suture ligature which represent nidus for infection.
Also, hemoglobin accumulates at the site of operation and this interfere with host defense mechanism by inhibiting leukocytes to phagocytose bacteria

The organisms found in postsurgical infection are those which can be found in the lower genital tract of normal a symptomatic women

Infection may be in the form of:
· Vaginal cuff abscess: in the area bet. vag. epith. and peritoneum following abd. or vaginal hysterectomy
or · Tuboovarian or isolated ovarian abscess (true abscess)

Isolated ovarian abscess without involvement of other pelvic organs are usually a manifestation of postsurgical infection.

(C) Primary ovarian abscess
Is an entity which is different from tuba ovarian abscess in which the wall of the abscess is composed of f.t. and ovarian parenchyma while in ovarian abscess, infection occur only in ovarian parenchyma.
Also, primary ovarian abscess is an unusual condition bacteria can gain access to ovarian parenchyma by haematogenous or lymphatic spread.
However, most primary ovarian abscess occur because bacteria present around the ovary gain access to the parenchyma through a break in the ovarian capsule either naturally by ovulation or by surgical procedure.

A primary ovarian abscess is usually unilateral but if bilateral, it indicates heamatogenous or lymphatic spread (from distant site e.g. tonsillitis).
The organism can reach the ovary from
· Fallopian tube
· Vagina during or after hysterectomy
· IUD assoc. infection
· Appendicitis, diverticulitis or any other condition causing peritonitis
A mixed flora of anaerobic and aerobic bacteria is usually present and actinomyces Israeli with sulfur granules are identified in few cases

Clinical presentation
A) Uncomplicated tuboovarian abscess
The same clinical picture of uncomplicated salpingitis differentiation require determination of an inflammatory adnexal mass

· The patient is usually in the 3rd or 4th decade
· 1/3 patients are nullipara
· 1/3 patients have history of PID or previous hospitalization for pelvic abscess
· Pelvic abscess in postmenopausal woman in usually assoc. with disease of intestinal tract such as ruptured appendix or sigmoid diverticulum

On examination
· Patient appears ill with temp. elevated
· She walks slowly with the hand on lower abdomen
· Abdominal distention and direct and rebound tenderness in the lower abdominal quadrant
· Pelvic examination is extremely tender with tender cervical mobility
· An irregular, tender, fixed inflammatory mass may be felt on one or both sides of the pelvis. the mass may be small or may extend out of the pelvis into the lower abdomen or it may dissect the rectovaginal septum and felt on rectovaginal examination

Diagnosis
1- ESR, WBCs
2- Laparoscopy: may be helpful but invasive
3- Non-invasive procedures :
- U/S, CT
- Radionuclide scanning

B) Ruptured tuboovarian abscess
· Symptoms
Acute progressive pelvic pain which is so severe that the patient can accurately identify the time and place of its occurrence identify the time and place of its occurrence

· Examination
- Patient appear ill, dehydrated
- Abdominal distention
- Absent intest. sound
- Signs of generalized peritonitis with shifting dullness
- Pelvic mass is felt in 50% of cases
- Fever, tachycardia, leucocytosis
- Culdecentesis ® purulent material

C) Postoperative pelvic abscess
[1] Vaginal cuff abscess or infected haematoma:
· Usually presents with fever and sensation of fullness or vaginal discomfort in the lower abdomen:
· Typically infected, foul smelling haematoma
it characteristically occur 48hr. postoperatively

2] True pelvic abscess
tend to present at a later date often after discharge from the hospital
It presents with fever, abdominal pain, tender palpable pelvic mass

N.B.: Characteristically, posthysterectomy adnexal mass are high in the pelvic. So, vaginal evacuation is not the optimal approach for the management of this abscess

Management of pelvic abscess
Whatever the etiological factor involved in the pathogenesis of pelvic abscess, the initial approach to the problem is the same
Once diagnosis has been made, the patient is admitted to hospital and conservative management is started. When a diagnosis of ruptured TOA is evident, early surgical intervention is indicated

ttt. consists of 3 lines
- Supportive therapy
- Antibiotic therapy
- Surgical intervention

[1] Supportive therapy
· Baseline biochemical and haematological investigations
· Rest in semifowler position
· I.V. fluids with electrolyte balance
· Analgesia

[2] Antibiotic therapy
the abscess is a unique environment characterised by:
· Low level of O2 tension which allow anaerobes to proliferate
· Circulatory compromise preventing antibiotics from reaching the area
· Poor phagocytosis by neutrophil
these factors are imp. in the resistance of these infections to antimicrobial therapy

Antibiotics given depend on sensitivities obtained the material obtained by culdecentesis or Bl. culture combination antibiotics is usually needed
· Coliforms are affected by
- aminoglycoside
- ampicillin
- cephalosporin
· Anaerobes are affected by
- metronidazole
- clindamycin
- chloramphenicol
so, combination of aminoglycoside or ampicillin + clindamycin or metronidazole
N.B. penicillin + chloramphenical were used (cheap and effective) effective against all org. except pseudomonas, but there is concern about the rare complication of aplastic anaemia
However, this complication does not occur if the dose not exceed 24gm

[3] Surgical intervention
Indications
· Ruptured TOA
· Diagnosis is in doubt
· No evidence of : response for 24hr
· Persistent generalized peritonitis for 24hr
· size does not ¯ by 48hr

Approaches
Clopotomy or laparotomy

* Colpotomy: done when 3 requirements
· Abscess in mid line or nearly so
· Abscess is cystic or fluctuant
· Abscess dissecting the rectovaginal septum or bulging in the posterior fornix
However, colpotomy will not cure all cases and about 1/3 of patients will require subsequent abdominal operation colpotomy is definitive curative procedure only in posthysterectomy abscess (cuff abscess) but in other abscesses, the chance of failure due to incomplete drainage of multilocular abscess is present

* Laparotomy
(A) unruptured pelvic abscess
the main approach for majority of patients when pelvic abscess is abdominal
· Midline subumblical incision: is made to allow exposure of the pelvis and extension to upper abdomen in case of ruptured abscess
· The operative procedure depend on the extent of pathology and etiology of the abscess
1- In postpregnancy infection
the uterus is usually involved. So, the ttt will be hysterectomy + BSO

2- In ascending infection
· More conservative surgery is needed and will depend on the site of the abscess
· Drainage of the abscess alone is not adequate and it is important to remove as much of the infected tissue to avoid recurrence of abscess
· The following alternatives may be done:
- Unilateral salpingectomy
- Unilateral salpingoophrectomy
- Bilat. salpingectomy
- Bilat. salpingoophrectomy
- Bilat. salpingectomy and unilat. oophrectomy
- Drainage only
rarely, hysterectomy is done

(B) Ruptured abscess
· Immediate laparotomy as delay for 24hr ® 80% mortality
· Identify the extent of pathology
· Ensure adequate lavage and drainage
· The affected andexal tissue is removed and hysterectomy is only performed if infection was following pregnancy with involvement of the uterus
· Intraoperative lavage with povidine iodine soln or normal saline with antibiotics
· Closed suction drainage at the pelvic cavity

MANAGEMENT OF ACUTE PELVIC INFLAMMATORY DISEASE .Green-top Guideline ,November 2008,RCOG

MANAGEMENT OF ACUTE PELVIC INFLAMMATORY DISEASE
This is the second edition of this guideline, which was previously published in 2003 under the same title.
1. Purpose and scope
Pelvic inflammatory disease (PID) is usually the result of infection ascending from the endocervix causing
endometritis, salpingitis, parametritis, oophoritis, tubo-ovarian abscess and/or pelvic peritonitis. While sexually
transmitted infections (STIs) such as Chlamydia trachomatis and Neisseria gonorrhoeae have been identified
as causative agents, additional STIs including Mycoplasma genitalium, anaerobes and other organisms may
also be implicated.PID is a common cause of morbidity and accounts for one in 60 general practitioner consultations by women
under the age of 45 years.6 Delays of only a few days in receiving appropriate treatment markedly increase
the risk of sequelae, which include infertility, ectopic pregnancy and chronic pelvic pain. Sequelae may also
have significant healthcare costs.9 This guideline applies to women requiring treatment for confirmed or
suspected acute PID being treated in an outpatient or inpatient setting by primary and secondary care
practitioners.
There are marked variations in the antimicrobial regimens used in the treatment of PID, reflecting uncertainty
in the optimal treatment schedule.10 The guideline contains recommendations for treatment and graded
evidence to support their use.
2. Identification and assessment of evidence
A Medline search was performed covering 1963 to August 2007 looking for the following terms in the title or
abstract: ‘pelvic inflammatory disease’, ‘adnexitis’, ‘oophoritis’, ‘parametritis’, ‘salpingitis’ or ‘adnexal disease’
(the dataset for 1963–86 was limited to Argonne Information Management journals and human subjects); citations were identified. A search of the Cochrane database revealed no directly relevant systematic reviews.
A search of the Cochrane controlled trials register using a search strategy of ‘pelvic inflammatory disease’,
‘adnexitis’, ‘oophoritis’, ‘parametritis’, ‘salpingitis’ or ‘adnexal disease’ identified 356 citations. The following
guidelines and reports were also reviewed: 2006 US Centers for Disease Control STD treatment guidelines,Royal College of Obstetrics and Gynaecology Study Group proceedings on PID 1996,1 2004 Health
Technology Assessment report, The Clinical Effectiveness and Cost Effectiveness of Antibiotic Regimens for Pelvic Inflammatory Disease, 2005 UK National Guidelines on Sexually Transmitted Diseases and 2007
European guidelines for the management of pelvic inflammatory disease.
The recommendations given in this guideline have been graded according to the guidance for the development of RCOG Green-top Guidelines.

3.Making a diagnosis of acute PID
3.1 Clinical
A low threshold for empiric treatment of PID is recommended because of the lack of definitive clinical
diagnostic criteria and because the potential consequences of not treating of PID are significant. In clinically severe cases, referral to hospital for treatment and further investigation is advisable.
The following clinical features are suggestive of a diagnosis of PID:
● bilateral lower abdominal tenderness (sometimes radiating to the legs)
● abnormal vaginal or cervical discharge
● fever (greater than 38°C)
● abnormal vaginal bleeding (intermenstrual, postcoital or ‘breakthrough’)
● deep dyspareunia
● cervical motion tenderness on bimanual vaginal examination
● adnexal tenderness on bimanual vaginal examination (with or without a palpable mass).
Clinical symptoms and signs lack sensitivity and specificity (the positive predictive value of a
clinical diagnosis is 65–90% compared with laparoscopic diagnosis but laparoscopy may also lack
sensitivity). The presence of excess leucocytes on a wet-mount vaginal smear is associated with
PID but is also found in women with isolated lower genital tract infection.
Laparoscopy enables specimens to be taken from the fallopian tubes and the pouch of Douglas and
can provide information on the severity of the condition. Although it has been considered the
gold standard in many studies of treatment regimens, 15–30% of suspected cases may have no
laparoscopic evidence of acute infection, despite organisms being identified from the fallopian
tubes. When there is diagnostic doubt laparoscopy may, however, be useful to exclude alternative pathologies.
Transvaginal ultrasound scanning may be helpful when there is diagnostic difficulty. When
supported by power Doppler, it can identify inflamed and dilated tubes and tubo-ovarian masses.
It may differentiate PID from acute appendicitis in a minority of cases but there is insufficient
evidence to support its routine use. Computed tomography24 and magnetic resonance
imaging25–27 can assist in making a diagnosis but the evidence is limited. A peripheral blood leucocytosis,
elevated erythrocyte sedimentation rate or C-reactive protein also support the diagnosis
and can provide a useful measure of disease severity but these are non-specific findings. There is insufficient evidence to support endometrial biopsy as a routine diagnostic test at present.
The differential diagnosis of lower abdominal pain in a young woman includes:
● ectopic pregnancy
● acute appendicitis
● endometriosis
● irritable bowel syndrome (and, less commonly, other gastrointestinal disorders)
● complications of an ovarian cyst, such as rupture or torsion
● urinary tract infection
● functional pain (pain of unknown physical origin).

Microbiological
Women with suspected PID should be tested for gonorrhoea and chlamydia.
Although not a prerequisite to justify initial treatment decisions, testing for gonorrhoea and
chlamydia in the lower genital tract is recommended. A positive result gives support to the clinical
diagnosis of PID and reinforces the need to treat sexual partners. The absence of confirmed
infection in the lower genital tract site does not exclude PID.
Testing for gonorrhoea should be with an endocervical specimen and tested via culture (direct inoculation on to a culture plate or transport of swab to laboratory within 24 hours) or using a nucleic acid amplification test (NAAT). If gonorrhoea is detected using a NAAT, an additional
endocervical swab should be taken for gonococcal culture to allow the reporting of antibiotic
sensitivities and revision of therapy if required (women at high risk of gonorrhoea should have an
endocervical swab for gonococcal culture taken at their first examination; for example, where the
woman’s partner has gonorrhoea, clinically severe disease, sexual contact abroad).
Testing for chlamydia should also be from the endocervix, preferably using a NAAT (such as polymerase chain reaction, strand displacement amplification).
Taking an additional sample from the urethra can increase the diagnostic yield for gonorrhoea and
chlamydia but is only recommended if the more sensitive NAAT is not available. A first catch urine
or self-taken vulvovaginal swab sample provides an alternative sample for some NAATs.
The absence of endocervical or vaginal pus cells on a wet-mount smear has a good negative
predictive value (95%) for a diagnosis of PID but their presence is non-specific (poor positive
predictive value (17%).
Other organisms, including M. genitalium have been associated with PID but routine screening
is not yet justified because of limited information on prevalence, natural history, treatment and cost
effectiveness.
Further advice on the appropriate testing for STIs is available from the National Screening and
Testing Guidelines for Sexually Transmitted Infections (www.bashh.org/guidelines).
4. Starting treatment
4.1 How should PID be managed in the outpatient setting?
Information on current and recent medication should be obtained.
Interactions between antibiotic therapy and hormonal contraception and other patient medications
should be assessed and appropriate action taken.
Outpatient antibiotic treatment should be commenced as soon as the diagnosis is suspected.
In mild or moderate PID (in the absence of a tubo-ovarian abscess) there is no difference in
outcome when women are treated as outpatients or admitted to hospital. It is likely that delaying treatment, especially in chlamydia infections, increases the severity of the condition and the risk of long-term sequelae such as ectopic pregnancy, subfertility and pelvic pain.

Outpatient antibiotic treatment should be based on one of the following regimens:
● oral ofloxacin 400 mg twice daily plus oral metronidazole 400 mg twice daily for 14 days
● intramuscular ceftriaxone 250 mg single dose,* followed by oral doxycycline 100 mg twice daily plus metronidazole 400 mg twice daily for 14 days.* Cefoxitin has a better evidence base for the treatment of PID than ceftriaxone but is not easily available in the
UK. Ceftriaxone is therefore recommended.
Broad-spectrum antibiotic therapy is generally required to cover N. gonorrhoeae, C. trachomatis and
anaerobic infection. Ofloxacin should be avoided in women who are at high risk of gonococcal
PID because of increasing quinolone resistance in the UK. Those women at high risk of acquiring
gonorrhoea include those whose partner has gonorrhoea, in clinically severe disease or if there is
a history of sexual contact abroad.
Metronidazole may be discontinued in those women with mild or moderate PID who are unable
to tolerate it, since its addition provides uncertain additional efficacy in this patient group.
Clinical trial evidence for the following regimen is less strong but it may be used as an alternative
to the treatments above:
● intramuscular ceftriaxone 250 mg immediately, followed by azithromycin 1 g/week for 2 weeks.
Although the combination of oral doxycycline and metronidazole (without ceftriaxone) has been
used to treat PID in the UK, there are no clinical trials adequately assessing its effectiveness and its
use in isolation is not recommended. Data supporting azithromycin monotherapy for PID is
also limited at present and its use without the addition of ceftriaxone is not recommended.
There are currently no randomised controlled trial data to support the use of an oral (rather than parenteral) cephalosporin as part of the treatment regimen. Tissue levels of the antibiotic are likely
to be lower following oral administration.
A detailed explanation of their condition should be provided to women, with particular emphasis on the
long-term implications for their health and the health of their partner(s). This should be reinforced with
clear and accurate written information.
When giving information to patients, the clinician should consider the following:
● an explanation of what treatment is being given and its possible adverse effects
● that following treatment fertility is usually maintained but there remains a risk of future infertility, chronic pelvic
pain or ectopic pregnancy
● repeat episodes of PID are associated with an exponential increase in the risk of infertility
● future use of barrier contraception will significantly reduce the risk of PID
● the need to screen her sexual contacts for infection to prevent her becoming reinfected
● clinically more severe disease is associated with a greater risk of sequelae
● the earlier treatment is given the lower the risk of future fertility problems.
A suitable patient information leaflet for PID is available at: www.rcog.org.uk/resources/public/pdf/Acute_
PID_2004.pdf.
4.2 What hospital treatment should be given and when should it be recommended?
Admission to hospital would be appropriate in the following circumstances:

surgical emergency cannot be excluded
● clinically severe disease
● tubo-ovarian abscess
● PID in pregnancy
● lack of response to oral therapy
● intolerance to oral therapy.
Inpatient antibiotic treatment should be based on intravenous therapy which should be continued until
24 hours after clinical improvement and followed by oral therapy.
Recommended regimens are:
● ceftriaxone 2 g by intravenous infusion daily plus intravenous doxycycline 100 mg twice daily,* followed by oral doxycycline 100 mg twice daily plus oral metronidazole 400 mg twice daily for a total of 14 days
* Oral doxycycline may be used if tolerated.
● intravenous clindamycin 900 mg three times daily plus intravenous gentamicin,* followed by either
● oral clindamycin 450 mg four times daily to complete 14 days
OR
● oral doxycycline 100 mg twice daily plus oral metronidazole 400 mg twice daily to complete 14 days.
* Gentamicin should be given as a 2 mg/kg loading dose followed by 1.5 mg/kg three times daily [or a single daily dose of 7 mg/kg may be substituted].
● intravenous ofloxacin 400 mg twice daily plus intravenous metronidazole 500 mg three times daily for 14 days.
The clinical trial data support the use of cefoxitin for the treatment of PID but this agent is not easily available
in the UK so ceftriaxone, which has a similar spectrum of activity, is recommended. An alternative thirdgeneration
cephalosporin would also be acceptable.
Intravenous doxycycline is available from IDIS World Medicines (+44 [0] 1932 824000). If parenteral
gentamicin is used then serum drug levels and renal function should be monitored.
The choice of an appropriate treatment regimen will be influenced by robust evidence on local antimicrobial
sensitivity patterns, robust evidence on the local epidemiology of specific infections, cost, the woman’s
preference and compliance and severity of disease.
Evidence of the efficacy of antibiotic therapy in preventing the long-term complications of PID is currently
limited.
4.3 Treatment in pregnancy and in young women
A pregnancy test should be performed in all women suspected of having PID to help exclude an ectopic
pregnancy. When the risk of ectopic pregnancy is judged clinically to be high, the pregnancy test should be
repeated 21 days after the date of last unprotected intercourse.
The risk of giving any of the recommended antibiotic regimens in very early pregnancy (before a positive
pregnancy test) is low, since significant drug toxicity results in failed implantation (UK National Teratology
Information Service).
PID is rare in women with an intrauterine pregnancy except in the case of septic abortion. In septic abortion,
the infective organism is unlikely to be a sexually transmitted pathogen. Cervicitis may, however, occur in a
pregnancy and is associated with increased maternal and fetal morbidity. Treatment regimens will be dependent
upon the organisms isolated. Drugs known to be toxic in pregnancy, such as tetracyclines, should be avoided.

A combination of cefotaxime, azithromycin and metronidazole for 14 days may be used. The risks associated
with metronidazole are uncertain but no confirmed associations with adverse outcomes have been reported.
Ofloxacin should be avoided, where possible, in young women, when bone development is still occurring.
However, this recommendation is based on data from animal studies and no problems have been reported in
human subjects, so the British National Formulary currently recommends that ofloxacin may be used in
children where other options are limited. Doxycycline can be safely used in children over the age of 12 years.
A particularly low threshold for diagnosing and treating PID in women under the age of 25 years is
appropriate, owing to the higher incidence of disease in this group and the potential impact on future fertility.
4.4 Treatment in a woman with an intrauterine contraceptive device
Consideration should be given to removing an intrauterine contraceptive device (IUD) in women
presenting with PID, especially if symptoms have not resolved within 72 hours.
The randomised controlled trial evidence for whether an IUD should be left in place or removed
in women presenting with PID is limited. Removal of the IUD should be considered and may be
associated with better short-term clinical outcomes but the decision to remove it needs to be
balanced against the risk of pregnancy in those who have had otherwise unprotected intercourse
in the preceding 7 days. Hormonal emergency contraception may be appropriate for some women
in this situation.
5. Other modes of treatment
Surgical treatment should be considered in severe cases or where there is clear evidence of a pelvic
abscess.
Consider drainage of an abscess and in noting its position, the possibility that the abscess may have
arisen from the appendix or colon.
Laparoscopy may help early resolution of the disease by division of adhesions and drainage of
pelvic abscesses. Ultrasound-guided aspiration of pelvic fluid collections is less invasive and may
be equally effective.
6. Management of sexual partner(s) of women with PID
When a sexually transmitted infection is either proven or likely to be the cause of PID, the current sexual
partner(s) should be contacted and offered health advice and screening for gonorrhoea and chlamydia.
Other recent sexual partners may also be offered screening. Tracing of sexual partners within a 6-month period of the onset of symptoms is recommended but this time period may be influenced
by the sexual history. The risk of detecting STIs in the partners of women with PID is high.Women should be advised to avoid intercourse until they and their partner have completed the treatment
course. Gonorrhoea diagnosed in their sexual partner should be treated appropriately and
concurrently with the index woman. Concurrent empirical treatment for chlamydia is
recommended for all sexual partners, owing to the variable sensitivity of currently available
diagnostic tests. If adequate screening for gonorrhoea and chlamydia in the sexual partner(s) is not
possible, empirical therapy for both gonorrhoea and chlamydia should be given.Currently recommended regimens are available at www.bashh.org. Tracing of sexual partners is not required
where a non-sexually transmitted pathogen has been clearly identified as the cause of infection.

Referral of the index woman and her partner to a genitourinary medicine/sexual health clinic is
recommended to facilitate contact tracing and infection screening.
7. Review of women with PID
In the outpatient setting, review at 72 hours is recommended, particularly for those with a moderate or
severe clinical presentation.
Failure to improve clinically suggests the need for further investigation, to exclude competing diagnoses, and
may require admission for parenteral therapy and/or surgical intervention.
Further review 4–6 weeks after therapy may be useful to ensure:
● adequate clinical response to treatment
● compliance with oral antibiotics
● screening and treatment of sexual contacts
● awareness of the significance of PID and its sequelae
● that a repeat pregnancy test is negative, if clinically indicated.
Repeat testing for gonorrhoea after treatment is recommended in those initially found to be
infected unless sensitivity testing of the isolate confirms sensitivity to the prescribed antibiotic.
Repeat testing for chlamydia and gonorrhoea is appropriate in those in whom persisting
symptoms, compliance with antibiotics and/or tracing of sexual contacts indicate the possibility of
persisting or recurrent infection.
A repeat chlamydia and gonorrhoea test is not otherwise required.
8. Women who are infected with HIV
Women with PID who are also infected with HIV should be treated with the same antibiotic regimens as
women who are HIV negative.
Women who are infected with HIV may have clinically more severe PID but respond equally well
to treatment as women who are not infected. Standard antibiotic treatment as outlined above is
therefore appropriate and hospital admission is only required for those with clinically severe
disease. Potential interactions between antibiotics and antiretroviral medication need to be
considered on an individual basis (information on drug interactions with antiretroviral drugs is
available at www.hiv-druginteractions.org).
Women with HIV should be managed in conjunction with their HIV physician.
9. Contraception options and PID
Women on hormonal contraception presenting with breakthrough bleeding should be screened for
genital tract infection, especially C. trachomatis.
The use of the combined oral contraceptive pill has usually been regarded as protective against symptomatic
PID. Retrospective case–control and prospective studies have, however, shown an association with an
increased incidence of asymptomatic cervical infection with C. trachomatis.61 This has led to the suggestion
that the oral contraception may mask endometritis.62

An IUD only increases the risk of developing PID in the first few weeks after insertion. One European
randomised trial compared efficacy and continuation rates of copper-containing IUDs and the levonorgestrelreleasing
intrauterine system (LNG-IUS). At 3 years, there were significantly fewer removals for PID in the
LNG-IUS group.
All women diagnosed with PID should be provided with information about future contraceptive options and
should be assisted in making an informed choice.
If a woman is likely to be at risk of future PID and requests an IUD for contraception, the LNG-IUS would
be the most appropriate choice
10. Auditable standards
Little is known about the long-term outcomes, in relation to future fertility, ectopic pregnancy and chronic
pelvic pain, following the treatment of PID. Appropriate short-term audit outcomes include:
1. Proportion of women receiving treatment with a recommended regimen – target 95%.
2. Proportion of women referred for tracing of sexual contacts – target 95%.
3. Proportion of named male contacts in STI associated PID confirmed to have been screened for infection and/or
treated – target 60%.
4. Proportion of women having an adequate sexual history documented – target 95%.
5. Proportion of women in whom microbiological investigations have been taken – target 90%.
For service organisation, please see: Royal College of Obstetricians and Gynaecologists. Standards in
Gynaecology. Report of a Working Party. 2008 [www.rcog.org.uk/resources/public/pdf/GYNStandardsWPR
(web)0608.pdf].

Antiphospholipid Syndrome and Pregnancy

Introduction :
Recognized for its associated thrombosis in the 1950s, antiphospholipid syndrome (APS) and lupus anticoagulant (LAC) are associated with pregnancy complications that include fetal loss, fetal growth restriction, preeclampsia, thrombosis, and autoimmune thrombocytopenia. It is characterized by an autoimmune process that is separate in many women from systemic lupus erythematosus (SLE) and other connective tissue diseases. Diagnosis requires clinical and laboratory findings with the clinical criteria being the primary method of diagnosis. Women with the clinical features should be tested for LAC and anticardiolipin (aCL) antibodies; most patients with APS have both LAC and aCL immunoglobulin G (IgG) antibodies.APS is classified as primary or secondary depending on its association with other autoimmune disorders. Primary antiphospholipid syndrome is diagnosed in patients demonstrating the clinical and laboratory criteria without other recognized autoimmune disease. Secondary antiphospholipid syndrome is diagnosed in patients with other autoimmune disorders such as SLE.
Antiphospholipid (aPL) antibodies belong to the large family of antibodies that react with negatively charged phospholipids (PLs) including cardiolipin, phosphatidylglycerol, phosphatidylinositol, phosphatidylserine, phosphatidylcholine, and phosphatidic acid.LAC and aCL predispose to clotting in vivo, predominantly by interfering with the antithrombotic role of PLs; thus, it is associated with clinical thrombosis, not bleeding. The aPL autoantibodies bind moieties on negatively charged PLs or moieties formed by the interaction of negatively charged PLs with other lipids, PLs, or proteins.

Pathophysiology :

The biologic effects mediated by the human aPL antibodies include
(1) reactivity with endothelial structures, which disturbs the balance of prostaglandin E2/thromboxane production;
(2) interaction with platelet PLs, with consequent up-regulation of platelet aggregation;
(3) dysregulation of complement activation; and
(4) interaction of aPL with phosphatidylserine exposed during trophoblast syncytium formation, which raises the possibility of a more direct effect of these autoantibodies on placental structures.
In patients with primary APS, the presence of the 3 aCL isotypes plus LAC has been associated with a higher number of recurrent spontaneous abortions compared with other possible combinations of aCL isotypes.
The association between aPL antibodies and particular human leukocyte antigen (HLA) alleles and HLA-linked epitopes has been reported in studies of patients with lupus erythematous (eg, HLA-DR7, HLA-DR4). The HLA-DR3 phenotypes seem to predispose to the formation of aCL antibodies and antinuclear antibodies (ANAs), but this has not been confirmed in patients. However, particular HLA alleles associated with recurrent miscarriage have not been reported.
Animals immunized with aCL or with the cofactor beta-2 glycoprotein I (b2GPI) develop clinical manifestations of APS, including fetal loss, thrombocytopenia, and neurologic and behavioral dysfunction, along with elevated levels of aPL antibodies.
aCL antibodies bind to b2GPI, or a complex formed by this b2GPI is a platelet adhesin glycoprotein and cardiolipin. Exposure of endothelial cells to anti-b2GPI antibodies and their corresponding peptides leads to the inhibition of endothelial cell activation, as shown by decreased expression of adhesion molecules E-selectin, intercellular adhesion molecule, and vascular cell adhesion molecule and of monocyte adhesion.
In vivo infusion of each of the anti-b2GPI antibodies into BALB/c mice followed by administration of the corresponding specific peptides prevents the peptide-treated mice from developing experimental APS. These fascinating results suggest that the use of synthetic peptides that focus on neutralization of pathogenic anti-b2GPI antibodies represents a possible new therapeutic approach to APS.
Passive transfer into naive mice of inherently heterogeneous aPL antibody populations, either affinity-purified or as part of whole immunoglobulin fractions, from humans with APS or autoimmune mice has been shown to induce growth retardation and fetal loss.

Frequency :
United States
Women have been reported to account for approximately 80% of patients with APS.The aPL antibodies account for 65-70% of cases of venous thrombosis in women with venous thrombosis in unusual sites (eg, cerebral portal, splenic, subclavian and mesenteric veins). The aPL antibodies are detected in approximately 2% of patients with nontraumatic venous thrombosis. Approximately 22% of women with APS have had venous thrombosis and 6.9% have had a cerebrovascular incident (over a median follow-up period of 60 mo); 24% of thrombotic events occurred during pregnancy or the postpartum period. The rate for thrombosis or stroke is 5-12%. These observations suggest that women with documented APS should not take estrogen-progestin combination oral contraceptives.SLE occurs in approximately 120 cases per 100,000 population and causes pregnancy complications in approximately 45 cases per 100,000 pregnant population.
Mortality/Morbidity
APS is one of the major causes of thrombosis and its complications in women. Arterial and venous thrombosis are both reported. Coronary artery occlusions are reported in patients with APS. Previous thrombosis in the face of the diagnosis of APS has been documented to have a rate of recurrence of 25% per year if untreated.
Maternal morbidity
Thrombosis, especially in patients with APS and a history of thrombosis is a major concern. Morbidity may also be associated with anticoagulation in patients treated with heparin or low molecular weight heparins in pregnancy. Women with APS have an increased incidence of preeclampsia, which is frequently prior to 34 weeks’, and severe preeclampsia requiring premature delivery. APS is also associated with infertility and pregnancy complications such as spontaneous abortions, prematurity, and stillbirths.
Maternal mortality
Mortality rates during pregnancy are not well characterized. Multiorgan failure has been described during pregnancy by Asherson[1 ]and during postpartum by Kochenour
Perinatal Morbidity
aPL antibodies are found in 10-15% of women at high risk for fetal growth restriction. Neonatal morbidity and mortality may be influenced by indicated preterm delivery for maternal severe preeclampsia or fetal growth restriction.Neonatal lupus dermatitis, a variety of systemic and hematologic abnormalities, and isolated congenital heart block have been
associated with APS and SLE.
Perinatal Mortality
Fetal deaths at or beyond 20 weeks' gestation may be attributed to APS involvement. The rate of fetal loss may exceed 90% in untreated patients who have APS. Therapy (including aspirin and heparin) can reduce the rate of fetal loss to 25%, as described by Cowchock et al.[3 ]
Sex
Most cases of APS (80%) are in women.
Age
APS is predominantly diagnosed in reproductive-aged women (ie, 15-55 y). This is similar to other autoimmune states.

Diagnosis :
History
The “International consensus statement for the diagnosis of antiphospholipid syndrome” was published in 1999 by Wilson et al.This serves as a set of criteria similar to the criteria for the diagnosis of other autoimmune disorders.
Diagnosis of antiphospholipid syndrome (APS) requires at least 1 clinical and 1 laboratory criterion.
Clinical criteria :
Vascular thrombosis: One or more clinical episodes of arterial, venous, or small-vessel thrombosis, occurring within any tissue or organ
Complications of pregnancy
-One or more unexplained deaths of morphologically normal fetuses at or after 10 weeks’ gestation
-One or more premature births of morphologically normal fetuses at or before 34 weeks’ gestation
-Three or more unexplained consecutive spontaneous abortions before 10 weeks’ gestation
Laboratory criteria
Anticardiolipin antibodies
- Anticardiolipin IgG or IgM antibodies present at moderate or high levels in the blood on 2 or more occasions at least 6 weeks apart
Lupus anticoagulant
- Lupus anticoagulant antibodies detected in the blood on 2 or more occasions at least 6 weeks apart, according to the guidelines of the International Society on Thrombosis and Hemostasis
Physical
APS is primarily a diagnosis based on clinical history and laboratory data. Some physical findings may be associated with primary APS, but patients with secondary APS are more likely to have findings on physical examination.
-Thrombosis or stroke - Possible residual neurologic findings
-Cutaneous manifestations
.These may include digital cyanosis, livedo reticularis, digital gangrene, and leg ulcers. The cause of these features remains otherwise unexplained.
.Other features related to cutaneous manifestations, with a cause that remains unexplained, include transient ischemic attacks or amaurosis fugax, positive result from the Coombs test, hemolytic anemia, chorea, and chorea gravidarum.
.Discoid rash (ie, erythematous raised patch with keratotic scaling and follicular plugging) is a criterion. Older lesions may be atrophic. Again, the cause remains unexplained.
.Photosensitivity with an unexplained cause is another criterion.
The following are physical findings that should be considered secondary to other autoimmune disorders and an appropriate evaluation should be undertaken.
-Arthritis: Patients may have nonerosive arthritis involving 2 or more peripheral joints, and the cause cannot otherwise be determined.
-Serositis: This may be (1) pleuritis or pleural effusion or (2) pericarditis or pericardial effusion, the cause of which cannot be explained.
-Renal disorder: Proteinuria of 0.5 g/d or the presence of cellular casts, without another cause, is a criterion for APS.
-Neurologic disorder: Criteria include seizures in the absence of other causes or psychosis in the absence of other causes.
-Hematologic disorder: Features, without an otherwise explainable cause, include
(1) hemolytic anemia with reticulocytosis,
(2) leukopenia of less than 4000 cells/mm3 on at least 2 occasions,
(3) lymphopenia of less than 1500 cells/mm3, or
(4) thrombocytopenia of less than 100,000 cells/mm3.
-Immunologic disorder: Again, the cause remains unexplained.
The clinical manifestations of SLE include the following:
.Skin lesions - 84-71%
.Arthritis - 63-95%
.Nephritis - 46-77%
.Raynaud phenomenon - 10-58%
.Neuropsychiatric features - 0-59%
.Lymphadenopathy - 0-58%
.Pleurisy - 37-56%
.Mucous membrane ulceration - 7-54%
.Pericarditis - 29-45%
.Splenomegaly - 9-18%
.Aseptic necrosis - 0-10%
.Clinical evidence of glomerulonephritis is found in more than 50% of cases. However, if biopsies are performed on all patients, the incidence of some nephritis may be as high as 90%. SLE is associated with encephalopathy and seizures, to a lesser degree with ischemic stroke, and, rarely, with subarachnoid hemorrhage.

Causes :
Like other autoimmune disorders, APS does not have a known etiology.Passive transfer of maternal antibodies mediate autoimmune disorders in the fetus and newborn. The mechanism of excess autoantibody production and immune complex formation is not well understood, although current investigation is focused on abnormal regulator functions and the possibility of a slow virus infection. In addition, certain genetic factors may be important, as indicated by a number of family and twin studies for systemic lupus erythematosus (SLE) and the demonstration of an increased frequency of HLA-DR2, HLA-DR3, and HLA-DR4 null alleles in patients with SLE.
Significant controversy still exists regarding the role of oral contraceptives in inducing SLE. Antinuclear antibodies (ANAs) associated with LP were reverted to negative when the drug was discontinued. Some patients using the intrauterine device complain of dysmenorrhea and recurrent infections, especially those taking prednisone and cytotoxic drugs. Although the incidence of SLE in families was initially believed to be no greater than in the general population, this is no longer thought to be true.
PL molecules are ubiquitous in nature and are present in the inner surface of the cell (ie, on the inner or outer surface of the cell membrane or intracellular organelles) and in microorganisms. Therefore, during infectious disease processes, including viral (eg, HIV, Epstein-Barr virus [EBV], cytomegalovirus [CMV], adenoviruses), bacterial (eg, bacterial endocarditis, tuberculosis, Mycoplasma pneumonia), spirochetal (eg, syphilis, leptospirosis, Lyme disease), and parasitic (eg, malaria infection), the disruption of cellular membranes may occur during cell damage. PLs release and stimulate aPL antibodies.
The SWISS PROT protein database revealed high homology between the hexapeptides that bind to ILA-1, ILA-3, and H-3 mAbs and the membrane particles of different bacteria and viruses. The sequence LKTPRV showed homology to 8 different bacteria (eg, Pseudomonas aeruginosa) and homologies to 5 types of viruses (ie, polyoma virus, human CMV, adenovirus). The sequence TL-RVYK shows homology to 8 different bacteria, including Haemophilus influenzae, Neisseria gonorrhoeae, and Shigella dysenteriae, and to viruses such as EBV and HIV. Therefore, data might support the theory predicting that epitope mimicry is involved in the propagation of the autoimmune status.
Autoantibodies include the following:
Antiphospholipid
Anticardiolipin
Antiphosphatidylinositol
Antiphosphatidylserine
Antiphosphatidylcholine
Anti–beta-2 glycoprotein I
Antinuclear antibody
Anti-DNA (double- or single-stranded)
Anti-Sjögren syndrome A antibody (Ro)
Anti-Sjögren syndrome B antibody (Ia)
Antibodies against microorganism(s) associated with infection or vaccination include the following:
Antibacterial PL
Antibacterial protein
Antiviral glycoprotein
Anti-Sjögren syndrome A antibody (Ro) and anti-Sjögren syndrome B antibody (Ia): These are associated with neonatal lupus erythematosus, including congenital complete heart block. These antibodies are usually present in patients with Sjögren syndrome.

Differential Diagnoses :
Preeclampsia
Thymic Tumors

Other Problems to Be Considered :
In women meeting the clinical criteria of early pregnancy loss, care must be taken to assure that the evaluation of spontaneous abortions prior to the 10 weeks’ gestation has included the appropriate evaluation to be considered unexplained.
Other causes of thrombocytopenia such as HIV infection, drug-induced thrombocytopenia, thrombotic thrombocytopenia, gestational thrombocytopenia, and preeclampsia should be considered. Other autoimmune disease should be ruled out in patients with thrombocytopenia.
Many manifestations of SLE can be seen in women with APS. A complete evaluation to exclude SLE as a primary disorder is appropriate if symptoms are present.

Laboratory Studies :

.Antiphospholipid syndrome (APS) is diagnosed when the patient has lupus anticoagulant (LAC) or IgG or IgM anticardiolipin (aCL) in medium-to-high levels, or both, on 2 occasions at least several weeks apart.
-Antiphospholipid (aPL) antibodies are detected by conventional and specific solid-phase or enzyme-linked immunoassays. Results are measured as GPL (IgG aCL), MPL (IgM aCL), or aPL (IgA aCL) units and reported in semiquantitative terms such as negative, low-positive, medium-positive, or high-positive.
-Isolated IgA aCL results are also of uncertain clinical significance and are not diagnostic of APS. An easy and reliable test would significantly help detection and follow-up of affected patients.
-Autoantibodies include antinuclear antibodies (ANAs), aCL antibodies, anti-DNA antibodies (single- or double-stranded), and anti-b2GPI.
.SLE is associated with lower serum complement levels measured either as total hemolytic complement activity CH50 or as levels of the third and fourth components of complement C3 and C4, respectively. Decreased levels of these are indicative of consumption by immune complexes. However, preeclampsia is associated with an increased serum complement level.
.Indications for testing for aPL antibodies include the following:
Obstetric indications
Unexplained fetal death or stillbirth
Recurrent pregnancy loss (3 or more spontaneous abortions with no more than 1 live birth)
Unexplained second or third trimester fetal death
Severe preeclampsia at less than 34 weeks’ gestation
Unexplained severe fetal growth restriction
Chorea gravidarum
Nonobstetric indications
Nontraumatic thrombosis or thromboembolism (venous or arterial)
Stroke, especially in individuals aged 24-50 years
Unexplained transient ischemic attack
Unexplained amaurosis fugax
Autoimmune thrombocytopenia
Autoimmune hemolytic anemia
Unexplained prolongation of a clotting assay
Transient ischemic attacks
Livedo reticularis
SLE or other connective tissue disorder
False-positive serologic test result for syphilis
.Laboratory criteria for the diagnosis of APS are as follows:
.LAC is detected by PL-dependent clotting assays, without correction with normal plasma. Results are confirmed by demonstrating PL dependency. The activated partial thromboplastin time (aPTT) is prolonged. Sera are screened for anticoagulant activity by mixing them with platelet-pool normal sera and assaying the aPTT. Several laboratory measurements are available for the assessment of LAC.
.For aCL or anti-b2GPI antibodies, an IgG isotype greater than 12-20 GPL units (medium- to high-positive) detected in a standardized assay using standard serum calibrators is indicative.
Hematologic and serologic values of APS are as follows:
Lupus anticoagulant
Prolonged clotting times with any of the following:
aPTT
Kaolin clotting time
Dilute Russell viper venom time
Plasma clotting time
These prolongations should be confirmed with one of the following:
Mixing studies with normal plasma, clotting time will remain prolonged with LA
Platelet neutralization test (recommended by some authorities
Anticardiolipin antibodies: Many aCL antibodies correlate poorly with the clinical manifestations of APS. At present, only IgG and IgM in moderate and high levels are recommended to be used in the diagnosis of APS.
False-positive results from the VDRL test may be present.
All studies need to be repeated in at least 6 weeks for confirmation before the diagnosis of APS is appropriate.

Imaging Studies :
Appropriate neurologic or imaging studies should be performed based on clinical findings (ie, in the presence of CNS symptoms, a CT scan or MRI).
Histologic Findings :
Histologically, 6 classes of lupus glomerulonephritis have been recognized by the World Health Organization.
Class I - Normal glomeruli observed with light microscopy; may show deposits with immunofluorescence or electron microscopy
Class II - Mesangial lesions
Class III - Focal proliferative glomerulonephritis
Class IV - Diffuse proliferative glomerulonephritis
Class V - Membranous glomerulonephritis
Class VI - Diffuse glomerular sclerosis

Treatment :

Medical Care
Pregnant women with antiphospholipid antibody syndrome (APS) are considered high-risk obstetric patients, and medical care is instituted with this in mind.
Obstetric care
Patients should be counseled in all cases regarding symptoms of thrombosis and thromboembolism and should be educated regarding, and examined frequently for, the signs or symptoms of thrombosis or thromboembolism, severe preeclampsia, or decreased fetal movement.
In patients with poor obstetric histories, evidence of preeclampsia, or evidence of fetal growth restriction, ultrasonography is recommended every 3-4 weeks starting at 18-20 weeks’ gestation.
Human chorionic gonadotropin (hCG) values in the first trimester can be followed to evaluate the viability of the pregnancy. If hCG levels are increasing normally (ie, doubling every 2 d) in the first month of pregnancy, a successful outcome is predicted in 80-90% of cases. However, when the increases are abnormal (ie, slower), a poor outcome is predicted in 70-80% of cases. Initiation of heparin in the face of a failing pregnancy should be undertaken with caution due to bleeding risks.
In patients with uncomplicated APS, ultrasonography is recommended at 30-32 weeks’ gestation to assess fetal growth. Lagging fetal growth may reflect uteroplacental insufficiency in patients with APS.
Anticoagulation with heparin is recommended in APS and pregnancy. Low molecular weight heparin (LMWH) may be used in these patients.
Importantly, counsel the patient regarding potential adverse effects of heparin. Heparin-induced osteoporosis occurs in 1-2% of cases.
Drugs such as chloroquine and cytotoxic agents are not recommended during pregnancy, and patients should stop taking these drugs several months prior to becoming pregnant.
Warfarin may be substituted for heparin during the postpartum period to limit further risk of heparin-induced osteoporosis and bone fracture.
Splenectomy during the early second trimester or at the time of cesarean delivery may be considered in patients with thrombocytopenia refractory to glucocorticoid therapy.
Bone density studies should be considered in patients receiving anticoagulation with heparin or LMWH due to the risks of osteopenia. This may be most important in women who have been treated in a previous pregnancy or are planning pregnancy.
Intravenous immunoglobulin (IVIG): Infused immunoglobulins may modulate aCL antibodies levels by 3 mechanisms.
Antiidiotypic antibodies may be present in the IVIG preparation. These antiidiotypic antibodies may bind autoantibodies to form idiotype-antiidiotype dimers, resulting in neutralization of autoantibody effects.
Antiidiotype antibodies may bind and down-regulate B-cell receptors, resulting in a decrease in autoantibody production.
Antiidiotype antibodies might bind receptors of regulatory T cells, resulting in suppression of lymphokine production and decreased activation of autoantibody-producing B cells.
Landry-Guillain-Barré-Strohl syndrome (LGBSS) of acute inflammatory demyelinating polyradiculoneuropathy can be seen in patients with APS and lupus.
Patients usually present with progressive bilateral and symmetrical muscle weakness accompanied by mild sensory symptoms, including paresthesia, numbness, and tingling. The disease can progress to involve the respiratory muscles, resulting in respiratory failure. Two thirds of the patients have a history of viral-like infections 1-3 weeks prior to the onset of symptoms.
Recently, CMV infection has been incriminated as a potential etiologic agent in some pregnant patients presenting with LGBSS.
Acute inflammatory demyelinating polyradiculoneuropathy is a rare disease with an incidence of approximately 1-1.5 cases per 100,000 LGBSS cases per year. LGBSS is exceedingly rare in pregnancy.
Nonobstetric care
Immunosuppressive agents are recommended for patients with SLE with secondary APS.
Thromboprophylaxis is recommended.
Patients should be evaluated for renal disease, (glomerulonephritis, end-stage renal disease), anemia, and thrombocytopenia.
Note the following:
The medications shown should not be used in the presence of contraindications.
Close obstetric monitoring of the mother and fetus is necessary in all cases.
The patient should be counseled in all cases regarding symptoms of thrombosis and thromboembolism.
Surgical Care
Patients with APS, especially secondary APS, may require surgical interventions for long-standing complications of their autoimmune disorder.
Cardiac valvular surgery is recommended in patients with severe aortic regurgitation due to the noninfectious vegetations that are seen as a result of APS.
Splenectomy is recommended in patients with the chronic form of idiopathic thrombocytopenic purpura and is associated with remission in approximately 75% cases.
Thromboprophylaxis is recommended for any abdominal or orthopedic surgery.
Manage thrombotic or hemorrhagic complications. Be aware of associated thrombocytopenia, and use laboratory methods of perioperative anticoagulation monitoring in the setting of prolonged clotting times.
Consultations
The patient should be informed about potential maternal and obstetric problems, including fetal loss, thrombosis or stroke, PIH, fetal growth restriction, and preterm delivery. Consultation with specialists in Maternal-Fetal Medicine and Rheumatology should be considered.
In women with APS and one or more prior thrombotic event, lifelong anticoagulation with warfarin may be advisable to avoid recurrent thrombosis. An assessment by a Rheumatologist or Hematologist may also be helpful.

Medication
In women with well-recognized obstetric APS, anticoagulant prophylaxis is recommended during pregnancy and the postpartum period. Pregnant women with APS are considered at risk for thrombosis and pregnancy loss. Data suggest low-dose aspirin and heparin (either unfractionated heparin or LMWH) are the treatments of choice for prevention of pregnancy loss in pregnant women with APS and previous pregnancy losses. Pregnant women with APS and a history of thrombosis but no pregnancy loss only require treatment with heparin. Treatment is optional for patients with no history of pregnancy loss or thrombosis.
Heparin compounds
Unfractionated intravenous (IV) heparin and fractionated subcutaneous (SC) LMWH are the 2 choices for initial anticoagulation therapy. Warfarin therapy may be initiated in the postpartum stage.
These are used in the treatment or prophylaxis of clinically evident intravascular thrombosis. Special precaution should be exercised in obstetrical emergencies or massive liver failure.
LMWHs may also be used. Similar to unfractionated heparin, LMWHs are a class of anticoagulants termed glycosaminoglycans. LMWHs are derived from unfractionated heparin but have smaller, more standard average masses than heterogeneous unfractionated heparin.
Unlike standard heparin, LMWHs have higher specificity for factor Xa and have fewer effects on platelet activity. As a result, LMWH may cause bleeding less often, while still retaining anticoagulant effects. LMWHs may be associated with less risk of heparin-induced osteoporosis.

Heparin, unfractionated
Indicated to decrease risk of thrombosis and pregnancy loss in pregnant women with APS.Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.
Dosing
Adult
APS with prior fetal death/recurrent pregnancy loss: 15,000-20,000 U/d SC divided q12h plus low-dose aspirinAPS with prior thrombosis or stroke: Adjusted dose heparin SC q12h to maintain aPTT within target rangeAPS without prior pregnancy loss or thrombosis: 15,000-20,000 U/d SC divided q12h (treatment optional)
Pediatric
Adolescents: Administer as in adults
Interactions
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity
Contraindications
Documented hypersensitivity; subacute bacterial endocarditis, active bleeding, history of heparin-induced thrombocytopenia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hemorrhage, monitor aPTT, adjust dose accordingly; caution in severe hypotension and shock; heparin-induced osteoporosis

Enoxaparin (Lovenox)
Indicated to decrease risk of thrombosis and pregnancy loss in pregnant women with APS.Prevents DVT, which may lead to pulmonary embolism in patients undergoing surgery who are at risk for thromboembolic complications. Enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, preferentially increases inhibition of factor Xa.
Dosing
Adult
APS with prior fetal death/recurrent pregnancy loss: 40 mg/d SC plus low-dose aspirinAPS with prior thrombosis or stroke: 1 mg/kg SC q12hAPS without prior pregnancy loss or thrombosis: 40 mg/d SC (treatment optional)
Pediatric
Adolescents: Administer as in adults
Interactions
Platelet inhibitors or oral anticoagulants such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding
Contraindications
Documented hypersensitivity; major bleeding, thrombocytopenia
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
If thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminases may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated or LMWH; 1 mg of protamine sulfate reverses effect of approximately 1 mg of enoxaparin if significant bleeding complications develop; heparin-induced osteoporosis; monitor target anti-Xa levels, adjust dose accordingly
Antiplatelet agents
Randomized controlled trials demonstrate improved fetal survival when pregnant women with APS and prior pregnancy losses are treated with low-dose aspirin plus heparin compared with low-dose aspirin alone.

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)
Antiplatelet effect indicated to decrease risk of thrombosis and pregnancy loss in pregnant women with APS. Inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. Used in low dose to inhibit platelet aggregation and improve complications of venous stasis and thrombosis.
Dosing
Adult
1-2 mg/d PO for antiplatelet effect; not to exceed 325 mg/d (low-dose aspirin)
Pediatric
Adolescents: Administer as in adults
Interactions
Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Contraindications

Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants

Special Concerns
Regarding corticosteroid therapy, administer supplementation to cover the labor or cesarean delivery in patients currently receiving steroids or those recently treated with these drugs.
No evidence indicates adverse effects related to breastfeeding, although breastfeeding is not recommended if high doses of cytotoxic or immunosuppressive agents are required.
Pregnancy in itself is not harmful to the mother or the baby unless the added work related to the newborn and the emotional stress in the family prove to be too much for a particular patient. Therapeutic abortions are generally not indicated in pregnant women with autoimmune disease.
Epidural anesthetic is not recommended if the mother has a marked drop in the maternal platelet count.
The use of forceps or the vacuum extractor should be individualized.

PREMENSTRUAL SYNDROME

Introduction :
Premenstrual syndrome (PMS) is a diverse constellation of cyclic physical and emotional symptoms, occurring monthly during the luteal phase of the menstrual cycle (ovulation to menstruation). This phase is followed by a symptom-free period of at least 1 week, beginning after the onset of menses. Of all the symptoms, the emotional and behavioral symptoms are the most devastating. In an attempt to define and treat the psychological symptoms, the American Psychiatric Association has described premenstrual dysphoric disorder (PMDD). PMDD requires the presence of at least one of 4 core symptoms (irritability, dysphoria, labile mood, tension) and at least 5 of 11 other symptoms. Symptoms must markedly impair functioning and interfere with normal activities.
I. Incidence.
It has been reported that 70% to 90% of the female population will admit to recurrent menstrual problems. Between 20% and 40% report some degree of temporary mental and physical dysfunction and 2% to 5% may be incapacitated.
PMS is cross-cultural and affects women of all races, socioeconomic status, and professions. There may be an increased incidence with age and major life stresses. Demographic data are contradictory concerning genetic contribution, effects of number of pregnancies, and educational level. Women with severe PMS may have a lifetime increased incidence of affective disorders.
II. Etiology.
Evidence supports the association of PMS with abnormal neurotransmitter response to normal ovarian function. Recent research has confirmed that women with PMS have normal levels of both estrogen and progesterone, are not vitamin or mineral deficient, have normal prolactin and thyroid levels, and are euglycemic. Of the possible mediators of ovarian steroid action in the central nervous system, serotonin, gamma-amino butyric acid (GABA) receptors, and beta-endorphins are the best studied.
A. Serotonin.
The association of serotonin with mood and appetite disturbances is well documented, and the sex steroidal hormones do modulate serotonergic activity. Women with PMS have significantly lower serotonin levels during the luteal phase, as measured in peripheral blood, compared with normal controls. This may be due to impaired postsynaptic serotonergic response in PMS patients. Compounds that increase serotonin levels have been shown to decrease symptoms of PMS.
B. Beta-endorphin
levels may be lower in PMS patients during both the periovulatory and premenstrual phases of the menstrual cycle. Substances that increase beta-endorphins improve PMS symptoms.
C. GABA receptors
The GABA receptors, associated with control of anxiety, are stimulated by progesterone, which may be a mechanism in the modulation of anxiety in PMS.
III. History.
PMS is a polysymptomatic disorder and the syndrome may last anywhere from 3 to 21 days. Symptoms do not all begin on the same day nor will women have the same symptoms each month or throughout their lives. The following is a partial list of symptoms:
A. Behavioral symptoms:
depression, irritability, tension, lethargy, mood swings, anger, uncontrolled crying, aggression, panic attacks, anxiety, social withdrawal, change in memory or concentration, change in libido, poor impulse control.
B. Physical symptoms
-Neurologic: migraines and other headaches, syncope, vertigo.
EtiologyMetabolic: breast tenderness, edema.
-Cardiovascular: palpitations, ectopic beats, paroxysmal tachycardia.
-Gastrointestinal: nausea, abdominal bloating, flatulence, constipation, diarrhea.
-Urinary: oliguria, urethritis, cystitis, enuresis, urinary retention.
-Dermatologic: acne, urticaria.
-Musculoskeletal: pain and swelling of the joints and muscles.
C. Chronic medical problems,
such as diabetes and asthma, as well as psychological disorders may worsen premenstrually, a condition termed premenstrual magnification.
IV. Physical examination.
A complete physical examination including a pelvic examination is necessary to rule out other causes such as ovarian cysts, fibroids, pelvic inflammatory disease, endometriosis, and thyroid disease. It is also important to perform a complete mental status examination to rule out psychopathology. There are no characteristic physical findings of PMS.
V. Investigative procedures.
The diagnosis of PMS depends on the temporal relationship of psychological and somatic symptoms with menstruation rather than the presence of symptoms alone. It is the recurring symptoms during the luteal phase followed by a symptom-free time that defines PMS. A thorough medical, sexual, and psychological history as well as physical examination and laboratory studies are necessary to identify PMS and to rule out other disorders.
A. Menstrual chart.
Evaluation should include a detailed diary of symptoms charted against the menstrual cycle .
The chart should show the length of the menstrual cycle, duration of bleeding, and regularity or irregularity of menstruation. By definition, PMS occurs only during ovulatory cycles.
Each symptom along with its severity can be charted each day. The patient should be sure to include eating patterns if they vary with the cycle.
A full three cycles are optimal for evaluation.
Posthysterectomy patients may still experience PMS if they retained their ovaries, so their 3-month chart will show the same characteristic pattern.
B. Laboratory tests
should be ordered as indicated by history and/or examination to rule out other disease as a source of the patient's symptoms.
VI. Management.
Since PMS represents an abnormal response to the physiologic ovulatory cycle, management can be directed to:
Altering the cycle.
Changing the body's response to the cycle.
Treating the symptoms themselves.
A. Self-help steps
Education is one of the most important components in the management of PMS.
Knowledge of the menstrual cycle, as well as female anatomy and physiology can aid in understanding this disorder.
It is also helpful to read the available literature on PMS.
Keeping a menstrual chart helps a woman achieve awareness of her menstrual cycle as well as her premenstrual symptoms.
Exercise. Regular aerobic exercise at least three or four times per week, continuing through the premenstrual phase, may reduce symptoms of PMS. This is especially true of the physical symptoms including breast tenderness, fluid retention, and abdominal cramping. Exercise has been shown to reduce stress and anxiety, increasing one's sense of well-being.
Stress management. Women should be encouraged to reduce the demands that they make on themselves and on others. Relaxation, visualization, and hypnosis are some other important methods of stress reduction. Supportive psychotherapy and reflexology may also be beneficial .
Diet and nutrition improves one's overall feeling of health and may be helpful with PMS. Recommended dietary changes include increasing complex carbohydrates and green vegetables and decreasing simple sugars, fats, and processed foods. Unfortunately, specific studies of the effect of diet on PMS have not demonstrated a benefit, with the exception of eliminating caffeine, which helps reduce breast tenderness and low salt/low fat diet, which improves fluid retention.
B. Food supplements
Vitamin B6. Pyridoxine is a coenzyme in the biosynthesis of serotonin and dopamine, probable mediators of PMS. Some studies have shown a benefit with vitamin B6 in doses well above the recommended daily allowance (RDA), starting at 25 mg twice daily and increasing to 100 mg per day. Higher doses to 300 mg have been studied but carry a significant risk of peripheral neuropathy.
Vitamin E in doses of 400 to 600 IU/day has, in some studies, alleviated the symptom of breast tenderness associated with PMS.
Calcium improves symptoms of water retention, abdominal cramps, and mood changes in doses of 1,000 mg/day. One study has also shown improvement with food cravings.
Magnesium supplementation, 300 to 500 mg daily during the luteal phase, has been shown to improve symptoms of mood changes and fluid retention in small randomized crossover trials.
There are now many PMS formulae that combine vitamins and mineral supplements. Of these only a few, Lurline PMS tablets and Optivite have been studied and shown to have some efficacy.
The use of cis-linoleic acid (evening primrose oil), 1,500 mg bid, is an old remedy for depression and anxiety symptoms of PMS. Randomized, double-blind trials have been unable to substantiate its efficacy.
C. Drug therapy.
Drug therapy can be tailored to alleviate specific symptoms or to obliterate the menstrual cycle itself.
Oral contraceptive pills (OCPs) are often used as a first-line treatment for premenstrual symptoms but few studies have substantiated efficacy except with some physical symptoms such as cramps and bloating.
Monophasic preparations may be more effective than triphasic combinations.
Patients should be warned that psychological symptoms could worsen when taking OCPs.
In the past, progesterone was widely used for PMS, but well designed studies do not demonstrate efficacy. The general popularity of using progesterone for PMS may be due to its mildly sedative properties.
Synthetic progestins (medroxyprogesterone acetate, norethindrone) are used as contraceptives or to regulate menstrual flow.
In some women, medroxyprogesterone acetate (Depo-Provera) eliminates the menstrual cycle and can in this way improve some of the physical symptoms of PMS.
Progestins should be used with caution in women with PMS because they can exacerbate psychological symptoms, especially anxiety and depression.
Gonadotropin releasing hormone (GnRH) agonists obliterate the menstrual cycle and are therefore very effective in controlling symptoms of PMS. Randomized trials have demonstrated significant improvement in PMS symptoms; however, psychological symptoms are not as consistently improved as physical symptoms.
These medications are expensive and must be used with add-back estrogen and progesterone to reduce menopausal side effects such as osteoporosis.
Use of GnRH agonists without add-back hormonal replacement must be limited to less than 6 months.
Leuprolide acetate, 3.75 mg IM monthly OR 11.25 mg q 3 months OR
Goserelin, 3.6 mg SQ implant monthly, OR
Nafarelin, 200 g bid intranasally, are the most commonly used preparations.
Selective serotonin reuptake inhibitors (SSRIs) are highly effective in the treatment of severe PMS. Multiple controlled double-blind studies have shown efficacy, with resolution of symptoms nearly immediately and in smaller doses than is normally used for depression.
Fluoxetine has been studied in the most detail and is effective in doses as small as 5 mg and up to 20 mg po qd. Efficacy has been shown with a daily dose throughout the month and also with treatment only during the luteal phase of the menstrual cycle (i.e., with symptoms). Although generally well tolerated, side effects include insomnia, anxiety, gastrointestinal disturbances, and sexual dysfunction.
Paroxetine, 5 to 30 mg/day, and sertraline, 25 to 150 mg/day, have not been as extensively studied as fluoxetine for PMS but are probably equally as effective.
Clomipramine, a tricyclic antidepressant with serotonin and noradrenaline reuptake inhibiting properties, has been successfully used to treat severe psychological symptoms of PMS.
Effective doses are 25 to 75 mg PO qd during the luteal phase of the menstrual cycle.
Side effects including fatigue, weight gain, nausea, seizures, and dry mouth may limit its usefulness.
Anxiolytics
Buspirone may be useful in patients with predominant symptoms of anxiety and it is neither sedating nor habit forming. The initial dosage is 5 mg tid, gradually increasing to cessation of symptoms with a maximum dose of 60 mg/day.
Alprazolam controls anxiety and irritability if given during the symptomatic period.
However, its use is associated with sedation, tolerance, and dependence and it should be used cautiously.
Dosage is 0.25 mg tid, increasing to a total daily dose of 4 mg. At the beginning of menses, the dose should be decreased by 25% each day.
Diuretics. Abdominal bloating and water retention are some of the most common symptoms of PMS. Despite this, actual weight gain and change in total body water have not been well demonstrated in studies. In this light, diuretics should be used with caution. Spironolactone, 25 mg tid or qid, during the luteal phase of the menstrual cycle may be effective for abdominal bloating and also may improve irritability, depression, and food cravings.
Danazol, a synthetic androgen, is effective in suppressing symptoms of PMS. However, its side effects, including weight gain and virilization may be unacceptable to patients.
D. Surgery.
Bilateral oophorectomy is rarely indicated in PMS treatment and should be reserved only for patients with severe PMS and after failure of all conservative measures. Complete resolution should be demonstrated with GnRH agonist suppression prior to undertaking surgery. Consideration should also be made of the number of years left until menopause.

Premature Rupture of Membranes (PROM) , Dr. Alaa Mosbah ,MD OBS&GYN

Definition:
It is rupture of membranes before onset of labour(PROM) .
Also rupture of membrane before 37 weeks gestation is called PPROM
Incidence:
10% of term pregnancies .
Preterm PROM complicates approximately 3 percent of pregnancies and leads to one third of preterm births
Aetiology:
The following factors are incriminated:
1. Cervical incompetence.
2. Polyhydramnios.
3. Multiple pregnancy.
4.Malpresentations as the presenting part is not fitting against the lower uterine segment .
5. Chorioamnionitis.
6. Low tensile strength of the membranes.A decrease in the collagen content of the membranes has been suggested to predispose patients to preterm PROM
7.those who have lower socioeconomic status, are smokers, have a history of sexually transmitted infections, have had a previous preterm delivery
Diagnosis:
The diagnosis of PROM requires a thorough history, physical examination, and selected laboratory studies. Patients often report a sudden gush of fluid with continued leakage. Physicians should ask whether the patient is contracting, bleeding vaginally, has had intercourse recently, or has a fever.
1- History: of gush of fluid per vaginum that moists vulval pads.
Drawback: Vulval pads can be moisted with urine or vaginal
discharge which can be mistaken with the amniotic fluid.

2- Nitrazine paper test:
The colour turns from yellow to deep blue due to alkalinity of the
amniotic fluid.
Drawback: blood, semen or vaginal infection are alkaline media give the same result.
3- Laboratory analysis: for creatinine, urea and uric acid in the fluid
sample.
Drawback: these components are present in the urine.
4- Fern test:
Visualization of fern-like pattern of dried amniotic fluid on a glass
slide under microscopy due to presence of protein.
Drawback: protein may be present in urine.
5- Sterile speculum examination:
to observe the escape of amniotic fluid from the external os.
6- Dye injection:
Through abdominal needle under ultrasonic guide into the amniotic
sac and observation of its passage through the external os or even in
the vulval pad.
Drawback: It carries risk of foetal trauma particularly if a large
amount of the amniotic fluid was drained.
7- Vernex, meconium or alpha-fetoprotein detection:
in the fluid sample is diagnostic.
8- Ultrasound:
is an ideal non-invasive technique for the detection of the residual amount of amniotic fluid. Oligohydramnios is diagnosed if the measurement of the largest bocket of the amniotic fluid is 1 cm or less . The largest bocket is usually present between the anterior shoulder and the neck.Or amniotic fluid index less than 5 cm .

Complications:
1. Preterm labour: with the risk of prematurity.
2. Infection: chorio-amnionitis, septicaemia and foetal pneumonia.
3. Foetal deformities and distress: due to oligohydramnios.
Management:
(1) Gestational age over 36 weeks:
- In absence of infection, foetal distress and abnormal lie,
wait for 24 hours as about 90% of patients with PROM will
pass into spontaneous labour. Prophylactic antibiotic can be
given during this period.
- PGE2 and / or oxytocin is used for induction of labour in
patients did not pass into labour after 24 hours.
(2) Gestational age between 34-36 weeks:
- In absence of infection and foetal distress, wait for 48
hours as rupture of membrane itself will accelerates lung
surfactant production and hence lung maturity.
- Induce labour after 48 hours with PGE2 and /or oxytocins.
- Prophylactic antibiotics is given during this period.
- Caesarean section is indicated in breech presentation < 36
weeks’ gestation.
(3) Gestational age between 28-34 weeks:
In absence of infection, the main aim is to manage the case
conservatively till the 35th week when lung maturity mostly occurs
and the baby can survive.
Conservative management as follow:

i) Rest in bed as long as there is escape of liquor
with restriction of efforts later on particularly
those that increase intra-abdominal pressure.
ii) Temperature is recorded every 4 hours.
iii) Observation for malaise, abdominal pain,
uterine tenderness and amount of escaped liquor
on sterile vulval pads.
iv) Leucocytic count and C-reactive protein may
be done every other day.
v) Prophylactic antibiotics may be given although
this is not advised by some authors as it may lead
to colonisation of resistant strains of organisms in
the genital tract.
vi) Tocolytic drugs : are given if uterine activity
starts.
vii) Corticosteroid therapy: is given for 48 hours
if labour was imminent or will be induced before
35 weeks.
(4) Gestational age less than 28 weeks:
There is little chance of foetal survival and the condition is usually considered as inevitable abortion.

RECOMMENDATIONS
The following recommendations and conclusions are based on good and consistent scientific evidence (Level A):
For women with premature rupture of membranes (PROM) at term, labor should be induced at the time of presentation, generally with oxytocin infusion, to reduce the risk of chorioamnionitis.
Patients with PROM before 32 weeks of gestation should be cared for expectantly until 33 completed weeks of gestation if no maternal or fetal contraindications exist.
A 48-hour course of intravenous ampicillin and erythromycin followed by 5 days of amoxicillin and erythromycin is recommended during expectant management of preterm PROM remote from term to prolong pregnancy and to reduce infectious and gestational age-dependent neonatal morbidity.
All women with PROM and a viable fetus, including those known to be carriers of group B streptococci and those who give birth before carrier status can be delineated, should receive intrapartum chemoprophylaxis to prevent vertical transmission of group B streptococci regardless of earlier treatments.
A single course of antenatal corticosteroids should be administered to women with PROM before 32 weeks of gestation to reduce the risks of respiratory distress syndrome (RDS), perinatal mortality, and other morbidities.
The following recommendations and conclusions are based on limited and inconsistent scientific evidence (Level B):
Delivery is recommended when PROM occurs at or beyond 34 weeks of gestation.
With PROM at 32 to 33 completed weeks of gestation, labor induction may be considered if fetal pulmonary maturity has been documented.
Digital cervical examinations should be avoided in patients with PROM unless they are in active labor or imminent delivery is anticipated.
The following recommendations and conclusions are based primarily on consensus and expert opinion (Level C):
A specific recommendation for or against tocolysis administration cannot be made.
The efficacy of corticosteroid use at 32–33 completed weeks is unclear based on available evidence, but treatment may be beneficial particularly if pulmonary immaturity is documented.
For a woman with preterm PROM and a viable fetus, the safety of expectant management at home has not been established.
Table: Management of Premature Rupture of Membranes Chronologically

Gestational Age
Management
Term (37 weeks or more)
Proceed to delivery, usually by induction of labor
Group B streptococcal prophylaxis recommended
Near term (34 weeks to 36 completed)
Same as for term
Preterm (32 weeks to 33 completed weeks)
Expectant management, unless fetal pulmonary maturity is documented
Group B streptococcal prophylaxis recommended
Corticosteroid—no consensus, but some experts recommend
Antibiotics recommended to prolong latency if there are no contraindications
Preterm (24 weeks to 31 completed weeks)
Expectant management
Group B streptococcal prophylaxis recommended
Single-course corticosteroid use recommended
Tocolytics—no consensus
Antibiotics recommended to prolong latency if there are no contraindications
Less than 24 weeks*
Patient counseling
Expectant management or induction of labor
Group B streptococcal prophylaxis is not recommended
Corticosteroids are not recommended
Antibiotics—there are incomplete data on use in prolonging latency.

Definitions:
Grades of Evidence
I Evidence obtained from at least one properly designed randomized controlled trial.
II-1 Evidence obtained from well-designed controlled trials without randomization.
II-2 Evidence obtained from well-designed cohort or case-control analytic studies, preferably from more than one center or research group.
II-3 Evidence obtained from multiple time series with or without the intervention. Dramatic results in uncontrolled experiments could also be regarded as this type of evidence.
III Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees.
Levels of Recommendations
Level A — Recommendations are based on good and consistent scientific evidence.
Level B — Recommendations are based on limited or inconsistent scientific evidence.
Level C — Recommendations are based primarily on consensus and expert opinion.

American College of Obstetricians and Gynecologists (ACOG). Premature rupture of membranes. Washington (DC): American College of Obstetricians and Gynecologists (ACOG); 2007 Apr. 13 p. (ACOG practice bulletin; no. 80). [103 references]

Progress of labour

Partograph

Partograph
•A partograph is a graphical record of the observations made of a women in labour
•For progress of labour and salient conditions of the mother and fetus
•It was developed and extensively tested by the world health organization WHO
Friedman's partogram devised in 1954 was based on observations of cervical dilatation and foetal station against time elapsed in hours from onset of labour. The time onset of labour was based on the patient's subjective perception of her contractility. Plotting cervical dilatation against time yielded the typical sigmoid or 'S' shaped curve and station against time gave rise to the hyperbolic curve.
•The partograph can be used by health workers with adequate training in midwifery who are able to :
- observe and conduct normal labour and delivery.
- Perform vaginal examination in labour and assess cervical diltation accurately
- plot cervical diltation accurately on a graph against time
•There is no place for partograph in deliveries at home conducted by attendants other than those trained in midwifery
•Whether used in health centers or in hospitals , the partograph must be accompanied by a program of training in its use and by appropriate supervision and follow up
Objectives

•early detection of abnormal progress of a labour
• prevention of prolonged labour
• recognize cephalopelvic disproportion long before obstructed labour
•assist in early decision on transfer , augmentation , or terminjation of labour
• increase the quality and regularity of all observations of mother and fetus
• early recognition of maternal or fetal problems
•the partograph can be highly effective in reducing complications from prolonged labor for the mother (postpartum hemorrhage, sepsis, uterine rupture and its sequelae) and for the newborn (death, anoxia, infections, etc.).

•early detection of abnormal progress of a labour
• prevention of prolonged labour
• recognize cephalopelvic disproportion long before obstructed labour
•assist in early decision on transfer , augmentation , or terminjation of labour
• increase the quality and regularity of all observations of mother and fetus
• early recognition of maternal or fetal problems
•the partograph can be highly effective in reducing complications from prolonged labor for the mother (postpartum hemorrhage, sepsis, uterine rupture and its sequelae) and for the newborn (death, anoxia, infections, etc.).
Partograph function

•The partograph is designed for use in all maternity settings , but has a different level of function at different levels of health care
• in health center, the partograph,s critical function is
to give early warning if labour is likely to be prolonged and to indicate that the woman should be transferred to hospital (ALERT LINE FUNCTION )
• in hospital settings, moving to the right of alert line serves as a warning for extra vigilance , but the action line is the critical point at which specific management decisions must be made
•other observations on the progress of labour are also recorded on the partograph and are essential features in management of labour
Components of the partograph

•Part 1 : fetal condition ( at top )
•Pqrt 11 : progress of labour ( at middle )
•Part 111 : maternal condition ( at bottom )
.Outcome
Part 1 : Fetal condition

•this part of the graph is used to monitor and assess fetal condition
•1 - Fetal heart rate
•2 - membranes and liquor
•3 - moulding the fetal skull bonesCaput

Basal fetal heart rate?
•< 160 beats/mi =tachycardia
• > 120 beats/min = bradycardia
• >100 beats/min = severe bradycardia
Decelerations? yes/no
Relation to contractions?
n Early
n Variable
n Late – -----Auscultation - return to baseline
> 30 sec è contraction
----- Electronic monitoring
peak and trough (nadir)è > 30 sec
membranes and liquor

•intact membranes ……………………………………….I
•ruptured membranes + clear liquor …………………….C
•ruptured membranes + meconium- stained liquor ……..M
•ruptured membranes + blood – stained liquor …………B
•ruptured membranes + absent liquor…………………....A

moulding the fetal skull bones

•Molding is an important indication of how adequately the pelvis can accommodate the fetal head
•increasing molding with the head high in the pelvis is an ominous sign of cephalopelvic disproportion
•separated bones . sutures felt easily ……………….….O
•bones just touching each other ………………………..+
•overlapping bones ( reducible 0 ……………………...++
•severely overlapping bones ( non – reducible ) ……..+++

Part11 – progress of labour

Cervical diltation
•Descent of the fetal head
•Fetal position
•Uterine contractions
•this section of the paragraph has as its central feature a graph of cervical diltation against time
•it is divided into a latent phase and an active phase
latent phase :

•it starts from onset of labour until the cervix reaches 3 cm diltation
•once 3 cm diltation is reached , labour enters the active phase
•lasts 8 hours or less
•each lasting < 20 sceonds at least 2/10 min contractions

Active phase :

•Contractions at least 3 / 10 min
•each lasting < 40 sceonds
•The cervix should dilate at a rate of 1 cm / hour or faster

Alert line ( health facility line )

•The alert line drawn from 3 cm diltation represents the rate of diltation of 1 cm / hour
•Moving to the right or the alert line means referral to hospital for extra vigilance

Action line ( hospital line )

•The action line is drawn 4 hour to the right of the alert line and parallel to it
•This is the critical line at which specific management decisions must be made at the hospital

Cervical diltation

•It is the most important information and the surest way to assess progress of labour , even though other findings discovered on vaginal examination are also important
•when progress of labour is normal and satisfactory , plotting of cervical diltation remains on the alert line or to left of it
• if a woman arrives in the active phase of labour , recording of cervical diltation starts on the alert line
• when the active phase of labor begins , all recordings are transferred and start by pltting cervical diltation on the alert line

Descent of the fetal head

•It should be assessed by abdominal examination immediately before doing a vaginal examination, using the rule of fifth to assess engagement
•The rule of fifth means the palpable fifth of the fetal head are felt by abdominal examination to be above the level of symphysis pubis
•When 2/5 or less of fetal head is felt above the level of symphysis pubis , this means that the head is engage , and by vaginal examination , the lowest part of vertex has passed or is at the level of ischial spines

Assessing descent of the fetal head by vaginal examination; 0 station is at the level of the ischial spine (Sp).

Uterine contractions

•Observations of the contractions are made every hour in the latent phase and every half-hour in the active phase
• frequency how often are they felt ?
• Assessed by number of contractions in a 10 minutes period
• duration how long do they last ?
Measured in seconds from the time the contraction is first felt abdominally , to the time the contraction phases off
•Each square represents one contraction
Palpate number of contraction in ten minutes and duration of each contraction in seconds

Part111: maternal condition

Name / DOB /Gestation
Medical / Obstetrical issues
Assess maternal condition regularly by monitoring :
•drugs , IV fluids , and oxytocin , if labour is augmented
• pulse , blood pressure
•Temperature
• Urine volume , analysis for protein and acetone

USING THE PARTOGRAPH POINTS TO REMEMBER

•It is important to realize that the partograph is a tool for managing labor progress only
•The partograph does not help to identify other risk factors that may have been present before labor started

•only start a partograph when you have checked that there are no complications of pregnancy that require immediate action
•a partograph chart must only be started when a woman is in labor,-- be sure that she is contracting enough to start a partograph
•if progress of labor is satisfactory , the plotting of cervical diltation will remain or to the left of the alert line

•when labor progress well , the diltation should not move to the right of the alert line
•the latent phase . 0 – 3 cm diltation , is accompanied by gradual shortening of cervix . normally , the latent phase should not last more than 8 hours
•the active phase , 3 – 10 cm diltation , should progress at rate of at least 1 cm/hour
•when admission takes place in the active phase , the admission diltation, is immediately plotted on the alert line

•when labor goes from latent to active phase , plotting of the diltation is immediately transferred from the latent phase area to the alert line

•diltation of the cervix is plotted ( recorded with an X , desent of the fetal head is plotted with an O , and uterine contractions are plotted with differential shading
•desent of the head should always be assessed by abdominal examination ( by the rule of fifths felt above the pelvic brim ) immediately before doing a vaginal examination
•assessing descent of the head assists in detecting progress of labor
•increased moulding with a high head is a sign of cephalopelvic disproportion

•vaginal examination should be performed infrequently as this is compatible with safe practice ( once every 4 hours is recommended )
•when the woman arrives in the latent phase , time of admission is 0 time
•a woman whose cervical diltation moves to the right of the alert line must be transferred and manged in an institution with adequate facilities for obstetric intervention , unless delivery is near

•when a woman ,s partograph reaches the action line , she must be carefully reassessed to determine why there is lack of progress , and a decision must be made on further management ( usually by an obesterician or resident )
•when a woman in labor passes the latent phase in less than 8 hours i.e., transfers from latent to active phase , the most important feature is to transfer plotting of cervical diltation to the alert line using the letters TR,
•Leaving the area between the transferred recording blank. The broken transfer line is not part of the process of labor
do not forget to transfer all other findings vertically

DR. Alaa

Elhawar Club, Mansoura

DR. Alaa mosbah

CONTRACEPTION

Introduction :
The contraceptive user has an array of methods from which to choose. Appropriate considerations include the user's age, need for concomitant protection against sexually transmitted infections, future plans for childbearing, health status, pattern of sexual activity, and feeling about method options. Method safety and efficiency are usually the two issues of greatest concern for users and clinicians. The morbidity for any methods of contraception is low.
The important trends in ensuring the safest possible use of contraception include the following:
Use of low-dose oral contraceptive products (i.e., ≤35 µg of estrogen, low-potency progestin).
Use of long-lasting progestins when estrogen may not be safely used.
Proper patient selection for the intrauterine device (IUD).
Use of barrier methods to decrease risk of sexually transmitted disease (STD), HIV, and hepatitis B virus transmission are sometimes used in addition to other contraceptives.
Careful counseling concerning sterilization including counseling the partner on the safety of vasectomy.
Use of emergency contraception (EC): postcoital.
Early recognition and diagnosis of pregnancy and ectopic pregnancy.
I. Oral contraceptives :
are the second most commonly used method overall and the most common method for patients younger than 30. The pill has undergone substantial changes since its development in the 1950s. Most important is the reduction in the amount of estrogen. Initially, pills contained 40 to 80 µg of ethinyl estradiol, whereas today 30 to 35 µg is the standard. This reduction of estrogen almost eliminates concern about cardiovascular risk in healthy nonsmoking women. Cardiovascular risk seems to be related to the thrombotic effect of estrogen, which is dose-related. At 35 µg the risk is not any higher than the baseline risk of a healthy woman. Figure 22.1 is a chart on relative potency of estrogens and progestins in currently available oral contraceptives.
A. Types of pills
Combined pills when used perfectly have a very low failure rate of approximately 0.1% to 3.0%. They provide a daily dose of estrogen and progestin for 21 days in a 28-day cycle. Almost all pills today are comparable in efficacy, side effects, and complications.
Estrogen acts by inhibiting FSH production and decreasing follicle development thereby limiting ovulation. It also may prevent implantation and potentiates the effects of progestins. Estrogen also stabilizes the endometrium.
Progestins inhibit luteinizing hormone (LH) release and, therefore, can interfere with ovulation. The endometrium atrophies, the cervical mucus becomes thick and hostile to sperm, and the fallopian tubes have decreased motility. Bleeding occurs when the estrogen and progestin are withdrawn, usually during the last 7 days of the 28-day cycle.
There are several different progestins used in oral contraceptives.
They are of varying potency but in each formulation potency is compensated by the dosage.
Progestins have an androgenic pharmacology and may affect lipid levels adversely; however, clinically this is rarely a problem.
Of the progestins, norethynodrel may produce estrogenic effects, and norethindrone acetate and norgestrel may produce antiestrogenic or androgenic effects or both. There had been some concern that the so-called newer progestins (gestodene, desogestrel, and norgestimate) present in third generation OCPs may incur higher thromboembolic risks. However, more recent data does not support this hypothesis .
Multiphasic preparations contain varying daily dosages of estrogen and progestin. Theoretically, this decreases the progestin dose and androgenic effects. Clinically, however, there is very little difference between the monophasic and multiphasic preparations.
The minipill contains progestin only and is taken continuously at the same time of day and with no cyclic interruption for maximum effectiveness. The preparation's main effects are on the endometrium, cervix, and fallopian tubes.
Failure rates of the minipill when it is used correctly are only slightly higher than combination pills, 0.5% to 3.0%.
It causes anovulation in only 40% to 60% of users.
Since the minipill has no estrogen, it is recommended for women who have a contraindication to the combined pill .
Minipills are often well tolerated by women who experience side effects, such as headaches, when using combined pills.
It is likely that some noncontraceptive benefits of pills, such as protection against pelvic inflammatory disease (PID), are mediated by progestin.
B. Contraindications and risk factors.
Certain systemic conditions contraindicate the use of the pill.
Women with absolute contraindication should never be given the pill.
For those with strong relative contraindications, risk and benefits should be weighed carefully.
C. Evaluation issues
When discussing options with the patient, it is important to determine whether or not she has any of the risk factors. It is also important to discuss lifestyle issues, noncontraceptive benefits, side effects, and severe complications. Recent evidence has confirmed that combined oral contraceptives are extremely safe. Some authors have suggested that pills should be available over-the-counter without a prescription.
Noncontraceptive benefits. The pill offers many benefits other than contraception and is used in the treatment of several clinical conditions. The following is a summary of these benefits:
Decreased menstrual flow, dysmenorrhea, and anemia.
Decreased fibrocystic changes of the breast with prolonged use.
Decreased risk of PID, although the risk of cervicitis may be increased.
Decreased acne.
Decreased ovarian and endometrial cancer risks. The risk of breast cancer may be slightly increased but tumors, when found, tend to be diagnosed earlier and are of a less aggressive type .
Decreased risk of ovarian cysts, although this may not be as true with the low-dose pills.
Decreased risk of rheumatoid arthritis.
Fewer ectopic pregnancies and abortions owing to its contraceptive effectiveness.
Lifestyle and other issues.
It must be stressed that pills do not provide protection from STDs, HIV, or hepatitis B transmission. Patients who are not mutually monogamous should be encouraged to also use a barrier method with the pill.
Family history should be explored to determine if occult risk factors exist .
Discussions with patients will reveal fears and misinformation that the clinician can correct.
A good understanding of the pill's benefits, risks, and method of use will increase compliance and effectiveness.
D. Dosage and type.
The axiom for determining pill dosage is to use the lowest dosage that provides effective protection from pregnancy.
Most women should be prescribed a 35-µg or less estrogen pill.
These pills contain the more potent ethinyl estradiol and may not have a markedly lower estrogenic effect than do pills containing 50 µg of mestranol.
Spotting or failure to have withdrawal bleeding are common problems associated with use of low-dose pills. Patients should be warned of these problems and advised that they often spontaneously resolve after three cycles.
Pills containing more than 50 µg estrogen (80 or 100 µg) are for the most part unavailable now. Pills containing 50 µg estrogen may occasionally be appropriate for women with severe acne, dysfunctional bleeding, or endometriosis.
Progestin-only pills may be the initial pill choice for postpartum or nursing mothers, women older than 30 to 35 years, or women who have vascular headaches.
The minipill is also a good choice for women who do not tolerate combined pills or for those who develop relative contraindications to the use of combined pills.
E. Instructions
Clinicians.
A thorough history including the foregoing risk factors, lifestyles, and considerations must be obtained.
A thorough examination including blood pressure, breast examination, Papanicolaou (Pap) smear and pelvic examination is done.
Be sure that every pill user is aware of the pill danger signs .
New users may benefit from an initial follow-up visit at 3 months to check blood pressure and review problems. Most users who discontinue use do so because of side effects. Thus, it is very important to emphasize that most of these side effects resolve spontaneously within the first 3 months of use .
Thereafter, annual examinations and Pap smears are appropriate.
For women older than 35 who may have risk factors, a blood sugar concentration and lipid panel should be checked. Healthy women with no family history do not need these tests.
Documentation of counseling and examination findings is essential.
It is important that the patient fully understands the method of taking the pill, the side effects, and the severe complications. She should know when and whom to call with any questions.
Patients.
Every pill user should memorize the five pill danger signs. The first letter of each symptom spells the acronym ACHES:
Abdominal pain.
Chest pain or shortness of breath.
Headaches.
Eye problems, such as blurred vision, flashing lights, or blindness.
Severe leg pain.
A pill user who develops a breast lump, notices growth or change in a mole, develops liver disease or jaundice, or becomes depressed should contact her clinician.
Pill users should know how to report problems to the clinician and know what to do if they experience bleeding, skip a period, or forget to take one or more pills.
A new pill user should start the first pack of pills within the first 5 days of menses.
Most can start on a Sunday, which makes it easy to remember and relegates menses to the weekdays.
If she cannot start within the first 5 days, a backup method for the first full cycle should be used.
Starting a package beyond the first 6 to 7 days may increase the failure rate.
In adolescents with a negative pregnancy test, an immediate start may be helpful to prevent forgetfulness. A backup method must be used for the first cycle.
Patients should take one pill a day at about the same time of day.
F. Sequelae
Pill hormones affect virtually every organ system, and about 40% of users notice side effects or noncontraceptive benefits. Severe complications are rare.
Complications and side effects. The major complications of pills are cardiovascular. These, however, are primarily limited to women older than 35 who smoke or have a history of other cardiovascular problems or diabetes.
Life-threatening complications:
Thrombophlebitis.
Deep pelvic vein thrombosis.
Pulmonary embolism.
Arterial thromboembolic events resulting in cerebrovascular accident or myocardial infarction.
Hepatic adenomas. These may regress after discontinuation of the pill.
Serious side effects include:
Hypertension.
Gallbladder disease.
Vascular headache.
Depression.
Other minor side effects, which usually improve with time, include:
Nausea.
Weight gain.
Breast tenderness.
Breakthrough bleeding.
Decreased libido.
Women who develop acne may want to discontinue use or change to formulations with lower androgen-potency progestins. Orthotricycline has been approved to treat acne.
Higher rates of cervical neoplasia (dysplasia, carcinoma in situ, and invasive carcinoma) have been reported for pill users. Whether this is an effect of the pill or of lifestyle is unclear. The pill can be continued with very careful follow-up.
Pill effects on subsequent fertility.
Resumption of ovulation is usually within the first 14 to 21 days of discontinuing the pill.
The pregnancy rate in the first 3 months lags behind that of users of other methods. However, within a year the rates are relatively the same.
There is no indication that infertility is increased by the pill.
Older data indicate that the higher dose pill may have caused a pregnancy rate lag of up to 42 months.
Noncontraceptive benefits. Use of the pill is associated with a decreased incidence of PID, ovarian and endometrial cancer, ectopic pregnancy, iron-deficiency anemia, rheumatoid arthritis, ovarian functional cysts, benign breast lumps, dysmenorrhea, and acne .
G. Clinical dilemmas
Optimal management of pill problems involves numerous clinical dilemmas.
Forgotten pills.
A woman who forgets to take one pill should double up the next day.
If two pills are missed, she should double up for 2 days and use a backup method of birth control until the next menstrual period.
If three or more pills are missed, the user should start a new pack of pills and use a second method of contraception as well.
If she is a Sunday starter, she may continue the pills until Sunday and then start a new package.
Breakthrough bleeding is a common occurrence in the first 3 months of starting the pill. If breakthrough bleeding persists beyond that time, a different formulation may be tried or a small amount of estrogen may be added in the first 7 days of the cycle (1.25 mg of conjugated estrogens or 1 mg of estradiol).
Skipped periods or amenorrhea. The pill's effect on the endometrium is dominated by progestin and causes atrophy. Amenorrhea may be a response to continued progestin stimulation.
If the patient takes the pills regularly and she is not concerned about the lack of a “withdrawal period,” nothing need be done. It may be advisable to check a pregnancy test, if there is any doubt about whether the pills are taken correctly.
If the patient is concerned, a period may be induced by adding estrogen, 1.25 mg of conjugated estrogens or 1 mg of estradiol for 21 days of the cycle. This can be done for one or two cycles to thicken the endometrial lining.
Alternatively, a patient may be switched to an oral contraceptive with a lower progestin potency.
Development of vascular headaches, hypertension, or cholestasis are reasons to discontinue the pill.
Development of cervical dysplasia is not a reason to discontinue the pill. Pap smear or colposcopy surveillance is necessary. These patients may be at risk for other STDs, HIV, and hepatitis B transmission and should be counseled to use a barrier method as well as the pill.
H. Special considerations
Adolescents may benefit in many ways by using the pill.
Cycles are regulated, are less painful, and have decreased blood loss.
There is less risk for PID, although the pill does nothing to mitigate against STDs, HIV, and hepatitis B transmission.
Adolescents who are not mutually monogamous should use a barrier method in addition to the pill.
Women older than 35 who are perimenopausal benefit from pill use.
The pill will regulate cycles.
There is increased bone density and less risk of rheumatoid arthritis.
It is an extremely effective method of birth control that should not be denied simply because of age.
“Morning-after pill” . Minipills may be given to women who have relative contraindications to the combination pills. It must be taken every day at the same time. If a pill is missed, a backup method must be used.
Postpartum and breast-feeding women also need effective protection.
Combination pills can be started after 3 weeks if postpartum and not breast-feeding.
A patient exclusively breast-feeding may start the minipill 6 weeks postpartum.
Combination pills are not recommended in women who are breast-feeding because estrogen can decrease the amount and quality of breast milk.
II. Injectable combination contraceptive :

A. Lunelle, a combination of medroxyprogesterone acetate and estradiol cypionate, has received Food and Drug Administration (FDA) approval as a monthly injectable contraceptive. In comparison to the oral combination pill, contraceptive effectiveness is very high since the problem of forgetting pills is eliminated. In an initial study over the course of 1 year, there were no pregnancies in 782 women.
B. Side effects
are expected to be similar to that of the OCP. There seems to be higher rates of irregular bleeding during the initial months of use when compared with corresponding rates in OCP users.
C. return to fertility
Compared with long-acting progestins, return to fertility after discontinuation of this method is more rapid. Ovulation can occur as early as 6 weeks after the last injection. For this reason it is also important to receive follow-up injections within 5 days of the prescribed 28-day injection schedule.
III. Long-acting progestin contraceptives :
Since 1992, long-acting injectable forms of progestins have been approved in the United States. Medroxyprogesterone acetate (Depo-Provera) has been used around the world for more than a decade. Levonorgestrel implants (Norplant system), silastic capsules that release progestin for up to 5 years, were approved in 1990. The mechanisms of action for these forms of progestin are the same as with the combined pill and the minipill. Progestin interferes with endometrial growth, cervical mucus production, and possibly fallopian tube transport. It may suppress LH surge and prevent ovulation but this is not consistent. About one third to one half of cycles are ovulatory. Effectiveness has been shown to be excellent, exceeding even that of sterilization in one large study.
A. Types of progestins
Norplant system is six silastic subdermal capsules that contain levonorgestrel.
Each capsule is 34 mm long and 2.4 mm in diameter. The levonorgestrel is very stable and is released over a period of 5 years. During the first year, 80 µg/day is released, which is comparable with the minipill and is about 50% of the progestin in the combined pills. Gradually, the release decreases to 30 to 40 µg/day. At 5 years, the amount released is not enough to provide adequate protection.
Very obese women may have relatively lower serum levels and, therefore, less contraceptive efficacy.
A modification of the Norplant system (Norplant II) has only two subdermal capsules. Implanon has only one subdermal capsule .
Depo-Provera is the depot form of medroxyprogesterone acetate. It is given as an injection of 150 mg every 3 months. The contraceptive effects may last up to 4 months.
B. Failure rate
The failure rates for either method are extremely low, from 0.2% to 0.3% in the first year. Most of the “failures” were in women who were pregnant at the time of insertion or injection. The Norplant failure rate increases with time until at 5 years it is as high as1.1%.
C. Contraindications and risk factors
are fewer than with the combined pills.
These methods may be safely used in women who may have contraindications to the combined pills (i.e., estrogen).
Theoretically, there are concerns with progestins' effects on lipid levels. However, studies do not show a significant change in lipids or carbohydrate metabolism.
D. Evaluation and counseling considerations.
Long-acting progestins have noncontraceptive benefits similar to those of the pill , except that there is no protection from ovarian cysts. In fact, ovarian cysts can occur more frequently.
E. Complications and side effects
Early animal research with Depo-Provera suggested increased breast tumors in beagle dogs. Worldwide use and many years of follow-up have alleviated fears of this severe complication. A multinational study showed a slightly increased risk ratio of 1.2 in women younger than 35 only in the first 4 years of use. Risks were not increased in women who had used this method longer than 5 years.
Serious side effects are rare. However, many side effects are such nuisances that patients discontinue use.
The most common side effect is irregular bleeding from the lack of estrogen's stabilizing influence on the endometrium.
Bleeding patterns are unpredictable.
Amenorrhea can occur.
Other side effects include:
Headaches.
Nausea.
Weight gain.
Acne.
Ovarian cysts.
Hyperpigmentation over the Norplant site.
Depression, which can be severe, more so with Depo-Provera than with Norplant implants.
Other considerations.
This method does not interrupt sex for contraception.
It provides no protection against STDs, HIV, or hepatitis B transmission.
Long-acting progestins are not as accessible as other methods. Norplant requires an appointment to have it inserted and removed.
In some cases it is costly because it involves a procedure charge.
Depo-Provera must be given every 3 months so patients must remember (or be reminded) to return regularly for injections.
There are no long-term effects on fertility. Most women ovulate in the first month after discontinuing this method. However, medium-range delays in ovulation (up to 9 months) can occur with Depo-Provera.
F. Instructions
Clinicians should discuss all of the foregoing considerations with the patient .
Some practitioners recommend a trial of a minipill before committing to the injection or Norplant system.
It is ideal to begin the progestin within the first 7 days of menses.
A pregnancy test is recommended before administering the first dose of Depo-Provera or inserting the Norplant.
The Norplant insertion procedure is not difficult and takes about 15 to 20 minutes. Wyeth-Ayerst can be contacted for training materials.
Removal of Norplant can take longer and may be complicated by an initial irregular placement or by a fracture of the silastic capsule.
Patients should be aware of possible side effects and may want to keep track of bleeding.
Patients should call in with any change in the bleeding pattern since a pregnancy test may be indicated.
G. Clinical dilemmas
If spotting or irregular bleeding continues, the patient may be treated with
Ibuprofen (Motrin), 800 mg PO tid for 5 days.
Conjugated estrogens, 1.25 mg PO or estradiol, 1 mg PO every day for 7 days.
Ethinyl estradiol, 20 µg PO every day for 25 days.
Methyltestosterone with conjugated estrogens (Premarin), 2.5 mg every day for 25 days.
Some clinicians use low-dose birth control pills such as ethinyl estradiol-norethindrone (Ovcon 35) for one cycle.
If all of the foregoing methods fail and the woman wishes to continue treatment, then a hysteroscopy and a D & C can be done to rule out intrauterine pathology.
A barrier method should be used with any estrogen-only method of treatment as it may decrease the effectiveness of the progestins by thinning cervical mucus.
If a patient develops amenorrhea, a pregnancy test should be obtained. The patient can be reassured that the method is still effective even without a period.
It is important to remember that many patients still ovulate while taking progestins. If there is any change in a regular pattern of bleeding, a pregnancy test is advised.
Headaches, severe acne, and depression may be indications for discontinuing this method.
H. Special considerations
Both Depo-Provera and Norplant may be used by lactating women.
Adolescents and women older than 35 may be well suited to one of these methods for the same reasons as those discussed for the combined pills .
Mentally disabled patients may particularly benefit from this method.
IV. IUDs :
have been used since the beginning of the twentieth century. This is a popular method of birth control worldwide but less so in the United States. With proper patient selection and counseling, products could be used more often. IUDs are believed to inhibit pregnancy by producing a local inflammatory response in the endometrium. This hostile environment is thought to be spermicidal and there is theoretical evidence that tubal motility is affected. It is important to realize that IUDs are thought to be contraceptive not abortifacient. Failure rates of any IUDs are low. The Progestasert fails between 2% and 3% of the time, whereas the failure rate for the CuT 380A is between 0.5% and 0.8%.
A. Types of IUDs
Nonmedicated IUDs are no longer available in the United States but some women still have them. Among the more common types are the Lippes Loop and the Saf-T-Coil. These types of IUDs work indefinitely and there is no need to remove and replace them.
Copper T-380A (ParaGard) is a copper-containing device in a T-shape, 36 mm long by 32 mm wide. It is currently approved for up to 10 years of use.
Progestasert contains progesterone that is released locally, has progestin (atrophic) effects on the endometrium, and affects the cervical mucus. This particular progestin IUD must be replaced every year.
Mirena is a new levonorgestrel-releasing IUD that has received FDA approval. This IUD can be used for up to 5 years.
B. Contraindications and risk factors
PID and pregnancy are absolute contraindications for use of an IUD.
The risk of developing PID for the first time while using an IUD is dependent on the sexual activity of the woman and her partner.
A woman in a mutually monogamous relationship will have little increased risk of developing PID while using the IUD.
A previous ectopic pregnancy is no longer considered an absolute contraindication.
The newer copper IUDs protect against ectopic as well as intrauterine pregnancy.
The Progestasert offers less protection against ectopic pregnancy.
Experimental levonorgestrel IUDs offer good protection against ectopic pregnancies, probably by interfering with ovulation..
C. Counseling considerations
The manufacturers of IUDs have developed extensive consent forms that the provider should review with the patient.
The best candidate for an IUD is a multiparous (proven fertility) woman involved in a mutually monogamous relationship.
As with the pill, it must be stressed that this method provides no protection against STDs, HIV, or hepatitis B transmission.
Wearing an IUD and contracting an STD can lead to severe PID and possibly abscesses.
Selecting the type of IUD. Most patients will prefer to have the longer lasting CuT 380A (ParaGard).
Progestasert may decrease the severity of dysmenorrhea and anemia in some women.
Mirena has the same benefits as Progestasert, with the additional advantage of needing replacement only once in 5 years instead of yearly.
Risks at the time of insertion include perforation and infection. There is about a 5% expulsion rate.
Patients should expect some cramping and discomfort for a few months.
There can also be heavy menses, spotting, or an increase in vaginal discharge.
These symptoms can be treated with standard doses of nonsteroidal antiinflammatory drugs.
Approximately 10% of patients will discontinue this method because of these problems.
Return of fertility is as rapid as with barrier methods. The endometrial cavity returns to normal almost immediately after removing the IUD.
D. Instructions
Clinicians should be well skilled in how to insert the different types of IUDs.
It is best to insert the IUD during menses or just after an abortion. This is not a strict rule as long as pregnancy has been completely ruled out.
If there is a suspicion of STDs, cultures need to be taken and results obtained prior to inserting the IUD.
Perform a bimanual examination to determine size and position of the uterus.
Grasp the anterior lip of the cervix with a tenaculum and sound the uterus slowly and gently.
Load the IUD into the inserter barrel and with slow steady traction on the tenaculum slide the IUD inserter barrel into the uterus.
Gently remove the inserter, being careful not to tug the IUD string.
Clip the strings about 3 to 5 cm from the os. Leaving them longer initially allows for some retraction over the next several days as the IUD becomes seated within the uterine cavity. If the strings are cut too short, the partner may feel them.
Paracervical injection of 10 to 20 mL of 0.5% lidocaine provides an effective anesthetic block for difficult or painful insertion. However, a paracervical block is usually not needed for insertion.
Since the risk of perforation is greatest at the time of insertion, patients should return in 2 to 3 weeks to have the placement checked and to rule out expulsion or perforation. At this return visit, preferably after a menses, the string length can be cut shorter if needed.
Patients. Be sure each patient knows how to check for her IUD strings and does so regularly. If the strings are absent or if a period is missed, the patient should contact the clinician.
A second method of birth control is recommended during the first 3 months after insertion.
Each user should know what type of IUD she has and when her IUD should be replaced.
Most important, she should memorize the IUD danger signs. The first letter of each sign spells the acronym PAINS.
Period late or missing.
Abdominal pain.
Increased temperature.
Noticeable discharge.
Spotting.
E. Sequelae
Potential IUD complications are listed in order of decreasing severity.
Infection is the cause of most IUD-associated hospitalizations and deaths. IUD users are two to eight times more likely to require hospitalization for PID than women using no contraception. Infection rates are highest among women at high risk for PID, including young women with multiple sexual partners in areas where STD rates are high.
IUD infection can occur without any obvious sign of systemic sepsis and without fever. Symptoms, such as abnormal discharge, bleeding, or pelvic pain, should be treated as infection until proven otherwise.
Because fertility impairment can be a consequence, IUD infection warrants immediate aggressive management.
Uterine perforation, embedment, or cervical perforation can occur silently (with no symptoms) and may be discovered when IUD removal is attempted or when unintended pregnancy occurs. Symptoms may include pain, bleeding, and disappearance of IUD strings.
Ultrasound is often helpful in determining the location of an IUD but may not be accurate for a woman with large fibroids.
Cervical perforation may occur as an IUD is being expelled.
The Dalkon Shield is not visible on x-ray films. Although it has been off the market since the 1980s, a few women may still have it.
Pregnancy. Whenever pregnancy occurs in an IUD user, the probability of ectopic pregnancy must be carefully evaluated. Although IUD use does not cause ectopic pregnancy, the IUD's effectiveness in preventing conception with ectopic implantation is lower than its effectiveness in preventing intrauterine pregnancy.
If pregnancy occurs, the IUD should be removed when the string is still visible.
If the string is not visible, patients should be counseled that there is a 50% spontaneous abortion rate and elective termination may be offered.
Ectopic pregnancy should always be considered and ruled out by ultrasound or D & C, if appropriate.
Lost IUD strings are a common complaint. In most cases the string may be seen inside the cervical canal. Narrow forceps can be used to probe the cervical canal in an attempt to bring the strings into view.
Consider pregnancy if the strings are not visible on careful examination. If pregnancy is ruled out, then a search must be made for the IUD.
Ultrasound will be able to determine if it is inside the cavity or if it has eroded into the myometrium.
IUDs that are totally inside the cavity may be left in place.
In many places worldwide, IUDs are routinely placed without strings.
If ultrasound is unable to identify the IUD, a three-way x-ray of the abdomen should be obtained to ensure that it is not floating in the abdominal cavity.
If the IUD is in the abdominal cavity, the patient should be referred for laparoscopic removal.
If the IUD is not seen on x-ray examination, most likely it was expelled without the patient's awareness. Remember that the Dalkon Shield is not visible on x-ray films.
Spotting and bleeding may vary depending on the type of IUD. Unusual spotting or cramping may represent pregnancy or mild infection and should always be considered prior to any treatment.
The progestin-type IUDs generally lead to hypomenorrhea, but long-time use can cause atrophy and irregular spotting.
Copper IUDs are more likely to cause irregular spotting and cramping than are progestin-containing ones. Nonsteroidal antiinflammatory drugs can decrease these problems:
Difficult removal of an IUD. Removal of the IUD during menses is generally easy. An IUD should be removed with gentle traction on the string.
In older IUDs, the string may pull off or the IUD may not move from its position, indicating that it may be partially embedded.
A narrow packing forceps may be used to grab the end of the IUD.
Sometimes, a paracervical block and cervical dilation may be necessary.
If this is unsuccessful, an IUD hook may be used inside the cavity.
A “Novak” curette, used for endometrial biopsies, is useful because of the serrations at the end of the curette.
The patient should be referred for hysteroscopic removal when other methods have failed.
IUD expulsion. Between 5% and 20% of users expel the IUD within the first year of use.
Expulsion or partial expulsion is often entirely asymptomatic. Symptoms may include the following:
Unusual vaginal discharge.
Cramping or pain.
Spotting.
Dyspareunia.
Lengthening of the IUD strings.
Feeling the plastic of the IUD.
Noting the passage of the IUD from the vagina.
Replacement of an IUD can be done in one office visit. Preprocedural antibiotic coverage, such as doxycycline 200 mg PO, may be used. Although a recent study showed no benefit to the use of prophylactic antibiotics in reducing pelvic infection rates in new IUD placements (18).
Cramping and pain should not be accepted as normal consequences of IUD use. The possibility of ectopic pregnancy or infection must be carefully evaluated. Increased menstrual cramping or intermittent cramping can occur, especially with larger IUDs.
F. Special considerations
Postcoital contraception. Insertion of a copper IUD within 5 days after unprotected intercourse provides effective postcoital contraception. This approach to morning-after treatment is logical only for women who wish to continue using the IUD as a method of contraception and who have no contraindications.
It is contraindicated in nulliparas, adolescents, and rape victims.
All of the previously discussed contraindications and risk factors must be considered .
Effectiveness has been reported to be >99%.
Newer, very effective, hormonal methods of postcoital or emergency contraception (EC) have been approved for safe and effective use by the FDA. These approaches make IUD insertion for this indication less attractive.
The IUD may be an ideal method for the perimenopausal patient who has completed her family and does not want to risk another pregnancy.
G. Clinical dilemmas
Most of the problems arising with an IUD in place can be mimicked by pregnancy. Therefore, always consider pregnancy.
Infection, especially PID, can occur in users of IUDs and may develop serious sequelae.
Be sure that the patient does not have an ectopic pregnancy.
Any patient with a suspicion of PID should be treated immediately and probably hospitalized.
Frank PID must treated with antibiotics.
After the first dose is given, the IUD should then be removed.
An ultrasound should be obtained, if an abscess cannot be ruled out on clinical examination.
If the infection seems to be limited to the cervix (i.e., cervicitis, asymptomatic positive Chlamydia or gonorrhea culture), it can be treated without removing the IUD and with very close follow-up.
Following an episode of PID, a woman should wait at least 3 months (preferably 1 year) for insertion of another IUD.
If future fertility is a goal, then should be avoided.
Uterine or cervical perforation.
When partial cervical perforation occurs, the IUD can usually be removed by using alligator forceps to push the device back into the uterine cavity and then removing the IUD by grasping it with forceps or pulling gently on the string.
In a nonpregnant woman, an IUD located outside the uterus (intraperitoneal) usually can be removed through a laparoscope.
Management of pregnancy. Obtain a serum pregnancy test to exclude ectopic or intrauterine pregnancy for any IUD user who has missed one or more periods. If pregnancy is intrauterine, the IUD should be removed because of the high risk (50%) of spontaneous abortion and, often, of associated infections. IUD removal reduces but does not eliminate the possibility of miscarriage.
If the strings cannot be seen or located in the cervical os, IUD removal cannot be attempted and therapeutic abortion should be considered.
If a woman decides to continue a pregnancy with an IUD in place, she should be warned about the 50% risk of spontaneous abortion and should be educated about signs of infection.
Ectopic pregnancy should always be considered and ruled out by ultrasound or D & C, if appropriate.
Most of the IUD-associated deaths have been the result of rapidly progressive infection with incomplete spontaneous abortion.
Management of lengthening string.
When an IUD is partially expelled, in many cases the string descends through the cervix and appears longer. The possibility of expulsion must be excluded before other causes are considered. Pelvic sonography and examination of the endocervical canal with a sterile swab can assist in this determination.
The string can also lengthen if, after insertion, part of the string remained in the uterine cavity and the clinician cut the string based on the segment visible in the canal.
Indications for IUD removal.
Pregnancy, pelvic infection, and partial expulsion are indications for immediate IUD removal.
Removal is also indicated when persistent pain is a problem, excessive bleeding causes a drop of 5% or more in hematocrit, or the patient requests removal.
An IUD can be removed at any time in the menstrual cycle. If the patient has had midcycle intercourse and the IUD is removed immediately thereafter, there may be some reduction in IUD efficacy for that cycle.
V. Barrier methods :
Although possibly more cumbersome than the methods already discussed, barrier methods, specifically condoms, have assumed new importance in this age of the potentially life-threatening STD—HIV—as well as other problematic STDs such as hepatitis B, HPV (human papillomavirus), HSV (herpes simplex virus), Chlamydia, and gonorrhea. It is important to explain to sexually active couples that prevention does require different or supplementary measures in conjunction with pregnancy prevention.
A. Diaphragm
The diaphragm acts as a barrier and serves as a receptacle to hold spermicide against the cervical os. Diaphragms are ineffective unless used with spermicide. Failure rates are related to the motivation of the patient and range from 6% to 18%. There are several types of diaphragms and familiarity with them will help the practitioner recommend the appropriate one to the patient.
Types of diaphragms. Each diaphragm is available in size increments of 5 mm.
Arcing-spring rim. This diaphragm provides the sturdiest of spring strengths; the rim arcs can be folded, thus facilitating insertion for some women. Available sizes range from 55 to 95 mm.
Two arcing-spring products, Koro-Flex and Bendex, fold at only two points along the rim.
The Ortho product, All-Flex, folds at any point, although it is less sturdy than the other two.
Flat-spring rim. This diaphragm has a thin rim, with gentle spring strength. The rim folds flat for insertion and is available in sizes 55 to 95. It is slightly harder than others to place correctly, but comfortable once placed behind the pubic bone.
Coil-spring rim. The coil-spring diaphragm has firm spring strength and is available in sizes 50 to 95. It folds flat for insertion and can also be used with an introducer.
Wide-seal rim. This diaphragm has an arcing-spring or a coil-spring rim with an additional soft flange along the inner edge to create a seal with the vaginal mucosa. It is available through Milex Products in sizes 65 to 85.
Contraindications and risk factors include the following:
Allergy to latex or spermicide.
Recurrent urinary tract infection.
Introital or pelvic pain.
Active lesions that interfere with comfortable fitting or insertion.
History of toxic shock syndrome (TSS) or colonization with Staphylococcus aureus.
Lack of medical staff to fit and instruct adequately on diaphragm use.
Inability of the patient to master correct insertion or removal.
Anatomic abnormalities. Diminished vaginal muscle tone, previous obstetric laceration, uterine prolapse, cystocele, rectocele, extreme and fixed retroversion, vaginal fistula, and vaginal septum may make diaphragm fitting or use impossible.
Fitting may not be accurate for a woman who has had a full-term delivery in the past 6 weeks.
How to determine correct size and fit. Select the largest rim size that is comfortable for the user. Since vaginal depth increases during sexual arousal, a diaphragm that is too small may slip out of place. On the other hand, a diaphragm that is too large may cause discomfort or recurrent urinary infection.
The anterior rim should tuck just behind the symphysis pubis and the posterior portion of the rim resides snugly in the posterior vaginal fornix.
The diaphragms or rings used for fitting should be washed with soap and water and then immersed in a 70% alcohol solution for 20 minutes after each use.
Many clinicians rely primarily on the arcing-spring diaphragm since it fits most women and is easy to insert. The arcing-spring diaphragm is also useful for a woman with a long and firm cervix.
The coil-spring or flat-spring diaphragm may provide a comfortable fit for a woman who has firm vaginal tone, who finds the arcing spring uncomfortable, or who has had problems with recurrent urinary infections.
Instructions.
Clinicians.
Be sure each user is able to insert and remove her diaphragm and can verify correct position by palpating her cervix.
Have her practice placement and removal while in the office.
Ensure that she is comfortable with the method and answer any questions.
The importance of spermicide and consistent use should be stressed. Spermicide must be used with initial coitus and replenished with subsequent acts without removal of the diaphragm.
Each patient should also be aware that TSS could occur with diaphragm use if not removed within 24 hours.
Patients.
Apply 1 tablespoon of spermicide cream or gel to the inner dome of the diaphragm and along the rim.
If the diaphragm is placed in the vagina more than 6 hours before intercourse, another applicator full of spermicide should be inserted.
Insert the diaphragm by pushing the rim downward and toward the back wall of the vagina. The rim should fit just behind the pubic bone and should reach back behind the cervix.
Always check to make certain the diaphragm is covering the cervix.
Leave the diaphragm in place for at least 6 hours after intercourse. If you have intercourse again during the 6-hour time, insert an applicator full of spermicide, but do not remove the diaphragm.
Remove the diaphragm any time after 6 hours, wash it with soap and water, and let it dry. It can then be reinserted with new spermicide or stored in its case until again needed.
Avoid leaving the diaphragm in place any longer than 24 hours, but do keep to the 6-hour minimum time.
Do not use talcum or perfumed powder or any petroleum products (e.g., Vaseline) on your diaphragm.
If you experience danger signs of possible TSS while using the diaphragm, contact your clinician immediately. The danger signs are:
Fever of 100°F or more.
Diarrhea and vomiting.
Muscle aches.
Rash (like sunburn).
Diaphragm size should be reassessed after childbirth, or when approximately 10% of body weight is gained or lost.
Sequelae.
Side effects. Overall, the diaphragm is a very safe method of contraception.
TSS is the most serious potential problem, but is very rare. A handful of TSS cases, however, have been reported in association with prolonged diaphragm placement. These cases did not arise during menses as is more typical for TSS. Any patient who experiences TSS danger signs must be evaluated promptly, which includes diaphragm removal, vaginal culture for S. aureus, and prompt antibiotic treatment when indicated.
Other problems that can occur with diaphragm use include
See section on spermicides discussed in C, below.
Recurrent cystitis.
The size of the diaphragm should be checked.
If size is not the problem, the patient should be counseled to void prior to and after intercourse.
In some cases an antibiotic may be given prophylactically [i.e., nitrofurantoin (Macrodantin), 50 mg PO, or sulfamethoxazole-trimethoprim (Bactrim or Septra), PO after coitus].
Allergic reactions to latex or spermicide. If the reaction is to the spermicide, try different brands. It may, in fact, be a reaction to perfume or other additives.
Irritation from spermicide.
Foul-smelling vaginal discharge when a diaphragm is left in place too long.
Recurrent candidiasis if the diaphragm is not thoroughly cleaned out and dried after use.
Pelvic discomfort from rim pressure.
Patient or partner discomfort. There are many ways this may manifest itself. There has to be a level of comfort in the relationship to incorporate the use of barrier methods. Furthermore, some patients may have physical discomfort with the diaphragm. If it is too small, the partner may notice it as well as it will move around in the vagina during coitus.
Noncontraceptive benefits. Use of a diaphragm and spermicide may provide significant protection against STDs. Their use is associated with a decreased risk of developing cervical dysplasia.
B. Cervical cap
The soft, thimble-shaped cup fits over the cervix and is held in place by suction. Pregnancy is prevented through the cap's action as a barrier over the cervix and by its ability to hold spermicide in place. The reported failure rate is similar to that of the diaphragm. Manufactured and long used in England, the Prentif cap was approved by the FDA for use in the United States in 1988.
The cervical cap has a deep dome with a groove inside the firm rim to aid suction and it is available in four sizes, ranging from 22- to 31-mm internal rim diameter.
Contraindications and risk factors are the same as for the diaphragm, with the following exceptions:
Cap use is contraindicated for a woman who has Pap smear evidence of HPV infection, cervical intraepithelial neoplasia, or cervical dysplasia.
Cap use should not be initiated if the woman has acute PID, acute cervicitis, or vaginal infection or has undergone cervical biopsy or cryosurgery within the past 6 to 12 weeks.
The cap should not be used during the first 6 weeks after full-term delivery, when vaginal bleeding is occurring after spontaneous or induced abortion, or during normal menses.
How to determine correct size and fit. Because of variations in normal anatomy and the limited number of cap sizes available, it is not possible to fit every patient satisfactorily. Only about 50% of women can use this method successfully.
The cap must fit snugly over the cervix and remains by suction.
The cap dome should be deep enough so that it does not rest on the cervical os.
The cap should not be easily dislodged with a fingertip.
The cap user should check carefully for cap dislodgment after intercourse.
Instructions are the same as for the diaphragm, with the following exceptions:
Spermicide is not necessary. If used, it should fill the dome of the cap one third full. Using spermicide may prolong the wearing time.
The cap should be left in place at least 6 hours after intercourse but can be in for up to 36 hours.
Sequelae.
Little is documented concerning possible side effects or complications of the cervical cap.
Reports have noted vaginal lacerations and abrasions caused by the Vimule cap (not currently available in the United States) and abnormal thickening of the vaginal mucosa, possibly a reaction to chronic irritation (2).
Other researchers have expressed concerns about pelvic infection, acute cervicitis, and abnormal Pap smears possibly linked to cap use.
Failures occur when the cap is dislodged during intercourse.
Any noncontraceptive benefits are likely to be similar to those afforded by diaphragm use .
C. Spermicides and the contraceptive sponge.
Spermicidal contraceptives consist of two components: an inert substance, such as foam, gel, cream, or in the case of the sponge (currently unavailable), polyurethane; and a spermicidal agent (non-oxynol 9). Spermicides immobilize and kill sperm. In addition, the sponge provides a barrier between the sperm and the cervical os and traps the sperm within the sponge. The typical failure rates are 21% to 28%.
Although contraceptive sponges have been discontinued, they may again become available. Spermicidal agents are often used in combination with condoms to provide an extremely effective method of contraception, with a failure rate possibly lower than 1:100 woman-years. In the United States, the active spermicidal agent for products is non-oxynol 9. This is a surface-active substance that destroys cell membranes of sperm. Currently, controversy exists as to the practical effectiveness of non-oxynol 9 in destroying many organisms that cause STDs. In the laboratory, the chemical is lethal to organisms that cause gonorrhea, genital herpes, syphilis, trichomonas, and HIV. However, the evidence that non-oxynol 9 decreases STD risks (including HIV) in human studies has been mixed. There is even some concern that frequent non-oxynol 9 use can irritate the mucosa of the vagina and skin of the vulva, possibly increasing susceptibility to HIV. Also, cystitis (discussed later) may be increased by non-oxynol 9 use, which allows for intravaginal proliferation of Eschericia coli, which is a frequent cause of cystitis .
Type of spermicidal method. All methods are available without prescription.
Foam. Used alone, there is a wide disparity between perfect-use effectiveness and actual-use effectiveness. Common mistakes include inconsistent or careless use, using too little foam, failing to shake the container vigorously enough, not placing the foam high enough in the vagina, and douching too soon after intercourse.
Cream and gel. When used alone, these are slightly less effective than other spermicides. Cream products have better dispersion to cover the cervix and vagina than do gels. Cream and gel are often used in conjunction with the diaphragm or cervical cap.
Suppositories and tablets dissolve over a period of 10 to 30 minutes after placement in the vagina but retain their full effectiveness for less than 1 hour. Mistakes arise from not allowing the tablet or suppository to dissolve, failing to remove the wrapper, placing the spermicide incorrectly, or having intercourse after the fully effective interval.
Contraceptive sponge. In the future, this method may again become available. The polyurethane sponge incorporates 1 g of nonoxynol-9. Approximately 200 mg of spermicide is released during the initial 24 hours of use. It has a concave dimple on one side that fits over the cervix and a woven loop to facilitate removal.
Contraindications and risk factors.
Contraindications to spermicide use include allergy to the active ingredient or base or physical inability to insert or use the product correctly.
Additional contraindications specific to sponge use include:
Anatomic abnormalities such as uterine prolapse, rectocele, cystocele, extreme uterine retroflexion, or vaginal septum when they interfere with placement or retention of the sponge.
History of TSS or vaginal colonization with S. aureus.
Prevention against STDs, HIV, and hepatitis B transmission is less ensured when these methods are used alone.
Instructions. Different formulations of spermicides have different effective times. Most must be placed within 1 hour of intercourse. The length of time protection lasts varies from 1 to 8 hours.
Correct use of a spermicide entails following package instructions carefully:
Removing the wrapper from tablets or suppositories.
Filling the applicator completely with foam, cream, or gel.
Placing the spermicide as close to the cervix as possible.
Applying additional spermicide for each act of intercourse.
Inserting the spermicide before intercourse.
Not douching for at least 6 hours after intercourse.
The sponge.
Correct use requires moistening the sponge with clean water, placing it over the cervix, and leaving it in place for at least 8 hours after intercourse.
The sponge should not be worn for longer than 24 hours.
Each user should learn the danger signs of TSS and know how to contact her clinician if these signs occur. TSS symptoms include high fever, rash, diarrhea, vomiting, and muscle aches.
Sequelae.
Spermicides.
Possible complications of spermicide use include irritation, allergic reaction, and failure of suppository or tablet to melt or foam.
Noncontraceptive benefits include decreased incidence of gonorrhea and trichomoniasis, augmented vaginal lubrication, and possibly some protection against cervical neoplasia.
Contraceptive sponge.
Sponge use involves the possible complications of spermicide .
Some users also experience dryness of the vagina and difficulty with removal or tearing of the sponge.
It is not known whether or not sponge use increases the risk of TSS.
Noncontraceptive benefits of the sponge include those listed for spermicides as well as absorption of vaginal secretions and ejaculate.
Clinical dilemma. When spermicide users experience an allergic reaction, the offending agent is often the perfume or base, although it may be the active spermicidal ingredient. Recommend a nonperfumed spermicide. Check the ingredients of the problem product and consider recommending one containing different ingredients.
D. Condoms
Mechanical barriers to cover the penis during intercourse have been used for hundreds of years. Synthetic condoms were developed after 1840. The popularity of condoms has made this the third most commonly used contraceptive method in the United States. Reported failure rates range from 2 to 12 pregnancies per 100 woman-years.
Types of condoms.
Most condoms are made of latex. About 1% are made from lamb cecum (“natural” skin condoms). Newer polyurethane (plastic) condoms are available and are also useful for those with latex allergy.
Condoms are available lubricated or nonlubricated, straight or tapered, and with or without reservoir tip. Some condoms have external ribbing.
Latex and plastic condoms can prevent transmission of all STDs, including the viral ones (HIV, HPV, HSV, hepatitis B), but natural or lambskin do not prevent transmission of viral STDs.
When protection against transmission of HIV is a consideration, latex condoms in conjunction with spermicide use are recommended. Skin condoms (natural) are more porous than latex, and small particles such as HIV may traverse the intact condom barrier.
Female condoms are available. These are pouches of plastic that line the vagina and cover the cervix.
Contraindications and risk factors.
Allergy to latex is a contraindication. Natural or plastic condoms can still be used.
Some men report difficulty maintaining an erection when using condoms, although others find that condom use is helpful for this.
Instructions. A new condom must be used for every act of intercourse and placed on the penis before any vaginal entry.
Patients should be instructed to place the condom on the erect penis before the penis touches the partner.
The end of the condom should extend beyond the tip of the penis and air should be removed to form a small receptacle.
Lubricants should be water-based only. Oil-based lubricants can weaken the condom.
After intercourse, the penis should be withdrawn while it is still erect, taking care to keep the bottom of the condom from coming off the base of the penis.
Jewelry, fingernails, and sex toys may tear the condom.
Average breaking rates for latex condoms are 1% to 2% and are greater for plastic, up to 7%. If breakage occurs, concomitant use of spermicides substantially decreases the risk of pregnancy.
Condoms should be stored in a cool, dry place and should not be reused.
Petroleum jelly can cause a condom to deteriorate.
Couples using condoms need to know about morning-after hormonal treatment.
Sequelae.
Complications.
The condom may reduce sensitivity of the glans penis. In some cases, use of the natural skin condoms may help.
Some users object to interruption in lovemaking to place the condom on the penis.
Very rarely, an allergic reaction to latex or lubricant can occur.
Noncontraceptive benefits. Condom use is one of the few opportunities for men to play an active role in contraception.
Condoms greatly reduce the transmission of STDs, hepatitis B, and HIV and diminish the likelihood of cervical cancer.
Condoms may also be of help in treatment of premature ejaculation and in preventing exposure to ejaculate for a woman who is allergic to her partner's semen or develops antibodies that cause infertility.
VI. Fertility awareness :
is also called natural family planning. The various methods include rhythm, basal body temperature (BBT), Billings (mucus) method, and the symptothermal methods. All these methods require periodic abstinence with unsafe days determined by physiologic changes that occur during a woman's menstrual cycle. Women who are well educated concerning their cyclic changes, have regular menses, are disciplined, and are willing to cope with possible pregnancy may have good success with fertility awareness. Some users choose to monitor several cyclic changes or combine fertility awareness with alternative contraceptive methods or both.
Failure rates range from 2% to 35%, depending on the method used and on whether alternative birth control was employed. Best success is reported for couples who abstain throughout the preovulatory phase and do not have intercourse until the fourth day after ovulation is clearly documented. Most failures occur because of intercourse during “early safe” days, when ovulation occurs a few days earlier than anticipated. Temperature and mucus changes do not predict ovulation accurately enough to avoid this problem.
VII. Sterilization :
is the most commonly used method of birth control in the United States. The pregnancy rates are 0.2 to 0.4 for tubal ligation and 0.15 for vasectomy per 100 woman-years. For the purpose of decision making about sterilization, these procedures should be considered irreversible.
A. Types of sterilization
Vasectomy.
This operation for men is a simple and safe procedure that prevents sperm passage by blocking the vas deferens. The clinician can ligate the vas deferens through a small incision of the scrotum.
Reversal is moderately successful. Depending on the type of vasectomy performed and the time interval to vasovasostomy, vasectomy reversal procedures can result in clinical success up to 50% of the time. Success diminishes if the vasectomy was performed over 10 years ago.
Tubal ligation. The fallopian tube can be blocked by ligation, coagulation, or mechanical occlusion with clips, bands, or rings. Tubal reanastomosis is generally less successful than is vasovasostomy and will be recommended only if a substantial portion of undamaged fallopian tube is available for repair. Reversal rates as high as 50%, however, have been reported for reanastomosis after clip ligation or surgical ligation with minimal damage. This rate is much lower when electrocautery has been used. The types of tubal ligation include the following:
Abdominal approach. More than 100 variations of abdominal tubal ligation have been developed. Two of the most commonly used methods are laparoscopy and minilaparotomy. Both procedures can be performed under local or general anesthesia.
For laparoscopy, one or two 1-in. incisions may be required, one for the laparoscope and one through which the tubes are grasped with forceps for coagulation or clip applications.
For minilaparotomy, a 2- to 3-cm incision approximately 3 cm above the symphysis pubis allows the surgeon to grasp the fallopian tube for ligation. Minilaparotomy is most feasible for patients with minimal abdominal wall fat.
Vaginal approach. The fallopian tubes can be approached by vaginal culdotomy or rarely by culdoscopy. Because of high complication rates, the advantages of an unobtrusive scar and rapid recovery are less attractive.
Hysterectomy. At one time, hysterectomy was the most common method of sterilization. This approach may be considered for women who are likely to require later hysterectomy because of known gynecologic disease but should not be a routine recommendation. Hysterectomy mortality is 10 to 100 times higher than that of tubal ligation, and the associated morbidity as well as cost in money and time is much greater.
B. Contraindications and risk factors
Ambivalence is a strict contraindication. Only a patient who wishes to terminate fertility should undergo sterilization. In reaching a decision, the possible impact of divorce or family tragedy should be considered. Remarriage is the most common reason cited for requesting reversal.
A patient who is obese, has cardiovascular disease, or has a serious medical condition that might increase anesthesia or surgery risks should be encouraged to consider alternative methods of fertility control.
C. Counseling
Every patient must understand that sterilization surgery is not 100% effective and that pregnancy can occur in rare cases. Because of the permanent and completely elective nature of sterilization surgery, informed choice and informed consent are crucial. The mnemonic BRAIDED has been developed for the essential components of informed consent counseling.
Benefits: It is effective and convenient.
Risk: Risk of method including consequences of method failure.
Alternatives: The patient must be informed about possible alternatives, including advantages and disadvantages of each.
Inquiries: Any questions the patient may have should be answered fully by the clinician.
Decision: The patient must feel free to decide against the proposed method, without implied pressure or coercion.
Explanation: The procedure planned must be explained in specific detail.
Documentation: Information provided to the patient should be entered in the medical record, along with a written consent form signed by the patient.
D. Sequelae
Male sterilization.
Vasectomy is a very safe procedure. Complications are generally minor and short term. Swelling, discoloration, and discomfort are common during the first few days after surgery.
More significant, but uncommon, complications are hematoma, granuloma, epididymitis, and wound infection.
One half to two thirds of men develop sperm antibodies after vasectomy, but the possible significance of this is unknown.
Approximately 0.4% of vasectomy procedures fail to terminate fertility. In most cases, failure is evident within a few weeks, as postoperative semen shows continuing sperm release.
Sperm counts should be obtained after 20 ejaculations and a repeat sperm count done at 2 months.
Approximately 10% will need to repeat the sperm count 1 to 2 months later to ensure that the count has decreased.
It is recommended that all men have a repeat sperm count 6 months after the vasectomy.
A backup method of contraception should be used until the semen no longer shows sperm release.
Female sterilization. Tubal ligation is also extremely safe. The greatest risk is in the type of anesthesia used with general anesthesia having the highest risk.
Complications of tubal ligation could involve damage to one or both ovaries or to the ovarian blood supply, and this could cause menstrual disturbance or a change in the hormonal milieu. Whether such problems can be linked to uncomplicated tubal ligation, however, has been an issue of controversy. Long-term follow-up in large case-control studies have found menstrual disturbances equally as frequent among controls as among sterilization cases.
Complications occur in fewer than 2% to 3% of women undergoing minilaparotomy and include infection, hematoma, uterine perforation, and bladder injury.
Complications are also rare with laparoscopy. The procedure can cause mesosalpingeal tear, bowel burn, uterine perforation, or hemorrhage.
Vaginal tubal ligation complication rates are approximately twice as high as those for laparoscopy or minilaparotomy, with infection and hemorrhage accounting for most of the problems.
Tubal ligation failure rates depend on the specific surgical method used.
Following laparoscopy, approximately 0.25% of patients experience failure. Ectopic pregnancy and pregnancy already established at the time of the surgery are the most common.
Postpartum tubal ligation, sterilization at the time of caesarean section delivery, and abdominal ligation by the Pomeroy method have somewhat higher failure rates.
VIII. Abortion :
Approximately 1.6 million abortions are performed annually in the United States; more than 90% are performed early in pregnancy using vacuum aspiration. Although the complication rate for abortion is as low as, or lower than, any other method of fertility control, very few women choose it as a primary fertility control method. Patient acceptance of effective contraception is extremely high at the time of unintended pregnancy, so birth control information and supplies are an important part of clinical management. Early identification and confirmation of pregnancy are also crucial tasks for all family-planning clinicians.
With the marked increase in ectopic pregnancy rate, early pregnancy identification can be lifesaving. Early confirmation also permits optimal initiation of prenatal precautions and care and early termination if abortion is the patient's decision. Abortion risks are lowest at approximately 7 to 8 weeks gestation and double for every 2-week delay thereafter. This method is not accepted in Islamic .
IX. Postcoital or EC :
has been mentioned in other sections. Practitioners need to be more aware of this option and feel comfortable using it. Patients need to be counseled that it is available as a backup if one of the foregoing methods is not used correctly (i.e., a failed condom). EC prevents ≈ 75% of expected pregnancies, probably closer to 95% when used within 24 hours of intercourse. In a recent review article about EC, Glasier thoroughly discusses the mode of action of these hormonal techniques and states, “The prevention of pregnancy before implantation is contraception and not abortion” . There is considerable current advocacy to make EC available without prescription in the United States. Evidence exists that this approach could reduce the unwanted pregnancy rate without risk to the users. There are two methods of postcoital contraception, hormonal and the IUD.
There are two main hormonal approaches to EC using either combination estrogen and progestin OCPs or progestin-only contraceptive pills. Together these are referred to as emergency contraceptive pills (ECPs). In 1997 the FDA declared the combination method of ECP use both safe and effective for use in pregnancy prevention. Previously studied, but not currently used, methods include danazol (an antigonadotropin) and high-dose estrogen-only regimens. It may be that antiprogesterone, mifepristone (RU-486), will be used for postcoital contraception. Effective contraception must be used within 72 hours of unprotected sex.
Combination estrogen and progestin methods include a large number of easily available formulations.
In all cases two doses are required, the first within 72 hours of intercourse, the second 12 hours after the first dose.
All use ethinyl estradiol 100 to 120 mcg and levonorgestrel 0.50 to 0.60 mg per dose. This is convenient because many conventional OCPs contain appropriate dosages of these hormones when taken in multiples.
For example, Ovral contains 50 mcg ethinyl estradiol and 0.25 mg levonorgestrel. Thus, taking two Ovral pills 12 hours apart provides the correct dose of ECPs.
Similarly, Lo/Ovral contains 30 mcg ethinyl estradiol and 0.15 mg levonorgestrel. Thus, four Lo/Ovral pills per each dose provides the correct dose.
One commercially available product, Preven, contains four tablets each containing 50 mcg of ethinyl estradiol and 0.25 mg levonorgestrel.
Progestin-only method. Currently, only one such method is commercially available; “Plan B,” which contains a single pill containing 0.75 mg of levonorgestrel, is taken within 72 hours of intercourse. This method was shown in a large multinational trial to be as effective as the combination estrogen and progestin regimen and may be preferred because of its low incidence of nausea and ease of single dosing.
The most common side effect of ECPs is nausea. Using combination pills, the incidence of nausea is 30% to 50% and approximately 20% have emesis. These rates drop by more than half with the progestin-only method. If vomiting does occur within 3 hours of either dose, some feel it should be repeated with an antiemetic.
Although the ECPs may slightly alter the expected menstrual interval, patients should expect to see their menses by 21 days after treatment. If the pregnancy ensues, the patient should be counseled appropriately concerning an undesired pregnancy. If she opts to continue the pregnancy, there is no evidence of teratogenic effects.
IUD placement within 5 days of conception can successfully prevent pregnancy with failure rates of less than 1%. .

SEXUALLY TRANSMITTED DISEASES , Dr. Alaa Mosbah MD OBS and GYN

Introduction :

Twenty or more infectious diseases may be transmitted by sexual contact. This chapter reviews those associated with cervicitis, gonorrhea and chlamydia, and those characterized by genital ulcers, syphilis, herpes, chancroid, lymphogranuloma venereum, and granuloma inguinale as well as the parasitic skin infestations, pediculosis pubis and scabies. Sexually transmitted diseases (STDs) often coexist. It is strongly recommended that whenever serologic testing is done, screening for syphilis (rapid plasma reagin test [RPR], HIV, hepatitis B surface antigen (HBsAg) and hepatitis C titer should be included routinely.

Classification:

BACTERIAL:

•Neisseria gonorrhea (gonorrhea)

Chlamydia trachomatis (Chlamydia)

•Treponema pallidum (Syphilis)

.Hemophilus ducreyi (Chancroid)

•Calymmatobacterium granulomatis (Donovanosis or granuloma inguinale)

•Gardnerella vaginalis (Bacterial vaginosis)

•Others: eg. Mycoplasma hominis , Ureaplasma urealyticum

VIRAL:

- Herpes simplex virus

- Human papilloma virus

- Hepatitis B virus

- HIV (AIDS)- Cytomegalovirus

- Molluscum contagiosum virus

PROTOZOAL: Trichomonas vaginalis (Trichomonal vaginitis)

ECTOPARASITES:

§Phthirius pubis (pubic lice infestation)

§Sarcoptes scabiei (scabies)

Consequences of STIs:

For women:

§Infertility

§Ectopic pregnancy

§Cervical cancer

§Adverse pregnancy outcomes ( prematurity, neonatal infection)

For children:

Eye infection

Blindness

For men :-Infertility

I. Gonorrhea.

Urogenital purulent inflammation is the most common form of infection with the gram-negative, intracellular diplococcus Neisseria gonorrhoeae, which has an avidity for columnar and transitional epithelium. Transmission is almost always by sexual contact, with a usual incubation period of 2 to 8 days. In the United States, an estimated 600,000 new infections are reported annually.

A. History.

The acute attack usually follows sexual exposure or a menstrual period. Symptoms include vaginal discharge, urinary frequency and dysuria, menstrual irregularity, and bilateral lower abdominal pain. An asymptomatic carrier state is common in both sexes. The incidence of asymptomatic gonorrhea in men has been estimated to be as low as 12% and as high as 50%. The estimated incidence for asymptomatic women ranges from 50% to 80%. Infections in other mucosal sites, such as the oropharynx and anorectal area, are usually asymptomatic, but may lead to complaints of pain and discharge. Hematogenous spread may occur, causing manifestations such as septic arthritis and skin lesions. The most common dissemination, however, is by mucosal passage to the fallopian tubes and ovaries, resulting in pelvic inflammatory disease (PID), occurring in 10% to 15% of infected women .

B. Physical examination.

In the asymptomatic case, the physical examination may be entirely normal. There may be a purulent discharge, or Skene's or Bartholin's glands may be inflamed. However, these are nonspecific signs, and the diagnosis is dependent on bacteriologic investigations. The classic presentation of acute gonococcal PID, with fever, abdominal and adnexal tenderness, and a purulent discharge, is often absent.

C. Investigative procedures

A Gram stain of urethral or cervical secretions is unreliable since there is a 60% to 70% false-negative rate in female patients.

Gonorrhea culture, on Thayer-Martin or equivalent medium. The culture should be placed in a candle jar since the organism is fastidious, requiring aerobic conditions with an increased carbon dioxide atmosphere to grow. Incubation should begin as early as possible. Depending on the history, cultures may also be required from the pharynx and rectum.

Enzyme immunoassay (ELISA), polymerase chain reaction (PCR), and ligase chain reaction (LCR) assays on endocervical or urine samples have largely replaced culture methods of diagnosis and are at least as accurate.

Serologic testing for syphilis should be done on all patients. HIV testing and screening for HBsAg and hepatitis C are strongly recommended.

Chlamydia testing should be done at the same time the gonorrhea culture is obtained.

D. Management.

Therapy is based on antibiotic sensitivity, site of infection, and concurrent STDs. Antibiotic resistance is mediated through two genetic mechanisms: chromosomal-mediated resistant N. gonorrhoeae and plasmid-mediated resistance. Two types of plasmids are important: one for penicillinase and one for high-level tetracycline resistance. Rectal infections are relatively refractory to amoxicillin and tetracycline, and pharyngeal infections to amoxicillin and spectinomycin. Chlamydia trachomatis is a common coinfective agent and should be covered with empiric therapy. A summary of the guidelines for treatment recommended by the Centers for Disease Control and Prevention (CDC), Atlanta, in 1998 follows.

Treatment of adults

Uncomplicated gonococcal infections are treated with empiric single-dose therapy consisting of ceftriaxone, 125 mg IM once. Mixing 1% lidocaine reduces the discomfort of the injection. Other recommended single-dose regimens include cefixime, 400 mg PO; or ciprofloxacin, 500 mg PO; or ofloxacin, 400 mg PO. Alternative regimens include spectinomycin, 2.0 g IM for patients who cannot tolerate cephalosporins or quinolones. Injectable cephalosporins that are also effective include ceftizoxime, 500 mg IM; cefotaxime, 500 mg IM; cefotetan, 1 g IM; and cefoxitin, 2 g IM. Oral cephalosporin regimens include cefuroxime axetil, 1 g PO; and cefpodoxime proxetil, 200 mg PO. These two regimens are less effective against pharyngeal infections. Other quinolone regimens include enoxacin, 400 mg PO; lomefloxacin, 400 mg PO; and norfloxacin, 800 mg PO. Many other antibiotics are effective, and this does not represent a comprehensive list of all suitable treatments.

All treatment regimens should include a single dose of azithromycin 1 g PO or a 7-day course of oral tetracycline or doxycycline to eradicate concurrent chlamydial infection, which has been documented in up to 45% of gonorrheal cases in some populations. These drugs are not considered adequate therapy for gonorrhea. Generic doxycycline costs a little more than tetracycline but provides the advantage of a 100-mg bid dosage unrelated to meals, compared with a 500-mg qid dosage between meals with tetracycline. The alternative regimen is erythromycin stearate, 500 mg; erythromycin ethylsuccinate, 800 mg; or erythromycin base, 500 mg PO qid for 7 days .

All patients should have a serologic test for syphilis and should be offered counseling and testing for HIV infection. Most patients with incubating syphilis (in who there is no clinical evidence and who are seronegative) may be cured by any of the foregoing regimens, with the exception of spectinomycin and the quinolones. Patients treated with these drugs should have a syphilis serologic workup in 1 month.

Pharyngeal infections should be treated with ceftriaxone, 125 mg IM. Those who cannot receive this drug should be treated with ciprofloxacin, 500 mg PO, as a single dose; and these patients require repeat culture 5 to 7 days later. Trimethoprim, 720 mg; sulfamethoxazole, 3600 mg PO once daily for 5 days may be an effective alternative therapy.

Sexual partners should be identified, examined, cultured, and treated presumptively.

Follow-up culture (so-called test of cure) following combined ceftriaxone-azithromycin or doxycycline therapy is not essential since treatment failure is rare. Reculture 1 to 2 months later (rescreening) detects both treatment failures and reinfections. Patients treated with other regimens and those with persistent symptoms should have cultures 4 to 7 days after completion of therapy.

Treatment failures after one of the recommended regimens are usually due to reinfection, indicating a need for improved contact tracing and patient education. Nevertheless, antibiotic sensitivities and chlamydial cultures are indicated. Additional treatment with ceftriaxone and azithromycin or doxycycline should be given.

Pregnant women should be treated with ceftriaxone, 125 mg IM, plus azithromycin 1 g PO or erythromycin base, 500 mg PO qid for 7 days. (Erythromycin stearate, 500 mg; erythromycin ethylsuccinate, 800 mg; or an equivalent may be substituted for erythromycin base). Tetracyclines (including doxycycline) and the quinolones are contraindicated in pregnancy because of possible adverse fetal effects. Pregnant women allergic to beta-lactams should be treated with spectinomycin, 2 g IM, followed by erythromycin. Test of cure is required for these cases.

Disseminated gonococcal infection (arthritis-dermatitis syndrome). The condition may be monoarticular or polyarticular. Skin lesions are commonly present with the arthritis. They begin as small red papules, evolving through vesicular and pustular stages to lesions with a necrotic center superimposed on a hemorrhagic base. Healing is usually spontaneous. Hospitalization is usually indicated, especially for those who cannot reliably comply with therapy or who have an uncertain diagnosis, purulent joint effusions, or other complications. Treatment schedules for this syndrome are included in the CDC guidelines but are outside the scope of this chapter.

Miscellaneous. The CDC guidelines also recommend schedules of therapy for infants born to mothers with gonococcal infections, for gonococcal ophthalmia in adults, and for neonatal infections. These are problems seldom encountered in a medical or gynecologic outpatient department. However, adolescents may be seen and should receive similar regimens. Children weighing more than 100 lb (45 kg) receive adult dosage while those weighing less receive dosages adjusted to weight. In all pediatric cases, the possibility of sexual abuse must be considered.

E. Sequelae.

The short-term and long-term complications and sequelae of gonococcal infections are mainly related to gonococcal PID .

II. Syphilis.

The infectious agent is a spirochete, Treponema pallidum. Spread is by sexual intercourse or by intrauterine transmission (congenital syphilis). The incubation period is usually 2 to 6 weeks, with a primary sore (chancre) appearing at the site of infection and remaining for 1 to 6 weeks. Manifestations of the secondary stage may appear 2 to 12 weeks later. During early latency (1–4 years), relapses with mucocutaneous lesions may occur. Thereafter, there are no relapses and the syphilis is noninfectious, except transplacentally. Late symptomatic syphilis is generally characterized by cardiovascular or neurologic disease, although any tissue can be involved.

The incidence of syphilis in the United States in 1995 was 9 cases per 100,000 population.

A. Early (primary, secondary, latent less than 1 year)

History. The primary chancre usually appears on the genitalia, mouth, or anus and is painless. The secondary stage may present with ulcerations of mucous membranes or skin eruptions. Frequently there is only a flulike syndrome with a fever, sore throat, and muscle pain. During the latent phase, the patient is generally asymptomatic. Nearly two thirds of patients pass through the primary and secondary stages without realizing it. The clinical spectrum of syphilis acquired in utero includes stillbirth, neonatal death, neonatal illness, and development of the stigmata of congenital syphilis in later life.

Physical examination. Chancres vary in appearance but the usual feature is that of a nontender clean-cut ulcer with an indurated base and an associated regional adenopathy. The secondary-stage skin lesions tend to be widespread and symmetric, with 60% to 80% of patients having lesions on their palms and soles. Cutaneous lesions tend to be maculopapular. Condylomata latum are intertriginous papules formed at areas of friction and moisture, such as the vulva. Mucosal or mucocutaneous lesions appear in 21% to 58% and include pharyngitis, tonsillitis, and the “mucous patch” (a papule with a central erosion found on the oral and genital mucosa). Lymphadenopathy is a very common finding in the secondary stage.

Investigative procedures. Dark-field microscopy of fluid expressed from lesions may demonstrate the organism. In practice, serologic tests are of major importance in diagnosis. Nontreponemal tests (Veneral Disease Research Laboratories test [VDRL] and RPR) are used for screening and may be repeated quantitatively as a guide to therapeutic response. The tests become positive 1 or 2 weeks after the appearance of the chancre. They are positive in approximately 66% of primary cases, in 99% of secondary cases, and in about 70% of late cases. These tests are nonspecific, with biologic false-positive results occurring in association with other infections and diseases (e.g., infectious mononucleosis, collagen vascular diseases). The titer is usually low (no more than 1:8), with a false-positive test. Treponemal tests (fluorescent treponemal antibody absorption test [FTA-ABS], Treponema pallidum immobilization test [TPI]) are specific, but are not quantitative, and remain positive even after adequate therapy. The treponemal tests, therefore, are used to confirm the diagnosis. The FTA-ABS test is positive in 85% of primary and 100% of secondary cases and may be the only positive test in tertiary cases. Positive serologic studies in the newborn may be passively acquired, but most physicians treat all VDRL-positive neonates. All patients with evidence of latent syphilis should have a lumbar puncture with a cerebrospinal fluid (CSF) VDRL to rule out neurosyphilis .

Management. The CDC recommendations (1998) are summarized as follows:

Drug therapy for early syphilis is benzathine penicillin G, 2.4 million units IM in a single dose. Penicillin-allergic patients should receive doxycycline, 100 mg PO bid; or tetracycline hydrochloride, 500 mg PO qid for 14 days. An alternative regimen is erythromycin, 500 mg PO qid for 14 days. Various ceftriaxone regimens may also be considered. Pregnant patients are treated similarly, but tetracyclines are contraindicated. Penicillin is the only acceptable therapy for the pregnant patient. Following documentation of penicillin allergy by skin testing, reactive patients should be desensitized and treated with penicillin. Desensitization should be performed in consultation with an expert and only where adequate emergency facilities are available.

Quantitative nontreponemal tests should be repeated at 3, 6, and 12 months after treatment. Pregnant women who are treated should have monthly tests until delivery.

Retreatment may be indicated if there is a fourfold increase in titer, an initial high titer fails to show a fourfold decrease within a year, or clinical signs persist or recur. Retreatment should consist of schedules recommended for late syphilis .Pregnant women who are treated and who do not show a fourfold decrease in titer in a 3-month period should be retreated.

Miscellaneous. Cases of syphilis should be reported within 48 hours of diagnosis to a local or state health department, which usually offers referral and follow-up services. Sexual partners are notified without identification of the index case.

Sequelae. One third of all untreated patients develop sequelae that are generally confined to the CNS and cardiovascular system.

B. Late (neurosyphilis, latent more than 1 year)

History, antecedent treatment, and previous serologic tests are important in establishing the diagnosis. Patients with latent symptomatic syphilis present with complaints relevant to the particular organs involved (see section II.B.2). The latent stage prior to clinical presentation ranges from 3 to 20 years.

Physical examination. The typical lesion of late syphilis is the gumma. These nodular ulcerative lesions can involve skin, mucous membranes, skeletal system, and viscera. Cardiovascular syphilis manifests with aortitis, aneurysm, or aortic regurgitation. Neurosyphilis may be asymptomatic or symptomatic, presenting as tabes dorsalis, meningovascular syphilis, or general paralysis of the insane. Iritis, choroidoretinitis, and leukoplakia may occur.

Investigative procedures. CSF VDRL should be done for clinical signs and symptoms consistent with a CNS lesion and for patients with syphilis of more than 1-year duration to exclude asymptomatic disease.

Management

Recommendations for therapy of cardiovascular, late benign syphilis, and syphilis of more than 1-year duration are as follows: benzathine penicillin G, 2.4 million units IM weekly for 3 weeks; or if penicillin-allergic, doxycycline, 100 mg PO bid, or tetracycline hydrochloride, 500 mg PO qid, for 30 days. Alternatively, if the patient is pregnant or unable to tolerate tetracyclines, desensitization in consultation with an expert may be indicated.

Neurosyphilis may be treated with aqueous crystalline penicillin G, 12 to 24 million units, administered as 2 to 4 million units q4h IV for 10 to 14 days. An alternative regimen is procaine penicillin, 2 to 4 million units IM daily, with probenecid, 500 mg PO qid, both for 10 to 14 days. After completion of these regimens, many authorities recommend the addition of benzathine penicillin G, 2.4 million units IM. Patients allergic to penicillin should be skin-tested and desensitized in consultation with an expert.

Up to 80% of patients treated during the late stages of syphilis remain seropositive indefinitely, although their titers should decrease over time.

The provider should keep in mind that the Jarisch–Herxheimer reaction can occur, producing fever, myalgia, tachycardia, and hypotension within 24 hours of treatment. Some authors recommend hospitalization of pregnant patients since this reaction places mother and fetus at increased risk.

III. C. trachomatis

is a bacterial intracellular parasite that causes a wide range of infections. In women, these include cervicitis, salpingitis, perihepatitis, and urethritis. There are 15 serotypes, and those associated with genital infection are D to K, whereas the L strains are associated with lymphogranuloma venereum. In the United States, approximately 4% to 5% of sexually active women carry Chlamydia in their cervix; and this site appears to play a central role in transmission, with the horizontal spread to male partners and the vertical spread to neonates. There are an estimated 4 million cases annually in the United States.

A. History.

Chlamydial cervicitis is frequently asymptomatic. However, a purulent discharge may be found. Dysuria and frequency (urethral syndrome) may be present. A history of nongonococcal urethritis in the male partner is associated with a 50% isolation of Chlamydia from the female partner. Neonates born to infected mothers have a 60% to 70% risk of infection, including a 10% to 20% risk of pneumonia and a 25% to 55% risk of conjunctivitis.

B. Physical examination.

Although the cervix may appear normal, there is often a significant increase in the incidence of cervical ectopy, erythema, and friability, as well as the presence of mucopus readily seen on a cotton-tipped swab. Mucopurulent cervicitis is caused by chlamydial infection in approximately 50% of cases.

C. Investigative procedures. Culture

is the only reliable way to establish the diagnosis. Endocervical samples are required and should be frozen if not cultured immediately. The organism must be grown in cell culture, and characteristic intracytoplasmic inclusions are identified after staining. If chlamydial cultures are not available, treatment should be given if the diagnosis is strongly suggested on clinical grounds. Direct tests for chlamydial antigen utilizing monoclonal antibodies, enzyme immunoassay, or a DNA probe are useful for screening high-prevalence populations. In low-prevalence groups, there are a significant number of false-positive results. Serologic testing is of little value.

D. Management.

Tetracycline, erythromycin, and azithromycin are highly effective, with cure rates approaching 95%. Additional drugs that have demonstrated activity against Chlamydia include sulfamethoxazole-trimethoprim, rifampin, clindamycin, ofloxacin, and amoxicillin.

The CDC-recommended regimens are azithromycin 1 g PO in a single dose or doxycycline, 100 mg PO bid for 7 days. Alternative regimens are ofloxacin, 300 mg PO bid for 7 days; erythromycin base, 500 mg PO qid for 7 days; erythromycin ethylsuccinate, 800 mg PO qid for 7 days; or sulfisoxazole, 500 mg PO qid for 10 days (this has inferior efficacy to other regimens) (3).

The CDC-recommended regimen for pregnant women azithromycin, 1 g PO or erythromycin base, 500 mg PO qid for 7 days. Alternative regimens include erythromycin base, 250 mg PO qid for 14 days or erythromycin ethylsuccinate, 800 mg PO qid for 7 days or 400 mg PO qid for 14 days. If erythromycin cannot be tolerated, amoxicillin, 500 mg PO tid for 7 to 10 days or clindamycin, 300 mg PO tid for 7 days, are recommended. Limited data exist on these regimens.

Sexual partners should be evaluated and treated.

Follow-up testing is unnecessary unless symptoms persist or reinfection is suspected. Pregnant patients, however, should be retested. At least 3 weeks must elapse after completion of therapy before retesting.

IV. Genital herpes simplex virus.

Venereal transmission through intercourse or orogenital contact is common for herpesvirus, a DNA virus. After the genital skin is inoculated, the virus infects peripheral nerve endings and travels to the lumbosacral dorsal root ganglia. A persistent, but subclinical, infection is established in the ganglion cells. Periodically, the virus becomes active and travels by peripheral nerves to the skin, inducing the characteristic focal recurrent lesion. Infections with herpesvirus type I or II are the most common cause of vesiculoulcerative lesions of the female genital tract. Type I generally causes oral lesions (fever blisters), and 75% to 80% of genital lesions are type II. However, these percentages vary with the population screened. About 50% to 70% of patients with primary infection experience recurrence. The attack rate (percentage of those who contract herpes simplex virus after exposure) for susceptible individuals is believed to be about 75%. There are an estimated 500,000 new cases in the United States annually, with more than 20 million episodes of recurrence.

A. History.

Incubation periods range from 1 to 30 days (median, 6–8 days). Generally, the presenting complaint is of blisters or ulcers on the vulva or severe vulvar pain. Much less often, severe dysuria, general malaise, fever, and enlarged inguinal nodes are the presenting features. The lesions typically evolve from vesicles to pustules to ulcers to crusts, with healing occurring over 14 to 21 days. They may be preceded by pruritus, burning, or hyperesthesia of the skin. Some patients may have no symptoms; thus it is not uncommon to miss the first infection. Recurrent infections are generally less severe than the primary infection and may be triggered by emotional stress, menses, intercourse, or may be totally unpredictable. Systemic symptoms rarely occur, and lesions last from 7 to 10 days. Recurrent lesions represent a reactivation of latent virus, not reinfection.

B. Physical examination.

Exquisitely sensitive vesicles and erosions of the labia, vaginal canal, perineum, and oropharynx may be found. Intense edema of the labia and urethra, as well as inguinal adenopathy may be present. Recurrent disease follows essentially the same course except that it is less debilitating, there are few ulcers, and adenopathy is seldom present. It is generally believed that there is no clinical difference between the lesions caused by the two virus types.

C. Investigative procedures.

The vesicles and ulcers characteristic of the disease are easily recognized, especially if there is a positive history. Cervical herpes virus is less obvious clinically. A Papanicolaou (Pap) smear of cervical herpes virus contains characteristic multinucleate giant cells in about 30% to 50% of patients. Definitive diagnosis can be confirmed by viral culture. Specimens should be taken using cotton-tipped or Dacron-tipped swabs placed in viral transport medium and held at 4°C until cultured. Direct detection of viral antigens using immunodiagnostic methods is available and provides sensitivities of 85% to 90%. These methods are much less sensitive in detecting asymptomatic viral shedding. Herpes virus antibodies appear within 4 days of primary infection and are present thereafter; therefore, they are not helpful in recurrent infection unless a change in titer is documented. Since herpesvirus is an STD, culture for gonorrhea and chlamydia infections and a serologic workup for syphilis, HIV, and hepatitis B and C should be obtained.

D. Management

General measures include keeping the vulva and perineum as dry as possible, wearing cotton underwear, and exposing the vulva to a heat lamp or a hair dryer, which may be soothing. Analgesics may be required because of pain and hypnotics may be required if there is interference with sleep. Occasionally, urinary retention may necessitate the use of an indwelling catheter. Sitz baths and local anesthetic creams may be helpful.

Specific measures. Oral acyclovir, valacyclovir, and famciclovir provide partial control of the symptoms and signs of herpes episodes but do not eradicate latent virus. Topical therapy is less effective and its use is discouraged. The CDC guidelines are as follows:

For first clinical episodes of genital herpes, the recommended regimen is acyclovir, 200 mg PO 5 times a day for 7 to 10 days or until clinical resolution. Alternatives are famciclovir 250 mg PO 3 times a day for 7 to 10 days or valacyclovir 1 g PO twice a day for 10 days. The dose of acyclovir is doubled for herpes proctitis and treatment is for 10 days, experience with famciclovir or valacyclovir in proctitis is lacking.

When treatment for recurrent episodes starts during the prodrome or within 2 days of lesion onset, limited benefit may result. The recommended regimen is acyclovir, 200 mg PO 5 times a day for 5 days or 400 mg PO tid for 5 days or 800 mg PO bid for 5 days. Drug therapy begun more than 2 days after onset of lesions has not been proven to be of benefit. Alternatives are famciclovir 125 mg PO twice a day for 5 days or valacyclovir 500 mg PO twice a day for 5 days.

Daily suppressive therapy reduces recurrences by at least 75% in patients having six or more episodes per year. Safety and efficacy have been reported for as long as 6 years. Asymptomatic viral shedding and the potential for transmission are not totally eliminated. After 1 year, therapy should be discontinued to reassess the rate of recurrence. The recommended regimen is acyclovir, 400 mg PO bid or famciclovir 250 mg PO bid or valacyclovir 500 mg PO bid or valacyclovir 1000 mg PO once a day.

For patients who have severe symptoms or complications that necessitate hospitalization, intravenous acyclovir shortens the median course of first episodes by approximately 7 days.

Acyclovir has not been adequately tested in pregnant or lactating women. Use in pregnancy is recommended only in the presence of life-threatening maternal infection. However, evidence of adverse effects has not been shown in ongoing registries, and therefore first clinical episodes in pregnancy may also be treated with acyclovir.

Patients should be counseled about the disease and advised to abstain from sexual intercourse while lesions are present. The risk of transmitting herpes simplex virus during asymptomatic periods is unknown. The use of condoms should be encouraged during all sexual exposures. Women also need to be instructed to inform their clinicians of their history of genital herpes early in pregnancy since serious neonatal infection may occur during parturition.

E. Sequelae.

In addition to a possible link with cervical neoplasia and neonatal infections, patients with the disease also have a high incidence of depression and sexual dysfunction. Much of the burden of this disease is of an emotional and social nature. Self-help groups, such as the American Social Health Association, may be of great assistance in helping herpes simplex virus patients cope with their problems.

V. Chancroid

is an ulcerating disease of the genital region caused by Haemophilus ducreyi. Its exact incidence is unknown, although clinical infection is rare in women. The incubation period is generally 4 to 7 days, the male to female ratio is 10:1.

A. CDC guidelines.

Chancroid is probably underreported because of the difficulty in proving the diagnosis. In an attempt to obtain more accurate incidence figures, the CDC has changed its reporting guidelines. The new case classification is:

Probable: a clinically compatible case with one or more painful genital ulcers and both

No evidence of T. pallidum by dark-field examination of ulcer exudate or by a serologic test for syphilis performed at least 7 days after the onset of ulcers.

Clinical presentation of the ulcer is not typical of a disease caused by herpes simplex virus, or an HSV culture is negative.

Confirmed: A case that is laboratory confirmed. Recently there has been a documented association of chancroid and HIV. The presence of HIV infection predisposes women to chancroid and increases the possibility of treatment failure.

B. History.

The patient usually presents with the complaint of a painful lesion.

C. Physical examination.

The initial lesion in women occurs on the fourchette, labia minora, urethra, cervix, or anus. Extragenital lesions may occur but are uncommon. Chancroid begins as an inflammatory pustule or papule that quickly ruptures to form a painful, nonindurated, shallow ulceration. Women tend to have multiple ulcers, with an average of four. The ulcer is 1 to 2 cm in diameter with ragged undermined edges, and the base is often covered with a purulent exudate. Approximately 1 week after the initial ulcer, lymphadenopathy, which is usually unilateral, develops in 50% of patients. This subsides without suppuration in more than half of the patients; however, if left untreated, the lymphadenitis may undergo unilocular suppuration. The involved nodes are inflamed and tender, and the overlying skin is erythematous. These nodes then break down, forming a single drainage sinus and/or fever may occur.

D. Investigative procedures

A presumptive diagnosis of chancroid may be made in the presence of a genital ulcer(s) with a negative examination for syphilis (dark-field examination, serologic tests, or both) and no evidence of herpesvirus during follow-up visits.

A definitive diagnosis is made by isolation of the organism from ulcers of lymph nodes on an appropriate selective medium, but the organism is difficult to culture.

DNA probes and the use of PCR may make diagnosis easier in the future.

E. Management

Drug therapy. Recommended regimens include azithromycin, 1 g orally; or ceftriaxone, 250 mg IM or ciprofloxacin, 500 mg PO bid for 3 days; or erythromycin, 500 mg PO qid for 7 days.

Fluctuant nodes should be aspirated through healthy adjacent skin as often as necessary to prevent the formation of a draining sinus. Incision and drainage of buboes may be necessary.

All sexual partners should be treated.

As with all STDs, examination should be undertaken for the presence of other STDs, HIV, and hepatitis B and C.

All patients should be counseled about the risk of transmitting chancroid and the risk of either transmitting or acquiring HIV and hepatitis B and C through sexual intercourse. Patients should be encouraged to abstain from intercourse until all lesions have healed. Condoms have also been shown to prevent the transmission of chancroid.

VI. Lymphogranuloma venereum

(LGV) is a granulomatous disease of the genital region that is primarily sexually transmitted. The causative organism is C. trachomatis, and the serotype is different from that which causes cervicitis. The incubation period is unknown. It is more common in men than women. LGV is rare in the United States, however, the actual prevalence is unknown.

A. History.

The presenting complaints may include a painless lesion, lymphadenopathy, lower abdominal pain, rectal bleeding, rectal purulent discharge, and proctitis with tenesmus, depending on the stage of development.

B. Physical examination

The initial lesion is a painless vesicopapule that appears on the external genitalia, vaginal walls, or cervix in women. It appears a few days to a few weeks after exposure. This quickly breaks down to form a small erosion that heals rapidly in men, but more slowly in women. As many as 50% of these lesions are asymptomatic and heal without scarring.

The secondary stage is characterized by lymphadenopathy, which is usually unilateral, but involves multiple nodes. This results in the formation of a large nodal mass with inflamed overlying skin. The involvement of inguinal and femoral nodes with a depressed area over the inguinal ligament (groove sign) is almost pathognomonic for LGV. These nodes then develop multiple foci of suppuration, followed by skin breakdown and formation of multiple draining sinuses (as opposed to chancroid, which has a single area of suppuration and one draining site). Genital mutilation often develops.

The inguinal adenopathy typically resolves after 2 to 3 months if untreated. However, in the tertiary stage involvement of internal nodes (perirectal and perivaginal) leads to an anorectal syndrome with lower abdominal complaints and proctitis with tenesmus, rectal bleeding, and a purulent discharge. This may lead to rectal strictures, elephantiasis of the labia, and rectovaginal fistulae. Although extragenital lesions are rare, LGV is associated with significant systemic signs such as fever, malaise, myalgias, and arthritis.

C. Investigative procedures

The diagnosis of LGV is best made by complement fixation titers, which are available through most laboratories. However, there is cross-reaction with other chlamydial serotypes. A fourfold increase in titer or a titer of greater than 1:64 should be considered diagnostic. A titer of 1:16 to 1:64 is suggestive, but can occur in individuals with other chlamydial infections. The organism can be recovered from nodal aspirations, but culture is technically difficult, expensive, and rarely available.

D. Management

Drug therapy. The recommended regimen is doxycycline 100 mg PO bid for 21 days. An alternative regimen is erythromycin 500 mg PO qid for 21 days.

As with chancroid, involved lymph nodes (buboes) should be aspirated through adjacent normal skin, and incision and drainage may be indicated.

Sexual contacts should be examined and treated.

Investigation for the presence of other STDs, including HIV and hepatitis B and C, should be undertaken.

VII. Granuloma inguinale

is generally considered a disease of tropical and subtropical regions. It is rare in the United States. The causative organism is an intracellular gram-negative bacterium, Calymmatobacterium granulomatis.

A. History.

The presenting complaint is usually of an enlarging painless ulcer.

B. Physical examination.

The initial lesion is a painless ulcer that has little undermining and is usually located on the labia or fourchette. There is no lymphadenopathy unless the lesion is secondarily infected. Occasionally, a deep granuloma may appear to be a fluctuant node. These “pseudobuboes” may erode through skin and slowly extend by local enlargement. Constitutional symptoms are absent. If left untreated, these lesions progress insidiously, often along skin folds, and take on a granulomatous appearance. The central portions of the ulcer may heal spontaneously, leaving gray, fibrous scars with active advancing borders. These scars can produce deformities and strictures. Long-standing lesions often produce elephantiasis-like enlargement of the labia and extensive ulceration of the perineum. Extragenital lesions can occur almost anywhere by direct spread, and systemic dissemination (presumably blood-borne) has been described. In advanced cases, general debilitation may lead to death. The incidence of squamous cell carcinoma is increased within the chronic ulcers.

C. Investigative procedures.

The diagnosis of granuloma inguinale should be considered in any genital ulcer lasting more than several weeks, especially in the absence of lymphadenopathy. The diagnosis is best made by finding the typical organisms (Donovan bodies) with histiocytes on stained smears or tissue sections from the edge of lesions. The tissue should be crushed and spread between two glass slides and stained with Wright's or Giemsa stain. The Donovan bodies exhibit bipolar staining and are commonly described as having a “safety pin” appearance.

D. Management

Drug therapy. The recommended regimens include doxycycline, 100 mg bid for 3 weeks or until all lesions have healed (from 2–12 weeks); trimethoprim-sulfamethoxazole DS (160/800) bid for at least 3 weeks; erythromycin, 500 mg qid for 2 to 3 weeks; or ciprofloxacin 750 mg PO bid for at least 3 weeks.

Sexual partners should be examined and treated.

Patients should also be examined for the presence of other STDs.

VIII. Pediculosis pubis.

The causative organism for pubic lice is Phthirus pubis (crab louse), which is different from body or head lice. Its life cycle is approximately 25 days and can be completed entirely on the human host. Soon after reaching maturity, impregnated females begin laying eggs (nits) that hatch in 7 to 8 days. Each egg is cemented to a single hair shaft.

Transmission is generally by direct body contact, usually sexual. The risk of transmission from fomites is negligible. Pubic lice are the most contagious STD known, and the risk of acquiring the infestation is approximately 95% after a single exposure. The incidence is higher in young women from 15 to 19 years of age and is higher in men older than 20 years. There is no racial difference. Although pubic lice can be transmitted without sexual contact, abuse should be considered in any infection in a child.

A. History.

The chief complaint of infested persons is pruritus and, because of autosensitization, it is not always localized to the affected sites. Patients may report seeing organisms move in their pubic hair.

B. Physical examination.

The louse is usually found in the pubic area, eyebrows, and eyelashes. Nits may be seen at the base of the hair shafts in these areas. Scratching may lead to secondary excoriations, which may predispose to lymphadenitis or pyoderma. The infested patient may also present with a symptomatic, bluish, nonblanching, nodular rash on the lower trunk and upper thighs, known as maculae ceruleae. This rash is believed to be either secondary to altered blood pigments in the patient or an excretory substance from the louse's salivary glands.

C. Investigative procedures.

A magnifying glass may be helpful in visualizing the lice or nits. They may also be placed on a slide with a drop of mineral oil and examined under the microscope. The lice look like miniature crabs.

D. Management

For pubic infestation, treatment with gamma benzene hexachloride (lindane [Kwell]), a solution of pyrethrins with piperonyl butoxide (RID), or a 1% permethrin creme rinse (Nix) is equally effective.

Lindane is available by prescription only, is absorbed through the skin, and can cause CNS toxicity (although this has been described only when it was used improperly or taken orally). It should not be used in pregnant or lactating women or on children younger than 2 years. The lotion is applied to the affected area, left on for 12 hours, and repeated in 1 week. The shampoo is massaged into the pubic hair and worked into a lather, left on for 4 minutes, and washed off. It is usually not necessary to repeat the application. Nits remaining after either treatment can be removed with forceps or a fine-toothed comb.

The pyrethrin solution is available without prescription and is poorly absorbed through intact skin, so it is apparently free of toxicity. Two ounces are massaged into dry pubic hair, left on for 10 minutes, and washed off. One treatment is all that is necessary, and remaining nits can be removed in the manner described previously. This is the treatment of choice in pregnancy and lactation.

1% permethrin creme rinse is available by prescription only. It should be applied to pubic hair and washed off after 10 minutes. This treatment should be repeated in 10 days, and remaining nits can be removed as discussed previously.

For infestation of the eyelashes, apply petrolatum bid for 8 days and remove the nits by hand.

Even though fomite transmission rarely (if ever) occurs, patients should be advised to wash and dry sheets, bedding, and clothing in the hot cycle. Sprays are available for use on inanimate objects, but are unnecessary and potentially dangerous and their use should be discouraged.

All sexual contacts should be treated simultaneously, and the patient should be examined for the presence of other STDs, including hepatitis B and HIV, since one third to one half of all patients have another STD.

Follow-up after 1 week if symptoms persist. Nonresponders should be retreated with an alternative regimen.

IX. Scabies infestation

is caused by the mite Sarcoptes scabiei. Like the crab louse, its entire life cycle can be completed on humans. The adult female burrows into the skin and remains there for life, approximately 30 days. She rapidly begins laying two to three eggs per day, which become adult mites in 10 days. However, fewer than 10% of the eggs become adults. The average patient with scabies only has 10 to 15 live adult female mites on the body at any time. The mites can survive for only 2 to 3 days at room temperature apart from humans. However, they can survive longer in warm humid areas such as nursing homes than in cool, dry climates.

Several different types of scabies have been described. These include scabies incognito, occurring in persons receiving steroids, which alter the clinical presentation; scabies in the clean, found in those with good hygiene and in whom physical findings are minimal; and nodular scabies, which present as reddish-brown pruritic nodules in the usual scabetic distribution and appear to represent a hypersensitivity reaction; Norwegian scabies, which is rare, highly contagious, and usually found in institutions with a propensity for mentally retarded and debilitated persons; and animal-transmitted scabies, with dogs as the major source of infection. All of these types are treated the same except the latter. The animal mite cannot complete its life cycle on the human host, so the infestation is self-limited (several weeks), and the animal must be treated to prevent reinfestation.

Transmission is by close personal contact, usually sexual. Scabies are rarely transmitted by fomites or by casual contact. It is more common in men than women.

A. History.

The primary symptoms are pruritus and a rash that is caused by sensitization to the mite. In primary infestation, it takes 4 to 6 weeks for these to occur, although in reinfestation, symptoms may appear within 24 hours. The pruritus is typically nocturnal. Since the immune system must be intact for a response, patients with a depressed immune system may not itch.

B. Physical examination.

The rash is usually symmetric and located primarily on the hands (especially finger webs and sides of digits), wrists, elbows, female breasts, waist, penis, and the lower portion of the buttocks. The pathognomonic lesion is the burrow, which is a short, wavy, dirty-appearing line. This lesion is seen very infrequently now even though the incidence of scabies is not decreasing. Excoriations of these lesions can lead to secondary infection.

C. Investigative procedures.

A presumptive diagnosis is made by observing the typical burrows in a symptomatic patient. A definitive diagnosis can be made by demonstrating the mite, the fecal pellets, or the burrow by special tests.

A drop of mineral oil can be placed on the skin lesions, which are then scraped with a scalpel blade and transferred to a slide for observation through the microscope.

The lesions can be moistened with alcohol, then scraped and transferred to a microscopic slide. Adding 20% potassium hydroxide to the slide and heating gently aids in clearing epidermal debris.

In the tetracycline test, a liquid tetracycline solution is applied to areas where burrows are usually found. After drying, the area is cleaned vigorously with isopropyl alcohol and then observed with a Wood's lamp. Burrows that have retained the tetracycline appear as yellow-green lines.

The ink test, similar to the tetracycline test, involves rubbing a fountain pen over the suspected area, then cleaning with alcohol, and looking for burrows that the ink has penetrated.

D. Management

Several treatments are effective.

Lindane (1%) lotion is applied thinly but thoroughly from the neck down and left on for 12 hours. The application is repeated in 1 week only for those with evidence of treatment failure or reinfestation. Lindane should not be used in pregnancy or lactation or in children younger than 2 years. Bathing prior to application is not recommended since it can potentiate absorption of the drug. The usual amount needed for adults is 30 mL.

Permethrin, 5% cream (Elimite), is an excellent scabicide and less toxic than lindane. This is used as a single application in the same way as lindane and washed off after 10 hours. Over-the-counter permethrim products are lower strength, designed to treat pediculosis, and are ineffective in the treatment of scabies.

Sulfur, as a 6% solution is applied nightly for 3 nights and washed off 24 hours after each application. Its efficacy and toxicity are not well established, and it is unpleasant to use.

Treatment should include brushing the formulation under the ends of the fingernails. In children and elderly patients, the face, head, and especially the postauricular fold should be included in treatment.

Bedding and clothing should be decontaminated via washing and hot cycle drying. Fumigation of living areas is unnecessary.

All persons in close personal contact with the patient should also be treated with one of the foregoing regimens.

For the pruritus, an oral antihistamine, such as hydroxyzine hydrochloride (Atarax), 25 mg tid; or diphenhydramine (Benadryl), 25 mg qid, as needed can be used simultaneously with the scabicide, or a 1% hydrocortisone cream can be used after treatment.

Female Sexual Dysfunction

Definition :
Female sexual dysfunction (FSD) is defined as a disorder of sexual desire, arousal, or orgasm, and/or sexual pain, which results in personal distress and has an impact on quality of life and interpersonal relationships. It is a compilation of problems that has both biologic and psychosocial components and is multifactorial in etiology.

Introduction :
Female sexual dysfunction (FSD) is defined as a disorder of sexual desire, arousal, and orgasm, and/or sexual pain that results in significant personal distress and might have an impact on the quality of life and interpersonal relationships . It affects approximately 4 out of 10 women in the United States, and according to the 1995 American College of Obstretricians and Gynecologists (ACOG) Technical Bulletin, sexual dysfunction occurs in as many as 35% of US women, with lack of libido being the most common symptom reported . Based on self-reported complaints from US census data, 10 million women between the ages of 50 and 74 report diminished lubri-cation, pain with intercourse, decreased arousal, and difficulty achieving orgasm . Several animal and human studies have documented that FSD is a progressive, age-related, hormone-sensitive condition .
A significant proportion of postmenopausal women are predisposed to experience FSD . In addition to the physical changes associated with menopause, FSD can significantly alter self-esteem and intimate relationships .
Female sexual dysfunction was previously thought to be caused by primarily psychological factors and interpersonal issues, and male sexual dysfunction was thought to be caused by physical and biologic changes. FSD, however, is a compilation of problems that has both biologic and psychosocial components. It is only recently that FSD has been considered to have a multifactorial etiology . Our improved understanding of normal female sexual function and age-related changes have helped us to better classify the types of dysfunction. FSD can also be associated with conditions that cause male erectile dysfunction, such as hypertension, smoking, elevated cholesterol, and pelvic surgery .
Models of Normal Human Sexual Functioning
In 1966, Masters and Johnson described the human sexual response that has remained a classic teaching model. This linear model, which focuses primarily on the vascular and neurologic changes, includes four stages: 1) excitement; 2) plateau; 3) orgasm; and 4) resolution.
Excitement refers to changes in the central nervous system(CNS) that cause vasodilation and increased blood flow to the genitalia. Several hormones play key roles in this process. The outcome of these complex physiologic processes results in lubrication and expansion of the vagina, increased labial girth, and exposure of the introitus, due to opening of the labia. A well-estrogenized vagina has prominent rugae, particularly in the lower third. These rugations allow the vagina to distend and increase frictional tension with coitus . The clitoris elongates and increases in diameter while the uterus elevates over the levator plate . Although the clitoris arises from the same embryologic structure as the penis, the genital tubercle, it lacks the bilaminar tunica albuginea and venous plexus. Therefore, during sexual stimulation the clitoris becomes engorged, but not erect. The uterus and cervix also add to lubrication by secreting mucus during this phase of stimulation.
Interruption of the vascular supply and innervation during pelvic surgery has remained a controversial issue in the topic of postoperative FSD. Ovarian atrophy and fibrosis of the vagina and clitoris can occur after disruption of the uterine vessels and removal of the uterus . Previous studies, however, have shown conflicting results of pelvic surgery on sexual function postoperatively . This might reflect the limited use of validated questionnaires rather than sexual dysfunctions related to pelvic surgery.
In older women, changes associated with excitement begin to diminish. Labial swelling and clitoral engorgement rarely occur in women older than age 60 . Vaginal lubrication, which usually takes seconds in young women, can take 1 to 3 minutes in women older than 40, if it occurs at all. The ability of the vagina to elongate, widen, and expand is reduced.
Excitement is followed by plateau, in the Masters and Johnson model. During this phase, the labia become engorged and the clitoris retracts. The Bartholin glands secrete fluid, and congestion of the outer third of the vagina occurs. The upper two thirds of the vagina expand, and pelvic--floor muscle tension builds. The combination of neurovascular injury and/or loss of muscular tone, due to birth trauma, surgery, menopause, vascular insufficiency, and aging in general can result in vaginal anesthesia, lack of orgasm with coitus, or coital incontinence .
Kaplan later modified this model by dividing the excitement phase into desire and arousal, and eliminating the plateau phase . In his model, desire results from neurogenic changes and arousal from vasogenic changes. The new diagnostic criteria for FSD are based on this revision.
Orgasm occurs when the levator ani muscles contract. This altered state of consciousness consists of 8 to 12 contractions of musculature at specified intervals, followed by vaginal and uterine contractions. Sensory afferent stimulation from the clitoris, labia, vagina, and periurethral glands travel to supraspinal structures. Adequate sensory information results in a discharge of central neurotransmitters and causes the contractile phase of orgasm. Some sensory information is also relayed to the cortical pleasure sites. The final result is massive release of muscular tension.
The postmenopausal uterus tends to be smaller and does not enlarge to premenopausal magnitude. Some women even experience painful contractions during orgasm .
Resolution was described by Masters and Johnson as the end of the sexual response and is characterized by pleasant, gradual diminishing of sexual tension following the above phases. Although this model accurately reflects the physiologic characteristics of the human sexual response, it is limited by the omission of social and psychological factors.
The biopsychosocial model postulates that biologic or physiologic processes alone cannot characterize female sexual response. It is, instead, a combination of biology, psychology, sociocultural influences, and interpersonal relationships. This model suggests that emotional intimacy, feeling emotional closeness, commitment, sharing, and tenderness to another person is often required for a woman to respond to sexual stimuli. This theory holds that a woman's sexual experience is initiated by a response to intimacy and a desire to share themselves emotionally and physically rather than being provoked by sexual fantasies or thoughts. Once the woman is emotionally aroused, she can then become sexually aroused, which will in turn lead her to sexual desire, and the ultimate culmination of the event for sexual reasons . Sexual arousal can be triggered by various stimuli ranging from conversation to music to direct physical contact. Therefore, a woman's lack of spontaneous sexual desire should not always be viewed as a dysfunction. There might simply be a lack of emotional connectedness to the person directing the sexual advances. Another point is that this model does not place orgasm as the goal of a sexual experience. Instead personal satisfaction, regardless of whether orgasm is reached, becomes the goal .
Physiology of Normal Sexual Function
Physicians, women, and their partners can comprehend abnormal sexual functioning once they appreciate the basic physiology behind normal sexual function. This usually begins with understanding the structures and bioactive substances involved in sexual function. There are several organs that are vital to a normal sexual response-the brain, however, is the center of the sexual universe. The five senses (smell, sight, sound, taste, touch) help to relay sexual images, fantasies, and ideas to the brain. The brain accepts these signals and translates them into messages the body can understand. These messages include signals to increase vascular blood flow and release sex hormones, such as estrogen, testosterone, and vasoactive substances.
The central nervous system is affected by both internal and external factors that result in a need or want to partake in sexual activity. The limbic and paralimbic systems emit signals that are responsible for a woman's arousal . Munarriz states that, in the biology of sexual function, desire consists of three areas: biologic, which is controlled in part by sex hormones and neurotransmitters; motivational roots, which are partly based on intimacy; and pleasure,relationship issues, and cognitive factors, such as risk and wish. Arousal results from central mechanisms, dreams, fantasies and thoughts, nongenital peripheral mechanisms, salivation, sweating, cutaneous vasodilatation, nipple erection, and genital engorgement.
Estrogen increases blood flow to the brain and the vagina. This might be related to estrogen's ability to stimulate the release of substances such as nitric oxide from endothelial cells, which act in a vasoactive manner to induce dilation. Levels of estradiol that are below 50 pg/mL have been correlated with sexual complaints . Decreased blood flow, sensation, and sex drive are all associated with low estrogen levels. In vivo studies in rabbits and rats have demonstrated that pelvic nerve stimulation causes a response that mimics genital arousal from sexual stimulation . Using these models, several studies have shown the importance of ovarian substances and hormones in modulating genital blood flow, vaginal lubrication, and vaginal tissue structural integrity . There is some evidence that this hormone might have effects on the urethral, vaginal, and clitoral blood flow through prevention of atherosclerotic plaque formation in the pelvic vasculature . Estrogen also increases vibratory sensation peripherally, and has a positive effect on nerve growth and nerve transmission .
Testosterone also serves an important role in women. Its concentration is 7 to 10 times higher in the brain than estrogen, and it is the primary precursor for estradiol biosynthesis in the brain . Testosterone is thought to work peripherally by either directly affecting arterial blood flow, or indirectly by increasing the availability of estrogen. Additionally, the hypothalamus, which controls sexual function and mood, contains dense estrogen and testosterone receptors. A study by DeCherney suggests that the testosterone receptors in the brain are linked to sex drive. The study implies that testosterone has a central role in controlling sex drive through receptor-mediated activities.
Normally, the clitoris and vagina are under the contractile tone of the pudendal, autonomic, and somatic nerves. Based on rabbit models, sexual stimulation results in release of neurogenic and endothelial nitric oxide (NO) . This might play a role in clitoral cavernosal artery inflow and helicine arteriolar smooth muscle relaxation during arousal .
Vaginal lubrication might be mediated by several neuro-transmitters, including NO and vasoactive intestinal peptide (VIP) .These substances modulate vascular and smooth muscle relaxation, causing capillary inflow that overwhelms normal sodium reabsorption, resulting in 3 to 5 mL of vaginal secretions. Smooth muscle relaxation that increases the length and caliber of the vagina, particularly in the distal two thirds, might also be due to these substances. Phosphodiesterase type V enzyme has been found in human clitoral cavernosal smooth muscle, which degrades cyclic guanosine monophosphate (cGMP) .Inhibition of this substance might result in relaxation of clitoral and vaginal smooth muscle and improve arousal .Other factors and hormones such as oxytocin and endorphins act on the brain to promote sexuality.
Diagnostic Classifications of Female Sexual Dysfunction
Inconsistency in classifying FSD has existed for years. In the past, many researchers created their own definitions for sexual disorders, which inevitably led to confusing and incongruent results. An attempt to address this issue was made through a panel of experts at the Consensus Development Conference on FSD in 1998 . The panel created a new classification of FSD that was published in the Journal of Urology, and reprinted with invited expert comment in the Journal of Sex and Marital Therapy [2001]. This system can be used in FSD caused by either medical or psychosocial etiologies, and it includes some modifications to the Diagnostic and Statistical Manual [of Mental Disorders] IV (DSM IV) system. Some experts would argue that this system is still based on the male linear model of sexual function . They argue that women can experience satisfaction and pleasure without experiencing every phase of the sexual response cycle. Our continuing quest to understand female sexual function and dysfunction might result in modifications of this classification system with time. The current system classifies the following disorders.
Hypoactive sexual desire disorder
Includes persistent or recurrent lack of sexual thoughts and/or receptivity to sexual activity, which causes personal distress. This can be secondary to medical causes (ie, endocrine) or related to psychological or emotional dis-orders. There are currently no validated, research-proven treatments for hypoactive sexual desire disorder, but lack of the estrogenic and androgenic effects on the female sex drive has been implicated as a possible cause.
Sexual aversion disorder
Sexual aversion disorder is the persistent or recurring phobic aversion to and avoidance of sexual contact with a sexual partner, which causes personal distress. This dis-order is usually caused by an underlying emotional or psychological problem, commonly physical or sexual abuse or childhood trauma.
Sexual arousal disorder
Sexual arousal disorder is the persistent or recurrent inability to attain or maintain sexual excitement, which causes personal distress. These disorders can be primarily physiologic in origin, resulting from insufficient vaginal lubrication, poor vascular blood flow to the genitalia, or neurologic etiologies. It can be secondary to medical/surgical therapy, pelvic floor disorders, and deficiencies in relaxation of pelvic floor musculature. This disorder can result from psychological factors, but is more commonly associated with organic factors. Sexual arousal disorder has been the focus of most of the basic science and clinical research in FSD.
Orgasmic disorder
Orgasmic disorder is defined as the persistent or recurrent loss of orgasmic potential after sufficient sexual stimulation and arousal, which causes personal distress. Orgasmic disorder can be primary (never achieved orgasm) or secondary, caused by traumatic nerve injury after pelvic floor surgery or spinal cord injury. There are several approaches to therapy, including addressing emotional trauma or medical/physical factors.
Sexual pain disorder
Sexual pain disorder is a persistent or recurrent genital pain associated with noncoital sexual stimulation, which causes personal stress. This disorder is further subtyped into dyspareunia, vaginismus, and other sexual pain disorder induced by noncoital sexual stimulation.
Clinical Evaluation of the Female Patient with Sexual Dysfunction
In the general gynecology or primary care setting, patients do not commonly present with FSD symptoms, even when a good rapport has been established. Many patients are reluctant to ask questions during evaluation, despite a high prevalence rate of FSD. For this reason, patients might be more comfortable answering questions presented on a standard history intake form. A recent study by Nusbaum et al. demonstrated the prevalence of sexual concerns in women seeking routine gynecologic care. Of the 964 (65%) respondents, 98% of this group reported one or more sexual concerns. Women might respond to an anonymous survey, but most women are hesitant to actively address these issues at annual examinations. This might be due to the perception or the actuality that the physician is too busy, or they are not approachable. Similarly, most health care providers fail to address sexual history as a part of the medical history. Societal, cultural, and religious values also play an important role in a woman's comfort level for discussing sexual function .
Once a problem is uncovered, clinicians might consider behavioral modification first. Reading articles/books on the symptoms can empower a woman and help educate the partner. Self-examination of the genitalia should be encouraged routinely. Educating a patient about their genital anatomy can help address body-image issues. Prolonged touching, both by a partner or the patient herself, can improve vaginal blood flow and potentially enhance orgasm. Changing routine sexual practices and experimenting with different places and positions can result in improved function for some. Creative thinking can help to bring excitement into a love life without significant medical intervention. Clinicians can focus on these techniques initially, instead of making a diagnosis.
Caregivers should also stress the importance of changes in lifestyle. Postmenopausal women who complain of decreased desire might benefit from aerobic training. Exercise, particularly strength training, has been shown to improve body image, decrease depression, and increase libido and levels of testosterone .Exercise of the pelvic floor also enhances pelvic blood flow, and possibly enhances orgasm by improving awareness . Smoking can decrease vaginal flow and worsen atherosclerotic disease in the aorto-iliac vessels.
For patients who have not benefited from behavioral modifications, a complete evaluation should be performed, including history, review of medications, completion of a sexual function questionnaire, a hormonal profile, when indicated, and physical examination. This examination should delineate if estrogen therapy is indicated and if there are painful trigger points.
Treatment of Female Sexual Dysfunction
Addressing FSD in a clinical setting should begin with an open discussion about the importance of nonpharmacologic therapies. Ultimately, the goal of therapy is to achieve satisfying and pleasurable experiences. The approach to therapy should start with identification of the disorders from a biologic or physical standpoint. Tantamount to defining the medical problem is to address relational, situational, and psychological issues. Couples should first engage in open conversation about their preferences in a way that is nonjudgmental or intimidating. Many couples benefit from short-term counseling to develop effective means of communicating. Couples should also address expectations of sexual frequency. It is important to educate patients and their partners that each sexual encounter does not have to culminate in orgasm to be pleasurable or satisfying.
Pain disorders
Addressing pain disorders should begin with obtaining a complete history of a woman's experiences. Depending on the population surveyed, between 20% and 66% of women have been sexually or physically abused at some point in their lives . Caregivers should specifically ask if date rape or forced intercourse during a steady relationship has occurred. Mental and verbal abuse, which is highly prevalent and underestimated, can also manifest as pain. Women who have been abused often dissociate from their bodies as a defense mechanism. Later in life, this can result in unconscious spasms or painful coitus.
A diagram of the female genital tract should be shown prior to examination. It is helpful for the caregiver to explain how the examination will proceed and for the woman to point out the painful area prior to examination. A mirror might be utilized while the examination is conducted. Begin with reviewing the external genitalia and asking again where the pain occurs. Women with vestibulodynia might have diffuse or local disease that causes pain on insertion. Patients with vaginismus involuntarily contract their pelvic floor even prior to examination or coitus. Both disorders can benefit from education, pelvic-floor physical therapy (including biofeedback and myofascial release), and psychological counseling, if indicated. The presence of endometriosis and/or pelvic adhesions can also cause deep or 'bump' dyspareunia, and thus might require medical or surgical intervention. In postmenopausal women with atrophic vaginitis, vaginal administration of estrogen has shown a clear benefit in decreasing pain on insertion, improving lubrication, and decreasing vaginal burning . Estrogen can be administered in a variety of methods: cream, tablet, or a ring. Some women also experience coincident changes in desire and arousal, which can result in pain if they are not fully aroused. A psychotherapist or a sex therapist can address relational issues. Patients should attend to situational factors such as fatigue and emotional exhaustion.
The presence of incontinence and/or prolapse does not prohibit women from functioning sexually and/or having satisfying activity . However, women undergoing procedures to correct incontinence and/or prolapse might experience complaints of pain postoperatively . Weber et al. demonstrated improved or unchanged sexual function after surgery for prolapse/incontinence, but higher rates of dyspareunia were noted after repair of the posterior wall. Routine repair of posterior wall defects should be challenged, owing to common patient complaints of pain and inability to have intercourse after such procedures.
Orgasm disorder
Women who have never achieved orgasm, primary anorgasmia, often need a referral to a sex therapist. Sociocultural values can inhibit a woman's ability to process pleasurable stimuli. Several techniques, such as sensate focus, systematic desensitization, and directed masturbation, have shown to be effective in treating primary and secondary anorgasmia and hypo-orgasmia . More women achieve orgasm with clitoral stimulation than from penile-vaginal intercourse. Caregivers should educate and reassure the couple that this is normal.
Secondary anorgasmia might be the result of depression or medications for depression. Switching to bupropion for women using selective serotonin-reuptake inhibitors (SSRIs) can be helpful. Bupropion has been shown to be more helpful than placebo in nondepressed women . The mechanism of action might be to increase NO synthase activity and subsequent NO availability .
Pelvic floor rehabilitation with Kegels, vaginal weights, and/or pelvic floor physical therapy can be used to strengthen pelvic-floor muscles and improve pelvic-floor blood flow and orgasm. Vaginal weights are useful in performing pelvic floor exercises, in that contraction of the pelvic floor musculature is required to retain the weight. The patient progressively moves through the weights until she can hold the heaviest weight in the vagina without any effort. Some women might benefit from sessions with a physical therapist and biofeedback. Home biofeedback units are also available. Recently, the FDA approved the EROS clitoral therapy device (EROS-CTD, St. Paul, MN). The device applies gentle suction to the clitoris and has been shown to improve orgasm, sensation, and lubrication in patients with and without FSD. Women who experience change in orgasm function after surgery or menopause might benefit from this device. Relational and situational variables can be dealt with by open communication between partners.
Arousal disorder
In the traditional model of sexual function, women become aroused after a desire or 'hunger' is initiated by sexual thoughts and fantasies. Recent research has indicated that this process is much more complex . Arousal involves 'a mind sexually awakened and a body physiologically prepared for sexual activity' in the context of emotional intimacy . Desire becomes a response to subjective awareness of this type of arousal. In women, the mere presence of genital congestion does not translate into sexual arousal. In fact, several studies have demonstrated an obvious disconcordance between genital arousal and subjective awareness of this physical process . Several reports have demonstrated increased vaginal pulse amplitude (VPA) with viewing erotic video, while reporting absent or minimal subjective arousal . This understanding can give patients and clinicians insight to treatment.
Postmenopausal women who complain of lack of lubrication and swelling might certainly benefit from vaginally administered estrogen. The role of oral estrogen is less clear. In vivo studies have shown estrogen prevents clitoral and vaginal fibrosis and, therefore, permits genital arousal . Although oral estrogens might improve end-organ function, they also increase sex-hormone binding globulin, which decreases free-testosterone and sexual desire. Sarrel reported that improvements of symptoms were seen at estradiol concentrations of more than 50 pg/mL. These levels also improved clitoral sensitivity and orgasm, and, in particular, increase desire and activity. Other studies have not validated improvement of arousal or orgasm with oral estrogen replacement therapy (ERT) . Premenopausal women who are lactating or on low-dose oral contraceptives might also benefit from short-term topical estrogen. These women are also the focus of sildenafil research on women who can achieve mental excitement but lack the genital stimulation.
Although sildenafil revolutionized male sexual dysfunction, research and reimbursement by third-party payers for women were, until recently, lacking, at best. Many women had hoped that this revolutionary sex drug would be equally effective for FSD. Current research demonstrates that patients and physicians must know who are appropriate candidates for this medical therapy. Several studies have been published that do not demonstrate improved sexual arousal. Laan et al. evaluated healthy premenopausal women without FSD. In this cross-over study, patients were given an oral 50-mg dose of sildenafil or placebo in the first session and the alternate in the next session. Despite significant increases in vaginal vasocongestion in the treatment group, there was no difference between the treatment group and the control group on subjective sexual arousal experience. In women with self-described FSD, Kaplan et al. reported changes in vaginal lubrication and clitoral sensitivity, but no significant improvement in sexual function. Conversely, Caruso et al. reported improved sexual arousal and sexuality with 25 mg and 50 mg of sildenafil in premenopausal women with arousal disorder. Basson et al. recently presented data from 577 estrogenized and 204 estrogen-deficient women with sexual arousal disorder. Patients were randomized to sildenafil 10 to 100 mg or matching placebo. Patients completed efficacy, satisfaction, and sexual function questionnaires. Neither group perceived an improvement in sexual response. Basson et al. pointed out that there might be subtypes of women with arousal disorder who might benefit from treatment: those with intact desire but limited genital function.
Sildenafil shows some promise in treating patients with antidepressant-associated sexual dysfunction (AASD). Approximately 30% to 70% of patients using SSRIs have AASD . In a review of the literature from 1989 to 1996, Shen et al. found that sildenafil reversed the AASD caused by SSRIs. The more recent studies have not focused on women, but do show improvement favoring sildenafil.
Sildenafil is not without risks. Several studies report headache, flushing, nausea, dyspepsia, and visual changes. The drug is also associated with sudden cardiac death and possibly stroke in high-risk patients.
Encouraging partners to uncover psychological and relational factors with a therapist or counselor can improve sexual experiences. Women with an arousal or desire disorder might benefit from viewing erotic videos with or without their partner. Increasing sexual fantasies might improve satisfaction and enjoyment in subsequent physical encounters.
Desire disorders
Disorders of desire are the most common presentation of FSD. A survey of 964 women presenting for annual examinations noted 67% of women complained of low desire . Dysfunction exists if a woman expresses a persistent or recurrent lack of sexual thoughts and/or receptivity to sexual activity, which causes personal distress. The development of desire results from the interaction of neurotransmitters and their target organs. The brain, however, is the central mediator of this process. Fantasies and sexual thoughts initiate the activation of this biochemical cascade in men. Women, however, seek out sexual stimuli in the context of emotional intimacy, based on the biopsychosocial model .Therefore, loss of this 'drive' is more commonly the result of alterations in intimacy, rather than biologic factors. Psychological, relational, or situational issues are factors that should be addressed before considering pharmacotherapy. If elucidated in the history, referral for professional counseling might be suggested. Many women experience a lack of desire due to the mental and physical exhaustion associated with daily activities and responsibilities. Emphasis on a healthy lifestyle, exercise, and rest are important to re-establishing desire.
Women who have undergone bilateral oophorectomy often complain of loss of desire. ERT improves vasomotor symptoms as well as atrophic vaginitis, but does not improve libido. ERT might actually cause or exacerbate loss of desire by increasing sex hormone binding globulin (SHBG) and decreasing free testosterone. Mixed results have been reported in postmenopausal women regarding testosterone replacement and improved desire . Rako suggests that testosterone deficiency can result in 1) global loss of sexual desire, lack of sexual fantasy and lack of sexual dreams; 2) decreased sensitivity to sexual stimulation in the nipples and in the clitoris; 3) diminished vital energy and sense of well-being. She states that even if total and free testosterone levels are normal, women who experience symptoms of depletion are candidates for replacement of testosterone. Rako also notes that women who undergo hysterectomy without adnexectomy might still suffer from testosterone depletion due to interruption of the uterine arteries and ovarian atrophy. This can have a profound effect, particularly for younger women who undergo hysterectomy, with or without oophorectomy. Premenopausal women using oral contraceptives can also benefit from testosterone replacement, because oral contraceptive pills decrease free testosterone levels.
There are many methods to replace testosterone, but there are no current guidelines for androgen therapy in FSD . Methyltestosterone and combined estrogen/testosterone are commonly prescribed by clinicians. Although these formulations are well tolerated, patients should be counseled on their effects on serum high-density lipoprotein (HDL) and liver function. Cosmetic effects such as acne and hirsutism can result, but irreversible virilization is rare. Transdermal testosterone replacement can also be administered. Shifren et al. showed a beneficial effect in a double-blinded, randomized, placebo-controlled, crossover-designed trial of 75 surgically induced menopausal patients. Supraphysiologic replacement improved measures of desire, orgasm pleasure, and general well being. Most studies showing benefit with testosterone report correction to premenopausal levels .

Evidence Based Management of Androgen Insufficiency in Women with Female Sexual Dysfunction

Evidence Based Management of Androgen Insufficiency in Women with Female Sexual Dysfunction

-In 2000, the International Consensus Development Conference on Female Sexual Dysfunction1 defined Sexual Desire Disorder as a persistent or recurrent deficiency of sexual fantasies or thoughts, and/or desire or receptivity to sexual activity accompanied by personal distress.

-The most severe form of this is sexual aversion disorder. The hallmark epidemiological study was done by Laumann2 and reported in J.A.M.A. in 1999. In all, 43% of women ages 18 to 59 years, suffer from some form of sexual dysfunction.

-The incidence of decreased libido remained constant in all decades studied at about 30-32%. How many of these women have decreased androgens is unknown. In a study in the UK, Dunn3 determined by postal questionnaire that 41% of women 18 to 75 years old had some form of sexual dysfunction.

As in men, decreased libido in women has been linked to decreased testosterone levels.

-Decreased sexual desire is multifaceted and often multiple causes are found in any single individual. Anxiety and depression have traditionally been linked to decreased libido, as well as relationship disorders. Acute and chronic illnesses, along with various medications have been implicated. Decreased sexual desire has been often noted to accompany the menopausal transition, and estrogen deficiency has been studied along with androgen deficiency.

-The Princeton Consensus Conference4 in 2002 defined female androgen deficiency as consisting of a pattern of clinical symptoms in the presence of decreased bioavailable testosterone and normal estrogen status. Besides decreased libido, changes in sexual function include decreased sexual receptivity and pleasure. As in men, decreased androgens may cause a diminished sense of well-being and unexplained fatigue and loss of energy. Vasomotor instability and decreased lubrication can occur even if the patient is adequately estrogenized. Decreased muscle strength and bone loss may also occur.

-In men, androgens are made primarily in the Leydig cells of the testicles.

-In women, half of the androgens and androgen precursors are produced in the ovary with the other half being derived from the adrenal glands. Also, half of the active androgens are produced by the peripheral conversion of precursors in various tissues. Therefore, damage to the pituitary gland, ovaries or adrenal glands will produce a deficiency. Also, blocking the function of these organs will impede their androgen production. Examples of this are cortisone, birth control pills, or even perimenopausal hormone replacement.

-Androgens have been given during menopause for many years. Greenblatt5 compared the effect of various combinations of androgens and estrogens during the menopause in 1950. The combination resulted in improved well-being and libido when compared to estrogen alone. Sherwin6, recently in 2002, summarized a number of randomized clinical trials showing that adding androgens to the standard estrogen replacement had added benefit to well-being, sexual desire and interest, frequency of intercourse, and frequency of orgasm.
-There are problems in considering the use of androgens in women. The use of testosterone for androgen replacement is not approved for use in the United States and in many other countries. There is a lack of knowledge on the exact normal range for testosterone by age, although we know that androgen precursors and testosterone decrease with age in both men and women. This is compounded by the lack of sensitive and specific testosterone assays in women. Because of this a free androgen index or a calculated free testosterone value is felt to be more precise.
Zumoff7, in 1995, published a curve showing decreasing testosterone levels in women from ages 20 to 50. There were only 33 women and none were screened for sexual difficulties. The mean testosterone levels declined from approximately 38 ng/dL at age 20 to approximately 12 ng/dL at age 50. There was no sudden decline associated with the menopausal years. Guay8 and colleagues recently presented the androgens values in 60 women for the same 30-year period, and these women were screened for sexual dysfunction, especially decreased libido. In doing this, and presumably eliminating some women with low testosterone from the normal pool, the normal range increases substantially. In this study, total testosterone ranged from 46 to 58 ng/dL for women aged 20-29 (n=17), 28 to 40 ng/dL for women aged 30-39 (n=23), and 27 to 39 ng/dL for women aged 40-49 (n=20). More normal range studies are needed with many more women to verify this finding.
-Products are being developed to deliver testosterone to deficient women. Shiffren et al9 studied women with impaired sexual function who were menopausal after oophorectomy. Testosterone or placebo was administered by transdermal patch to the women who were receiving standard estrogen replacement. The total testosterone was raised above the normal range despite the SHBG decreasing, but the free and bioavailable testosterone remained within the normal range. Sexual frequency and orgasm increased significantly with the testosterone, along with an increase in well-being and mood. No adverse effects on skin and lipids were noted but the study did have a high placebo response as well as possible supraphysiological levels of total testosterone and dihydrotestosterone at the higher treatment dose level. The study did confirm that testosterone therapy augmented the standard estrogen replacement in menopause and actually did have added benefits, especially in the area of sexual function.

Very few studies have been done in premenopausal women complaining of sexual dysfunction. Guay et al10 studied women, ages 20-49, who appeared healthy but who complained of sexual dysfunction. They, and an age-matched group of women with no sexual complaints, had regular menses and were taking no medications or birth control pills. The two groups were separated significantly by a sexual function questionnaire.

-The women complaining of sexual dysfunction had significantly lower adrenal androgen precursors and testosterone levels than their age-matched controls. This included decreased levels of pregnenolone, 17-OH pregnenolone, DHEA-S, total testosterone and free testosterone. The cortisol part of adrenal gland function remained quite normal.

-Goldstat, et al11, also studied premenopausal women complaining of decreased libido. They were found to have testosterone levels in the lower third of the presumed normal range for young women. These women received testosterone cream or placebo for 12 weeks. The women on testosterone therapy had significantly increased well-being as well as increased sexual desire and activity. The mean decrease in a depression inventory score approached significance. Androgens play an important role in general well-being and energy as well as in sexual function, but more research is needed in developing the data and tools needed to outline androgen deficiency more precisely.

References:

Basson R, Berman J, Burnett A, et al. Report of the international consensus development conference on female sexual dysfunction: definitions and classifications. J. Urol 2000; 163: 888 - 893.
Laumann EL, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA 1999;10: 537-545.
Dunn KM, Croft PR, Hackett GI. Sexual problems: a study of the prevalence and need for health care in the general population. Family Practice 1998; 15: 519-524.
Bachmann GA, Bancroft J, Braunstein G, et al. Female androgen insufficiency: the Princeton consensus statement on definition, classification, and assessment. Fert. & Ster. 2002; 77: 660-665.
Greenblatt RB, Barfield WE, Garner JF, et al. Evaluation of an estrogen, androgen, estrogen-androgen combination and a placebo in the treatment of the menopause. J. Clin. Endocrinol. Metab. 1950; 10: 1547-1552.
Sherwin BB. Randomized clinical trials of combined estrogen-androgen preparations: effect on sexual functioning. Fert. & Ster. 2002; 77: S49.
Zumoff B, Strain G, Miller L, et al. Age-related decrease in total testosterone in women. J. Clin. Endocrinol. Metab. 1995; 80: 1429-1430.
Guay A, Munarriz R, Jacobson J, et al. Serum androgen levels in women aged 20-49 years with no complaints of sexual dysfunction. Int. J. Imp. Res. 2004; 16: 112-120.
Shifren JL, Braunstein GD, Simon JA, et al. Transdermal testosterone treatment in women with impaired sexual function after oophorectomy. N Eng J Med 2000;343: 682-688.
Guay A, Jacobson J, Munarriz R, et al. Serum androgen and androgen precursor hormone levels in women with and without sexual dysfunction. Int. J. Imp. Res.: J. Sex. Med. 2004; 16: 121-129.
Goldstat R, Briganti E, Tran J, et al. Transdermal testosterone therapy improves well-being, mood and sexual function in pre-menopausal women. Menopause 2003; 10: 390-398.

DR. Alaa mosbah M.D OBS& GYN

Cesarean section

Caesarean Section (C.S)

Caesarean Section (C.S)

Definition:

An operative procedure to deliver a viable foetus or more (i.e. after 28 weeks or 20 weeks according to the (ACOG) through an abdominal and uterine incisions.

Incidence:
increased from 5% in 1970 to 25% in 1990 due to:
1.Procedures as high forceps and difficult mid forceps are
abandoned in favour of C.S.
2. Increased C.S delivery in breech presentation.
3. Destructive operations are abandoned in favour of C.S.
4.Decreased morbidity and mortality due to C.S encourages its
use.

5. Increased repeated C.S due to increased primary C.S.

Indications:
(A) Maternal indications:
1. Contracted pelvis and cephalopelvic disproportion (see before).
2.Pelvic tumours especially if impacted in the pelvis or cancer
cervix.
3. Antepartum haemorrhage .
4. Hypertensive disorders with pregnancy .
5. Abnormal uterine action .
6. Previous uterine scar as hysterotomy or metroplasty.
7. Previous successful repair of vesico-vaginal fistula.
8. Previous caesarean section if,
i- the cause of the previous section is permanent e.g.
contracted pelvis.
ii- previous section was upper segment.
iii- suspected weak scar as evidenced by:
- History of puerperal infection after the previous
section.
- Hysterosalpingography or hysteroscopy done
after the previous section reveals a defect in the
scar.
- Vaginal bleeding during current labour.
- Marked tenderness over the scar during current
labour.
iv- Associated conditions as antepartum haemorrhage or

malpresentations.

(B) Foetal indications:
1. Malpresentations and malposition .
2.Prolapsed pulsating cord or foetal distress before full cervical
dilatation.
3. Diabetes mellitus (see before).
4.Bad obstetric history as recurrent intrauterine foetal death in last
weeks of pregnancy or repeated intranatal foetal death.
5.Post-mortem C.S. done within 10 minutes of maternal death
to save a living baby.

Contraindications:
1- Dead foetus: except in;
- Extreme degree of pelvic contraction.
- Neglected shoulder.
- Severe accidental haemorrhage.
2- Disseminated intravascular coagulation: to minimise blood loss.
3- Extensive scar or pyogenic infection in the abdominal wall e.g. in

burns.

Types of Caesarean Section:
(A) According to timing:
1.Elective caesarean section: The operation is done at a
pre-selected time before onset of labour, usually at completed 39 weeks .
2.Selective caesarean section: The operation is done after onset of labour
(B) According to the site of uterine incision:
1.Upper segment caesarean section (classical C.S.): The incision
is done in the upper uterine segment and it is always vertical.
2.Lower segment caesarean section (LSCS) : It is the
commoner type. The incision is done in the lower uterine
segment and may be transverse ( the usual) or vertical in the following coditions :
i- Presence of lateral varicosities.
ii- Constriction ring to cut through it.
iii- Deeply engaged head.
(C) According to number of the operation:

1. Primary caesarean section: for the first time.
2.Repeated caesarean section : with previous caesarean
section(s).
(D) According to opening the peritoneal cavity:
1.Transperitoneal : The ordinary operation where the peritoneal
cavity is opened before incising the uterus.
2.Extraperitoneal: The peritoneal cavity is not opened and the
lower uterine segment is reached either laterally or inferiorly
by reflecting the peritoneum of the vesico-uterine pouch . It is
indicated in case of infected uterine contents as

chorioamnionitis.

Advantages of elective C.S:
1.Pre - operative good preparation as regard sterilisation and
antiseptic measures, fasting and bowel preparation.
2. The risk of puerperal sepsis is minimised.

3. The operation is scheduled and working is in ease.

Disadvantages of elective C.S:
1. The risk of immaturity of the foetus or its lung is present.
2. Higher incidence of respiratory distress syndrome.
3. The lower segment may be not well formed.
4. Postpartum haemorrhage is more liable to occur.
5.Imperfect drainage of lochia as the cervix is closed so it
should be dilated by the index finger introduced abdominally through the uterine incision
Procedure of Lower Segment Caesarean Section:
Anaesthesia: General inhalation anaesthesia with nitrous oxide
+ oxygen ( the most commonly used) , epidural, spinal or
rarely local infiltration anaesthesia.

Position : Tilting the patient 15o to the left in the dorsal
position minimise the aorto-caval compression.
Skin incision: pfannenstiel ( transverse suprapubic) incision is
the most commonly used, but midline or paramedian vertical
suprapubic incisions may be used. If the patient had a previous
C.S incise in the same incision with trimming of the fibrosed
edges of the wound to help good healing.
Pfannenstiel incision has a better cosmetic appearance, better healing and less
incidence of incisional hernia but it is more time consuming associated with
more blood loss and gives less exposure.
The subcutaneous fat is incised.
The anterior rectus sheath is incised transversely in case of
pfannenstiel incision and longitudinally in case of vertical
incisions.
The rectus muscles : are separated in the midline in pfannenstiel
incision or retracted laterally in case of vertical incisions. The parietal peritoneum: is opened vertically.
The uterus is centralised, the bowel and omentum are packed off
with moist laparotomy pads, however this is usually
unnecessary.
The loose peritoneum over the lower uterine segment is held and
incised transversely, for about 10 cm in a semilunar fashion with
its edges directed upwards.
The bladder is dissected downward and is retained behind a
Doyne retractor placed over the symphysis.
A stay suture may be taken superficially in the lower segment
below the assumed site of uterine incision to help in its
identification after evacuation of the uterus.
he uterus is incised : in the same semilunar fashion by one of
the following methods:
A semilunar mark is made by the scalpel cutting
partially through the myometrium for 10 cm. A short
(3cm) cut is made in the middle of this incision mark
reaching up to but not through the membranes. The
incision is completed by the 2 index fingers along the
incision mark. If the lower uterine segment is very
thin , injury of the foetus can be avoided by using the
handle of the scalpel or a haemostat ( an artery
forceps) to open the uterus.
The short ( 3cm) middle incision may be enlarged by a
bandage scissors over 2 fingers introduced into the
uterus to protect the foetus.
Membranes are ruptured by toothed or Kocker’s forceps. The head is delivered by :
i- introducing the right hand gently below it and lifting it
up helped by fundal pressure done by the assistant,
ii- using one blade of the forceps or,
iii- using Wrigley’s forceps.
If the head is deep in the pelvis it can be pushed up vaginally by
an assistant.
The Doyen’s retractor is removed after the hand or forceps blade
is applied and before head extraction.
Suction for the foetus is carried out before delivery of the head.
In breech or transverse lie the foetus is extracted as breech.
The placenta is removed.

Closure of the uterine incision is done in 3 layers.
- The first is a continuous locking suture taking most of the
myometrium but not passing through the decidua to guard
against endometriosis and weakness of the scar.
- The second is a continuous or interrupted one inverting
the first layer.
- The third is a continuous or interrupted layer to close the
visceral peritoneum of the uterus. Closure of visceral
and/or parietal peritoneum is omitted by some surgeons.

The abdomen is then closed in layers

Upper Segment Caesarean Section :
Indications:
1.Dense adhesions, extensive varicosity or myoma in the lower
uterine segment making its exposure or incising through it
difficult.
2. Impacted shoulder presentation.
3. Anterior placenta praevia.
4. Defective scar in the upper segment.
5. Cancer cervix.
6. Rapid delivery is indicated.
7. If a concomitant tubal sterilisation will be done.
8. Previous successful repair of high vesico-vaginal or
cervico-vaginal fistula.
9. Post-mortem hysterectomy.

Procedure:
Abdominal incision: is vertical.
Uterine incision : 10 cm vertical incision is made in the midline
of upper uterine segment without incising the peritoneal coat
separately as it is adherent in the upper segment.
Extraction of the foetus: as a breech in cephalic presentation.
The last layer of the uterine incision closure includes the
superficial part of the myometrium with the peritoneal covering.
The remainder of the procedure is as lower segment C.S.
Special problems encountered during caesarean section:
(I) Anterior placenta praevia:
Try to pass beside the placenta to reach the foetus if this is impossible cut
through it but severe bleeding will result which may affect the foetus.
(II) Narrow uterine incision:
Extension of the lower uterine segment incision may be done by:
a- "J" shaped or hockey-stick incision : i.e. extension of one end of the
transverse semilunar incision upwards.
b- "U"- shaped or trap-door incision: i.e. extension of both ends upwards.
c- An inverted T incision: i.e. cutting upwards from the middle of the
transverse incision. This is the worst choice because of its difficult
repair and poor healing.
Advantages of the lower segment over the upper segment operation:
1.Less blood loss: due to less vascularity and the placental bed
is away from the incision.
2. Easier to repair.

3. The resultant uterine scar is stronger due to:
a- Better coaptation of the edges as the lower segment is
thin.
b- Better healing as the lower segment is more passive
during puerperium.
c- The scar is distant from the subsequent site of placental
implantation which may penetrate it.
So subsequent rupture uterus is less (0.2% versus 2% in
upper segment).
4. Less subsequent adhesions to the bowel and omentum.
5. Less liability to acute gastric dilatation and paralytic ileus.
6. Less liability to peritonitis due to better peritonization and
healing.
Mode of Delivery in Subsequent Pregnancies:
The rule that "caesarean always caesarean" had been replaced since a long time
by "caesarean always hospital delivery". If the cause of the previous section is
not permanent as contracted pelvis, vaginal delivery can be tried.
Caesarean Hysterectomy:
Hysterectomy is carried out after caesarean section in the same sitting for one
of the following reasons:
1- Uncontrollable postpartum haemorrhage.
2- Unrepairable rupture uterus.
3- Operable cancer cervix.
4- Couvelaire’s uterus.
5- Placenta accreta cannot be separated.
6- Severe uterine infection particularly that caused by Cl. welchii.
7- Multiple uterine myomas in a woman not desiring future pregnancy although

it is preferred to do it 3 months later.

Caesarean Sterilisation:

Tubal sterilisation is usually advised during the fourth caesarean section.

Complications of Caesarean Section:
(I) Operative:
1- Primary maternal mortality is 4 times that of vaginal delivery which
may be due to:
i- shock .
ii- Anaesthetic complications particularly Mendelson’s
syndrome
iii- Haemorrhage usually due to extension of the uterine
incision to the uterine vessels, atony of the uterus or DIC.
2- Injuries to the bladder or ureter.
3- Foetal injuries.
(II) Post-operative:
(A) Early:
1. Thrombosis and pulmonary embolism.
2. Acute dilatation of the stomach and paralytic ileus.
3. Wound infection, puerperal sepsis and burst abdomen.
4. Chest infection.
(B) Late :
1. Rupture of the uterine scar.
2. Incisional hernia.

Deep Vein Thrombosis in Pregnancy

Introduction :
Deep vein thrombosis (DVT) is a rare but serious complication that can occur during pregnancy. Thromboembolic events can include venous thrombosis of the leg, calf, or pelvis, and also the most serious and life-threatening complication: pulmonary embolism (PE). Thromboembolic events during pregnancy and postpartum are a leading cause of maternal mortality in the United States and in the United Kingdom .
Pregnancy is recognized as a physiological state that substantially increases the risk of thromboembolic disease and its complications; a pregnant woman has a five times greater risk of thrombi formation than a non-pregnant woman of similar age
Incidence and Risk Factors :

The reported incidence of DVT in the literature varies widely. The incidence of venous thrombosis as approximately 1:1000–2000 pregnancies. Other sources report the incidence to be lower . The prevalence of thrombosis varies with the mode of delivery and the gestational length of the pregnancy . Risk factors for forming a DVT include advanced age, prolonged bed rest or immobility, pelvic or leg trauma, obesity, coagulation disorders, and certain chronic diseases . Risk factors that may be influenced by pregnancy include preeclampsia, Cesarean section, instrument-assisted delivery, hemorrhage, multiparity, and varicose veins . Women with a previous history of a thromboembolic event are at increased risk during their pregnancy as are women who have hereditary or acquired thrombophilias such as Factor V Leiden.
Thrombophilia is a disorder in which there is a tendency for the formation of thrombi or clots. It is estimated that 15% of the general population has a thrombophilia reports that in the presence of thrombophilia the maternal risk for thrombosis is increased by a factor of 8. According to . approximately 50% of all episodes of venous thromboembolism in pregnancy and postpartum are linked to acquired and congenital thrombophilias. Management of pregnant women with thrombophilia is based on individual assessment of risk factors and history . Although a comprehensive discussion about thrombophilias and pregnancy is beyond the scope of this article, interested readers should view the reference list for appropriate articles that discuss thrombophilias in more detail.
Thromboembolic disease may occur at any point in pregnancy. ,in a review of 165 cases of thrombosis over 15+ years, found that DVT occurred more frequently during the antepartum period than the postpartum period. One hypothesis for this is that women working outside the home during pregnancy must sit for prolonged periods of time, thus increasing their risk. Concerning where thrombosis is more often seen in pregnancy, most cases of thrombosis in the legs are in the ileofemoral veins than the calf veins . Clots located in the deep veins such as the ileofemoral veins are more likely to cause pulmonary embolus than those of the superficial veins of the legs . Approximately 90% of thrombi are located on the left side, which may be related to the anatomy of the veins and arteries on the left side . The enlarging uterus may provide additional compression on the vessels and further reduce venous flow .
Pathophysiology :

In 1999, Rosendaal reported that thrombosis is a multicausal disease in which risk factors, acquired and congenital, dynamically interact, rarely occurring without risk factors. Pregnancy unquestionably places certain women in a higher risk category. In the 1800s, Virchow described a triad of predisposing factors for thrombosis that still exist today: Venous stasis, endothelial or vascular damage, and hypercoagulability . Venous stasis exists as a normal course of pregnancy; the gravid uterus exerts mechanical compression on the inferior vena cava and pelvic veins as it enlarges, and the effects of some hormones, such as progesterone, increase venous distensibility . In addition, vascular and endothelial damage can occur during the course of a normal or instrumental vaginal delivery or during a Cesarean delivery. Intravenous catheters or medications may also cause vessel wall injury .
Hypercoagulability is a normal physiologic change in pregnancy, and might be so because the body is preparing for control of blood loss after delivery of the placenta. Fibrinogen levels double during pregnancy in preparation for the separation of the placenta and the development of a fibrin layer in its place .In addition, clotting factor levels (Factors V, VII, VIII, IX, X, XII) increase during pregnancy .
Although levels of Protein C remain normal, levels of Protein S decrease in pregnancy. Consequently fibrinolytic activity (the splitting up or dissolving of clots) decreases from inhibitory substances produced by the placenta. Although the levels of some coagulation factors do not change remarkable during pregnancy (i.e., the platelet count), by 3 weeks postpartum the levels of affected coagulation factors return to normal. The risk of developing a thrombosis continues until approximately 12 weeks postpartum.
Diagnosis of DVT and PE :

In the general population, diagnosis of DVTs is difficult and clinical findings can be unreliable, leading to delays in diagnosis and treatment which can be life threatening. The reason for the difficulty in diagnosis is that approximately one-half of all DVTs are asymptomatic. The physical signs of DVT will depend upon the development of collateral circulation, location, and size of the thrombus, and the degree of vessel obstruction. The pregnant woman poses significant challenges to diagnosis, based on expected body changes. Swelling, aches, and pains in the lower extremities are common by the second and third trimesters, and those are the symptoms of DVT. When examining a lower extremity for DVT diagnosis, a 2 cm difference between calf measurements in the affected and unaffected leg is common. Pain, heat, redness, tenderness, edema, changes in skin color, and a palpable cord may be seen. The woman may have a positive Homan’s sign (dorsiflexion of the foot which produces pain in the calf or popliteal area), although this is not present in all women with DVT. Phlegmasia alba dolens (white leg) or phlegmasia cerula dolens (blue leg) may develop with obstruction of the large veins. In postpartum women, it is more common to have phlegmsasia alba dolens (milk leg), which creates the milky white appearance in the affected leg, occurring due to spasms of the arterioles .
Diagnostic tests used in evaluating a suspected case of thrombosis include venography, impedance plethysmography (IPG), and Doppler ultrasound. Venogram has been considered the gold standard for making the diagnosis of DVT, but is invasive and involves using contrast dye to visualize the veins in the legs. Because the use of dye and radiation involve potential risk to the mother and the fetus, noninvasive tests should be used as initial screening tools for pregnant women, although noninvasive tests could miss thrombi of the pelvic veins.
Ultrasound, a noninvasive procedure, used in combination with Doppler analysis, can be an appropriate screening test for DVT. Doppler combined with ultrasound is known as the duplex study; real -time imaging provides visualization of vessels, and Doppler measures change in blood flow through the vessels. Doppler imaging is more sensitive to the veins in the femoral or popliteal area than the calf. Another test is impedance plethysmography, a non-invasive test that measures change in venous volume through electrical resistance; however, it is not very specific for the distal veins of the legs.
Pulmonary thrombi that embolize from DVTs may present as an acute event. Symptoms may include dyspnea, tachypnea, color changes, air hunger, anxiety, chest pain, tachycardia, cough, changes in heart sounds, rales in the lung fields, and hemoptysis, with dyspnea and tachypnea being the predominant presenting signs. Because PE can occur and can be life threatening, any patient with a suspected or confirmed DVT should be monitored for PE.
Diagnostic work-up for suspected PE includes arterial blood gas sampling, ventilation-perfusion scan, angiography, chest radiography, and electrocardiogram. Many of these tests are nonspecific. Blood gas sampling with a SpO2 <>90%. Scans with high probability are good indicators, but low or intermediate probabilities are less useful clinically. Pulmonary angiography is more invasive, and does expose the fetus to minimal radiation. Angiogram is useful if other noninvasive tests are inconclusive.
Women who develop DVT or PE during or after their pregnancy should have a thrombophilia work-up. Testing that may be ordered may include Factor V Leiden, Anti-thrombin III, prothrombin gene mutation, Protein C and S, Lupus anticoagulant, and Anticardiolipin antibodies (ACOG, 2000b). The American College of Obstetricians and Gynecologists (2000a) recommends individualized thromboprophylaxis for all pregnant women who are at high risk for developing thrombosis.
Treatment :

Treatment for confirmed or suspected cases of DVT or PE is immediate anticoagulation therapy. The goals of treatment in the pregnant woman are to reduce morbidity and mortality and to protect the fetus. Anticoagulation is started when there is a high suspicion that either a DVT is present or PE is possible. Anticoagulant agents are used to prevent the extension of existing clots and the formation of new thrombi. Drugs used include unfractionated heparin, low molecular weight heparin (LMWH), and warfarin (Coumadin). Each drug prevents the blood from clotting normally at different points during the clotting sequence. Traditionally, unfractionated heparin has been the gold standard for treatment of acute thrombosis and for thromboprophylaxis during pregnancy. However, LMWH is being used with increased frequency.
Heparin works by inhibiting the formation of thrombin and fibrin thereby reducing clot formation and extension and is the preferred treatment for pregnant women because it does not cross the placental barrier and therefore does not affect the fetus. However, heparin does have potential side effects. The mother is at risk for osteoporosis, thrombocytopenia, and hemorrhage. The risk of osteoporosis may be related to dosing and length of treatment . Heparinization for active thromboembolitic disease may vary between institutions and practitioners. Treatment protocols may vary but the literature supports management of DVT/PE in the pregnant woman with intravenous unfractionated heparin for 5–10 days followed by subcutaneous injections of heparin every 12 hours. Intravenous infusion dosing is based on achieving a therapeutic range of the activated partial thromboplastin time (aPTT) at 1.5–2 times normal. Several protocols are available in the literature; . The usual concentration is heparin 25,000 units per 250–500 cc. An initial bolus is given, usually 5000–10,000 units, and then a maintenance dose of approximately 800–1200 units is continued. The aPTT is measured every 6 hours until therapeutic and then testing can be done daily thereafter. The therapeutic range of the aPTT is generally between 60–80 seconds but may vary. Periodic testing of platelet counts should be done for patients on prolonged therapy. Long-term heparin use is known to cause osteoporosis as well as thrombocytopenia, but these side effects appear less often with LMWH use . Oral calcium supplements should be given to minimize the potential for osteoporosis development.
The switch to subcutaneous heparin injections after initial heparinization is controversial. Antepartum patients with DVT, especially thrombi in the iliac or femoral veins that are more likely to embolize, may benefit from more precise anticoagulation. Some advocate continuing heparin infusion during the antepartum period because it is difficult to achieve therapeutic levels with subcutaneous injections. Anti-Xa levels measure the therapeutics of subcutaneous heparin. The target range is usually 0.2–0.70µ/ml. Unfractionated heparin infusions may be desirable for those patients who may be clinically unstable or when delivery may be imminent.
LMWH is being used with increasing frequency as a result of clinical research demonstrating safety and efficacy during pregnancy . It has the advantage of being administered once daily and has a longer half-life, but is more expensive than traditional therapy. LMWH also appears to cause less osteoporosis and heparin-induced thrombocytopenia . Enoxaparin (Lovenox) and dalteparin (Fragmin) are two of the most widely used LMWHs. LMWH works by inhibiting factor Xa in the clotting cascade thereby preventing the formation of thrombi. Dosing of the LMWH is based on weight and rounded to the nearest available prepackaged dose. The usual dose for Lovenox is 1 mg/kg every 12 hours. A dose of 40 mg is reported to be effective for pregnancy.
Recommendations for dosing with LMWH depend upon the basis for requiring anticoagulation and the practitioner’s preference. Once daily dosing may provide sufficient coverage for prophylaxis in a patient with no previous thrombophilia history or event, whereas twice-daily dosing may be needed to achieve therapeutic levels in a patient with active thrombolic disease or event. Chan et al. (2001) suggest that twice daily dosing of LMWH may be needed in the pregnant woman because physiological changes such as increases in glomerular filtration rate metabolize the drug more quickly. Patients being treated for an acute event may benefit from testing of therapeutic levels. Antifactor Xa levels can be obtained 4 hours after administration to monitor dosing requirements.
Warfarin (Coumadin) can be used as well but it is traditionally used in the postpartum period, and for specific diseases such as for women with artificial heart valves. Warfarin does cross the placenta and can have tetratogenic effects. During the first 6 to 9 weeks gestation, warfarin has been shown to cause fetal embryopathy such as limb and nasal hyperplasia, scoliosis, stippling of the bone epiphyses, microcephaly, and nasal hypoplasia, and should not be used. At any point in the pregnancy, warfarin has been documented to place the fetus at risk for central nervous system and eye abnormalities as well as hemorrhage. Additionally, there is a risk of placental abruption. Therefore, warfarin should be considered for long-term use in pregnant women who have prosthetic heart valves and have contraindications to heparin therapy. Warfarin works by inhibiting the formation of several vitamin K-dependent clotting proteins. Historically, it is started shortly after heparin therapy is initiated and most recently it is being used with LMWH. Dosing is individualized and is titrated to achieve a target range of the International Normalized Ratio (INR) of 2.0 to 3.0. Heparin is usually discontinued after the INR reaches >2.0. It takes approximately 2 to 7 days for the body to deplete the stores of clotting proteins and the INR to be near the therapeutic range. Treatment is usually continued for at least 3 to 6 months or longer if indicated. Warfarin is safe for women intending to breastfeed in the postpartum period. Small amounts of warfarin will be transmitted through the breast milk to newborns; therefore, parents should be aware of potential side effects to the newborn. Parents should be taught to observe the infant for bleeding, bruising, or the development of petechia. Any of these changes should be reported to the pediatrician .
Thrombectomy and vena cava filter are two treatment options that are less widely used. Vena caval filter is considered for pregnant woman to prevent pulmonary embolization from unstable venous clots. The filter is used for patients who continue to have recurrent pulmonary emboli despite adequate heparinization or who may be unstable and anticoagulation is contraindicated. Thrombectomy is usually limited to severe cases with massive PE or limb-threatening disease.
Superficial venous thrombosis is typically seen in the superficial veins of the calf, usually associated with varicosities and intravenous insertion sites. The risk of embolization is rare. Treatment includes rest, elevation, analgesia, and elastic compression stockings.
Management in Labor :

Women receiving anticoagulation in labor should be cared for by providers skilled in high-risk care. Management of the pregnant woman on anticoagulants during the intrapartum period is dictated by the reason for the therapy; therefore, the treatment will vary. Patients who are receiving thromboprophylaxis can usually have their heparin therapy discontinued during labor, but LMWH has a longer half-life and needs to be discontinued sooner. If needed, anticoagulation therapy can be restarted 4 to 6 hours postpartum, with the exception of women with mechanical heart valves or serious thrombophilia.
Therapeutic heparin infusions during labor can be continued, and the rate adjusted to maintain the aPTT at 1.5x’s normal. This mode of treatment is ideal for those patients who are at increased risk of hemorrhage (i.e., placenta previa or placental abruption).
Regional anesthesia is not recommended for women on LMWH, for the literature raises concerns about reports of hematoma formation in nonpregnant patients receiving heparin after epidural placement . Consultation with the anesthesia service is recommended. For planned inductions or Cesarean deliveries, dosages of LMWH can be timed so that peak levels are achieved before anesthesia is needed. Certain patients receiving LMWH can be switched to heparin injections toward the pregnancy’s end so that regional anesthesia is an option in the event of spontaneous labor or induction. In general, at least 4 hours should pass after unfractionated heparin is administered and at least 12 to 24 hours since the last dose of LMWH is given before regional anesthesia can safely be given. If epidural anesthesia is given, LMWH can usually be restarted at least 3 hours after the catheter is removed.
After delivery, many women will be restarted on anticoagulation for 6 to 12 weeks postpartum. Women who had been treated for active thrombosis during pregnancy may have therapy continued longer than 12 weeks, and may be treated up to 6 months or longer.
Nursing Implications :

Treatment modalities will vary between practitioners, but nurses can be active in educating patients about risk factors, prevention, and treatment options for thromboembolic disease .Patients being treated for active thrombosis will need prolonged anticoagulation therapy. Whether it be for treatment of active disease or for prophylaxis, patient compliance is essential for successful anticoagulation, and nurses can be essential in helping women to understand the necessity of continued treatment. In addition to educating women about pharmacologic treatment for or prevention of thrombosis, nurses must teach women about signs of clots, side effects of drug treatment, self-injection techniques, labor support, prevention of complications such as embolization and postthrombolic insufficiency, and when to seek medical attention. Nursing care should include not only teaching but frequent assessments for bleeding from anticoagulant therapy and complications resulting from DVT/PE.
The woman who has active thromboembolic disease or who is receiving anticoagulation poses challenges to any perinatal nurse. Education must be offered to pregnant and postpartum women, especially those women with additional risk factors such as obesity, preeclampsia, or hypertension. Women taking warfarin will require specialized teaching on drug interactions and dietary restrictions. Women should also be counseled to take adequate calcium supplementation and perform weight-bearing exercise as tolerated while taking heparin to lessen the potential for heparin-induced osteoporosis.
Bleeding is a major side effect of any anticoagulant used. Special attention should be paid to monitoring for bleeding and educating the patient about the risk of bleeding and the need to notify the healthcare provider immediately if bleeding should occur. Women in active labor should be assessed frequently during labor and postpartum for abnormal bleeding. Protamine sulfate can be used to reverse the effects of both LMWH and unfractionated heparin; therefore, it should be readily available minutes to prevent hypotension. Long-term therapy with heparin should consist of periodic testing of the platelet count. Women receiving heparin therapy who present in labor or for evaluation should have the platelet count measured.
Properly fitting antiembolitic stockings or elastic compression stockings promote the fluid movement of blood through the veins of the leg by exerting pressure. Women who are on prolonged bed rest, are undergoing Cesarean section, or are at high-risk due to obesity or preeclampsia should be fitted for elastic stockings in knee or thigh length. Knee-length stockings are generally believed to be easier to apply and to fit properly, thereby being more effective. Stockings that are too loose provide no compression; those that are too tight may promote venous stasis. Proper fit is best obtained by measuring the calf diameter and selecting a size that corresponds to the manufacturer’s recommendations. The stockings should be removed once per day and the legs inspected. Other devices that can be used to reduce the pooling of blood in the venous system are external pneumatic compression and venous foot pumps. Women on bed rest should be taught to perform active and passive resistance exercises to prevent muscle wasting and promote venous return.
Postpartum women who will be taking warfarin need extensive teaching about the drug and its effects. Warfarin interacts adversely with many prescriptions and over the counter medications. Patients should be instructed to call their physician before taking other medications, and to limit foods rich in Vitamin K (e.g., broccoli, lettuce, spinach). If the woman desires more children, she should be warned about possible tetratogenic effects to the fetus while she is taking the drug, and the essential nature of birth control during this time. Women taking warfarin must be told to notify their physician if they do become pregnant or plan to conceive while taking warfarin. As with any medication or anticoagulant, the patient should be aware of possible side effects including bleeding from the gums, dark or red stool or urine, heavy menses, heavy bleeding from cuts; patients should be advised to notify their healthcare provider should any of these side effects occur.

External version

The aim :
1. To detect cephalo-pelvic disproportion.
2. Cephalic delivery is safer for the mother and foetus.

Success rate:
50-70%.
Indications
Breech presentation ,transverse lie
Do not perform this procedure before 37 weeks.
Technique :
• Have the woman lie on her back, and elevate the foot of the bed.
• Listen to and note the fetal heart rate. If there are fetal heart rate abnormalities (less than 100 or more than 180 beats per minute), do not proceed with external version.
• Palpate the abdomen to confirm presentation and position of the fetal head, back and hips.
• To mobilize the breech, gently lift the lowest part of the fetus from the pelvic inlet by grasping above the pubic bone (Fig P-5 A).
• Bring the head and buttocks of the fetus closer to each other to achieve forward rotation. Rotate the fetus slowly by guiding the head in a forward roll as the buttocks are lifted (Fig P-5 B–C).
• Listen to the fetal heart rate. If an abnormality is detected:
- Have the woman turn on to her left side;
- Give oxygen at 4-6 L per minute by mask or nasal cannulae;
- Reassess every 15 minutes.
• If the procedure is successful, have the woman remain lying down for 15 minutes. Counsel her to return if bleeding or pain occurs or if she believes the baby has returned to the previous presentation.
• If the procedure is unsuccessful, try again using a backward roll (Fig P-5 D).
• If the procedure is still unsuccessful and fetal heart rate is good, tocolytics may increase the chances of successful version. Give:
- terbutaline 250 mcg IV slowly over 5 minutes;
- OR salbutamol 0.5 mg IV slowly over 5 minutes.
• If the procedure is still unsuccessful, attempt version again after 1 week or if the woman presents in early labour with breech or transverse lie.
• If they are fetal heart abnormalities:
- Turn the woman onto her left side;
- Reassess the fetal heart rate every 5 minutes;
- If the fetal heart rate does not stabilize within the next 30 minutes, deliver by caesarean section .
Causes of failure:

1- Large sized foetus.
2- Oligo - or polyhydramnios.
3- Short umbilical cord.
4- Uterine anomalies as bicornuate or septate uterus.
5- Irritable uterus. Tocolytic drugs may be started 15 minutes before the procedure to overcome this.
6- Obesity.
7- Rigid abdominal wall.
8- Frank breech because the legs act as a splint.
Contraindications:
1- Contracted pelvis.
2- Multiple pregnancy.
3- Hydrocephalus.
4- Antepartum haemorrhage.
5- Uterine scar.
6- Hypertension as the placenta is more susceptible to separation.
7- Elderly primigravida.
8- Ruptured membranes.

9-Anaesthesia during version is contraindicated as pain is a safeguard against rough manipulations.
Complications:
1- Accidental haemorrhage due to separation of the placenta.
2- Rupture of membranes .
3- Preterm labour.
4- Foetal distress.
5- Cord presentation or prolapse.
6- Entangling of the cord around the foetus.
7- Isoimmunization in Rh-negative mothers due to foeto - maternal transfusion.

HOW TO PERFORM THE COLPOSCOPIC EXAMINATION

Prepare your patient.
Obtain informed consent and answer her questions. Assure her you will attempt to minimize pain (often a consuming worry) and will use "numbing medicine" (if appropriate). Make sure to know the pregnancy status of your patient. Ibuprofen 800 mg may be offered thirty minutes prior to procedure (be careful on empty stomach), but decreases cramping better if given the night before and morning of the procedure.
A bimanual exam should have been done with the annual exam. If a bimanual examination is needed, perform it here. Quickly examine the vulva for obvious condylomata or other lesions. If cervical biopsy is well tolerated and things are going well, examine the vagina/vulva after the biopsies as the speculum is withdrawn. The excess vinegar from the cervical exam will often stain the vulva. The vulva also can be examined at the time your patient returns for follow-up and/or definitive treatment.
Insert the speculum.
Consider the use of vaginal side wall retractors, a Penrose, or glove thumb with obese or multiparous women with vaginal redundancy (pregnancy too, if you develop colposcopy skills with pregnant patients). Warm the speculum with water (never lubricants), of course.
Examine the cervix.
Is the cervix inflamed or infected-looking? An active cervicitis confounds colposcopic detail. Do cultures if necessary. Repeat Pap only if this is critical information. Even a correctly performed Pap smear may irritate the cervix and often causes bleeding. Gently blot (not wipe) away any excess mucous using normal saline. Look for leukoplakia and abnormal vessels.
Apply 5% acetic acid with a cotton ball held in a ring forceps or a rectal swab. This gently applies lots of vinegar quickly and without trauma. Repeat application every five minutes, as the vinegar effect is only temporary. Warn patients, "this may burn a little." Calling the solution "acetic acid" may help increase the patient's perception of burning. Calling it "vinegar" usually will not.
Start with low power (typically 5x). Scan the entire cervix with white light. Use a vinegar-soaked Q-tip to help manipulate the cervix and transformation zone into view if necessary. The tenaculum is almost never necessary to move the cervix. Kogan endocervical speculum can greatly aid the examination of the distal endocervical canal if necessary. Use higher magnification to carefully document abnormal vascular patterns. The green filter can help find vascular areas.
Is colposcopy satisfactory?
The entire transformation zone, including the entire squamocolumnar junction, must be visualized. The borders of all lesions also must be entirely seen (not disappearing into the canal for instance) for visualization to be adequate. The uncooperative patient or severely flexed uterus with inadequate visualization are potential causes of inadequate colposcopy. Inadequate colposcopy with cytologic evidence of dysplasia frequently requires cervical cone biopsy for work-up. Mentally map abnormal areas. Remember that colposcopic observation's main goal is to highlight areas for biopsy. It is not, per se, a diagnostic tool. However, acetowhite areas that have sharp geographic boarders and a dimension of thickness or roughness are likely to be histologically more severe. Furthermore, all other things being equal, the presence of vessel atypia in any lesion implies more severe dysplasia. Use the following parameters to grade severity of lesions:
Mild acetowhite epithelium < Intensely acetowhite
No blood vessel pattern < Punctation < Mosaic
Diffuse vague borders < Sharp demarcated borders
Follows normal contours of the cervix < "humped up"
Normal iodine reaction (dark) < Iodine-negative epithelium (yellow)
Leukoplakia - usually a very good (condylomata) or a very bad sign (SCC)
Atypical vessels - usually cancer
Lugol's solution (Schiller's test).
May be used by the beginning colposcopist or at any time when further clarification of potential biopsy sites is necessary. It need not be used in all cases. The sharp outlining afforded by Lugol's iodine (Schiller's test) can be dramatic and very helpful. Iodine staining does not interfere with histology. Lugol's solution is often very helpful on the vagina and proximal vulva (non-keratinized skin). It can be used to thoroughly and simultaneously examine the entire vagina for glycogen-deficient areas, which correlate with HPV and/or dysplasia in non-glandular mucosa. It is often reserved for difficult cases when a non-cervical source of cervical Pap smear atypism is suspected (as in "normal cervical colposcopy" with dysplasia on Pap smear or normal ECC histology).
ECC and ECB
If desired, apply topical benzocaine (Hurricaine) solution to the entire face of the cervix using a cotton ball. It will usually be effective in 30 to 45 seconds.
Perform an endocervical curettage (ECC) or endocervical brushing (ECB) if indicated.
Use a Kevorkian curette (preferably without a basket) and scrape the canal, 360 degrees, twice. The sample appears as a coagulum of mucus, blood, and small tissue fragments. Use ring forceps or a cytobrush to gently retrieve the sample. Submit on paper and label "ECC." Do not do an ECC on pregnant patients.
Alternatively, a cervix Pap smear brush (the "pipe-cleaner type brush") may be placed into the os and spun around 5 times. The resulting tissue and blood coagulum may be submitted as a histological specimen in formalin. A short drinking straw may also be placed over the brush to act as a sheath to protect the brush from contamination by the ectocervix while the device is being introduced or withdrawn. Place the brush inside of the straw and place the straw against the os. Then advance the brush, obtain the sample, and withdraw the brush back into the straw for removal. This results in sensitivity about the same as the Kevorkian curette but a higher specificity.
Perform cervical biopsy
Begin by mentally mapping a biopsy strategy. Biopsy posterior areas first to avoid blood dripping over future biopsy sites. The cervix can be manipulated with a Q-tip or hook if necessary to provide an adequate angle for biopsy. Three mm deep is typically all that is necessary. Always include the area with vessel atypism in at least one biopsy site. It is not necessary to include normal- appearing tissue with biopsy samples (i.e., biopsy the margins of lesions). Beginning colposcopists can enhance their skills by initially separating samples from difference biopsy sites in different bottles and subsequently correlating them with colposcopic impression. If bleeding is profuse from a particular site and more biopsies are needed, apply a Q-tip to the area and proceed with the next biopsy. Do not apply Monsel's solution until all biopsies are completed. Monsel's will ruin good histology.
Apply pressure and Monsel's solution to bleeding sites. The Monsel's should be as thick as toothpaste to be most effective. Swab out the excess Monsel and blood debris, which appears as a nasty black substance that eventually will pass and may cause alarm (and potential late night phone calls).
Gently remove the speculum and view the vaginal wall collapse around the receding blades of the speculum. Are any abnormal areas apparent? Have the patient rest supine for at least several minutes and then sit up slowly and rest again. Fainting and light-headedness are not uncommon.
Carefully draw and label a picture of lesions and biopsy sites. Correlate the pictures with the submitted samples, if placed in different containers.
Provide careful post-procedure instructions
Advise no douching, intercourse, or tampons for 1-2 weeks (or until return visit). Patients are instructed to return for foul vaginal odor or discharge, pelvic pain, or fever. Tylenol, ibuprofen, or Aleve may be used for cramps (if any). Otherwise, follow-up is usually in 1 to 3 weeks to discuss histology results.

COLPOSCOPIC TERMINOLOGY

Introduction
In the past decade, major changes in our understanding of the epidemiology and science of cervical carcinoma has yielded efforts to develop a unified terminology to be used throughout the international scientific community. The International Federation of Cervical Pathology and Colposcopy (IFCPC) approved a basic colposcopic terminology at its Seventh World Congress in Rome, May, 1990.This outline summarizes this terminology. These terms should be used to describe findings during the colposcopic examination.
OUTLINE OF COLPOSCOPIC TERMINOLOGY
I. Normal colposcopic findings
Original squamous epithelium
Columnar epithelium
Normal transformation zone
Squamocolumnar Junction (SCJ)
Squamous Metaplasia
II. Abnormal colposcopic findings
1.Within the transformation zone
A. Acetowhite epithelium
.Flat
.Micropapillary or microconvoluted
B. Punctation
C.Mosaic
D.Leukoplakia
E.Iodine-negative epithelium
F.Atypical vessels
2.Outside the transformation zone, e.g., ectocervix, vagina
A. Acetowhite epithelium
.Flat
.Micropapillary or microconvoluted
B.Punctation
C.Mosaic
D.Leukoplakia
E.Iodine-negative epithelium
F.Atypical vessels
III. Colposcopically suspect invasive carcinoma
IV. Unsatisfactory colposcopy
Squamocolumnar junction not visible
Severe inflammation or severe atrophy
Cervix not visible
Entire lesion not seen
V. Miscellaneous findings
Non-acetowhite micropapillary surface
Exophytic condyloma
Inflammation
Atrophy
Ulcer
Other

Vulvodynia /DR. Alaa Mosbah MD OBS&GYN

Introduction & Classification :
In 2003, the International Society for the Study of Vulvovaginal Disease (ISSVD) revised its definition of the frequently used and well-accepted term “vulvodynia.” The new classification acknowledges that vulvar pain can be attributed to diagnosable disorders such as infections, dermatologic disorders, neoplastic processes, and neurologic disorders. The other category is vulvodynia, pain not related to a specific, identifiable disorder. Vulvodynia is often described as a vulvar discomfort with sensations of burning, irritation, or rawness. In addition, the ISSVD further expanded its classification of vulvodynia into generalized and localized pain. These categories are further subdivided to provoked pain or unprovoked pain. Additionally, there is a category for pain that is both provoked and unprovoked (mixed). Vestibulodynia (previously termed vestibulitis) is a pain localized to the vestibule. The suffix “-itis” has been excluded from the recent ISSVD terminology because studies found a lack of association between excised tissue and inflammation. Other terminologies have classified vestibulodynia as primary or secondary; in the primary subset, the pain has been present since the first tampon use or intercourse, and with secondary vestibular pain, women have had painless tampon insertion or intercourse, then the vestibular pain develops at a later time.
Epidemiology :
Until recently, the epidemiology of vulvodynia was largely unknown. The prevalence of vulvodynia has ranged from estimates of as low as 200,000 women in the United States to as high as 15% of women based on a report from a general gynecologic practice population. A study from 1998 reported 1.3% in a female genitourinary medicine clinic population had vulvodynia. A more recent study by Danielsson and coworkers evaluated 3017 women aged 20 to 60 years participating in a screening program for cervical cancer who answered a questionnaire about possible painful coitus. The prevalence was 9.3% for the whole group (13% for women aged 20-29 and 6.5% for women aged 50-60). Women with pain localized to the vestibule (vestibulodynia) have been characterized as white, young (mean age, 32 years), and nulliparous. However, a recent study, performed in 2003, estimated the prevalence of chronic unexplained vulvar pain in an ethnically diverse population-based sample of women. Approximately 16% of respondents (4915 women) reported chronic burning, knife-like pain, or pain on vulvar contact that lasted for at least 3 months or longer. Chronic vulvar pain on contact decreased with increasing age, but the cumulative incidence of chronic burning and knife-like pain was similar across all ages. Contrary to earlier assessments, white and black women reported a similar lifetime prevalence. However, Hispanic women were 80% more likely to experience chronic vulvar pain than were white and black women.
The Etiology of Vulvodynia :
Exactly what causes vulvodynia is unknown, but it most likely occurs from a variety of sources. Proposed etiologies include abnormalities of embryologic development, increased urinary oxalate excretion, genetic and/or immune factors, hormonal factors (association with oral contraception use or menopause), infection (human papillomavirus [HPV] and candida), inflammation, and neuropathies. There may be several different diseases with similar symptoms that are related to vulvodynia.
In the past decade, many of the early theories about vulvodynia have not been substantiated. The majority of recent studies do not support an association with HPV, particularly in pain that is localized to the vestibule. The role of candidiasis in this condition is uncertain. Similarly, the role that inflammation plays in the development of localized vulvar dysesthesia is unclear. Histopathologic specimens from patients with vestibulodynia have been compared with control subjects and similar findings have been found in each population. Many control subjects have nonspecific inflammation. Several papers that mention inflammation and inflammatory cytokines show inconsistent results. Bohm-Starke and colleagues found a low expression of the inflammatory markers cyclooxygenase 2 and inducible nitric oxide synthase in the vestibular mucosa of women with localized vestibular pain as well as in healthy control subjects. A few clinicians believe that vulvodynia occurs directly as a result of psychologic or sexual dysfunction. This viewpoint, however, is rejected both by most patients and by the majority of those working in the field. On the other hand, almost all agree that the presence of chronic pain such as occurs in vulvodynia can secondarily affect a patient's psychologic well-being.
A consensus has been emerging among thought leaders (most recently at an National Institutes of Health [NIH]-sponsored conference on vulvodynia in April 2003) that generalized, nonprovoked vulvodynia is described most accurately when it is thought of as a complex regional pain syndrome (CRPS), similar to other CRPS such as fibromyalgia and interstitial cystitis.
Like women with other CRPS, women with vulvodynia exhibit enhanced systemic pain perception, a process known as central nervous system sensitization. Second, women with vulvodynia are more likely to have other CRPS such as interstitial cystitis. This may be explained by another phenomenon common to CRPS known as “wind-up” in which there is a progressively increasing activity in dorsal horn cells of the spinal cord after repetitive activation of primary afferent C-fibers. Another study found a significant decrease in estrogen receptor expression in the vestibular mucosa of women with vestibulodynia.
Treating Vulvodynia
Numerous treatments have been used for the various forms of vulvodynia, including vulvar care measures; topical, oral, and injectable medications; biofeedback and physical therapy; a low oxalate diet with calcium citrate supplementation; and surgical treatments. Other kinds of treatment include acupuncture, hypnotherapy, topical nitroglycerin, and botulinum toxin, but they are not discussed here. It is important to recognize that rapid resolution of vulvodynia is unusual even with appropriate therapy. Whereas a 100% improvement rate is desired in all patients, most women with vulvodynia do not reach that level. They report markedly less pain at follow up, although many are not cured.
Vulvar Care Measures
Common suggestions for minimizing irritation include the use of 100% cotton underwear during the day and not wearing underwear at night while sleeping. We counsel patients to avoid vulvar irritants and douching, and to use mild soap for bathing without applying soaps to the vulva. We recommend against using facecloths for washing; the interlabial sulci and vestibule can be cleaned easily with water and gentle touch. If menstrual pads are irritating, 100% cotton pads may be helpful. Adequate lubrication for intercourse is recommended. Many different lubricants exist with various bases such as Slippery Stuff, Femglide, Astroglide, Femigel (Australian Bodycare, Denmark) (natural product from tea trees), K-Y Jelly, Lubrin (Aurora Pharmaceuticals, Australia) (a suppository), Moist Again, Replens, Sylk (made of Kiwi fruit vine and purified water), Surgilube, Vielle, vitamin E oil, Crisco oil, and saliva. Some patients find the lubricants to be irritating, particularly some of the commercial lubricants. Many patients have an allergic reaction to lubricants that contain propylene glycol. Natural oils are also used by some patients (olive, sweet almond, sesame, rose hip, grape seed, and wheat germ). Ice packs or other forms of cold application are helpful in some patients, but these produce irritation when overused. Cool gel packs may be useful. Rinsing the vulva after urination may be helpful in some cases. The area then should be gently patted dry. The use of hair dryers is irritating and should be avoided. After bathing in a tub or shower, we advise patients to pat dry the genital area. If the skin is dry, emollients (such as vegetable oil or plain petrolatum) may be used topically to hold moisture and improve the barrier function.
Topical Therapies For Vulvodynia
Some patients find relief from vulvodynia with topical anesthetics. All topical anesthetics may cause initial burning and stinging on application; the discomfort lasts for a few minutes until the area is numb. The longer the ointment is on the area, the deeper the anesthesia .
The most commonly prescribed topical medication is lidocaine (Xylocaine) jelly 2% or ointment 5%. This can be applied as often as required for symptomatic relief and 30 minutes before sexual activity for those women with dyspareunia (ointment preferred). EMLA (eutectic mixture of local anesthesia, comprising lidocaine and prilocaine) LMX 4 (Ferndale Laboratories, Ferndale, MI), and LMX 5 (lidocaine 4% and 5%) are also used by some patients. The sexual partner may experience numbness as well. When a topical anesthetic is used, the sexual partner should avoid oral contact.
The long-term use of overnight topical lidocaine has been suggested as a specific therapy for vulvodynia, with a theory that the regular application of lidocaine to interrupt the painful impulses may minimize feedback amplification of pain and allow for healing. The use of overnight lidocaine has been studied in an open label trial by Zolnoun and colleagues. Patients were instructed to apply a copious amount of 5% lidocaine ointment to the affected area at bedtime and were asked to place a cotton ball generously coated with the 5% lidocaine ointment in the vestibule to assure continuing overnight application. They were instructed to use the treatment nightly for 8 or more hours every night. Of 61 women with vestibulodynia, 76% were able to have intercourse after therapy as compared with 36% at baseline (mean, 7 weeks) with significantly less pain during sexual activity.
Benzocaine, which is the anesthetic in Vagicaine and Vagisil, is a sensitizer and can cause an allergic contact dermatitis, which is why we do not recommend their use in patients with vulvodynia. Similarly, diphenhydramine, Benadryl, is in many topical anesthetic and antiitch preparations, and because it is another common sensitizer, we do not recommend it. Some patients benefit symptomatically from the application of plain petrolatum, Vaseline, perhaps because it minimizes friction of skin folds.
Estrogen has been used both topically and in an intravaginal ring with variable results. Other topical medications that patients have used include capsaicin, atropine, nitroglycerine, and Traumeel .
Some patients with specific point tenderness have responded to topical doxepin. For some patients with localized pain, a combination of topical amitriptyline 2% and baclofen 2% in a water-washable base has been useful.
Topical therapies that patients describe as not having significant benefit for vulvodynia are important to note to avoid possible local side effects and ultimate aggravation of symptoms. Although topical corticosteroids logically should improve the pain of vestibulodynia, they generally do not improve this condition. The use of chronic topical corticosteroids on the vulva occasionally produces steroid dermatitis, characterized by erythema and burning. Likewise, some clinicians have used topical testosterone for vulvodynia, thinking that a subclinical vulvar dermatosis is a possible causative factor. However, this medication is irritating to many and useful for very few. Topical antifungal medications are used empirically by many clinicians for presumed superimposed yeast because early theories as to the cause of vulvodynia included possible hypersensitivity to candida species. Topical antifungal therapy generally does not improve vulvodynia beyond the soothing properties of some vehicles, and superimposed irritant discomfort is more likely for women using it.
Oral Treatments for Vulvodynia
Antidepressants
Antidepressants have been used for the treatment of many chronic pain conditions. A common treatment of vulvodynia is the use of an oral tricyclic antidepressant such as amitriptyline, Elavil, nortriptyline, Pamelor, and desipramine, Norpramin ; all 3 have been used to treat many pain conditions thought to have a neuropathic etiology. Whereas tricyclic antidepressants have traditionally been used for generalized vulvodynia, they are also useful in the treatment of localized pain. In a report of 33 women being treated at a vulvodynia clinic, 15 had a complete response to tricyclic antidepressants for the treatment of vulvodynia (both generalized and localized). The mechanism of action is believed to be associated with blocking reuptake of norepinephrine and serotonin transmitters, although the mechanism may actually be from the anticholinergic effects. These drugs affect sodium channels and the N-methyl-D-aspartate (NMDA) receptor.
If a healthcare provider and patient choose this treatment of vulvodynia, it may be important to emphasize its effect on pain rather than its effect on depression to enhance patient compliance.
Tricyclic Antidepressant Dosage For Vulvodynia
The dosages of tricyclic antidepressants used for vulvodynia are significantly less than those used for depression. Amitriptyline is often used as a first-line agent, although many healthcare providers prefer nortriptyline and desipramine, because they tend to have fewer side effects than amitriptyline (which include dry mouth, drowsiness, and constipation) . All are dosed in a similar fashion. We recommend starting patients at a low dose and increasing the dosage slowly until a nightly dose is reached that relieves symptoms. Patients should take this medication approximately 2 hours before bedtime. It is started at 5 to 25 mg nightly (use 5-10 mg for elderly patients) and increased by 10 to 25 mg weekly, not to exceed 150 mg per night. Tricyclic medications are available as syrups so that very small doses can be used to start patients who are sensitive to these medications.
Should patients elect to stop taking these drugs, they should be weaned off them gradually and warned against stopping them too suddenly. This medication should not be used in patients with abnormal heart rates (tachycardia) or in patients taking monoamine oxidase (MAO) inhibitors.
Patients on tricyclic antidepressants should not be pregnant, intend to become pregnant, or breast feed while using these drugs; appropriate contraception should be used for patients of reproductive age if they are sexually active. It is important to remember that these medicines will add to the effects of alcohol and other central nervous system depressants. Patients should avoid more than one drink of alcohol daily while on this medication.
Other antidepressants have been used for pain control. Many providers have prescribed selective serotonin reuptake inhibitors (SSRIs) for women with vulvodynia, but in general, SSRIs have not proven effective for pain relief for a majority of women. However, a newer class of medications called selective serotonin and norepinephrine reuptake inhibitors (SSNRIs) have been effective in treating vulvodynia. These include venlafaxine, Effexor XR, and duloxetine, Cymbalta .
Preclinical studies have shown that venlafaxine and its active metabolite, O-desmethyl-venlafaxine (ODV), are potent inhibitors of neuronal serotonin and norepinephrine reuptake and weak inhibitors of dopamine reuptake. Venlafaxine and ODV have no significant affinity for muscarinic cholinergic, H 1-histaminergic, or (alpha) 1-adrenergic receptors in vitro. Pharmacologic activity at these receptors is hypothesized to be associated with the various anticholinergic, sedative, and cardiovascular effects seen with other psychotropic drugs. It is started at 37.5 mg daily and increased to 75 mg daily, if needed. With all of the antidepressants discussed, adequate time for a treatment trial must be given before abandoning them, as long as the side effects are tolerable. Often, full pain relief response is not seen until 4 or more weeks of antidepressant use.
Cymbalta is a newer medication that is early in its use for pain control. It is U.S. Food and Drug Agency (FDA)-approved for diabetic peripheral neuropathic pain as well as major depression. For pain control, it is started at 30 mg by mouth daily and gradually increased to 60 mg per day in a single dose.
Anticonvulsants
Gabapentin (Neurontin) and carbamazepine (Tegretol) have been used to treat chronic pain conditions, including vulvodynia . Gabapentin comes in 100-mg, 300-mg, 400-mg, 600-mg, and 800-mg tablet sizes. Generally, it is started at 300 mg orally per day × 3 days, then 300 mg orally twice a day × 3 days, and then 300 mg orally 3 times per day. It can gradually be increased to 3600 mg orally total daily. Ideally, gabapentin is given in a 3-times-a-day dose, but if the patient is unable to comply with that, it can be given in a twice-a-day dose. No more than 1200 mg of gabapentin should be given in a single dose. Gabapentin tends to have fewer side effects than the tricyclic antidepressants. The adverse effects of gabapentin include somnolence and dizziness and, less commonly, gastrointestinal symptoms and mild peripheral edema. Monitoring and dosage adjustment are required for these side effects, but usually the drug does not need to be discontinued. Gabapentin can cause or increase gait and balance problems in older patients, and may have an effect on cognitive impairment. For patients with renal insufficiency, we recommend a careful dose adjustment. It may take 3 to 8 weeks for gabapentin to become effective for pain control; like with antidepressants, it takes time to work and for patients to develop a tolerance to side effects from the drug. Topiramate, Topamax and oxcarbazepine, Trileptal, also anticonvulsants, may also be used for treating vulvodynia instead of carbamazepine.
Biofeedback and Physical Therapy
Biofeedback and physical therapy are currently used in the treatment of vulvodynia, both for the patient with localized pain as well as the patient with generalized pain. Biofeedback can help patients devise strategies for confronting and reducing pain, especially if vaginismus is also present. This is a common finding in patients with vestibulodynia. Patients with vestibular pain in general have increased resting tone and decreased contraction tone of the pelvic floor muscles. With the aid of an electronic measurement and amplification system or biofeedback machine, an individual can view a display of numbers on a meter, or colored lights to assess nerve and muscle tension. In this way, it is possible to develop voluntary control over those biologic systems involved in pain, discomfort, and disease. The time required for physical therapy and biofeedback as well as the frequencies of visits will vary with each person. Success rates in the 60% to 80% range have been reported.
Intralesional Injections
Generally speaking, topical steroids do not help patients with vulvodynia, although occasionally, a trigger point injection may be beneficial. Trigger-point steroid and bupivacaine injections have been successful for some patients with localized vulvodynia. It is recommended that not over 40 mg triamcinolone acetonide be injected monthly. To administer this treatment, we suggest combining the steroid with bupivacaine (large-area use 0.25% bupivacaine; small-area use 0.5% bupivacaine), drawing the triamcinolone acetonide into the syringe before the bupivacaine to prevent contamination of the triamcinolone. Inject the combined drugs into a specific area or use them as a pudendal block. Generally, patients do not tolerate more than 3 or 4 injections. Another regimen has been reported that uses submucosal methylprednisolone and lidocaine.
Interferon Therapy
Interferon-alpha, a naturally occurring protein produced by leukocytes, improves the immune system, decreases inflammation, and inhibits mast cells. A study of 214 patients treated with a series of 12 intravestibular injections of 1.5 million units of interferon-alpha showed an overall 42% success rate.
Low Oxalate Diet With Calcium Citrate Supplementation
Oxalates are found in foods such as spinach, beets, wheat bran, peanuts, chocolate, and tea. Oxalate appears in the urine from eating these foods, but also by degradation of microbes in the intestines, intestinal permeability, endogenous (internal) synthesis within the body by the liver and other tissues, and the kidneys' handling of oxalate. Although controversial, the use of oral calcium citrate along with a low oxalate diet may help some women. Because oxalate is an irritating substance, vulvar burning may be associated with elevated levels of oxalates in the urine. Hyperoxaluria has been treated with calcium citrate, which has a chemical structure similar to oxalate and competes with it in the tissues. The significance of oxalates to vestibulodynia has been questioned.
Surgical Treatment of Vulvodynia
Vestibulectomy
The most important criterion for surgical success in treating vulvodynia is identifying the proper surgical candidate. Before vestibulectomy, it is important to evaluate the patient for vaginismus, which may occur in 50% to 60% of patients with vestibulodynia. Vaginismus, if present, should be treated before surgery, because surgery is generally less successful in this subgroup of patients. Treatment of vaginismus includes using vaginal dilators and different types of physical therapy. Sexual counseling may aid a patient's recovery by reducing vaginismus and improving poor sexual arousal, which can develop after long-term dyspareunia.
Surgical Excision
Surgical excision is generally thought of as the last treatment option for patients with vestibulodynia, but this opinion varies among specialists. Excision of the vulvar vestibule has had a variety of success rates. It is our opinion that although vestibulectomy has a high success rate in some studies, this surgery should be reserved for women with longstanding and severe localized vestibular pain when all other managements have not brought adequate pain relief, because many women find adequate relief with other less invasive treatments.
Surgical Techniques
Various surgical techniques are used for the treatment of vestibulodynia unresponsive to all other therapies. We categorize surgical correction of introital dyspareunia of vestibulodynia into the 3 groups: 1) local excision, 2) total vestibulectomy, and 3) perineoplasty. Vestibuloplasty, which involves denervation of the vestibule using incision, undercutting, and closure of the mucosa without excision of the painful tissue or increasing the caliber of the introitus, has been found ineffective, most likely because either removal of the painful tissue or the generation of increased introital dimensions is required for relief of dyspareunia caused by vestibulodynia.
1.Local Excision :
This technique requires precise localization of small painful areas at the time of surgery, which are outlined with a marking pen before administering anesthesia to the area. The tissue is then excised and closed in an elliptical fashion. It may be necessary to undermine the margins of contiguous tissue for sufficient closure.
2.Total Vestibulectomy :
Vestibulectomy is most often performed under spinal or general anesthesia. The patient should undergo testing with a cotton swab before anesthesia while in the operating room to outline the areas of pain . Often pain may be in the majority of the vestibule. The incision may need to approach the periurethral area and extend from the opening of Skene's ducts to the perineum . Excision of the periurethral area should occur with caution not to compromise the angle of the urethra . The incision is carried down laterally along Hart's line to the superior portion of the perineum. The incision should extend above the hymeneal ring. The intervening skin, mucous membrane, hymen, and adjacent tissue are removed. The minor vestibular glands are excised and Bartholin's ducts are traversed in the dissection (however, it is rare to see a cyst develop after vestibulectomy). The vagina is undermined, mobilized, and brought down to cover the defect . The defect should be closed in 2 layers using absorbable 3-0 and 4-0 sutures .
3.Perineoplasty :
In the perineoplasty procedure, the vestibulectomy is performed and includes removal of tissue on the perineum, usually terminating just above the anal orifice. Again, the vaginal mucosa is undermined and advanced to cover the defect.
Complications in vestibulectomies include blood loss, wound infection or separation, granulation tissue, chronic fissuring, Bartholin's duct cyst formation, decrease in lubrication, and continued pain.
4.Surgery For Pudendal Nerve Entrapment :
When the pudendal nerve is entrapped, and the patient has failed guided nerve blocks, tricyclic antidepressants, anticonvulsants, and physical therapy, surgical treatment is an option. Because there are a variety of surgical approaches used for nerve entrapment, we recommend finding a surgeon with particular expertise in this procedure when surgery is indicated.
Psychologic Effects of Vulvodynia
The psychologic impact of chronic pain is well documented. Feelings of hopelessness, depression, and anxiety are common. These feeling are compounded in sexual pain disorders such as provoked vestibulodynia. Unfortunately, even when vulvar pain resolves, the psychologic and sexual dysfunction often persists. Therefore, in addition to treating the biologic processes of vulvar pain, it is imperative to concurrently treat the associated psychosexual and relationship dysfunction. At our institutions, the authors have found that it is essential to have a multidisciplinary team involving physicians, nurses, sex therapists, psychologists, and couple therapists to adequately treat the biologic, psychologic, and social aspects of vulvar pain.

Multiple Births , DR. Alaa Mosbah , M.D OBS&GYN

Background: Multiple births are defined as more than one fetus being born of a pregnant woman. Since 1970, incidence of multiple births has been increasing because of more widespread use of assisted reproductive technologies to treat infertility. Multifetal pregnancies are high-risk pregnancies with a number of associated fetal and neonatal complications. Researchers have studied twins in an attempt to separate the influence of genetic and environmental factors on both fetal and postpartum development.
Pathophysiology: Multiple births include twins and higher order multiples (eg, triplets, quadruplets). The 2 types of twins are monozygotic and dizygotic.
Two sperm fertilizing 2 ova produce dizygotic twins, which sometimes are called fraternal twins. Separate amnions, chorions, and placentas are formed in dizygotic twins. The placentas in dizygotic twins may fuse if the implantation sites are proximate. The fused placentas can be separated easily after birth.
Monozygotic twins develop when a single fertilized ovum splits during the first 2 weeks after conception. Monozygotic twins also are called identical twins. An early splitting (ie, within the first 2 days after fertilization) of monozygotic twins produces separate chorions and amnions (dichorionic/diamniotic). These dichorionic twins have different placentas that can be separate or fused. Approximately 30% of monozygotic twins have dichorionic/diamniotic placentas.
Later splitting (ie, during days 3-8 after fertilization) results in monochorionic/diamniotic placentation. Approximately 70% of monozygotic twins are monochorionic/diamniotic. If splitting occurs even later (ie, during days 9-12 after fertilization), then monochorionic/monoamniotic placentation occurs. Monochorionic/monoamniotic twins are rare; only 1% of monozygotic twins have this form of placentation. Monochorionic/monoamniotic twins have a common placenta with vascular communications between the 2 circulations. These twins can develop twin-to-twin transfusion syndrome (TTTS). If twinning occurs beyond 12 days after fertilization, then the monozygotic pair only partially split, resulting in conjoined twins.
Triplets can be monozygotic, dizygotic, or trizygotic. Trizygotic triplets occur when 3 sperm fertilize 3 ova. Dizygotic triplets develop from one set of monozygotic cotriplets and a third cotriplet derived from a different zygote. Finally, 2 consecutive zygotic splittings with 1 split result in a vanished fetus and monozygotic triplets.
It is important to evaluate the placenta(s) after the birth of all multifetal pregnancies in order to determine zygosity.
Frequency:
In the US: The birth rate of monozygotic twins is constant worldwide (approximately 4 per 1000 births). In contrast, dizygotic twinning is associated with multiple ovulation, and its frequency varies among races within countries and is affected by maternal age (increases from 3 in 1000 in women younger than 20 years to 14 in 1000 in women aged 35-40 years, declining thereafter) and parity. In the United States, the overall incidence of twins is approximately 12 per 1000, and two thirds are dizygotic. The birth rate of dizygotic twinning is highest for African Americans (10-40 per 1000 births), followed by Caucasians (7-10 per 1000 births) and Asian Americans (3 per 1000 births). The rate of higher order multiple births also has increased recently, which has been attributed to in vitro fertilization and embryo transfer. Naturally occurring triplet births occur in approximately 1 per 7000-10,000 births; naturally occurring quadruplet births occur in 1 per 600,000 births.
Internationally: The birth rate of monozygotic twins is constant worldwide (approximately 4 per 1000 births). Birth rates of dizygotic twins vary by race. The highest birth rate of dizygotic twinning occurs in African nations, and the lowest birth rate of dizygotic twinning occurs in Asia. The Yorubas of Western Nigeria have a frequency of 45 twins per 1000 live births, and approximately 90 percent are dizygotic.
Mortality/Morbidity: Multifetal pregnancies are high-risk pregnancies. The fetal mortality rate for twins is 4 times the fetal mortality rate for single births. The neonatal mortality rate for twins is 6 times more than the neonatal mortality rate for single births. Higher order multiple births have even greater mortality rates in comparison to twin and single births.
A high incidence of low-birth weight infants, due to prematurity and intrauterine growth retardation (IUGR) and their associated complications, contribute to this problem. Twins have increased frequency of congenital anomalies, placenta previa, abruptio placenta, preeclampsia, cord accidents, and malpresentations, as well as asphyxia/perinatal depression, group B streptococcal (GBS) infections, hyaline membrane disease, and TTTS.
Race: The frequency of naturally occurring twin births varies by race. Black women have the highest birth rate of twins, followed by Caucasian and Hispanic women. Asian women have the lowest birth rate of twins.
Age: Maternal age has no effect on monozygotic twin births. Advanced maternal age (>35 y) is associated with increased risk of dizygotic twins. Incidence of naturally occurring twin births has increased recently because of the trend to delay childbearing to later years.
History: Most multifetal pregnancies are diagnosed prenatally. Maternal complaints of excessive weight gain, hyperemesis gravidarum, and/or sensation of more than one moving fetus; use of ovulation-inducing drugs; or family history of dizygotic twins should alert caregivers to the possibility of a multifetal pregnancy.
Physical: Women with multifetal pregnancies may have a uterine size inconsistently large for dates and may experience accelerated weight gain. On auscultation, more than one fetal heart rate may be heard.
Causes: Risk factors for multifetal pregnancy can be divided into natural and induced. Risk factors for natural multifetal pregnancy include advanced maternal age, family history of dizygotic twins, and race. Induced multifetal pregnancies occur following infertility treatment via the use of ovulation-inducing agents or gamete/zygote transfer.
Lab Studies:
CBC: In TTTS the donor twin is frequently anemic at birth. The recipient twin is polycythemic at birth.
Calcium: Hypocalcemia is common in premature infants, especially the donor twin in TTTS.
Glucose: Hypoglycemia is common in premature infants, especially if TTTS is present.
Bilirubin: Hyperbilirubinemia may develop in polycythemic infants from TTTS.
Imaging Studies:
Maternal ultrasonography confirms most multiple gestation pregnancies.
Neonatal head ultrasound: Premature infants from multifetal pregnancies are susceptible to intraventricular hemorrhage and periventricular leukomalacia.
Medical Care: Medical care of the woman with multiple gestation pregnancy is beyond the scope of this chapter.
Medical care of infants from multiple gestation births depends on complications.
The usual method of delivery for higher order multiple births (eg, triplets, quadruplets) is cesarean delivery.
Cesarean delivery is also the usual method of delivery for twins in the following situations:
Breech/vertex presentation with the possibility of interlocking twins
Monoamniotic twins
Conjoined twins
Congenital anomalies that threaten increased neonatal morbidity in a twin
Delivery room management of infants from multifetal pregnancies requires adequate personnel skilled in neonatal resuscitation. Infants from multifetal pregnancies are at increased risk of birth asphyxia and respiratory distress syndrome (RDS). Such infants may require bag mask ventilation and endotracheal intubation in the delivery room.
Partial exchange transfusion may be necessary in donor or recipient twins from TTTS.
Partial exchange transfusions are used to increase hemoglobin concentrations in anemic donor twins while maintaining euvolemia. Small aliquots (5-15 cc) of packed red blood cells (RBCs) are infused (usually via an umbilical venous catheter) following removal of an equal volume of the infant's blood until a desired hemoglobin is attained. The transfused packed RBCs should be appropriately cross-matched, cytomegalovirus (CMV) negative, and irradiated.
Partial exchange transfusions are used to decrease hemoglobin concentrations in polycythemic recipient twins while maintaining euvolemia. Small aliquots (5-10 cc) of fresh frozen plasma are infused (usually via an umbilical venous catheter) following removal of an equal volume of the infant's blood until a desired hemoglobin is attained.
Consultations: A woman with multiple gestation pregnancy may benefit from a consultation with a perinatologist. A neonatologist may be involved in the postnatal care of multiple birth infants, particularly if the births are premature or if congenital anomalies are present.
Complications:
Prematurity: Infants from multifetal pregnancies are more likely to be born prematurely and require neonatal intensive care. Approximately 50% of twin deliveries occur before 37 weeks' gestation. The length of gestation decreases inversely with the number of fetuses present. Infants from multifetal pregnancies represent 20% of very low birth weight infants.
Hyaline membrane disease: Twins born at less than 35 weeks' gestation are twice as likely to develop hyaline membrane disease (HMD) as single birth infants born at less than 35 weeks' gestation are. Incidence of HMD is greater in monozygotic than in dizygotic twins. Concordance rate for HMD (ie, both twins have HMD) is greater in monozygotic than in dizygotic twins. If the twins are discordant for HMD, then the second twin is more likely to develop HMD than the first twin.
Birth asphyxia/perinatal depression: Newborns from multiple gestation pregnancies have an increased frequency of perinatal depression and birth asphyxia from a variety of causes. Umbilical cord entanglement, locked twins, a prolapsed umbilical cord, placenta previa, and uterine rupture can occur and result in asphyxiation of an infant. Occurrence of cerebral palsy is 6 times more common in twin births and 30 times more common in triplet births than in single births. Monochorionic/monoamniotic twins are at highest risk for cord entanglement. The second-born twin is at greatest risk for birth asphyxia/perinatal depression.
GBS infections: Early onset GBS infections in low birth weight infants are nearly 5-fold greater than in average weight singletons.
Vanishing twin syndrome: Early ultrasound diagnosis has revealed that as many as one half of all twin pregnancies result in the delivery of only a single fetus. The second twin vanishes. Intrauterine demise of one twin can result in neurologic sequelae in the surviving twin. Acute exsanguination of the surviving twin into the relaxed circulation of the deceased twin can result in intrauterine CNS ischemia.
Congenital anomalies/acardia/twin reversed arterial perfusion sequence: Congenital anomalies more commonly develop in twins than in a single fetus. CNS, cardiovascular, and GI defects occur with increased frequency. Monozygotic twins have increased incidence of deformations secondary to intrauterine space constraints. Common deformations in twins include limb defects, plagiocephaly, facial asymmetry, and torticollis. Acardia is a rare anomaly unique to multiple gestation. In this condition, one twin has an absent or rudimentary heart. Twin reversed arterial perfusion (TRAP) sequence occurs when an acardiac twin receives all of the blood supply from the normal "pump" twin. This only occurs in monochorionic twins. Blood enters the acardiac twin in a reversed perfusion manner. Blood enters this fetus via an umbilical artery and exits via the umbilical vein. The excessive demands on the normal "pump" twin can cause cardiac failure in that twin.
Twin-to-twin transfusion syndrome: This syndrome occurs in monochorionic/monoamniotic or monochorionic/diamniotic twins. Vascular anastomoses in the monochorionic placenta result in transfusion of blood from one twin (ie, donor) to the other twin (ie, recipient). One classification scheme separates TTTS into severe, moderate, and mild forms.
Severe TTTS presents early in the second trimester at 16-18 weeks' gestation. A difference of more than 1.5 weeks' gestational size between twins occurs. Severe TTTS has a 60-100% mortality rate. Polyhydramnios develops in the sac of the recipient twin because of volume overload and increased fetal urine output. Oligohydramnios develops in the sac of the donor twin because of hypovolemia and decreased urine output. Severe oligohydramnios can result in the stuck twin phenomena in which the twin appears in a fixed position against the uterine wall.
Moderate TTTS develops later at 24-30 weeks' gestation. Although a fetal size discrepancy of more than 1.5 weeks' gestation occurs, polyhydramnios and oligohydramnios do not develop. The donor twin becomes anemic, hypovolemic, and growth retarded. The recipient twin becomes plethoric, hypervolemic, and macrosomic. Either twin can develop hydrops fetalis.
Mild TTTS develops slowly in the third trimester. Polyhydramnios and oligohydramnios usually do not develop. Hemoglobin concentrations differ by more than 5g/dL. Twin sizes differ by more than 20%. Polycythemic twins can develop hyperviscosity syndrome and hyperbilirubinemia after birth.
Frequency:
In the US: Monozygotic twins occur in 3-5 per 1000 pregnancies. Monozygotic twins can be monochorionic or dichorionic. Approximately 75% of monozygotic twins are monochorionic. Only monochorionic twins are at risk for TTTS. TTTS occurs in 5-38% of monochorionic twins.
Mortality/Morbidity: Severe TTTS has a 60-100% mortality rate. Mild-to-moderate TTTS is frequently associated with premature delivery. Morbidity and mortality depend upon the gestational age of the twins at delivery. The more premature the twins are at birth, the higher the incidence of morbidity and mortality. Fetal demise of one twin is associated with neurologic sequelae in 25% of surviving twins.
History:
Women with twin pregnancies who develop TTTS frequently complain of a rapidly enlarging abdomen over 2-3 weeks as polyhydramnios develops.
Other complaints include preterm labor and premature rupture of membranes.
Physical: TTTS can be considered in pregnant women carrying twins if they develop a rapidly increasing fundal height. After birth, TTTS can be considered if significant differences in the appearance of monozygotic twins exist.
Donor twin
Small for gestational age - More than 20% smaller than recipient twin
Pallor
Poor peripheral perfusion
Recipient twin
Large for gestational age - More than 20% larger than donor twin
Plethoric and ruddy
Jaundice
Hydrops fetalis can be present in either twin in TTTS. These infants have subcutaneous edema, a distended abdomen, and respiratory distress.
Causes: TTTS occurs in monozygotic, monochorionic twin pregnancies when an anastomosis between placental vasculature exists.
Other Problems to be Considered:
Hydropsfetalis PolycythemiaPolycythemia PolyhydramniosOligohydramniosAnemia of the newborn
Lab Studies:
CBC count: The donor twin is frequently anemic at birth, whereas the recipient twin is frequently polycythemic at birth.
Calcium: Hypocalcemia is frequently present in the donor twin.
Glucose: Hypoglycemia may be present in either twin.
Creatinine: Either twin may have evidence of renal dysfunction.
Platelet count: Thrombocytopenia can occur in either twin.
Bilirubin: Hyperbilirubinemia may develop in the polycythemic recipient twin.
Imaging Studies:
Head ultrasound: Premature twins are susceptible to intraventricular hemorrhage and periventricular leukomalacia.
Echocardiogram: Myocardial dysfunction, myocardial hypertrophy, valvular insufficiency, and pericardial effusions can be detected in either twin.
Renal ultrasound: Abnormal renal echogenicity may be present in either twin and indicates hypoxic-ischemic cortical necrosis.
Abdominal ultrasound: Ascites may be present if hydrops fetalis occurs.
Chest x-ray films: Pleural effusions and cardiomegaly may be present if hydrops fetalis occurs.
Medical Care: A detailed description of medical care of the pregnant woman carrying twins with TTTS is beyond the scope of this review. Medical care of twins after birth is directed toward problems related to prematurity, anemia, polycythemia, and hydrops fetalis.
Severely anemic donor twins may require packed RBC transfusions or partial exchange transfusions.
Polycythemic recipient twins may require partial exchange transfusion to lower serum hematocrit levels.
Newborns with hydrops fetalis may require mechanical ventilation, thoracocentesis, pericardiocentesis, and paracentesis
Complications:
Neurologic sequelae
Intrauterine demise of one twin can result in neurologic sequelae in the surviving twin.
Acute exsanguination of the surviving twin into the relaxed circulation of the deceased twin can result in intrauterine CNS ischemia.
Prognosis:
Outcome is dependent upon gestational age at birth. The lower the gestational age at birth the greater the risk for long-standing neurologic or pulmonary sequelae. Catch-up growth occurs postnatally in most of the smaller donor twins.

Conjoined twins: Incomplete late division of monozygotic twins produces conjoined twins. Conjoined twins are connected at identical points and are classified according to site of union.
Thoracopagus - Joined at chest (40%)
Xiphopagus/omphalopagus - Joined at abdomen (34%)
Pygopagus - Joined at buttocks (18%)
Ischiopagus - Joined at ischium (6%)
Craniopagus - Joined at head (2%)
Intrauterine growth retardation: Birth weights of twins are smaller than weights of corresponding singletons. However, when combined, birth weights of twins are greater than weights of corresponding singletons. Most of the deficit of birth weight occurs in the final 8-10 weeks of pregnancy. Birth weight discrepancies of more than 20-25% are considered discordant. Discordant birth weights occur in 10% of twins. The cause of discordant birth weights among twins is the difference between each twin's placental surface area or TTTS. Discordant birth weights among triplets are more common than discordant birth weights between twins. Approximately 30% of pregnancies with triplets have a birth weight discordance of more than 25%.
Prognosis:
The prognosis of infants born from multiple gestations depends upon the complications that develop. Some studies have reported that the risks of death, chronic lung disease, and grade III/IV intracranial hemorrhage were similar in twins and singletons. Other studies have reported a higher incidence of complications such as necrotizing enterocolitis, retinopathy of prematurity, and patent ductus arteriosus in infants from multiple gestation versus singletons.

MANGEMENT OF TWIN PREGNANCY:

It consists of 4 main items:
I- Antepartum management.
II- Intrapartum management.
III- Postpartum management.
IV-Management of complicated twin pregnancy.

I-Antepartum Management:
[A]. OBJECTIVES:
The main objectives of antepartum management in twin pregnancy are;
1- Prevention of preterm labor, achieved through:
i- Bed rest
ii- Prophylactic tocolysis.
iii-Ambulatory uterine contraction monitoring ( home uterine activity monitoring).
iv-Infection surveillance & control.
v- Plus or minus prophylactic cervical cerclage.
vi-Betamethazone , 12mg IM daily for 2 consecutive days, (repeated every week), starting at 28 weeks, ending at 34 weeks, for every case at risk of preterm delivery.

2-Evaluation of fetal growth, achieved through:
i- Serial ultrasound measurements every 3-4weeks after 16weeks gestation.
ii- Antepartum fetal surveillance using NST, BPP.
iii- Amniocentesis & lung maturity tests. In cases of concordant twins, one sac is examined & the results applied for both fetuses. In cases of discordant twins, determination of maturity should depend on the tests of the larger fetus ( the discordant twin ”the smaller” shows premature lung maturity due to chronic distress).

3- Determination of the best mode of delivery.

[B]. FOLLOW UP SCHEME:
1-Antenatal visits:
Made every 2weeks, in each visit the following parameters should be confirmed:
i- Blood pressure evaluation.
ii-Proteinuria estimation.
iii- Uterine fundal growth.
iv- Fetal movement.

2-Ultrasound examination:
Made every 3-4 weeks to evaluate fetal growth & detect fetal complications.

3-Vaginal & bladder infection should be recognized & properly treated.
4-Vaginal examination:
Made in every visit starting from 22 weeks or even earlier in complicated cases. The aim is to evaluate the lower uterine segment & cervical length. If the lower segment is bulging & the cervix is less than 0.5 cm long, tocolysis is indicated.
The examining finger should never be introduced through the cervical canal to avoid infection & preterm labor ( from prostaglandin release).

5-Bed rest:
- Starts at 22 weeks in uncomplicated twin pregnancy. In complicated cases (e.g. hydramnios, increased uterine activity & discordant growth) it starts earlier or once complication is diagnosed.
- The patient should stop working & rest in lateral decubitus position at least for 2 hours each morning & sleep 10 hours per night.

II- Intraparum management: [management of twin delivery]
[A]. PREREQUESITES:
Due to the many complications that are common in twin pregnancy (e.g. preterm labor, uterine dysfunction, abnormal presentation, prolapse of the cord, pre-mature separation of the placenta & postpartum hemorrhage) the following prerequisits should be taken:
1- Continuous fetal monitoring for both fetuses simultaneously all the time of labor.
2- Blood transfusion products should be readily available.
3- Intravenous infusion system with wide caliber i.v. cannula. The rate of infusion is 120 ml / hr. lactated Ringer & 5% dextrose.
4- Ampicillin 2 g i.v. / 6hr. especially in preterm labor.
5-A trained obstetrician skilled in intrauterine manipulations should be present.
6- An experienced anesthetist should be available on call.
7- For each fetus, 2 people; one is skilled in resuscitation, should be available.
8-Delivery area should provide adequate space for the teamwork.
9-Operative theater should be alarmed & ready for cesarean section at any time.

[B]. ROUTE OF DELIVERY:
The presentation of the 1st twin is the main determining factor. According to ACOG recommendations (1989), vaginal delivery is only indicated in:
1-Vertex- vertex presentation.
2-Vertex –non vertex ( controversial especially with prematurity).
When the 1st fetus is non-vertex, cesarean section is the route of choice for delivery.

[C]. INDUCTION OF LABOR:
Indications:
1-Severe preeclampsia.
2-Severe hyperemesis.
3-Severe maternal respiratory distress due to over- distension.
4-Severe pain due to over-distension.
Methods:
1- Cesarean section ( unless the fetuses are grossly premature & hopeless).
2- Amniotomy alone; initiates labor & improve uterine contractions due to reduction of the uterine size.
3-Amniotomy & pitocin drip.

[D]. ANALGESIA & ANESTHESIA:
1- Vaginal delivery:
(a). Spontaneous vaginal delivery:
i-Pudendal nerve block (+) nitrous oxygen.
ii- Epidural analgesia or caudal block (in non-hypertensive patients).

(b). Intrauterine manipulations: fluthane or isoflurane inhalation (they may ↑ blood loss).

2-Cesarean Section:
i-Balanced general anesthesia or,
ii-Conduction analgesia; epidural or spinal.

[E]. VAGINAL DELIVERY OF THE SECOND TWIN:
- Continuous fetal monitoring.
-Combined vagino-abdominal exam immediately following delivery of the 1st twin.
- Management differs according to presentation of the 2nd twin as follows:
1-Cephalic: moderate fundal pressure & rupture of membranes, waiting for spontaneous delivery, provided that no fetal distress. If fetal distress occurs, instrumental delivery is indicated (vacuum or forceps), or cesarean section.

2-Breech: as cephalic (see above), or breech extraction under general anesthesia if fetal distress occurs.

3-Transverse: the following are done in sequence:
i-External cephalic version (under ultrasound guidance), then delivered as cephalic. If fails,
ii- External podalic version (under ultrasound guidance), followed by breech extraction. If fails,
iii-Internal podalic version & breech extraction. If fails,
iv-Cesarean delivery for the 2nd twin.
Also cesarean section may be indicated when fetal distress appears from monitoring FHR at any stage.

[F]. CESAREAN SECTION IN TWIN PREGNANCY:
Incidence: in the USA, it is 40% ( 60% primary C.S, & 40% repeat C.S.).
Indications:
1-Uterine dysfunction especially hypotonic inertia.
2-Twins in uterus didelphys.
3-Non-vertex presentation of the 1st twin.
4-Fetal distress shown from fetal monitoring (1st or 2nd twin).
5-Discordant twins.
6-Prolapsed pulsating cord.
7-Birth weight ≤ 1500g (with hopeful chance for survival).
8-Locked twins.
9- Severe preeclampsia & unfavorable cervix.
10-Other indications, as in singleton pregnancy.

III. Post partum management: [ third stage management]
- Postpartum hemorrhage is common in twin than in singleton delivery & usually is atonic due to uterine over-distension. Hence the following measures should be instituted immediately following delivery of the placenta:
1-Oxytocin 30 iu in 1000 ml of lactated Ringer’s solution in dextrose 5%.
2-Ergometrine 0.5-1mg in 1000 ml of lactated Ringers solution.
3- Prostaglndin infusion ( PG –F2α).
4- Prostaglandin analogue ( misoprestone; cytotec tablets), given 400-600μg [ 2-3tablets] per rectum have proved effective in prevention of atonic postpartum hemorrhage.
5-Other measures including, gentle uterine massage, vaginal exploration for tears & manual exploration of the uterine cavity for placental remnants or uterine rupture especially if intrauterine manipulations were done for delivery of the 2nd twin.

IV. Management of Complicated twin Pregnancy & Delivery:
The management is individualized & have been discussed under each complication (see before).

MULTIPLE GESTATION WITH TRIPLETS OR MORE
Incidence:
- In the USA, the incidence of triplets was 1: 6000births, while that of quadreplets was 1: 41 million births.
- Recently the incidence is increased after administration of ovulation induction for the management of infertility as follows: with gonadotropins is 20% ( 75% twins & 25% more), with clomiphene the incidence of multiple pregnancy is 10%.

Complications:
Every thing that has been said about twin pregnancy is applied to gestations with higher number with increased perinatal morbidity & mortality especially preterm delivery (85%) & neonatal death (20%).

Management during pregnancy:
All measures applied to twins are applied here plus 2 specific procedures; selective termination & selective reduction.
1- Selective Termination:
- It is selective destruction of a twin or higher-order multiple gestation fetus with identified congenital anomalies during the 2nd trimester or earlier.
- It is usually done by intra-thoracic or intr-afunic (umbilical cord) injection of potassium chloride or air embolism under ultrasound guidance.
- The best results were obtained with potassium chloride, before 20weeks, in non presenting fetus.

2-Selective fetal reduction:
- Here there is no congenital anomalies detected & the procedure is performed just to reduce the number of fetuses to avoid complications that may result with higher numbers, hence improving the survival of the remaining fetuses.
-The procedure was 1st developed by Berkowitz (1988), to reduce the number of fetuses resulted from IVF.
-The technique is the same as described above in selective termination.

Informed Consent:
An informed consent should be taken from the parents before any of the two procedures is performed. The consent should contain the information about the complications of both procedures which include the following:
1-Abortion of the remaining fetuses (13%).
2-Abortion of the wrong (normal) fetus in twins.
3-Retention of a genetic or structurally abnormal fetuses after a reduction in number.
4-Damage without death to a fetus.
5-Preterm labor of the remaining fetuses.
6-Development of discordant twins or growth restricted fetuses.
7-Maternal complications such as infection, hemorrhage, or DIC (due to retained products of conception).

Management of Labor:
All prerequisites of twin delivery is applied here.
Mode of delivery:
1- Cesarean section : is advocated by most obstetricians (especially in USA) to avoid complications of fetuses. They reserve vaginal delivery to conditions with markedly immature fetuses or maternal complications that make CS hazardous to here.
2- Vaginal delivery: Intentional vaginal delivery for triplets is advocated by Wildshut (in Netherland,1995), & by Dommergues(in France,1995).
Discordant growth:
Definition: it is presence of difference in weight of 20% or more of the larger twin’s weight between both twins ,i.e. the smaller twin(discordant) is less in weight by ≥20% of the larger twin’s weight.

Classifications:
(A). Depending on the magnitude of difference in weight;
Grade I discordancy: the difference is 15- 25%.
Grade II discordancy: the difference is > 25%.
(B). Depending on the order of birth of the smaller twin:
Discordant- first
Discordant- second

Incidence: discordant growth affects 15-29% of twin pregnancies.
Causes:
1- Unequal placental mass;
- Affect both mono- and di-chorionic twins but more in dichorionic twins.
-Gives a typical example for asymmetrical IUGR due to defect in transfer of substances from the mother to the fetus.
- Usually discovered by ultrasound after 24 weeks with asymmetric measurements (see diagnosis).
- In severe cases the FHR monitoring shows fetal distress. Acidosis may be also found.
2-Genetic syndromes:
- Affect both mono-and di-chorionic twins but more in monochorionic twins.
-Gives a picture of symmetric IUGR.
- Usually discovered by ultrasound at 16-20 weeks, with associated neural tube defects (NTD), cardiac anomalies, and chromosomal defects.
-In severe cases FHR monitoring shows distress.
3-Twin-to-twin transfusion syndrome:
Growth discordancy due to this phenomenon is limited to monochorionic twins(see later).

Antenatal Diagnosis of Discordant Growth:
(A). Ultrasound examination:
1-BPD: presence of difference of ≥6mm. (not accurate).
2- HC : ,, ,, ,, ,, ≥ 5%.
3- AC: ,, ,, ,, ,, ≥ 20mm.
4- EFW:,, ,, ,, ,, 15-20%.(see definition).

(B). Doppler ultrasound:
Presence of difference in S/D ratio > 15% plus difference in EFW >15% → the best method for diagnosis.

Management of Discordant Growth:
I. Antenatal Management:
The management differs depending on the cause:
(A). Unequal placental mass;
1-Follow up of the smaller twin by frequent NST & amniotic fluid volume estimation.
2-Weekly injection of betamethazone (12mg/12hr./2 doses) in anticipation of preterm labor.
3-Delivery of both twins: is the best management when signs of fetal distress arise. Elective delivery is seriously considered at 34weeks, and definitely indicated at 36weeks.

(B). Genetic syndromes:
Treatment depends on the nature of the defect & possibility of re-corrective therapy.

(C). Twin-to-twin transfusion syndrome:
Treatment consists of serial amniocentesis of the hydramniotic sac (for more details see later).

II. Route of delivery :
The route of delivery in discordant growth is controversial; there are two opinions:
1- Elective cesarean section whatever gestational age & presentation.
2-Selective approach; vaginal delivery is allowed if the cervix is ripe, presentation is vertex- vertex , and EFW of the discordant fetus is ≥1500gm.

Prognosis of discordant growth:
- Poor prognosis; many of them die due to congenital anomalies or prematurity.
- Survivors suffer morbidity with physical & intellectual sequelae.
-Prognosis is more worse for the discordant-2nd twin .

Single Fetal Demise:
Definition: It is the death of one twin in-utero.
Incidence: It occurs in 3-4% of all twin pregnancies.
Complications:
Depends on the gestational age at which the single fetal demise occurs;
(A). If occurs before 14weeks:
-No maternal risks.
-No risks on the living fetus. The dead fetus is compressed resulting in what is called ‘fetus papyraceus’ or ‘vanishing twin’ .
(B). If occurs after 14 weeks:

I-Maternal complications:
The most serious complication is DIC occurring ≥3 weeks following fetal demise. It affects 25% of those mothers, so periodic monitoring of hemostatic system is necessary in patients who continue pregnancy via evaluation of the items of DIC profile [ fibriogen, FDP, PT, PTT, Platelet count, and D-dimer]. For more details see the chapter of accidental hemorrhage.

II- Fetal complications:
(1). Neurological damage:
-Affects 20% of the survivors.
-Occurs due to transfer of thromboplastin from the dead twin producing thrombotic arterial occlusion that affect mainly the anterior & middle cerebral arteries of the survivor twin causing multicystic encephalomalacia.
-It is not exactly known when this complication occurs following fetal demise.
(2). Renal cortical necrosis:
- It is another sequela that may result from thrombotic arterial occlusion but with less frequency.

Management:
The management depends on the gestational age (GA) when diagnosis of the condition is made;
1-Conservative management:
-Indicated when GA is ≤ 28 weeks [morbidity is more when the fetus is delivered].
-Management consists of periodic monitoring of maternal hemostatic system & follow up of the survivor with ultrasound or MRI.
2- Induction of labor:
- Indicated when ;
(a). GA is 34weeks or more when diagnosis has made.
(b). 24-48 hours from diagnosis & the GA is more than 28 weeks [ this delay is required for the corticosteroid given to enhance fetal lung maturity].

Twins pregnancy

Abdominal Ultrasound

Monoamniotic twins

Abdominal U.S

Pregnancy in bicornuate uterus

TVS done by DR. Alaa Mosbah

HYDROPS FETALIS

Definition & Classification:
Fetal hydrops is defined as the extra-cellular accumulation of fluid in the fetal tissues & serous cavities. The condition has multiple etiologies but it can be generally classified into 2 main categories:
1- Immune hydrops fetalis: when there is evidence of circulating antibodies against fetal RBCs’ antigens in the maternal serum.
The condition is also known as;
· Erythroblastosis fetalis; the name is derived from accelerated erythroblastosis in the fetus in response to hemolysis of the fetal RBCs by the maternal antibodies.
· Rh (Rhesus) isoimmunization; the name is derived from the presence of anti-Rh antibodies produced by the Rh –negative mother against the Rh-positive fetus.

2- Non-immune hydrops fetalis: when there is no evidence of circulating antibodies against fetal RBCs’ antigens in the maternal serum.

Historical Review:
1- Ballantyn (1892); established the clinico-pathological criteria for diagnosis of hydrops fetalis.
2- Diamond (1932); reported that fetal anemia characterized by numerous circulating erythroblasts was associating this syndrome.
3- Landsteiner & Weiner (1940); discovered Rhesus factor in rhesus monkeys.
4- Finn (1961) & Freda (1963); developed effective maternal prophylaxis.
ERYTHROBLASTOSIS FETALIS
Etiology & Pathogenesis:
- Erythroblastosis fetalis is a disease in which the fetal RBCs are hemolysed by maternal iso-antibodies that are able to cross the placenta (being IgG). Iso-antibodies are antibodies capable of reacting with RBCs from the same species (iso-), but not with RBCs of the same individual who produced the antibodies (i.e. not auto-).

- About 97% of cases of erythroblastosis fetalis are caused by maternal isoimmunization against the Rh-D antigen present on the fetal RBCs.

- The other 3% are caused by immunization against other antigenic groups on fetal RBCs such as C, c, E, e, K, k, Fya, M, and Jka.

- Maternal iso-immunization may result from:
1- Passage of fetal Rh-positive RBCs into the blood stream of the Rh-negative mother in the course of pregnancy, especially at the time of delivery (i.e. feto-maternal transfusion).
2- Transfusion of Rh-positive blood to an Rh-negative female.

-Antigen-antibody reaction (type II hypersensitivity) will result leading to hemolysis of fetal RBCs & fetal hemolytic anemia with the following consequences:
1- Fetal heart failure.
2- Massive fetal edema (hydrops fetalis).
3- Intrauterine fetal death.
4- Neonatal hyperbilirubinemia.

Pathophysiology:

- The inheritance of blood group antigens occurs according to Mendelian laws except the group Xga , which is X-linked & co-dominant (i.e. both alleles are expressed in the heterozygous individual).

- The Rh system is formed of 6 genes, 3 carried on each chromosome. Tree of them are dominant (C,D,E) & 3 are recessive (c,d,e). the most important is the D gene which confers to the individual the characteristic of being Rh-positive.

- Rh –positive individual may be homozygous (DD), or heterozygous (Dd), whereas the Rh-negative person is only homozygous (dd).

- Homozygous Rh-positive (DD) father when matted with Rh-negative (dd) mother, 100% of offsprings are Rh-positive. Whereas heterozygous (Dd) father when matted with Rh-negative (dd) mother, 50% of offsprings are Rh-positive.

- Other Rh antigens (C, E) may rarely initiate erythroblastosis fetalis. Other antigens as Kell (K), Duffy (Fy), Kidd (Jk), usually cause isoimmunization via prior blood transfusion rather than pregnancy.

- Lewis antigens (Le) do not cause erythroblastosis fetalis & not synthesized in the RBCs membrane, but absorbed into it.
During normal pregnancy, fetal RBCs cross the placenta in 5% of patients during the 1st trimester & in 47% of patients by the end of the 3rd trimester. However in most cases, the number of fetal - RBCs is small & insufficient to cause primary immune response. Hence the incidence of isoimmunization during the course of the 1st Rh- incompatible pregnancy is less than 1%.

- At the time of delivery, although passage of fetal blood into maternal circulation is the rule not the exception, only 10-15% of Rh-incompatible pregnancies are isoimmunized i.e. there is low index of sensitization. The causes of low index of sensitization are;
1- Size of the inoculum. The inoculum is the fetal blood into the maternal circulation. The greater the size of the inoculum, the greater the possibility of sensitization. However some mothers have been immunized by as small as 0.25ml of fetal Rh-positive blood.
2- ABO incompatibility. When there is ABO incompatibility between the Rh-negative mother & Rh-positive fetus, the frequency of sensitization is decreased by 50-75%. This is because maternal anti-A & anti-B antibodies will destroy the fetal Rh-positive RBCs before they can elicit immune response.
3- Nonresponders. About 30-35% of Rh- negative individuals can not be immunized by Rh-positive antigens. This characteristic seems to be genetically controlled but depends on the amount of the inoculum to a certain degree.

Primary immune response:
- Incidence: 1% during pregnancy & 10-15% during delivery.
- Once elicited, IgM is formed followed by IgG.
- The time between feto-maternal bleeding & initiation of primary immune response is exactly unknown, but usually several weeks. So, prophylactic administration of D-immunoglobulin to mothers shortly after delivery inhibits the immune response. If the administration is delayed up to 2 weeks, it is protective in 50% of cases.

Secondary immune response:
Once Rh-isoimmunization has been initiated, mothers produce large amounts of antibodies in response to small amounts of fetal RBCs leaking into maternal circulation in subsequent pregnancies (type II hypersensitivity). This is the reason that the 1st baby usually escapes.

Anti- Rh immunoglobulins:

IgM
Complete antibody
Appears 1st.
Large molecular weight.
Can not cross the placenta.
Can not produce erythroblastosis
Agglutinate RBCs suspended in saline at 4-20ºC

IgG
Incomplete antibody.
Appears later.
Small molecular weight.
Can cross the placenta.
Can produce erythroblastosis
Agglutinate RBCs suspended in medium containing albumin or Coomb’s serum at 37ºC.
Clinical Picture:
Depends on the severity of fetal hemolysis & may include the following:
1- Congenital hemolytic anemia.
2- Congestive heart failure.
3- Ascites, serous effusions, peripheral edema (i.e. hydrops fetalis).
4- Placental hypertrophy.
5- Hepatomegaly, splenomegaly; due to congestive heart failure & extra-medullary hematopoiesis.Neonatal jaundice & Kernicterus. Kernicterus is the deposition of bilirubin in the basal ganglia of the neonatal brain. Since the neonatal liver can not effectively handle the large amounts of pigment released during the hemolytic process, neonatal jaundice & kernicterus results. During the intrauterine life, the accumulation of the billirubin pigment is prevented due to its removal via 1- placental circulation & metabolism in maternal liver, so jaundice & kernicterus never occur antenatally.

MANAGEMENT:
There are 2 types of patients who are managed differently:
1- Rh- non-immunized patient.
2- Rh –immunized patient.

[I]-Management of Rh- negative Non-Immunized Patient
The Rh-negative non-immunized group is formed by primigravida & multipara patients who do not have detectable isoantibodies in the initial prenatal evaluation. The management should include:
[A]. Assessment of chances for immunization.
[B]. Measures to detect isoimmunization in current pregnancy.
[C]. Prophylaxis in the antepartum & immediate postpartum period.

ASSESSMENT OF CHANCES FOR IMMUNIZATION:
This is done by doing blood typing for the partner:
1- If he is Rh-negative, the infant will be Rh-negative & no need for further testing.
2- If he is Rh- positive, the infant is Rh-positive in 50% of cases (if the father is heterozygous), or in 100% of cases (if the father is homozygous), with a possibility of isoimmunization.

MEASURES TO DETECT ISOIMMUNIZATION IN CURRENT PREGNANCY:
This is achieved by doing antibody screening at 20, 24, and 28 weeks of gestation.
1-If screening is positive at any time, the patient is managed as immunized (see later). During sensitization screening ‘detection of Rh- antibody titer’ any positive titer is considered ‘ sensitized’ except in patients with previous administration of D-Ig in prior pregnancy, the patient is considered sensitized if the titer is more than 1:4.

2-If screening is negative at all times, anti-D immunoglobulin is given at 28 weeks, with no need for further testing. At delivery it is necessary to determine the mother’s eligibility to receive a 2nd dose of anti-D Ig in the immediate postpartum period. The 2nd dose is indicated in the following conditions:
i- Infant is Rh-positive.
ii- Direct Coomb’s test on umbilical cord blood is negative (i.e. infant’s RBCs are not covered by irregular antibodies).
iii- A cross-match between the anti-D & mother’s RBCs is compatible.
- Although D-Ig administration at 28 weeks seems to be cost-ineffective, it decreases the incidence of isoimmunization in the 3rd trimester from 2% to 0.2 %.

PROPHYLAXIS WITH D- IMMUNOGLOBULIN:
-The usual dose is 300 μg given IM, usually in the 1st 72 hours postpartum. This dose is capable of neutralizing the potential antigenicity of 30ml of fetal blood (=15ml of fetal RBCs), and prevent isoimmunization in 90% of cases. The remaining 10% of cases in whom the anti-D Ig is ineffective probably as a result of large fetomaternal transfusion.

- A large fetomaternal transfusion occurs in 1:500 deliveries & should be suspected in the following conditions:
1- Birth of a pale baby. 2- Fetal hemoglobin < 10g.
3- Abruptio placentae 4- Midforceps operations & traumatic deliveries.
- Detection of fetomaternal bleed is made by “ Kleihauer- Betke test” which is based on the fact that an acid solution ( citric acid phosphate buffer pH 3.5) elutes the adult but not fetal hemoglobin from RBCs. Thus the fetal erythrocytes appear in the blood smear stained dark red & surrounded by colorless ghosts (adult erythrocytes without hemoglobin). This test can detect as little as 0.2ml of fetal blood diluted in 5 liters of maternal blood.

- Kleihauer – Betke test is useful only to evaluate the volume of large fetomaternal hemorrhage
(and hence the amount of D-Ig required) but not useful & should not be used to determine the need for D-Ig administration, as about 50% of Rh-negative mothers who become sensitized have a negative postpartum test. The need of the mother to be given the D-Ig is determined by cross-match between the anti-D & the maternal RBCs.

- D-Ig can be given up to 2 weeks postpartum with 50% protective value.

- Indications of D- Ig administration:
1- At 28 weeks gestation in Rh- negative non-sensitized patients (optional).
2- At postpartum period in Rh- negative non-sensitized patients.
3- Following abortion (spontaneous or induced).
4- Following ectopic pregnancy or molar pregnancy.
5- Following amniocentesis.
6- Following cordocentesis.
7- Following chorionic villus sampling ( CVS).
[ In all these cases the patient must be Rh-negative & non-sensitized].
[II]. Management of Rh-negative Immunized Patient:
The management is based on adequate use of 4 diagnostic procedures, which are:
A. Maternal serum antibody titers.
B. Fetal assessment by ultrasound.
C. Amniotic fluid bilirubin determination.
D. Fetal blood sampling ( cordocentesis).

MATERNAL SERUM ANTIBODY TITERS:
- Only useful in follow up of patients in their 1st immunized pregnancy because:
1- The correlation between antibody titer & fetomaternal bleeding only exist in the 1st immunized pregnancy & lost in subsequent pregnancies.
2- Following the initiation of immunization, the serum antibody concentration is very low & rarely exceeds the critical level. The critical level means that no death resulting from erythroblastosis has occurred within 1 week of delivery when the antibody titer was at that level or lower. The critical level is variable in different laboratories; may be 1: 16, 1:32, or 1:64, so the obstetrician should use the same laboratory for all of the antibody titer determinations.

- Patient in their 1st immunized pregnancy should have antibody titer every 4 weeks.

- Patients with the following conditions should not be monitored with antibody titers but should be managed on the basis of spectrophotometric analysis of the amniotic fluid :

1- Past obstetric history of fetal or neonatal erythroblastosis (even if their titer do not exceed the critical level). This is because past obstetric history is the predominant indicator of the fetal outcome.

2-Initial testing reveals antibody titer ≥ critical level.

3- During follow up; the titer reaches or exceeds critical level, or there is a significant rise in the titer ( 2 tube dilution) in 2 consecutive tests even if the high dilution does not reach the critical level (e.g. titer ↑ from 1:4 to 1:32 with a critical level 1:64).

-Management will be as follows:
1- Antibody titer always below the critical level up to 36 weeks:→
Delivery at term (38-40 weeks) & expect normal or slightly affected baby. The patient is not allowed to pass term.

2- Antibody titer less than the critical level up to 32 weeks & significantly elevated at 36 weeks: →Amniocentesis for Δ OD 450, PG, and L /S ratio;
· Mature fetal lungs → delivery.
· Immature fetal lungs & elevated bilirubin ( Δ OD more than 0.05) → 2 options ( depending on circumstances );
a). Glucocorticoids for 24 hour & delivery after 48 hours. OR,
b). Fetal blood sampling & Intrauterine transfusion ( IUT) if the fetus is anemic.
· Immature fetal lungs & low bilirubin ( ∆ OD less than 0.05)→ Repeat amniocentesis after 1 week & delivery once lungs are mature.

3- Antibody titer above the critical level at any time before 36 weeks: → Follow up with amniotic fluid analysis & cordocentesis (see later).
FETAL ASSESSMENT BY ULTRASOUND:
-High resolution, level II ultrasound is necessary for management of sensitized Rh- negative patient aiming to:
1- Clear visualization of the fetal structures.
2- Early diagnosis of fetal ascites, pericardial effusion, liver enlargement, and placental swelling.

- Some investigators believe that the accuracy of ultrasound in detecting signs of fetal hemolytic disease is better than that of amniotic fluid bilirubin measurement. However, other investigators proposed the following objections for using ultrasound as the main indicator of fetal hemolytic disease:
1- Fetal hydrops usually develops when fetal hematocrit is < 20% , therefore, ultrasound will detect only advanced degrees of anemia.
2- Amniotic fluid bilirubin determination & cordocentesis can detect fetuses with moderate & severe hemolysis when ultrasound evauation is still normal.
3- In many cases, the onset of hydrops is sudden & its detection by ultrasound will require frequent evaluations.

AMNIOTIC FLUID ANALYSIS:
- It is mandatory in the management of Rh- negative immunized gravida in all her pregnancies except the 1st sensitized one.
- Amniotic fluid (AF) analysis includes spectrophotometric analysis to determine bilirubin level & assess fetal lung maturity by detecting phosphatidyle glycerol (PG) and lecithin / sphengomyeline ratio (L / S ratio).
- Spectrophotometric analysis of AF is a reiable method for evaluating the severity of fetal hemolytic disease & determination of the optimal time for IUT or delivery.
- Traditional amniocentesis was performed initially at 26 weeks because :
1- The limit of fetal viability was at 26 weeks before the development of modern trends of neonatal intensive care.
2- The Liley graph (1961) used to evaluate the severity of sensitization beginning at 27 weeks.

- Nowadays, amniocentesis may be performed at any time after 16 weeks in patients with:
1- High antibody titer ≥ critical level.
2- History of previous history.
3- Ultrasound evidence of signs of fetal hydrops.

- Principles of amniocentesis:
1- Tap site is selected by ultrasound avoiding the placenta & cord.
2- Bladder is emptied.
3- Antiseptic solution e.g. povidone iodine 10% ( Betadine®) at puncture site.
4- Anesthesia ; local infiltration with Xylocaine 2% may be used.
5- Needle ; 22 gauge, 3.5- 7 inch long needle is used.
6- Aspirate : 5-10 ml of amniotic fluid are aspirated. The sample is kept in brown bottle to protect from light which destroys bilirubin content.
7- Centrifugation, filtration & spectrophotometric analysis are all done.
8- Spectrophotometric analysis: when normal AF is examined in a spectrophotometer using water as a blank, the optical density (OD) readings between 350&650nm form an almost straight line. If AF contains bilirubin, the OD readings will show a peak at 450nm, and the size of the peak will be proportionate to the amount of pigment in the fluid. Rather than continuous scanning between 350&650nm, most laboratories measure the OD at 375, 450 & 525 nm.
1- Results : are blotted on a semilogarithmic paper & a straight line is drown between the readings at 375 &525nm. The difference the point at which the line crosses the 450nm mark (expected value) & the actual reading at this wave length is the delta optical density 450 (Δ OD 450) that is used by the clinician for patient management purposes.
2- When using AF analysis in the management of Rh-negative sensitized patients, the obstetrician must keep in mined these 2 important points:
(a). Bilirubin content of normal AF; Bilirubin concentration increases from 10th to 17th week, remains stable ( plateau) until 26th week, then decreases thereafter to term.
( b). Problems with amniocentesis;
i- Preterm labor: is a rare side effect, instead there is usually mild uterine contractions lasting for 30-45 minutes & subside spontaneously. If remains, β- mimetics are indicated (e.g. turbotaline 250mg S.C.).
ii- Bloody taps; is a term that reserved for gross, visible contamination of AF with fetal or maternal blood ( mostly maternal). If fluid is grossly contaminated with blood comes out of the needle, the best thing to do is to let the fluid escapes to see if spontaneous clearing occurs. If the hematocrit value of AF after clearing is > 5%, the OD450 reading will be distorted & should not be used for patient management. No value of giving D-immunoglobulin when there is a bloody tap in Rh- negative sensitized patient.
iii- Infection; is a rare complication of amniocentesis that may result in chorioamnionitis & preterm delivery. Aseptic technique during amniocentesis will minimize infection.
iv- Fetal distress; is rare with wide oscillation in base-line FHR for 1-2 hours & usually disappear spontaneously. However, if combined with bloody tap & the FHR is sinusoidal, this is indicator of fetal anemia as a result of fetal hemorrhage (tap).
v- Aspiration of urine; the patient is asked to empty her bladder before the procedure. A drop of fluid is smeared & examined under the microscope for ferning. Amniotic fluid ferns while urine does not .
vi- Meconium staining of AF; meconium causes a marked rise in Δ OD 450 value, and this change does not disappear after centrifugation. For this reason Δ OD 450 value from meconium- stained specimens should not be used for patient management.
vii- Polyhydramnios; when found with erythroblastosis fetalis, it indicates deterioration of fetal status. It gives false low Δ OD 450 that may be misleading when evaluating the severity of the disease. If polyhydramnios is suspected or diagnosed, the total volume of AF should be determined using 51Cr , Evans blue, or sodium para-amniohippurate, and OD450 value should be corrected for dilution.
viii- Multiple pregnancy; each fetal sac should be evaluated separately. One ml of indigocarmine is injected into the sac entered 1st under ultrasound guidance.
Management Based on Δ OD 450 values: According to Liley graph, there are 3 zones:
1-Zone 1:
- Δ OD 450 value is < 0.09.
- No immediate danger of IUFD.
- The procedure should be repeated in 4 weeks.
- If the value remains in zone 1, delivery at term ( 38-40 weeks) & birth of normal or mildly affected baby is anticipated.

1- Zone 3:
-Δ OD 450 is > 0.15
- There is danger of immediate IUFD.
- Cordocentesis must be done, if there is severe fetal anemia ( hematocrit < 30%)→ IUT is performed.
- If fetal lungs are mature, delivery is the best choice.

3- Zone 2:
- ΔOD value is between 0.09 and 0.15
- The procedure is repeated in 1 week;
- If the value decreases to zone 1( decreasing trend ) , management is as zone 1.
- If the value increases to zone 3 ( rising trend ), management is as zone 3.
- If the value remains in zone 2 ( horizontal trend), the procedure is repeated in another week & if horizontal trend continues, cordocentesis & evaluation of fetal hematocrit with exception of fetuses with adequate indices of fetal lung maturity who are delivered immediately.

NB; There are 2 methods for evaluation other than the Liley graph:
1- Robertson method (1969): similar to Liley but it has the advantage of greater individualization of care by using amniocentesis intervals of 1,2,3,4 weeks depending on ΔOD 450 value & gestational age.
2- Freda method (1965): uses the net value ( not the delta value) of OD at 450nm. Freda correlated these absolute values with the bilirubin concentration in the AF & the fetal status at birth.

CORDOCENTESIS:
- Fetal blood sampling “cordocentesis” was 1st introduced by Daffos in 1983 & changed dramatically the management of Rh- sensitized patients.
- It is done after 18 weeks gestation, but best after 24 weeks.
Values of cordocentesis:
1- Measurement of fetal hematocrit & hemoglobin concentration to determine the severity of hemolysis & the need for IUT ( hematocrit < 30%).
1- Determination of fetal blood group & Rh- type.
2- Direct Coomb’s test.
3- The same technique for cordocentesis is used for direct intra-vascular intra-uterine transfusion, a technique that allowed successful treatment of hydropic fetuses unresponsive to transfusions into the fetal peritoneal cavity.

Indication for cordocentesis:
The main indication for cordocentesis is Rh- negative sensitized patients with amniotic fluid bilirubin values in zone 3 or high zone 2 after 26 weeks of gestation. It may be used instead of amniocentesis between 16- 26 weeks ( AF analysis is not reliable at this age).

Technique of cordocentesis:
For fetal blood sampling or transfusion, the site of the placental insertion of the cord is identified using high resolution ultrasound & color flow mapping. Then, under ultrasound guidance, a needle is introduced into the umbilical vein. It does not need maternal sedation & can be performed as an outpatient procedure.

Complications: few including;
1- Feto-maternal hemorrhage; with massive increase in antibody & worsening of hemolytic process.
2- Thrombosis of umbilical vessels; leading to vasospasm & fetal bradycardia.
3- IUFD; occurs in 1.5% of cases after 24 weeks & in 5% before 24 weeks.

INTRAUTERINE TRANSFUSION ( IUT):
- First introduced at 1963 & is carried out under real-time ultrasound guide.
- There are 2 types: ( both using O-ve blood)
(A). Intraperitoneal transfusion:
- The blood ( O-ve) is injected into the peritoneal cavity of the anemic fetus ( hematocrit < 30%) which is then transported by the lymphatics into fetal circulation.
- It is done in cases where direct intra-vascular transfusion is contraindicated or failed.
- It is easier technique than direct IUT.

(B). Direct intravascular transfusion:
- Following the same technique for cordocentesis, the blood is directly injected into the umbilical vein of the anemic fetus.
- It is the procedure of choice & can reverse fetal hydrops.
- It results in 85% good outcomes in compromised fetuses.
Contraindications:
1- Failure to obtain fetal blood sample after several attempts.
2- Difficult approach to umbilical cord; posterior placenta & maternal obesity.

Complications:
Are the same as in cordocentesis.

EARLY DELIVERY & USE OF GLUCOCORTICOIDS:
- Delivery is the best option for management of Rh- negative sensitized patient if the following circumstances exist:
1- Pregnancy is 32 weeks or more, with
2- Δ OD 450 value is in Liley’s zone 3 or high zone 2, and
3- Mature fetal lungs as evidenced by L/S ratio ≥ 2.2 or PG ( phosphatidyl glycerol ) present in the amniotic fluid.
- Glucocorticoids ( 12 mg betamethazone IM daily for 2 days, followed by delivery 24 hours from the 2nd dose) should be given to patients with amniocentesis results indicating the need for IUT or immediate delivery ( zone 3 or high zone 2) & the fetal lungs are immature.

NON- IMMUNE HYDROPS FETALIS (NIHF)
Definition:
NIHF is defined as the extracellular accumulation of fluid in tissues & serous cavities, without evidence of circulating antibodies against RBCs antigens. Sonographic examination must demonstrate fluid accumulation in at least 2 sites.

Incidence:
- The overall incidence is 1: 1500 to 1: 3500 live births.
- Before introduction of anti-D gamma globulin prophylaxis in 1960, 80% of cases of hydrops fetalis were caused by Rh- isoimmunization. However, nowadays NIHF constitutes 75% of all cases of hydrops seen in developed counteries.

Causes:
Approximately 120 separate fetal causes have been reported in association with NIHF including the following:
1. Cardiovascular diseases (20%):
- cardiovascular malformations,
- cardiac arrhythmias,
- cardiovascular neoplasms.
All lead to fetal congestive heart failure & finally hydrops fetalis.
NB. Arrhythmias are treatable with good prognosis, while others are not.

2. Idiopathic NIHF (15%):
Despite thorough investigations as many as 15-30% of NIHF are classified as idiopathic.

3. Chromosomal abnormalities ( 10%):
- The most common are trisomy 21( Down) & Turner syndrome. Others include trisomies 13, 16, and 18, triploidy, mosaicism, and balanced translocations.
- The underlying mechanisms responsible for development of hydrops are; cardiovascular anomalies, hypoalbuminemia, and lymphatic malformations associated with chromosomal anomalies.

4. Cystic hygroma (10%):
It is a malformation of lymphatic system characterized by single or multiloculated fluid filled cavities in the fetal posterior cervical aspect plus webbing of the neck & postnatal buffiness of the limbs. It may result from some chromosomal abnormalities e.g. Turner syndrome.

5. Hematological disorders: α – thalassemia major ( 10%):
- Causes severe fetal anemia & high output cardiac failure.
- Transmitted as autosomal recessive trait ( i.e. both parents must have the trait ).
- It is screened for by hemoglobin electrophoresis of the parents.

6. Pulmonary malformations (5%): e.g.
- Cystic adenomatoid malformation of the lung.
- Chest wall hamartoma.
- Extra-lobar intra-thoracic lobe sequestration.
- Congenital diaphragmatic hernia.
1. Infection (5%):
-The causative organisms are the “PRATSCHEC” agents; Parovirus, Rubella, AIDS, Toxoplasma, Syphilis, Cytomegalovirus, Herpes virus, Echovirus, & Coxackievirus.
- The commonest virus is parovirus B-19, which causes severe anemia but it does not cause fetal malformation. Parovirus B-19 causes what is called the “fifth disease”.
- The 2nd common is cytomegalovirus which has the following criteria for diagnosis; IUGR, microcephaly, cerebral echogenic densities & positive maternal IgM titers. The best method for diagnosis is the viral culture from fetal blood or amniotic fluid.
- AIDS virus have not been reported in association with NIHF.

2. Miscellaneous infrequent causes: include the following;
· Skeletal dysplasia.
· Multiple pregnancy.
· Gastrointestinal anomalies.
· Mendelian syndromes.
· Umbilical anomalies.
· Maternal disease.
· Fetomaternal hemorrhage.
· Placental tumors.
· Genitourinary anomalies.
· Lysosomal storage disorders.
· Fetal hepatic neoplasms.

Diagnosis:
- It is primarily ultrasound diagnosis. The common sonographic findings include:
1) Polyhydramnios.
2) Skin edema greater than 5mm in thickness.
3) Ascites.
4) Placental enlargement.
5) Pericardial or pleural effusions.
6) Cardiomegaly .

- It is recommended that NIHF not be diagnosed when fluid accumulation is limited to ONE body cavity. However, since a unique fluid accumulation may be the first sign of developing NIHF, follow up ultrasound examination is warranted.
- Once the diagnosis has been made, a complete work-up should be performed, including the following:
1- History:
- Family history of chromosomal anomalies.
- History of exposure to teratogens or infections during pregnancy.

2- Blood analysis “ maternal”:
(a) Blood grouping & typing.
(b) Antinuclear antibody (ANA) screening.
(c) Glucose screening.
(d) Hemoglobin electrophoresis.
(e) Viral antibody titers.
(f) Kleihauer’s test.
(g) Glucose-6-phosphate dehydrogenase defeciency screening.

3- Level II ultrasound examination.
4- Cordocentesis for:
(a) Fetal karyotype & blood grouping.
(b) Blood count & hemoglobin.
(c) Blood gases.
(d) Blood cultures.
(e) Viral antibody titers.
(f) Liver function & metabolic testing.

1- Fetal echocardiography for structural malformations.

Prognosis:
- Prognosis is generally poor; the perinatal mortality rate ranges from 40% to 98% depending on the cause.
- Prognostic factors include:
1- Cause of hydrops; anatomic malformations have the worst prognosis.
2- Karyotype.
3- Severity of anemia.
4- Fluid collection; amount & location.

- Factors associated with NIHF & contribute to poor prognosis are (4 P):
1-Preeclampsia. 2- Preterm labor.
3- PROM. 4- Postpartum hemorrhage due to retained placenta.

- The best prognosis with spontaneous resolution of hydrops is found in:
1- Cytomegalovirus (CMV) infection.
2- Cardiac arrhythmias without structural malformations.

- Recurrence of NIHF is low except if the cause is genetic.

Management:
-Management must be individualized as it depends on:
1- The cause of hydrops.
2- The prognosis.
3- Counseling of the parents.
- Management plan is usually as follows:
1- Before viability ( < 20weeks): Termination of pregnancy is an option.

2- After viability ( > 20 weeks): 2 options;
A. Expectant management; in cases with severe anatomic malformations or chromosomal anomalies.

B. Active management; in cases with treatable problems as parovirus anemia & fetal arrhythmias. The treatment modalities include the following:

1) Amniocentesis: to relief maternal discomfort & prevent preterm labor.
2) Fetal paracentesis & thoracocentesis: to minimize the possibility of dystocia during labor & facilitate resucitation of the neonate.
3) Intrauterine transfusion: to treat the parovirus-induced anemia.
4) Fetal intra-peritoneal injection of red blood cells & albumen.
5) Fetal thoraco-amniotic shunting in cases of pleural effusion.

Investigation and treatment of couples with recurrent miscarriage

Evidence-based clinical guidelines for theinvestigation and treatment of couples with recurrent miscarriage

Royal College of Obstetricians and Gynaecologists, 2003

Genetic factors
· All couples with a history of recurrent miscarriage should have peripheral blood karyotyping performed. The finding of an abnormal parental karyotype should prompt referral to a clinical geneticist. (C)
· In all couples with a history of recurrent miscarriage cytogenetic analysis of the products of conception should be performed if the next pregnancy fails. (C)
Anatomical factors
· All women with recurrent miscarriage should have a pelvic ultrasound to assess uterine anatomy and morphology. (√)
Cervical weakness
· Cervical cerclage is associated with potential hazards related to the surgery and the risk of stimulating uterine contractions and hence should only be considered in women who are likely to benefit. (B)
Endocrine factors
· Routine screening for occult diabetes and thyroid disease with oral glucose tolerance and thyroid function tests in asymptomatic women presenting with recurrent miscarriage is uninformative. (√)
· There is insufficient evidence to evaluate the effect of progesterone supplementation in pregnancy to prevent a miscarriage. (A)
· There is insufficient evidence to evaluate the effect of human chorionic gonadotrophin (hCG) in pregnancy to prevent miscarriage. (A)
· Prepregnancy suppression of high luteinising hormone (LH) concentration among ovulatory women with recurrent miscarriage and polycystic ovaries who hypersecrete LH does not improve the live birth rate. (A)
· Polycystic ovary morphology itself does not predict an increased risk of future pregnancy loss among ovulatory women with a history of recurrent miscarriage who conceive spontaneously. (B)
· There is insufficient evidence to assess the effect of hyperprolactinaemia as a risk factor for recurrent miscarriage. (A)
Immune factors
Antithyroid antibodies
· Routine screening for thyroid antibodies in women with recurrent miscarriage is not recommended. (B)
Antiphospholipid syndrome
· To diagnose antiphospholipid syndrome (APS) it is mandatory that the patient should have two positive tests at least six weeks apart for either lupus anticoagulant or anticardiolipin (aCL) antibodies of IgG and/or IgM class present in medium or high titre. (C)
· Currently there is no reliable evidence to show that steroids improve the live birth rate of women with recurrent miscarriage associated with aPL when compared with other treatment modalities; their use may provoke significant maternal and fetal morbidity. (A)
· In women with a history of recurrent miscarriage and antiphospholipid antibodies (aPL), future live birth rate is significantly improved when a combination therapy of aspirin plus heparin is prescribed. (A)
· Pregnancies associated with aPL treated with aspirin and heparin remain at high risk of complications during all three trimesters. (B)
Alloimmune factors
· Immunotherapy, including paternal cell immunisation, third-party donor leucocytes, trophoblast membranes and intravenous immunoglobulin (IVIG), in women with previous unexplained recurrent miscarriage does not improve the live birth rate. (A)
Infective agents
· TORCH (toxoplasmosis, other [congenital syphilis and viruses], rubella, cytomegalovirus and herpes simplex virus) screening is unhelpful in the investigation of recurrent miscarriage. (C)
· Screening for and treatment of bacterial vaginosis in early pregnancy among high risk women with a previous history of second-trimester miscarriage or spontaneous preterm labour may reduce the risk of recurrent late loss and preterm birth. (A)
Unexplained recurrent miscarriage
· Women with unexplained recurrent miscarriage have an excellent prognosis for future pregnancy outcome without pharmacological intervention if offered supportive care alone in the setting of a dedicated early pregnancy assessment unit. (C)
Grades of recommendations
A
Requires at least one randomised controlled trial as part of a body of literature of overall good quality and consistency addressing the specific recommendation.
B
Requires the availability of well controlled clinical studies but no randomised clinical trials on the topic of recommendations.
C
Requires evidence obtained from expert committee reports or opinions and/or clinical experiences of respected authorities. Indicates an absence of directly applicable clinical studies of good quality.
Good practice point
√
Recommended best practice based on the clinical experience of the guideline development group.

Luteal phase defect

Definition :
Abnormal C.L. function with insufficient progesterone production. The deficiency may be in the amount or duration of progesterone secretion.
Incidence: it is common in :
· Old age · Patients with endometriosis
· Infertile patients · History of recurrent preg. loss
· Hyperprolactinemia · Clomiphene citrate users
Types
1) Inadequate luteal phase : inadequate amount of progesterone
2) Short luteal phase
3) A luteal cycle
4) Clomiphene citrate associated or GNRHa associated due to prolonged pit. downregulation
5) Halban’s disease
Physiology: the development of normal C.L depend on:
(1) Intact hypoth.–pit. system with proper synthesis of gonadotropins
(2) Development of the necessary receptors in the follicles
(3) Estrogen production is critical in development of mature follicle and subsequent C.L
(4) FSH / LH ratio is essential and a ratio of 1.0 is proper. Higher or lower ratio is assoc. with poor follicular phase, follicular growth and hence C.L.
(5) Hormonal mileu inside and around the growing follicle is important which influences its growth and biologic function necessary for C.L.
(6) Towards the end of preovulatory phase of the follicle, there is ¯ed FSH receptors and ed LH receptors in granulosa cells
Aetiology :
As the C.L. is a continuum of follicle, any factor which affect the follicular growth will affect C.L. function
(1) Central factors: (hypothalamo – pit) : the most imp.
May result in suboptimal level of FSH early in the cycle
® inadequate tonic LH and inadequate LH surge
® alteration of LH/FSH ratio
It may result from
1- Heritable factors in CNS
2- Psychic trauma
3- Nutritional or chronic diseases
(2) Primary ovarian defect :
Abnormal ova, or insufficient no. of follicles or inadequate response to gonadotrpoin as in premenopause
Affect steroidogenesis(3) Hyperandrogenemia
Leads to dysfunction of hypoth pit
Also directly interfere with follicular growth
(4) Hyperprolactinemia: affect steroidogenesis
(5) Endometriosis: PG F2a ® luteolytic effect
(6) Clomiphene
may be related to inadequate gonadotropin and not due to the medication
(7) Defect in receptor synthesis of the endomet. and defect in endomet. tissue response to normally circulating levels of steroids
(8) Metabolic effect: ¯ed O2
inadequate Bl. oxygenation as associated with Fallot’s tetralogy ® abnormal steroidogenesis
Clinical effects:
1- Infertility 3.5%
2- Recurrent 1st T. abortion 35%
3- DUB. (irregular shedding)
Diagnosis
1) BBT chart: can not establish diagnosis as thermogenic response differ in individuals. However, it is suggested when there is ( abbreviated BBT chart – slowly rising temp)
2) PEB: correlated with BBT
The most frequently used. It should be done close to the next menstruation 1-2 days prior to menses from the fundus. PEB. taken during menses is unreliable. It is taken on the least 2 occasions .
Endomet. histology 2 or more days out of phase i.e the histologic pattern precede the expected pattern by 2 or more days .
3) Serum progesterone
Single assay is less valuable because
· bell – shaped of postovulatory progesterone
· pulsatile secretion
· variation from patient to patient and from cycle to cycle
Assessment by daily progesterone in luteal phase is accurate but expensive and inconvenient
It is better to do 3 progesterone assays in day 4,6,8 prior to next menses. In normal cycle the sum > 15ng/ml
N.B.: Urinary pregnanediol is unreliable clinically to assay luteal function as it is subject to errors resulting from wide individual variation of progesterone that is metabolized and excreted as pregnanediol

An accurate etiology diagnosis is required which is not always possible in ordinary clinical practice.
However it is imp. to check for
. Central pathway
. Nutritional disease
. Emotional tension
. Ch- illness
. Metabolic disease
. Hyperprolactinemia, hyperandrogenism

Short luteal phase
< 10 days the interval bet. the LH peak and the onset of menses
· The pattern of FSH and LH secretion during menstrual cycle is normal
· The mean FSH level and FSH/LH ratios are ¯ed
· The inter cycle of FSH is ¯ed
· The peak conc. of progesterone are lower and occur earlier
If endomet. biopsy is performed and the histology of the endomet. is correlated with LH peak or BBT shift, the endomet. response will be in phase.
It is uncertain if the short luteal phase plays a significant role in infertility but if the defect is severe, follicular development and corpus luteum function would be grossly abnormal and infertility would result.
It is suggested to be due to defective follicular maturation 2ry to gonadotropin secretion
Treatment of short luteal phase: FSH
Is directed towards ing the extent of FSH stimulation very early in the menstrual cycle by
· Clomiphene starting from 2nd day of cycle
· If failed ® low doses of HMG starting 1st day of cycle

Treatment of luteal phase defect: 5 modalities are available for ttt of inadequate LPD
1- Progesterone
2- HCG
3- Clomiphene
4- HMG
5- Bromocriptine
[1] Progesterone therapy
· Progesterone suppository : 25mg intravaginally twice daily
· Progesterone in oil: 12.5mg IM. daily
· Micronized progesterone: 200mg oral twice daily
treatment started on the day of BBT rise and continues until menses begin if pregnancy occur ®continued until 10th week gestation
[2] Parentral HCG
2500 – 500 IU every other day beginning the day of BBT rise and continued as before.
This therapy is less successful than progesterone bec. it can’t maintain an abnormal C.L.
However, it can be used only in patients whose lesions are mild and are central in origin.
The successful end point of therapy is a normal endomet. as evidenced by PEB.
[3] Clomiphene citrate
Although recommended by some, it also has been incriminated as causing ovulatory cycles with luteal phase insufficiency treatment begun with 50mg on day 2 and continued for 5 days used to provide early surge of FSH
Progesterone assay should be repeated during treatment cycle to verify correction .
If normal, the same dose continued. If not it is ed sequentially in 50mg/day increments in successive cycles until correction is achieved.
[4] HMG
Used if Clomiphene failed
start with 1-2 ampoules/day starting on day 2 cycle patient are monitored as anovulatory patients
[5] Bromocriptine
Used in both hyperprolactinemic with LPD and those whose prolactin levels were normal. The results are superior in those who are hyperprolactinemic .

Abruptio placenta

Definition :(AP) is the premature separation of the implanted placenta from the uterine wall.
A. Epidemiology.
The incidence varies from 1 in 86 to 1 in 206 births. AP has a recurrence rate of 5–17% after an episode in one previous pregnancy and 25% after episodes in two previous pregnancies.
B. Etiology.
Although many cases continue to be idiopathic, AP is associated with maternal hypertension, advanced maternal age, multiparity, cocaine use, tobacco use, chorioamnionitis, and trauma. Rarely, rapid contraction of an overdistended uterus may lead to abruption, such as with rupture of membranes with polyhydramnios or delivery of an infant in a multiple gestation.
C. Clinical manifestation.
The amount of external bleeding can vary from none to massive hemorrhage. The presence of blood in the basalis stimulates uterine contractions, which results in abdominal pain. Fetal and maternal mortality rates vary depending on the location and size of the hemorrhage.
D. Maternal complications
Hemorrhagic shock leading to ischemic necrosis of distant organs
Disseminated intravascular hemorrhage
Couvelaire's uterus (extravasation of blood into uterine muscle) leading to uterine atony. Rarely, Couvelaire's uterus may lead to uterine atony and massive hemorrhage, which necessitates aggressive measures such as selective arterial embolization or cesarean hysterectomy to control the bleeding.
E. Fetal complications
include hypoxia leading to fetal distress, death, growth restriction, prematurity, anemia, and major malformations.
F. DiagnosisHistory and physical examination. Classically, AP
presents with vaginal bleeding and acute onset of constant abdominal pain, whereas placenta previa presents with painless vaginal bleeding. A vaginal examination should not be performed unless both placenta previa and vasa previa have been ruled out. Maternal vital signs, fetal heart pattern, and uterine tone should be monitored. Fundal height can also be followed to look for concealed hemorrhage.
Ultrasonography. Although ultrasonography is relatively insensitive in diagnosing AP, a hypoechoic area between the uterine wall and placenta may be seen with large abruptions.
Pelvic examination. If placenta previa is ruled out, perform a speculum examination to look for vaginal or cervical lacerations and evaluate vaginal bleeding. If there is a discharge that is suspicious for infection or the cervix is friable, obtain a wet prep, potassium hydroxide (KOH), and cervical cultures for gonorrhea and chlamydia.
Laboratory tests. If the clinical presentation is suspicious for AP, the following tests may be performed: complete blood cell count with a hematocrit and platelet count, prothrombin/activated partial thromboplastin time, fibrinogen and fibrin degradation product levels, blood type and screen (type and crossmatch determination should be considered depending on severity of bleeding), and Betke-Kleihauer test.
In addition, two bedside tests can be performed. A “poor man's clot test” consists of placing a specimen of whole blood in a red-top tube. If a clot does not form within 6 minutes or forms and lyses within 30 minutes, a coagulation defect is most likely present. To determine if vaginal blood is maternal or fetal in origin, an Apt test may be performed at the bedside. This test consists of mixing vaginal blood with potassium hydroxide. If the blood is maternal in origin, it will turn brown. If it is fetal in origin, no changes will occur because fetal hemoglobin is more resistant to changes in pH. This may prove helpful in distinguishing between placenta previa and vasa previa.
G. Management.
The management of AP depends on the fetus's gestational age and the hemodynamic status of both patient and fetus. Standard management for all patients includes establishment of intravenous access with two large-bore catheters, fluid resuscitation, blood type and crossmatch determination, and continuous fetal monitoring. Rho(D) immunoglobulin should be administered to Rh-negative individuals. In addition, maternal vital signs should be recorded frequently. A Foley catheter should be placed to monitor urine output, which should be more than 0.5–1.0 mL/kg/hour.
Term gestation, maternal and fetal hemodynamic stability. One should plan for vaginal delivery with cesarean section reserved for the usual obstetrical indications. If the patient does not present in labor, induction of labor should be initiated.
Term gestation, maternal and fetal hemodynamic instability. Aggressive fluid resuscitation as well as transfusion of blood products and coagulation factors should be performed as appropriate. Once maternal stabilization is achieved, cesarean section should be performed unless vaginal delivery is imminent.
Preterm gestation, maternal and fetal hemodynamic stability. Eighty-two percent of patients who are at less than 20 weeks' gestation can be expected to have a term delivery despite evidence of placental separation. Only 27% of patients who present after 20 weeks' gestation, however, will have a term delivery.
Preterm, absence of labor. These patients should be followed closely with serial ultrasonographic examination for fetal growth starting at 24 weeks' gestation. Steroids should be administered to promote fetal lung maturity. If at any time maternal instability arises, delivery should be performed after appropriate resuscitation. Otherwise, labor should be induced at term or if testing shows signs of fetal compromise.
Preterm, presence of labor. If both maternal and fetal hemodynamic stability are established, tocolysis may be used in selective cases, particularly cases of extreme prematurity. Magnesium sulfate is preferred over the β-sympathomimetic agents (terbutaline sulfate) because it has fewer cardiovascular side effects. The β-sympathomimetics may mask the physiologic signs of shock. If maternal or fetal hemodynamic status is compromised, delivery should be performed after appropriate resuscitation.
Preterm gestation, maternal and fetal hemodynamic instability. Delivery should be performed after appropriate resuscitation.
Abruptio placentae and abdominal trauma
Whenever abdominal trauma has occurred, AP must be ruled out. In the absence of vaginal bleeding, uterine contractions, or uterine tenderness, 2–6 hours of continuous
fetal heart monitoring may be adequate. If any of these signs are present, then 24 hours of observation is warranted. The laboratory studies mentioned earlier can be performed as well. Rho(D) immunoglobulin should be administered within 72 hours of the trauma to Rh-negative unsensitized patients.

Evidence-based Guideline for the Management of Uterine Fibroids

Assessment

· Asymptomatic women with fibroids where the uterine size is less than 16 weeks in
size (and where other causes of pelvic mass have been excluded) do not need
further investigations but should be advised to seek medical advice if symptoms
occur (D).
· Asymptomatic women with fibroids >16/40 should have specialist referral to
discuss options including observation (D).

· Women who have fibroids detected during pregnancy should be referred to a
specialist for a consult but do not require additional surveillance unless symptoms
arise during the pregnancy (D).
· Although there is no evidence that asymptomatic women with a fibroid uterus
greater than 20 weeks will have future health problems, hysterectomy or
myomectomy is an option (D).
· Transvaginal sonohysterography (TVSH) should be considered prior to
hysteroscopy in women where intrauterine pathology such as submucous fibroids
and polyps are suspected as diagnostic hysteroscopy can be avoided in up to 40%
of women (A).
· Transvaginal ultrasound of the endometrium is accurate in excluding endometrial
hyperplasia but is often unable to distinguish submucosal fibroids and polyps (A).
· Transabdominal ultrasound may be required for uteri greater than 12 weeks' size
as these will be beyond the reach of the transvaginal ultrasound (D).
· Transvaginal ultrasound and transvaginal sonohysterogram are both more
accurate in diagnosing the location of fibroids than hysteroscopy (A).
· When recommending hysteroscopy the following should be considered:
Ø Normal saline should be used as it offers advantages (shorter and less
discomfort) over carbon dioxide instillation (A).
Ø Local anaesthetic should be offered as either a paracervical block,
uterosacral block or uterine instillation (A).
· There is insufficient evidence to recommend magnetic resonance imaging (MRI)
scanning as an initial diagnostic test for uterine pathology (D).
· MRI should be considered for women in whom the location or nature of the fibroids
remains uncertain after transvaginal ultrasound and transvaginal
sonohysterography or who wish to avoid the possible discomforts of a TVSH (D).

· There is insufficient evidence to recommend CT scanning in the assessment of
fibroids (D).
Medical Treatments
· Progestogens should not be recommended in the treatment of uterine fibroids as
there is insufficient evidence of benefit (D)
· Oral contraceptives are not effective in shrinking uterine size but may reduce
menstrual blood loss with a resultant improvement in haematocrit (C).
· Hormone replacement therapy (HRT) should not be used to treat fibroids as it is
not effective in reducing uterine fibroid size (A).
· Women who bleed while on continuous combined HRT and who are known to have
fibroids should have adjustments made to their HRT by either decreasing the
oestrogen dose or increasing the progesterone dose (D)
· Transdermal oestrogen formulations should not be given to women with fibroids
(A).
· RU486 is effective in reducing uterine fibroid size without causing a reduction in
bone mineral density (D)
· Danazol should not be recommended as initial treatment for fibroids as it is not as
effective as gonadotrophin-releasing hormone analogues and has androgenic side
effects which limit its use (C)
· Gestrinone is effective in reducing uterine and fibroid size but androgenic side
effects may limit its use (A)
· Nonsteroidal anti-inflammatory drugs (NSAIDs) are not effective as a treatment for
women with fibroids in reducing heavy menstrual bleeding (B)

· Gonadotrophin-releasing hormone analogue (GnRHa) treatment effectively
reduces uterine and fibroid size but unpleasant side effects and a reduction in bone
mineral density limit its sole use to 6 months (A).
· Gonadotrophin-releasing hormone (GnRH) analogue treatment for 3 months
followed by combined ‘addback’ therapy (oestrogen plus progestin) result in fibroid
shrinkage and are an alternative for women who have contraindications to surgery
or who do not wish to undergo. Once therapy stops then the fibroids will return to
pretherapy size. (B)
· There is insufficient evidence to recommend progestogen-releasing intrauterine
systems to reduce uterine fibroid size (C)
Surgical Management
· Administration of GnRH analogues for 2 to 4 months prior to surgery for uterine
fibroids is recommended for women with a large uterus (> 18 weeks size) or preoperative
anaemia (B).
· Women who are diagnosed with submucous uterine fibroids and heavy or
abnormal menstrual bleeding should be offered hysteroscopic ablation or resection
as an alternative to hysterectomy (C).
· Women with subserous and intramural fibroids associated with symptoms such as
heavy menstrual bleeding and pressure symptoms should be offered a
myomectomy as an alternative to hysterectomy (D).
· Laparoscopic myomectomy should not be undertaken in women who wish to
conceive because of case reports suggesting increased risk of uterine rupture (D).
· There is insufficient evidence to recommend the routine use of adhesion barriers
(B)

· There is insufficient evidence to recommend the routine use of vasopressin in
reducing operative blood loss . (C).
· There is insufficient evidence to support the introduction of laser induced interstitial
thermotherapy, myolysis or cryomyolysis technique (D).
· Embolisation of uterine fibroids may be an effective alternative to myomectomy or
hysterectomy but RCTs are awaited (D).
· The low incidence of leiomyosarcoma discovered incidentally in asymptomatic
women with uterine fibroids does not support operative management of fibroids as
prevention of leiomyosarcoma (D).
· The decision whether a hysterectomy or myomectomy is undertaken is dependent
on: the woman’s preference, the age of the woman, the desire to retain
reproductive potential and the position and number of the fibroids (D).
· Women with fibroids associated with symptoms such as heavy menstrual bleeding
and pressure symptoms should be offered a myomectomy as an alternative to
hysterectomy (D).
· Women who have fibroids detected during pregnancy should be referred to a
specialist for a consult but do not require additional surveillance unless symptoms
arise during the pregnancy (D).

Endometrioma by TVS

Endometrioma

Kissing ovaries by TVS

Severe endometriosis

DR. Alaa Mosbah . Research

Elgomhoria newspaper

Uterosacral endometriosis

Ovulatory dysfunction

Prediction and detection of ovulation:
During an ovulatory cycle, a complex series of endocrinologic, biophysical and structural events occur and can be monitored by:
[1] Clinical methods : which include
a- BBT
b- Measurement of changes in the quality, quantity and ionic concentration of cervical mucus
c- Alteration in the proportion of superficial and parabasal cells in vaginal epith. (vag. cytology)
[2] Chemical monitoring:
a- Measurement of LH, FSH, E2 and progesterone or their metabolites in serum/or urine
b- Measurement of steroids in saliva
c- Histologic changes in the endometrium
[3] Physical monitoring
a- Ovarian ultrasound to assess no. of follicles and their growth
b- Electrical resistance in saliva or vaginal secretion

These techniques are used to:
· Detect ovulation
· Monitor ovulation induction
· Predict ovulation in order to time coitus or insemination
(A) Clinical methods
1] BBT
The thermogenic shift, esp. if it is abrupt and preceded by a nadir, measures a response to the production of progesterone by C.L.
A slight but significant in progesterone production usually precedes the LH peak, but this early rise is usually insufficient to cause a BBT shift.
Although in most women BBT can be interpreted correctly, the system has a number of problems:
· The day of ovulation may vary from one cycle to another
· The day of shift may precede or follow the day of follicle rupture by > 2 days
· BBT shifts altered by many factors
Because most BBT shifts occur after ovulation, the technique can be used only for purpose of confirmation

2] Measurement of changes in quality and quality and ionic concentration of cervical mucus
The preovulatory E2 rise causes the cervical os to open widely with simultaneous in cervical mucus production and a change in the character of mucus.
Midcycle mucus is clear, a cellular and has high water concentration and high spinnbarkiet.
Usually mucus of this good quality is present only during the preovulatory period and precedes the rise in serum E2 level by days .
The changes in cervical mucus, together with those in BBT. form the basis of symptothermal method of natural family planning. However, in some cases there is mucus of good quality well before ovulation and in other women, cervical mucus production remains inadequate despite a normal E2 peak.
An objective method of assessing changes in cervical mucus quantity and ionic content is reflected in the vaginal electrical resistance
3] Vaginal cytology
To detect alteration in the proportions of superficial and parabasal cells. The preovulatory E2 rise causes an in no. of superficial cells present in the vaginal epithilium and a proportionate decline in the no. of parabasal cells .
Because these changes lag behind those in serum by 3 or 4 days, the cornification index or karyopyknotic index is not sufficiently sensitive to predict impending ovulation.Also, alteration in the vaginal flora can prevent the normal epithelial responses
(B) Chemical monitoring
· Measurement of LH: (monoclonal antibody)
for purpose of hormonal testing, an antibody which can bind specifically and tightly to one certain hormone (antigen) can detect very small amounts of the hormone. Until recently, most antibodies have been produced by immunizing animal against the hormone and using their serum as the source of antibody.
These antibodies are not always useful as diagnostic tests because a mixture of antibodies usually is produced by many different B lymphocytes responsible for antibody production. Although a mixture of antibodies can be separated into individual, more specific components, cell lines capable of producing a single type of antibody have been developed.
The cells derived from multiplication of one hybrdome cell all produce the same antibody, called monoclonal antibody.
Because one antigen can trigger the formation of many different antibodies, many different monoclonal antibodies can be produced against one individual antigen.
Each monoclonal antibody then can be evaluated for its specificity and affinity for that antigen, and the best antibody can be selected and used to detect accurately the desired hormone in blood or urine.
Monoclonal antibody technology has been available for detecting LH in lab. But now available as ovukit used to detect the LH surge in urine which is semiquantitative test which takes about 1hr. to complete. The preovulatory surge of LH with the ovukit is defined as color change that equal or exceed the color intensity generated in the 35mIU/ml LH standard testing of the midday 10.00-20:00 specimen is most likely to detect the LH surge.
The ovuquick is a modified version of ovukit and requires only 4 min.
The semiquantitave method of determining the LH surge allows the patient and physician to predict when the probable ovulation will occur within 12-24hr.
Disadvantages
The occasional LH surge that is not followed by ovulation and instances of luteinized unruptured follicle syndrome will not be detected.
The purpose of these is to predict ovulation so that coitus can be timed or insemination planned.
Because these tests predict ovulation shortly before it occurs, they can not be used as a method of contraception.
· Measurement of E2
Follicular maturation is associated with ed production of E2 from the granulosa cells.
The exponential rise in serum E2 conc. leads to an E2 peak that induces LH peak and precedes it by 12hr. Serum tests for E2 can be used to monitor oocyte maturation and to predict ovulation
Disadvantages
The tests are expensive and inconvenient as multiple visits are needed and results are not available for 8-24hr.

N.B.: It appears that the BBT, U/S, and at home tests for LH surge are best techniques to predict and confirm the occurrence of ovulation
(C) Physical monitoring
Ultrasound
Real time U/S can be used to monitor follicle maturation and rupture and is the only technique available to determine in which ovary, the dominant follicle is developing and to verify that ovulation had occurred.
Imaging started in 10th day in 28 day cycle and continued daily. Each ovary is scanned in transverse and longitudinal planes. When it reaches 12-14mm, an oblique scan is also obtained . Evaluation of follicular growth may be limited to measurement of the largest diameter of the largest follicle or extended to calculation of follicular volume which is more accurate and may be mandatory in patients with overdistended bladder or pelvic adhesions which may cause follicular compression .
· Criterion of follicular maturation
Progressive enlargement of the dominant follicle in all diameters Estimates of largest mean follicular diameter have ranged from a mean of 10mm 5 days prior to ovulation to a mean of 21mm on the day of ovulation .
The rate of change is exponential during this time period
· Criteria of the actual occurrence of ovulation
1- Disappearance of the follicle
2- Replacement of the dominant follicle by irregular cystic structure decreasing in size .
3- Filling in of the follicle with ultrasonic echoes
4- Collapse of the follicle followed by emergence of the C.L. cyst which may exceed 40mm in diameter
5- Each of these changes be accompanied by fluid in Douglas pouch

Ovulatory dysfunction

· Normal ovarian function
1- Follicular maturation
2- Selection of the dominant follicle
3- Ovulation
4- Corpus luteum formation

Approximately 30-40% of infertility patients present with ovarian dysfunction
· Evaluation of ovarian dysfunction
History
1- Menstrual pattern
- Amenorrhea
- Oligomenorrhea
- Polymenorrhea
2- History of medical disease or surgery
3- history of drugs
Examination
1- Height (short stature as in Turner’s syndrome)
2- Weight (obesity as in PCO)
3- Thyroid gland
4- Breast examination
5- Fascial and body hair
6- Gynecological examination
Investigations
· Midluteal progesterone (4-10 days before onset of next menses)
· FSH, LH, prolactin, testosterone, TSH
· Progesterone withdrawal test
· Skull x ray in case of high PRL or low gonadotropin
·Chromosomal karyotyping in primary amenorrhea or OV failure
· Pelvic U/S: to detect genital anomalies in amenorrhea and in PCO
Diagnosis
Group (I) hypothalamo-pit failure
· Characterized by:
1- 1ry or 2ry amenorrhea
2- Low pit. gonadotropin FSH, LH
3- PRL normal
4- Progestagen test –ve (no endogenous estrogen)
5- CT skull exclude space occupying lesion
· Examples:
1- Anorexia nervosa
2- Psychological stress (acting through neuropeptides)
3- Kallaman’s syndrome (isolated gonadotropin deficiency)
4- Sheehan’s syndrome (postpartum pit. necrosis)
· Treatment :
ttt of anorexia nervosa by psychotherapy and weight gain
ttt of psychological factor by psychotherapy
the other causes are treated by either GnRh or gonadotorpin

Group (II) : Hypothalamo-pit. dysfunction
· Charact. by:
1- Regular cycles, oligonenorrhea or even amenorrhea
2- Midluteal progesterone is low
3- FSH, LH in normal range
4- PRL normal
5- Progestogen test +ve
6- Serum testosterone levels may be elevated
· Examples
1- PCO, the classical example (with its criteria)
2- CAH: classical or non classical
3- Adrenal tumours
4- Androgen producing ovarian tumours
· ttt:
PCO ® induction of ovulation
CAH ® corticosteroid therapy
OV. tumours and adrenal tumours ® removed
Group (III) : ovarian failure
· Charact. by:
1- Amenorrhea
2- –ve progestogen test
3- ed FSH
· Examples:
1- Turner syndrome: 45 X 0
The ovaries are streak and they contain oocytes during early intrauterine life. These oocytes fail to be surrounded by granulosa cells and undergo rapid rate of degeneration. So, by the age of puberty, no functioning follicles are left
2- Pure gonadal dysgenesis: 46xx or Sweyer’s synd. 46xy where the y chromosome is defective and does not express the testis determining factor
3- Premature ovarian failure: i.e. ovarian failure before the age of 40 y. may be due to :
- Autoimmune disorder
- Genetic factor
- Infection (mumps)
- Irradiation
- Cytotoxic drugs
- Idiopathic
· Treatment: the only real ttt of these patients is IVF using donated eggs. Also, they should be given HRT
Group (IV) congenital or acquired genital tract disorders
· Charact. by
1- Amenorrhea
2- Normal levels of FSH, LH
3- Normal PRL
4- –ve gestagen test and –ve estrogen test
5- Normal 2ry sex characters
· Examples:
1- Congenital: imperforate hymen, T. vaginal septum and Rokitansky – Kauster – Hauser syndrome
2- Acquired: the classical example is Asherman’s syndrome
· Diagnosis: U/S , laparoscopy, hysteroscopy
· Treatment:
Group (V): hyperprolactinemia with a space occupying lesion
· Charact. by:
1- Menstrual disturbances
2- PRL ed
3- Pit. adenoma on CT scan (microadenoma – macroadenoma)
4- Neurological and ophthalmologic ex.
· Treatment: dopamine agonist as bromocriptine
Group (VI) Hyperprolactinemia with no space occupying lesion
· Charact. by:
1- Menstrual disturbances
2- PRL ed
3- no space occupying lesion
· Examples:
1- Hypothyroidism
2- Ch. renal failure
3- Severe liver disease
4- Drugs
- O.Cs
- Dopamine depleting agents (reserpine)
- Dopamine receptor blocking agents (phenothiazines)
· Treatment: Bromocriptine
Group (VII): Amenorrhea with space occupying lesion in the hypothalamo – pit region with normal or low PRL
· Charact. by:
1- Amenorrhea
2- ¯ FSH, LH
3- PRL normal
4- –ve Progestogen test
· Example: the most common tumour in the pit in childhood and adolescence is craniopharyngioma
Neurological and ophthalmological ex. is required
· Treatment: depending on symptoms, size and location of the tumour ® surgery may be required

N.B.: Relation of prolactin to menstrual function:
-Upper limit of normal 15ng/ml
-15-30ng/ml. difficult to define and require repeated determination
-Level > 50ng/ml ® amenorrhea
-Level 30-50ng/ml ® minor alteration of menstrual function:
- Luteal phase defect
- Anovulatory cycle

Amniotic Fluid Meconium

Meconium is derived from the Greek mekonion a word for poppy juice or opium

FORMATION AND COMPOSITION OF MECONIUM
-Meconium is first eyident in the fetal intestine at approximately 70- 85 days' gestation

-It is composed primarhy of water (72- 80%) , primary bile acids

MECONIUM IN AMNIOTIC FLUID
-The degree of tissue stain with meonium depends on (I) meconium concentrations (2) length of exposure
(3) the nature of the exposed tissues

-Vernix : stains yellow in 12 hours
-Finger nails stain yellow in ; 4-6 hours
-Surfrace staining of the placenta within 1 hour
-Umbilical cord staining after l hour with 5% meconium and at 15 minutes with 1% meconium
-Meconitum in pulmonary macrophages suggests antepartum aspiration

-Meconium have (1) Direct VC effects on umbilical vein due to bile acids
(2) Enhance the ability of amniotic funid to sustain bacterial growth

EFFECTS OF MECONIUM ON PULMONARY MATURITY TESTING

1-Meconium has a variable effect on L/S ratio ,it may interfer with phospholipid fraction and raising
the L/S ratio or it may increase sphingomyelin concentration due to cellular debris so decrease L/S

2-PG determination by immunologic method not affected by meconium

ULTRASONOGRAPHIC DETECTION OF MECONIUM-STAINED AMNIOTIC FLUID

1-A.F.appear echogenic or particulate.The positive predictive value of echogenic was only l0 %

2-Diagnosis of Fetal meconium peritonitis , it is a chemical inflammation of the peritoneum caused by
the escape of sterile meconium through a perforation in the bowel
The potential etiologic mechahisms include:
• Intestinal atresias
• Congenital bowel malrotation anomalies
. Volvulus
• Intussusception
• Cystic fibrosis

Diagnosis
• Increased echogenicity of the bowel
• Acoustic shaddowing suggesthlg calcifications
• Polyhydramnios
• Ascites
• Dilated intestinal loops filled with fluid
Amniocentesis to rule out chromosomal abnormalities ,cystic fibrosis and to check fetal lung maturity

THEORIES OF MECONIUM PASSAGE
1-Maturation Theory
-Because it is seldom passed before 34 weeks, its presence in amniotic fluid may reflect gastrointestinal
maturity in late gestation
-Transit time through the fetal small intestine decreases as gestation advances. In the 32-week fetus
transit time to the colon 9 hours compared with 4 .5 hours in the term fetus.
-Immaturity of intrinsic and extrinsic innervation of the bowel may impair the ability of the
premature fetus to pass meconium

2-Theory of Fetal Distress

-Meconium was released when the oxygen saturation of the umbilical vein was below 30 % , it is
passed in response to parasympathetic stirnulation during cord compression
-Amniotic fluid meconium was present more than twice as biophysical profile (BEP) score was
(6 or less) than normal .

3-Role of Intestinal Hormones
-Motilin is an intestinal polypeptide that stinmlate motor function in the colonic smooth muscles . Mean
motilin levels in cord venous blood are highe in term than in preterm infants. A fourfold inerease in
cord plasma motilin level in term infants with abnormal fetal heart rate.

-The relatinship between meconium passage and motilin may help to explain the passage of' meconium
in the preterm fetus

INCIDENCE, ASSOIATIONS, AND PERINATAL OUTCOME

I -Second-Trimester Passage of Meconium

-Discolored A. fluid is encoutered in approximately 2% of genetic amniocenteses .Perinatal outcome is
favorable in more than 90 % of patients. Most patients with stained fluid had clear fluid at the time of
delivery, indicating the transient nature
-The green -stained or brown - stained second-trimester amniotic fluid usually contains degraded blood
pigments rather than meconium and biochemical testing or spectrophotometric analysis.

II-Third-Trimester Passage of Meconium

-The incidence varies from 2 – 11 %. The management of' the high-risk patient is controversial , the
fetus shomd undergo additional antenatal evaluation if delivery is not imminent.

II-Intrapartum Meconium

-The incidence is between 7% - 22% , it approaches 40 % in post-term gestation
-Risks of perinatal morbidity and mortality, especially when accompanied by abnormal FHR patterns
as decreased baseline variability and f'ewer FHR accelerations.Late decelerations are not necessary
present .

-The relationship to low Apgal scores and acidosis remains controversial.

IV-MECONIUM CONSISTENCY

- Thick meconium is associated with a higher incidence of poor fetal outcome compared with thin
staining.
- Thick meconium is often deseribed as "pea-soup," particulate, viscous, and opaque, in contrast with
watery, translucent, lightly-stained thin meconium.
-"Early" passage of meconium (passed during or before the active phase of' labor) carried a greater risk
than "late" passage (passed during the second stage, after clear fluid had been noted).

-The presence of meconium per se does not imply fetal distress during labor unless other parameters
support such a contention. The most important clinical value of meconium-stained amniotic fluid is
to alert the obstetrician to look further for signs of fetal compromise. The obstetrician should initate
suction of the infant's oropharynx at delivery and the need to alert the pediatric staff

MECONIUM ASPIRATION SYNDROME AND ITS PREVENTION

-This term refers to the presence of meconium below the vocal cords and in the lungs. When amniotic
fluid contains meconium, meconium is found below the vocal cords in approximately one third of
neonates
- Fetal breathing (gasping in particular) is the mechanism by which meconium enters the lungs.
- It develops in 2 - 8% of infants delivered through meconium-stained amniotic fluid .
- In its mild form, it may present with neonatal tachypnea associated with normal pH and low Pco2,
resolying within 2-3 days.
-In its more severe form, the syndrome present as hypoxemia, acidosis, and respiratory failure within
minutes to hours after birth.

-The pathophysiology involve a combination of mechanical Obstruction and Chemical pneumonitis of
the small airways by particulate meconium inhaled at the time of the infant's first breath .
-Pulmonary vascular spasm lead to pulmonary hypertension and right-to-left shunting through the
patent foramen ovale or ductus arteriosus.
-Hypoxia may lead to convulsions, renal failure, DIC, and heart failure .
-The death rate is up to 40% in some studies.

DELEE AND TRACHEAL SUCTIONING

-Suctioning of the fetus immediately after delivery of the head and before delivery of the thorax, with
Selective tracheal intubation and suctioning
-Unfortunately, even the most vigorons suctioning before the first breath does not remove meconium
already aspirated into the lungs before birth

ASPHYXIA, PULMONARY ARTERY HYPERTROPHY, AND MECONIUM
Hypoxia, pulmonary hypertension anal ptrsistent fetal circulation are the hallmarks of MAS.AMNIOINFUSION FOR MECONIUM

-The amnioinfusion experienced a sixfold decrease in the incidence of meconium visualized helow the
vocal cords.
-The benefit of amnioinfusion is not related to the meconium per se but, rather, to alleviating umbilical
cord compression and variahle fetal heart decelerations, thereby restoring normal fetal oxygenation

Intrauterine Fetal Death

DIFINITION

* WHO defines fetal death as death prior to the complete expulsion or extraction from its mother
of a product of conception, irrespective of the duration of pregnancy.

The death is indicated by the fact that after such separation the fetus does not breathe or show any other
evidence of life, such as beating of the heart, pulsation of the umbilical cord, or definite movement of
voluntary muscles.

Fetal deaths are classified
-Early if they occur at less than 20 weeks' gestation
-Intermediate if they occur between 20 and 27 weeks' gestation
-Late if they occur at 28 weeks' gestation or greater.

*In developing nations, fetal mortality is calculated only on the basis of deaths at 28 weeks'
gestation or greater

* In the United States
Abortions, defined as intrauterine deaths which occur at less than 20 completed weeks .

Missed abortions refer to those in which fetal products are retained for some prolonged period of
time, usually 4 to 8 weeks.

Fetal deaths are classified as antepartum or intrapartum, depending on whether they occur prior to or
after the onset of labor.

The incidence of IUFD
- 9/1000 live births
- Higher fetal mortality rates are noted in [ very young (<15>35 years
old) mothers, in unmarried mothers, in male fetuses, and in multiple gestations.]

DIAGNOSIS OF FETAL DEATH

1- Patient's signs and symptoms.
Lack or cessation of fetal motion, absence of uterine growth on serial examinations, and inaudible
heart sounds on auscultation were suggestive, but not specific.

2- Radiologic findings included the "halo sign" created by scalp edema, overlapping of the cranial
bones (Spalding's sign) , and abnormal angulation of the fetal spine.
Finding of intravascular gas within the fetus (Robert's sign), it results from decomposition of fetal
blood , it may be found in the first days following third trimester death; however, it is not present in
all cases.

3- Real-time ultra sound With the real-time ultra sound equipment, the diagnosis of fetal death is
simple and reliable, with 100 percent sensitivity and specificity
Signs of fetal death
- Failure to detect cardiac activity
- Absence of fetal motion,
- Overlapping skull bones,
- Scalp and skin edema, and intrafetal gas
- No motion other than the pulsation of the maternal aorta.
Conditions Associated With Fetal Death
-Chromosomal abnormalities, congenital anomalies, and hypoxia are the major causes of fetal
death

-The earlier the gestational age at which death occurs, the more likely there is to be a
chromosomal abnormality .
- As pregnancy advances, fetal hypoxia and congenital anomalies are more likely to be the cause of
death.

I-Chromosomal
1-Numerical abnormalities
Autosomal trisomies (e g, trisomy 13, 18, and 21)
X-chromosomes monosomy
Triploid and tetraploidy
2-Structural abnormalities
Robertsonian translocations
Unbalanced reciprocal translocations

II-Congenital malformations
1-CNS abnormalities
Neural tube defects
Hydrocephalus
2-Cardiac abnormalities
Structural defects
Arrhythmias
3-Abdominal wall defects
Omphalocele
Gastroschisis
4-Genitourinary
Bilateral renal agenesis
Obstructive uropathy (posterior uretheral valves)
5-Skeletal abnormalities
Dwarf ism
Arthrogryposis

III- Infectious causes
1-Bacterial
Group B streptococci
Listeria monocytogenes
Ascending infection secondary to rupture of membranes
SyphiIis
2-Mycotic
Candida albicans
Coccidiomycosis
3-Parasitic infections
Malaria
Chaga's disease ( Trypanosoma Druze)
Toxoplasmosis
4-Viral
Cytomegalovirus
Coxsackie B3
Ru bella
Mumps
Parvovirus
Herpes simplex virus 2

IV-Immunologic causes
1-Isoimmune-mediated
Anti-D isoimmunization
Others (anti-Kell, anti-Duffy, anti-C, anti-E, etc.)

2-Autoimmune
Antiphospholipid antibodies
Lupus anticoagulant
Anticardiolipin antibodies
Anti-SSA antibodies (causing heart block)
Systemic lupus erythematosus

V-Maternal conditions
Diabetes
Hypertension
Trauma (fetomaternal hemorrhage)
Drug abuse

VI-Placental/umbilical cord
Placenta abruption/infarction
Placenta previa
Umbilical cord knots/strictures
Cord entanglement
Cord hemangiomas
Cord prolapse

VII-Other fetal causes
Intrauterine growth retardation
Postmaturity

DIAGNOSTIC EVALUATION OF FETAL DEATH
-Knowing the cause of fetal death is important for several reasons
First, it aids the parents in understanding what led to the demise of their fetus, and alleviates them of
any self-imposed guilt.
Second, the parents may be counseled to the recurrence risks for the specific condition.
Third, subsequent pregnancies may be managed with closer fetal surveillance.

I - Maternal history
II- Physical examination
III- Ultrasound

-Confirm fetal death
-Assess gestational age at the time of death (rely on long bones, e.g., femur, humerus)
-In multiple gestation, look for evidence of
- Twin-to-twin transfusion syndrome - Dividing membrane
-Twin-embolization syndrome in the surviving fetus

-Search for congenital anomalies (e.g., cystic hygroma, neural tube defects, abdominal wall defects,
renal agenesis, obstructive uropathy)

-Assess intrauterine environment
Placental localization (e.g., placenta previa)
Evidence of abruption (retroplacental clot)
Evidence of infection (e.g., syphilis, parvovirus B19 ) or erythroblastosis (placental thickness)

-Amniotic fluid volume
Decreased in IUGR, obstructive uropathies, or renal agenesis
Increased with congenital and chromosomal abnormalities as well as diabetes

- Abdominal pregnancy should be ruled out (uterine wall should surround the fetus)

IV-Amniocentesis at the time of diagnosis rather than waiting for delivery for karyotype and
amniotic fluid cultures for Listeria, cytomegalovirus, and other aerobic or anaerobic
organisms.

V-Laporatory tests (HbA1c, VDRL, TORCH titers, parvovirus B19 serology ,
Kleihauer-Betke , ANA , lupus anticoagulant, anticardiolipin antibodies, urine toxicology for
drugs )

VI- After delivery
-Once delivery has occurred, all products of conception should be carefully examined.
-If THE FETUS is delivered intact, careful photographs should be taken.
-If any dysmorphic features are present, they should be photographed in detail.
-Consultation with a geneticist.

-Placental tissues should be examined by a pathologist for evidence of thrombi,
infarcts, inflammation, villitis, erythroblastosis, parasitic infestation, etc.
-Placental cultures for Listeria monocytogenes should be obtained
-For chromosomal studies, fetal blood obtained by cardiac puncture, and a tissue biopsy from the
fetal thigh . In special circumstances, muscle biopsies may be required.
-When a metabolic disturbance is suspected, fetal serum and/or urine should be obtained.
-If skeletal dysplasia is suspected, radiologic examination in the form of plain x-rays, or computed
tomography, magnetic resonance imaging, or xeroradiography.

MANAGEMENT

-The mother and physician must choose between expectant management awaiting spontaneous
onset of labor or uterine evacuation by any of the medical or surgical modalities .

I- Expectant management
- 80 percent of patients go into labor within 2 weeks and coagulopathy develops if the dead fetus is
retained within the uterus for at least 5 weeks

-Weekly assays of serum fibrinogen levels
- About 4 weeks after fetal death, fibrinogen levels begin to decline at a rate of 20 to 85 mg/dL per
week, fibrinogen levels above 100 mg/dL are not associated with disturbances in clot formation
- Once the coagulation defect is identified, steps should be undertaken to promptly evacuate the uterus
of the retained products of conception.
Expectant management has two major disadvantages.
First, it is often emotionally unacceptable for the parents.
Second, it may place the mother at significant risk for development of coagulation defects due to
hypofibrinogenemia

II- Methods of uterine evacuation

A- Surgical techniques : cervical dilatation and uterine emptying by sharp or suction curettage; rarely,
hysterotomy or hysterectomy .

B - Medical techniques : prostaglandins (or analogues) administered intraamniotically, intravaginally, or
parenterally, and intravenous oxytocin .

1 - When the uterus is less than 13 weeks' size, dilatation and curettage is the method of choice
2 - From 13 to 16 weeks' gestation, either dilatation and evacuation or prostaglandins .
3 - At gestational ages greater than 16 weeks, prostaglandin administration (parenterally, vaginally,
or intraamniotically)
Prostaglandins are approved by FAD for management of fetal death up to 28 weeks' gestation.
4 -If the cervix is favorable, induction of labor by oxytocin infusion .

A-Surgical Techniques

@- Dilatation and Evacuation

@-Hysterotomy, Hysterectomy, and Laparotomy
Indications
- Coexisting gynecologic disease as ovarian tumor
- Abdominal pregnancy

-Performing a hysterotomy subjects the mother to significant morbidity, increased chance of mortality,
and a much longer recuperative period. Moreover, pregnancies following hysterotomies are
frequently associated with increasing the likelihood of uterine rupture

N.B- While the intraamniotic instillation of aborti facients should not be used in cases of fetal
death due to the presence of necrotic tissue, which increase the chance of rapid absorption
of the infused agent as well as infection and coagulopathy.

B - Medical techniques

1- Prostaglandins

PGE2 and PGF2a, are potent uterine stimulants
They can be administered oral, intraamniotic, intramuscular, intracervical, intravaginal, and most
recently, intrafetal.

I - INTRAVAGINAL PROSTAGLANDINS
- PGE2 vaginal suppositories are effective for terminating a pregnancy beyond 12 weeks'
gestation. The 20-mg Suppositories are approved by (FDA) for the management of intrauterine fetal
death up to 28 weeks' gestation

Prostaglandin E2 are contraindicated in patients with

- Known hypersensitivity to dinaprostone
- Patients with acute pelvic infection.
- Patients with active cardiac, pulmonary, renal, or hepatic disease.
- If contraindications to labor are present, such as previous classical cessarean section,
placenta previa, maternal cardiac failure, or invasive cervical carcinoma.

Side effects
- 67 percent experience nausea and / or vomiting; therefore, pretreatment with antiemetics is
recommended
- 40 percent experience diarrhea, they should be premedicated with antidiarrheals
- Transient temperature elevations of greater than (1.1°C) occur in 50 percent of patients
- Less frequent (10 percent) side effects include headache, shivering, chills, and transient
diastolic blood pressure decreases of greater than 20 mmHg.
- Uterine rupture and cervical lacerations
- Approximately 15 percent of patients will have incomplete evacuation of their placentas

II- INTRAVENOUS PGE2

- A solution of prostaglandin E2 , 5 ug/mL in 0.9% saline is infused intravenously, starting at a rate
of 0.125 mL/ min (0.625 ug / min).
- After 1 h, the infusion rate is increased to 0.5 ml/ m ,if satistactory uterine contractions are not
present.
- Not approved in the United States for use
-The induction to delivery time is shorter for the PGE2 group

III-INTRAMUSCULAR

-A 15-methyl PGF2 a analogue, known as Prostin / 15 M (Upiohn) is approved in the United States
for use as an intramuscularly injected abortifacient.
-After premedication with antiemetics and antidiarrheals, a dose of 250 ug (1 mL) is injected deep
IM and repeated at 1. 5 - to 3 .5 h intervals.
-The success rates 90 to 100 percent, all have delivered after one or two injections.

-The major disadvantage is the need for repetitive, painful injections.
It is preferred in the presence of ruptured membranes or a significant vaginal infection

IV-INTRAAMNIOTIC PG2 Fa
Technique.
-An amniocentesis is performed with an 18to 20-gauge spine needle, and a small amount of amniotic
fluid is aspirated to ensure intraamniotic location.

-A test dose of 5 mg (1 ml.) of PG F2 (supplied as 5 mg /mL in 20-mg and 40-mg vials) is slowly
injected to detcrmine any idiosyncratic or hypersensitivity response, or signs or symptoms such as
vomiting, pain, or bronchospasm. The test dose should be injected over 5 min.
- If no adverse reactions develop, 35 mg more are injected over at least 7 min (5 mg/min).

-The intraamniotic route of administration for any abortifacient (e.g., urea, saline, or prostaglandins) in
cases of fetal death is not recommended
1- Rapid absorption may occur and serious complications may result.
2- If an immediate adverse reaction develops there is no way to reverse the medication
-Approximately 97 percent of patients will deliver within 48 h.
- Complications uterine rupture and cervical lacerations

V- INTRAUTERINE EXTRAAMNIOTIC

Technique
- Inserting a Foley catheter (16F) into the cervix after cleansing the vagina with povidone-iodine
-The balloon is inflated when the catheter tip has passed the internal cervical os.
- A test dose of 125 ug of the PGE2 is instilled into the catheter followed by 250 ug in 10 min.
Thereafter, 375 ug of the PGE2 solution is injected every 2 h until delivery.
Advantages

-Dose of PGE2 administered is significantly less , the side effects are less
- It avoids painful intramuscular injections or amniocentesis.
-Oxytocin augmentation is rarely required
- Fever and gastrointestinal symptoms occur less often.

- This method is effective and safe and compares favorably to PGE2 vaginal suppositories

VI- INTRACERVICAL PGE 2

- PG gel is used for
1-Ripening the cervix prior to surgical evacuation of the uterus
2-Treatment of the unfavorable cervix before induction of labor at term
3-Ripen thc cervix for induction of second-trimester abortions

-It may be helpful when inducing the patient with an intrauterine fetal death beyond 28 weeks'
gestation, especially when the cervix is unfavorable for induction.

-Gastrointestinal side effects were minimal.

VII-INTRAFETAL PGF2 a
- A new route was recently in the elective termination of a hydropic fetus with a cystic hygroma
at 21 weeks' gestation, 40 mg of PGF2 a was injected into the cystic hygroma because there was
severe oligohydramnios.

VIII - ORAL PROSTAGLANDINS

- Both PGE2 and PGF2a, when administered orally, are effective in inducing uterine activity in
pregnant women and have been used to induce labor at or near term.

-Much larger doses are required to induce labor, gastrointestinal side effects, especially severe
diarrhea, make this route of administration unacceptable for use in the management of fetal
death.

2- Oxytocin

- To induce labor with oxytocin after 28 weeks gestational age.
- Oxytocin should be administered in lactated Ringer's solution rather than aqueous dextrose, to
avoid water intoxication due to the antidiuretic properties of oxytocin.
-If the cervix is unfavorable, pretreatment with either laminaria tents or PG gel
-If induction is initially unsuccessful, serial induction over 2 to 3 days may be effective.
FETAL DEATH IN MULTIPLE GESTATIONS

-It occurs in approximately 0.5 to 1.0 percent of twin gestations.
-It probably occurs more often in monochorial placentations.

RISKS
1-FETAL
-The surviving fetus may be exposed to the same factors that resulted in the death of the sibling as
maternal hypertension, diabetes, autoimmune disease, or intrauterine infection.

-Risk of intrauterine disseminated intravascular coagulation and the twin embolization
syndrome.[ renal cortical necrosis and cerebral necrosis, which might result in multicystic
encephalomalacia.]. Fortunately, this syndrome is uncommon, with an estimated risk of 0.5 percent.

MATERNAL
- Maternal intravascular coagulopathy.

EVALUATION
1-Ultrasound to determine if there is one common placenta or two separate placentas.
- If fetal sex is different, dizygocity and thus dichorionic placentation is assured.
- In monchorionic placentation , signs of twin embolization syndrome in the surviving twin should
be sought, such as ventriculomegaly, microcephaly, porencephaly, and renal cortical necrosis.

2-Weekly assays of fibrinogen, fibrin split products, prothrombin time, partial thromboplastin
time, and platelet count.

3- Intense fetal surveillance (e.g., twice weekly NST / biophysical profile)

MANAGEMENT

1- When occurs at or near term, treatment consists of
-Reversal of anticoagulation abnormalities with blood products
- Immediate uterine evacuation.

2- When occurs remote from term, the risks of prematurity of the living infant(s) may indicate
pregnancy prolongation , heparin therapy may be utilized

3- If a cause of death is not medically correctable, delivery of the survivor(s) should be undertaken.

4 - If a treatable maternal condition (e.g., maternal diabetes) exists, intensive fetal surveillance

5- In dichorionic placentation setting there is no risk for fetal DIC in the survivor

EMOTIONAL ASPECTS OF INTRAUTERINE DEATH

- The health care provider plays a significant role in assisting parents and families through the delivery
and postpartum period and even after the patient returns home .

- Subsequent pregnancies are often marked by strong anxiety and ambivalence.

Embryology of the Genital Tract

-The reproductive organs in the female consist of external genitalia, gonads, & internal duct system
between the two.

-The genital organs develop close to those of the urinary tract. Both arise in intermediate mesoderm
on each side of the root of the mesentery underneath the coelomic epithelium

-The pronephros, a few transient excretory tubules in the cervical region, appears first. These
tubules quickly degenerate, but its caudal end persists and open at the cloaca.

-Connection will ultimately be established between this duct and some of the tubules of the
mesonephros which soon appears and the duct is known as the mesonephric duct.

-The mesonephros, a second primitive kidney, develops as a long prominent swelling bulging into the
dorsal wall of the coelom in the thoracic and upper lumbar regions

ORIGIN OF THE MULLERIAN DUCTS

1-DEVELOPMENT OF THE UTERUS AND TUBES

-At the 4 th week after fertilization, the mullerian ducts first appear lateral to each wolffian duct as
invaginations of the dorsal coelomic epithelium.

-Each bud penetrates the mesenchyme lateral and parallel to each wolffian duct. As the solid buds
elongate, a lumen appears in the cranial part, beginning at each coelomic opening & it extend gradual
to the caudal growing tips of the ducts.

-At the 6 th week, the caudal end of each duct crosses the ventral aspect of the wolffian duct

-The paired ducts continue to grow in a medial and caudal direction until they meet in the midline and
become fused together in the urogenital septum

-At the 8 th week, the duct extends caudally until it reaches the urogenital sinus of the now subdivided
cloaca . The blind end of the duct projects into the posterior wall of the urogenital sinus as the
Mullerian tubercle

FATE
-The site of invaginations forms the fimbriated ends of the fallopian tubes
-The most cranial parts remain separate and form the fallopian tubes
-The cranial point of fusion is the site of the future fundus of the uterus
-The caudal segments fuse to form the uterus and part of the vagina
-During the 4th month, proliferation of mesenchyme around the fused portion of the ducts leads to the
development of the thick, muscular walls of the uterus and cervix.

-The origin of the endocervical mucosa is controversial
-Fluhmann postulated that the upward growth of the vaginal squamous epithelium, that he believed
was of sinus origin, extended into the endocervix with subsequent columnar transformation.
-Most authors favor a mullerian origin for the endocervical mucosa.

-In any discussion of the embryology of the cervix, mention should be made of the importance of
mesonephric remnants
-These structures are found as minute tubules or canaliculi in the lateral cervical wall
-They are lined with nonciliated simple columnar or cuboidal cells that have translucent cytoplasm
and large, round nuclei.

-Bizarre tumors, both benign and malignant, may arise from these remnants

2-DEVELOPMENT OF THE VAGINA
-The vagina is formed from the lower end of the uterovaginal canal and the urogenital sinus
-A solid vaginal cord results from proliferation of the cells at the caudal tip of the fused mullerian ducts
-The cord gradually elongates to meet the bilateral endodermal evaginations (sinovaginal bulbs)
-Sinovaginal bulbs extend cranially to fuse with the caudal end of the vaginal cord, forming vaginal
plate

-Subsequent canalization of the vaginal cord occurs, followed by epithelialization with cells derived
mostly from endoderm of the urogenital sinus
-The vagina develops under the influence of the mullerian ducts and estrogenic stimulation

THEORIES: The origin of stratified squamous epithelium, remains in dispute.
-Koff ( 1933) suggested that the lower 5th is derived from the urogenital sinus and the remainder from
the transformed mullerian epithelium

-Blumer (1957) proposed that the sinus and mullerian epithelium are histologicalty distinct and that the
vaginal epithelium is derived completely from sinus epithelium

-Forsberg, ( 1965) using histochemical methods, postulated a wolffian origin for the vaginal lining.

-Parlmey ( 1974) stated that only the upper 1/3 of the vagina is formed from the mullerian ducts and
that the lower vagina develops from the vaginal plate of the urogenital sinus

3-DEVELOPMENT OF THE GONADS

-The development of the human gonads has a triple origin from:
1. The coelomic epithelium of the genital ridge.
2. Underlying mesoderm.
3. Primitive germ cells which come from an extragonadal source.

DEVELOPMENT
Indifferent stage
-The gonad begins as a bulge on the medial aspect of the mesonephric ridge
-There is proliferation of the cells of the coelomic epithelium beneath which is a concentration of
mesenchymal cells.
-Cords of coelomic epithelium projects into the substance of the developing gonad, breaking up the
mesenchyme into loose strands interdigitating with these cords

-During these early stages large numbers of big, primitive germ cells can lying between the cords

-Gradually the germ cells become evident within the sex cords and the cells themselves are reduced in
size.
-The coelomic epithelium gives rise to the sex cords and the primitive mesenchymal tissue gives rise
to the supporting tissue between.

DIFFERENT stage
-The gonad that is to become an ovary passes from the indifferent stage into one of differentiation and
growth, and later, into the stage of follicle formation and stromal development

-By 8 weeks cords beneath the outer cellular layer increase greatly in size and are sometimes called
the secondary sex cords

-The epithelial cells of the secondary cords are called the pregranulosa cells that undergo active
proliferation and the germ cells becoming considerably reduced in size. This growth phase continues
until some 14 weeks

-The stage of follicle formation and stromal development follows. Fetal stromal cells develop from
the mesenchyme in the region of the ovarian hilum at first and gradually spread peripherally until they
permeate the whole ovary by 32-34 weeks

-In the absence of the developing stroma, oocytes become encapsulated by a ring of pregranulosa
cells
-Disintegration of oocytes that do not succeed in encircling themselves with a capsule of pregranulosa
cells

-Once the stroma has spread throughout the primitive ovary, the primary follicles develop a capsule
of stroma cells and the pregranulosa cells become granulosa cells. These cells secrete a fluid which is
first retained within the cell membrane, but ultimately accumulates in the follicular cavity

-The stroma cells of the follicular capsule differentiate into theca cells

The Origin of Ova

-It arise in the endoderm. Primitive germ cells in the epithelium of the yolk sac migrate along the
endoderm of the yolk sac into the duct, into the site of the primitive gonad

-The total population of germ cells reached a peak of 6, 800 000 at 5 months. By the time of birth the
number had fallen to 2 000 000 of which 50% were atretic

Development of External Genitalia

-The primitive cloaca is subdivided by a transverse septum into an anterior urogenital portion and
posterior rectal portion, begins at 4-5 weeks and is complete around 7 weeks

-On the external surface of the embryo, the genital tubercle forms a conical projection encircling the
anterior end of the cloacal membrane; the tubercle is present before cloacal division is complete

-A medial pair of eminences, the genital folds, and a lateral pair, the genital swellings, are then
formed by proliferation of mesoderm around the lower end of the urogenital sinus

-The bladder and urethra are formed entirely from that portion of the vesicourethral division of the
urogenital sinus above the Mullerian tubercle
-The pelvic and phallic divisions of the sinus lead to the formation of the vestibule
-The genital tubercle becomes the clitoris
-The genital folds remain separate as the labia minora and the genital swellings enlarge to become the
labia majora

CLASSIFICATION OF UTEROVAGINAL ANOMALIES

-The 1988 American Fertility Society (AFS) classification of uterovaginal anomalies comprises 4 groups

CLASS I . DYSGENESIS OF THE MULLERIAN DUCTS
CLASS II. DISORDERS OF VERTICAL FUSION OF THE MULLERIAN DUCTS
CLASS III. DISORDERS OF LATERAL FUSION OF THE MULLERIAN DUCTS
CLASS IV. UNUSUAL CONFIGURATIONS OF VERTICAL-LATERAL FUSION DEFECTS

Class I. Dysgenesis of the Mullerian Ducts
-It includes agenesis of the uterus and vagina (the Mayer-Rokitansky-Kuster-Hauser syndrome)

Class II. Disorders of Vertical Fusion of the Mullerian Duct

-Due to faults in the junction between the mullerian tubercles & the urogenital sinus.
-They include:
-Transverse vaginal septum: classified as either
obstructed or
unobstructed
-Cervical agenesis or dysgenesis
Class III. Disorders of Lateral Fusion of the Mullerian Ducts

-They can be:
Symmetric-unobstructed as with the double vagina, or
Asymmetric-obstructed, as with unilateral vaginal obstruction it almost invariably are associated
with absence of the ipsilateral kidney

A-Asymmetric-obstructed with unilateral vaginal obstruction it is associated with absence of the
ipsilateral kidney
1. Unicornuate uterus with a noncommunicating rudimentary horn
2. Unilateral obstruction of a cavity of a double uterus
3. Unilateral vaginal obstruction associated with double uterus
B-Symmetric-unobstructed

1. Didelphic uterus
a. Complete longitudinal vaginal septum
b. Partial longitudinal vaginal septum
c. No longitudinal vaginal septum
2. Septate uterus

a. Complete
I) Complete longitudinal vaginal septum
2) Partial longitudinal vaginal septum
3) No longitudinal vaginal septum

b. Partial
l ) Complete longitudinal vaginal septum
2) Partial longitudinal vaginal septum
3) No longitudinal vaginal septum
3. Bicornuate uterus
a. Complete
1) Complete longitudinal vaginal septum
2) Partial longitudinal vaginal septum
3) No longitudinal vaginal septum
b. Partial
1) Complete longitudinal vaginal septum
2) Partial longitudinal vaginal septum
3) No longitudinal vaginal septum

4. T-shaped uterine cavity (diethylstilbestrol related)

5. Unicornuate uterus

a. With a rudimentary horn
1) With endometrial cavity
a) Communicating
b) Noncommunicating
2) Without endometrial cavity
b. Without a rudimentary horn
Class IV. Unusual Configurations of Vertical-Lateral Fusion Defects
-This includes combinations of uterovaginal anomalies and other disorders
-Unusual configurations of vertical-lateral fusion defects can be seen with abnormalities of the lower
urinary tract.
AMERICAN FERTILITY SOCIETY CLASSIFICATION OF MULLERIAN ANOMALIES
Classification Anomaly

Class I Segmental, mullerian agenesis-hypoplasia
A. Vaginal
B. Cervical
C. Fundal
D. Tubal
E. Combined anomalies

Class II Unicornuate
A. Communicating
B. Noncommunicating
C. No cavity
D. No horn

Class III Didelphus

Class IV Bicoruate
A. Complete (division down to internal os)
B. Partial

Class V Septate
A. Complete (septum to internal os)
B. Partial
Class Vl Arcuate

Class Vll DES related

DISORDERS OF VERTICAL FUSION
I-TRANSVERSE VAGINAL SEPTUM

-Incidences vary from 1 in 2000 to 1 in 70,000
-It is due to incomplete fusion between the mullerian duct & the urogenital sinus
-It varies in thickness and can be located at any Ievel in the vagina
-46 % occur in the upper vagina, 40% in the midvagina, and 14% in the lower vagina
-It is associated with few urologic anomalies
-There may be associated congenital anomalies as urinary tract anomalies, coarctation of the aorta,
ASD, and malformations of the lumbar spine

-The lower surface of the septum is covered by squamous epithelium. The upper surface is covered by
glandular epithelium, which is transformed into squamous epithelium by a metaplasia after correction
of the obstruction
CLINICAL PICTURE
@-In neonates & young adults

-Hydrocolpos develops in the upper vagina & creates a large pelvic and lower abdominal mass
-It displaces the bladder anteriorly & the ureters laterally leading to hydroureters & hydronephrosis,
compresses the rectum and indirectly compress the vena cava and produce cardiorespiratory
failure
-The septum should be removed through a perineal approach

@-In adults
-Hematocolpos develop, symptoms include severe cyclic lower abdominal pain, no visible
menstrual discharge if the septum is complete
-Central lower abdominal and pelvic mass
-A septum large enough to allow pregnancy to occur can cause dystocia during labor
-Pelvic examination per rectum revealed a cervix and a normal-sized corpus

Surgical Technique for a Transverse vaginal Septum
-Transverse incision is made through the vault of the short vagina
-A probe is introduced through the septum after a portion of the barrier has been separated by sharp
and blunt dissection.
-Palpation of a urethral catheter anteriorly and insertion of a double-gloved finger along the anterior wall
of the rectum posteriorly so that the bladder and rectum can be avoided during this procedure

-A soft foam rubber vaginal form covered with a sterile latex sheath can be placed in the vagina and
removed in 10 days, it can be worn for 4 to 6 weeks until complete healing occurred

HIGH TRANSVERSE VAGINAL SEPTUM
-A space is created between the rectum and bladder to permit identification of the obstructed vagina
-A probe is passed through the fundus of the uterus to tent out the vaginal septum and enable the
surgeon to excise it from below and resect it safely.
-The operator can probe the mass with an aspirating needle to identify old menstrual blood.
-The upper vagina is then opened and the septum excised

-If the distance between the septum and the upper vagina is too great an indwelling acrylic resin form
consisting of a bulbous end and a channel through which menstrual blood can drain is placed into th
vagina
-Vaginal dilatation daily for 2 to 4 months to prevent contracture
-An alternative may be a split-thickness graft to bridge the gap

-Hurst and Rock described aspiration of the hematocolpos under ultrasound guidance to relieve the
acute pain and delay surgery
-Or continuous OCs to delay recurrence of hematocolpos.

II-CONGENITAL ABSENCE OR DYSGENESIS OF THE CERVIX
-It is an infrequent anomaly, it is often in association with absence of a portion or all of the vagina
-Retention of menstrual blood initiates symptoms of cyclic lower abdominal pain
-Diagnosis
-Ultrasonography
-Magnetic resonance imaging

-Anatomic Variations of Congenital Cervical Anomalies
I-Cervical aplasia (lack a uterine cervix)
II-Cervical dysgenesis, can be described as 4 subtypes:
1. Intact cervical body with obstruction of the cervical os
2. Cervical body consisting of a fibrous band of variable length and
3. Stricture of the midportion of the cervix
4. Fragmentation of the cervix

-Associated anomalies of the urinary tract are rare
-Variable portions of the vagina can be atretic
-Cervical obstruction is most often associated with a vagina of normal length.

Treatment
-Many authors recommend hysterectomy as an initial procedure for a patient with a functioning
uterine corpus and congenital absence of the cervix and vagina
-Hysterectomy can eliminate problems such as cryptomenorrhea, sepsis, endometriosis, and multiple
operations. It may be possible to conserve the ovaries
-Vaginoplasty with a split-thickness graft

III-DISORDES OF LATERAL FUSION
-Failures of lateral fusion of the two mullerian ducts cause vaginal anomalies that are grouped as
obstructed or unobstructed.

The Unobstructed Double Uterus (Bicornuate, Septate, or Didelphic Uterus)

-Complete failure of medial fusion of the two mullerian ducts can result in complete duplication of the
vagina, cervix, and uterus
-Partial failure of fusion can result in a single vagina with a single or duplicate cervix and complete or
partial duplication of the uterine corpus

Historical Development of Surgical Procedures

-Ruge, in 1882, first reported excision of a uterine septum in a woman who had suffered two pregnancy
losses
-Paul Strassmann of Berlin and later Erwin Strassmann, his son, began studies in 1936 & reported
in 1953

Diagnosis of Uterine Anomalies
-Presence of abnormal uterine contour during pregnancy, caused by a combination of fetal
malpresentation and an anomalous uterus
I -Ultrasonography, hysterography, or laparoscopy
-Hystcrosalpingography
-It must be taken at right angles to the axis of the uterus
-It is best done under fluoroscopy
-Double‑contour pelvic pneumoperitoneum‑hysterography
-IVP

Uterine Anomalies and Reproductive Faiture
-The etiology remains unclear
-Presence of a uterine septum can lead to abortion because of diminished intrauterine space for fetal
growth or because of implantation of the placenta on a poorly vascularized septum.
-Associated cervical incompetence, LPD, and distortion of the uterine milieu

-The chance for a live born child increases with each pregnancy loss

THE DIDELPHIC UTERUS
-Diagnoses easily on routine pelvic examination by identification of two complete cervices and perhaps
also a longitudinal vaginal septum (75%)
-Patient with a longitudinal vaginal septum will usually, but not always, have a didelphic uterus
-The didelphic uterus is associated with the best possibility of a successful pregnancy (fetal
survival rate is 60% without metroplasty)

-There is some increase in perinatal mortality, premature birth, breech presentation, and CS
-It should not be considered an appropriate indication for metroplasty. Not only is this procedure
technically difficult, but it can result in cervical incompetence or cervical stenosis.

THE SEPTATE UTERUS
-Most patients evaluated for repeated abortion and found to have a septate uterus

-25% of patients have associated vaginal septum
-Fetal survival rates are higher after septate uterus repair than after other repairs. 95% became
pregnant postoperatively, and 77% delivered a liveborn child

-AFS class VA uterus (a double cervix and uterine cavity with a single fundus) can result from a
rotation abnormality during the descent of the mullerian ducts
The dextrorotating mullerian ducts overrotate In every patient with a complete septate uterus, the left
cervix is higher than the right
Uterine Anomalies and Menstrual Difficulties
-Dysmenorrhea & abnormal and heavy menstrual bleeding occur more frequently with any form of
double uterus and relieved after unification operations

-Dysmenorrhea and menorrhagia are inappropriate indications for uterine unification

Uterine Anomalies and Infertility

-Erwin Strassmann stated that primary infertility could be cured in 60% of patients with uterine anomaly
-Non uterine causes of infertility must be ruled out before metroplasty
-Even if no other cause of infertility, this may be an appropriate indication of metroplasty

Surgical Technique for Uterine Unification

1-TRANSCERVICAL LYSIS OF THE UTERINE SEPTUM
-The septum can be electrosurgically incised or resectoscope
-A regimen of danazol or a GnRh agonist for 2 months to reduce the amount of endometrium that can
obscure the surgeon's view during the procedure
-The septum is electrosurgically incised by the cutting loupe of the resectoscope
-If excessive bleeding, use of IU Foley catheter as tamponade & removed in 4-6 hour
-Allow pregnancy after 2-months
-Delivery may be vaginal

2-THE MODIFIED JONES METROPLASLY

-The abdomen is opened through a transverse incision
-To facilitate manipulation a traction suture is placed through the top of the septum
-No attempt is made to stain the uterine cavity with methylene blue
-Hypotensive anesthetic techniques in combination with the tourniquets will allow operation with
negligible blood loss.
-The uterine septum is surgically excised as a wedge. The incisions begin at the fundus of the uterus
usually within 1 cm, and sometimes even less, of the insertion of the fallopian tubes

-After the wedge is removed, the uterus is closed in three layers with interrupted stitches 2-0
nonreactive suture on an atraumatic tapered needle

-The inner layer of stitches must include 1/3 of the thickness of the myometrium, the knot is tied within
the endometrial cavity

-The sutures are placed anterior first and then posterior. After the first few stitches are placed , the
second layer is started to avoid tension
-The third layer of stitches in the serosa both anteriorly and posteriorly
-If a double cervix is present, the physician should not attempt to unify the cervix because an
incompetent cervical os will be the result

-Postoperative hysterogram films often show small dog‑ears that are left over tags from the original
bifid condition of the uterus. It do not seem to interfere with function

-Delay 4 to 6 months before attempt of pregnancy is advised

3-THE TOMPKINS PROCEDURE
-A single median incision divides the uterine corpus and septum in half.
-The incision is carried inferiorly until the endometrial cavity is reached.
-Each Iateral septal half is then incised to within 1 cm of the tubes.
-No septal tissue is removed. The myometrium is reapproximated

-Advantages of the Tompkins technique: it is simpler, it conserves all myometrial tissue and leaves
the uterotubal junction in a more normal & lateral position, and that it provides better results

NB Cases of broad uterine septum can benefit from the wedge metroplasty.
THE STRASSMANN MBTROPLASTY
-It is not easily adapted to the septate uterus, it is the procedure of choice for unification of the two
endometrial cavities of an externally divided uterus, both bicornuate and didelphic

-The rectovesical ligament is attached anteriorly to the bladder, folds over and is attached between
the uterine cornua, continues posteriorly in the cul‑de‑sac, and ends with its attachment to the anterior
wall of the sigmoid and rectum. This ligament must be removed before a unification procedure can be
performed

-Tourniquets are used
-The two uterine cornua are incised on their median sides along their longitudinal axes, deeply
elongated to expose the uterine cavities

-Inferiorly, the incision is carried far enough to join the two sides into a single endocervical canal. If it
appears that a deeper incision will compromise the competence of the cervix, then a double cervical
canal can be Ieft.

-The suture technique for joining the two sides is the same as for the modified Jones procedure.

-Uterine suspension can be performed if necessary
-Presacral neurectomy should be considered only in patients with severe midline dysmenorrhea.

-The cervix should be dilated for proper drainage from the uterine cavity

-Ringer lactate containing heparin and corticosteroid can be used for peritoneal lavage throughout the
procedure

Cervical Incompetence Associated With a Double Uterus
-When a patient with an anomalous uterus, becomes pregnant, she must be watched closely for
evidence of cervical incompetence

-Cervical cerclage is used mostly in patients with a partial bicornuate uterus

-The cervical incompetence, not the uterine anomaly, is the proper indication for cerclage in these
patients.

-Some reproductive losses from a uterine anomaly might be prevented by cerclage

-Delivery should be by CS if the cervix will cause dystocia as in a double or septate cervix

Mode of Delivery After Metroplasty

-The scar formed after unification is as strong as if not stronger than the scar formed after CS. why?
Endomyometritis is a common complication after CS but is not a complication of uterine unification
-Despite evidence that the uterine scar heals securely after unification operations, it is recommend
to perform elective cesarean section in all patients after abdominal metroplasty

DES Uterine Anomalies

-The T‑shaped uterus is the most commonly seen
-Cervical cerclage may be indicated in some patients.

UNICORNUATE UTERUS

-It can be present alone or with a rudimentary horn or bulb on the opposite side
-The rudimentary anlage (uterine muscle bundle or bulb) can communicate directly with the unicornuate
uterus.
-Most rudimentary horns are noncommunicating (90%)

Associated Anomalies
-Urinary tract anomalies are often associated with a unicornuate uterus
-On the side opposite the unicornuate uterus, there may be a horseshoe or a pelvic kidney or the
kidney may bd hypoplastic or absent.

-The orifice of the mullerian duct develops at about the level of the fourth thoracic vertebra (T4) in
the embryo. The tip subsequently migrates along the course of the mullerian duct into the pelvis

-Malpositions of the ovary and tube occurs
Reproductive Performance
-The reproductive performance is similar to that of the didelphic uterus
-In cases of unicornuate uterus with a noncommunicating rudimentary uterine horn, there is danger of
pregnancy in the rudimentary horn from transperitoneal migration of sperm or ovum from the opposite
side

-Signs and symptoms of ectopic pregnancy will develop with rupture of the horn. Rupture is associated
with sudden and severe intraperitoneal hemorrhage and shock.
-Perform cerclage as indicated

LONGITUDINAL VAGINAL SEPTUM
-Failure of fusion of the lower miillerian ducts that form the vagina can result in a vagina with a
longitudinal septum
-The septum can be partial or complete
-In cases of didelphic uterus with a longitudinal vaginal septum, one uterine hemicorpus is usually
better developed than the other.

-The septum should be removed (when the patient is not pregnant) unless there is a contraindication.

B-ASYMMETRIC OBSTRUCTION OF THE UTERUS OR VAGINA
@-Unicornuate Uterus and Noncommunicating Uterine Anlage Containing Functional
Endometrium
-One mullerian duct develops normally, while the opposite mullerian duct fails to develop or develops
incompletely, then a relatively normal unicornuate uterus is found on one side and the cervix,
musculature, uterine cavity, endometrium, fallopian tube, blood supply, and ligamentous attachments
are absent or hypoplastic to a varying degree on the other side.

-If a rudimentary uterine horn does not communicate externally but have an endometrium-lined uterine
cavity, the symptoms of obstructed menstruation may begin soon after menarche and severe
dysmenorrhea will be present

-Diagnosis should be made as soon as possible, because retrogrrade menstruation and pelvic
endometriosis will develop
@-Unilateral Obstruction of a Cavity of a Double Uterus
-One cavity communicate with a cervix and the other did not. This could be an example of unilateral
failure of cervical development

-The patient complained of severe dysmenorrhea that appeared shortly after the menarche
-A tense, cystic mass was palpable in the right half of the pelvis
-The operation, described by Jones, consisted of making an incision through the anterior wall of the
cystic right portion of the uterus. The entire septum was excised and the uterus was reconstructed by
anastomosis of the two cavities.
@-Double Uterus With Obstructed Hemivagina and Ipsilateral Renal Agenesis
CLASS IV: UNUSUAL CONFIGURATIONS OF VERTICAL-LATERAL FUSION DEFECTS
-Mullcrian duct anomalies can occur in association with a variety of other problems

Ultrasound in obstetrics /DR. Alaa Mosbah , M.D OBS & GYN

- Obstetric ultrasound is the use of ultrasound scans in pregnancy. Since its introduction in the late I950's ultrasonography has become a very useful diagnostic tool in Obstetrics.
- Currently used equipments are known as real-time scanners, with which a continuous picture of the moving fetus can be depicted on a monitor screen. Very high frequency sound waves of between 3.5 to 7.0 megahertz (i.e. 3.5 to 7 million cycles per second) are generally used for this purpose. They are emitted from a transducer which is placed in contact with the maternal abdomen, and is moved to "look at" (likened to a light shined from a torch) any particular content of the uterus. Repetitive arrays of ultrasound beams scan the fetus in thin slices and are reflected back onto the same transducer. The information obtained from different reflections are recomposed back into a picture on the monitor screen (a sonogram, or ultrasonogram). Movements such as fetal heart beat and malformations in the fetus can be assessed and measurements can be made accurately on the images displayed on the screen. Such measurements form the cornerstone in the assessment of gestational age, size and growth in the fetus.

The main uses of ultrasonography are in the following areas:
1- Diagnosis and assessment of early pregnancy:
The gestational sac can be visualized as early as four and a half weeks of gestation and the yolk sac at about five weeks. The embryo can be observed and measured by about five and a half weeks.

2- Threatened miscarriage.
The viability of the fetus can be documented in the presence of vaginal bleeding in early pregnancy. A visible heartbeat could be seen and detectable by pulsed Doppler ultrasound at 6 weeks and is usually clearly visible by 7 weeks. If this is observed, the probability of a continued pregnancy is greater than 83 percent. Missed abortion and blighted ovum will usually give typical pictures of a deformed gestational sac and absence of fetal poles or heart beat. Ultrasonography is also useful in the early diagnosis of ectopic pregnancies and molar pregnancies.

3- Determination of gestational age and assessment of fetal size
Fetal body measurements reflect the gestational age of the fetus. This is particularly true in early gestation. In patients with uncertain last menstrual periods, such measurements must be made as early as possible in pregnancy to arrive at a correct dating for the patient. In the latter part of pregnancy measuring body parameters will allow assessment of the size and growth of the fetus and will greatly assist in the diagnosis and management of intrauterine growth retardation (IUGR).

The following measurements are usually made:
a) The Crown-rump length (CRL)
This measurement can be made between 7 to 13 weeks and gives very accurate estimation of the gestational age. Dating with the CRL can be within 3-4 days of the last menstrual period.
b) The Biparietal diameter (BPD)
The diameter between the 2 sides of the head. This is measured after 13 weeks. It increases from about 2.4 cm at 13 weeks to about 9.5 cm at term. Different babies of the same weight can have different head size, therefore dating in the later part of pregnancy is generally considered unreliable.
c) The Femur length (FL)
Measures the longest bone in the body and reflects the longitudinal growth of the fetus. Its usefulness is similar to the BPD. It increases from about 1.5 cm at 14 weeks to about 7.8 cm at term.
d) The Abdominal circumference (AC)
The single most important measurement to make in late pregnancy. It reflects more of fetal size and weight rather than age. Serial measurements are useful in monitoring growth of the fetus.

4- Placental localization.
Ultrasonography has become indispensible in the diagnosis or exclusion of placenta praevia, and other placental abnormalities as in diabetes, fetal hydrops, Rh isoimmunization and severe intrauterine growth retardation.
5- Multiple pregnancies.
In this situation, ultrasonography is valuable in determining the number of fetuses, the chorionicity, fetal presentations, evidence of growth retardation and fetal anomaly, the presence of placenta praevia, and any suggestion of twin-to-twin transfusion.
6- Hydramnios and oligohydramnios.
Excessive or decreased amount of liquor (amniotic fluid) can be clearly depicted by ultrasound. In both these situations, careful ultrasound examination should be made to exclude intrauterine growth retardation and congenital malformation in the fetus such as intestinal atresia, hydrops fetalis or renal dysplasia.
7- Fetal malformation.
Many structural abnormalities in the fetus can be reliably diagnosed by an ultrasound scan, and these can usually be made before 20 weeks. Common examples include hydrocephalus, anencephaly, myelomeningocoele, achondroplasia and other dwarfism, spina bifida, exomphalos, Gastroschisis, duodenal atresia and fetal hydrops. With more recent equipment, conditions such as cleft lips/ palate and congenital cardiac abnormalities are more readily diagnosed and at an earlier gestational age.
First trimester ultrasonic 'soft' markers for chromosomal abnormalities such as the absence of fetal nasal bone, an increased fetal nuchal translucency (the area at the back of the neck) are now in common use to enable detection of Down syndrome fetuses. Ultrasound can also assist in other diagnostic procedures in prenatal diagnosis such as amniocentesis, chorionic villus sampling, cordocentesis (percutaneous umbilical blood sampling) and in fetal therapy.

8- Other areas.
Ultrasonography is of great value in other obstetric conditions such as:
a) confirmation of intrauterine death.
b) confirmation of fetal presentation in uncertain cases.
d) evaluating fetal movements, tone and breathing in the Biophysical Profile.
d) diagnosis of uterine and pelvic abnormalities during pregnancy e.g. fibromyomata and ovarian cyst.

Transvaginal Scans
With specially designed probes, ultrasound scanning can be done with the probe placed in the vagina of the patient. This method usually provides better images (and therefore more information) in patients who are obese and/ or in the early stages of pregnancy. The better images are the result of the scan head's closer proximity to the uterus and the higher frequency used in the transducer array resulting in higher resolving power, Fetal cardiac pulsation can be clearly observed as early as 6 weeks of gestation. Vaginal scans are also becoming indispensable in the early diagnosis of ectopic pregnancies. An increasing number of fetal abnormalities are also being diagnosed in the first trimester using the vaginal scan. Transvaginal scans are also useful in the second trimester in the diagnosis of congenital anomalies.

Doppler Ultrasound
The doppler shift principle has been used for a long time in fetal heart rate detectors. Further developments in doppler ultrasound technology in recent years have enabled a great expansion in it's application in Obstetrics, particularly in the area of assessing and monitoring the well-being of the fetus, and the diagnosis of cardiac malformations. Doppler ultrasound is presently most widely employed in the detection of fetal cardiac pulsations and pulsations in the various fetal blood vessels. Doppler examinations can be performed abdominally and via the transvaginal route. The power emitted by a doppler device is generally greater than that used in a conventional 2-D scan.

3-D Ultrasound
The scan requires special probes and software to accumulate and render the images, and the rendering time has been reduced from minutes to seconds. A good 3D image is often very impressive. Volumetric measurements are more accurate. Present evidence has already suggested that smaller defects such as spina bifida, cleft lips/palate, and polydactyl may be more lucidly demonstrated. Other more subtle features such as low-set ears, facial dysmorphia or clubbing of feet can be better assessed, leading to more effective diagnosis of chromosomal abnormalities. The study of fetal cardiac malformations is also receiving attention. The ability to obtain a good 3D picture is nevertheless still very much dependent on operator skill, the amount of liquor (amniotic fluid) around the fetus, it's position and the degree of maternal obesity, so that a good image is not always readily obtainable.

The Schedule of scanning
There is no hard and fast rule as to the number of scans a woman should have during her pregnancy. A scan is ordered when an abnormality is suspected on clinical grounds. Otherwise a scan is generally booked at about 7 weeks to confirm pregnancy, exclude
ectopic or molar pregnancies, confirm cardiac pulsation and measure the crown-rump length for dating. A second scan is performed at 18 to 20 weeks to look for congenital malformations, exclude multiple pregnancies and to verify dates and growth. Placental position is also determined.

Safety of ultrasound
Harmful effects in cells of experimental animals or humans have not been demonstrated in the large amount of studies that have so far appeared in the medical literature due to the use of diagnostic ultrasound in the clinical setting. Apparent ill-effects such as low birth weight, speech and hearing problems, brain damage and non-right-handedness reported in small studies have not been confirmed or substantiated in larger studies from Europe. The greatest risks arising from the use of ultrasound are the possible over- and under- diagnosis brought about by inadequately trained staff, often working in relative isolation and using poor equipment.

ACOG Guidelines on Antepartum Fetal Surveillance

Techniques of Antepartum Fetal Surveillance
Several techniques for antepartum fetal surveillance currently in use are discussed in the ACOG bulletin. These include fetal movement assessment, nonstress test, contraction stress test, fetal biophysical profile, modified biophysical profile and umbilical artery Doppler velocimetry.
FETAL MOVEMENT ASSESSMENT
Fetal movement assessment occurs when the mother perceives a diminution in fetal movement. The mother counts fetal "kicks" as a means of antepartum fetal surveillance. The optimal number of movements and the ideal duration for counting movements have not been determined; however, numerous protocols have been reported and appear to be acceptable.
CONTRACTION STRESS TEST
The contraction stress test is based on the response of the fetal heart rate to uterine contractions. It is believed that fetal oxygenation will be transiently worsened by uterine contractions. In the fetus with suboptimal oxygenation, the resulting intermittent worsening in oxygenation will, in turn, lead to the fetal heart rate pattern of late decelerations. Uterine contractions also may provoke or accentuate a pattern of variable decelerations caused by fetal umbilical cord compression, which in some cases is associated with oligohydramnios.
The contraction stress test is interpreted by the presence or absence of late fetal heart rate decelerations, which are defined as decelerations that reach their nadir after the peak of the contraction and that usually persist beyond the end of the contraction. The results of the contraction stress test are categorized in the ACOG bulletin as follows:
* Negative. No late or significant variable decelerations.
* Positive. Late decelerations following 50 percent or more of contractions (even if the contraction frequency is fewer than three in 10 minutes).
* Equivocal-suspicious. Intermittent late decelerations or significant variable decelerations.
* Equivocal-hyperstimulatory. Fetal heart rate decelerations that occur in the presence of contractions that are more frequent than every two minutes or last longer than 90 seconds.
* Unsatisfactory. Fewer than three contractions in 10 minutes or a tracing that is not interpretable.
Relative contraindications to the contraction stress test usually include conditions that are associated with an increased risk of preterm labor and delivery, uterine rupture or uterine bleeding. According to ACOG, these conditions include the following:
* Preterm labor or certain patients at high risk of preterm labor.
* Preterm membrane rupture.
* History of extensive uterine surgery or classic cesarean delivery.
* Known placenta previa.
NONSTRESS TEST
In the nonstress test, the heart rate of the fetus that is not acidotic or neurologically depressed will temporarily accelerate with fetal movement. Heart rate reactivity is believed to be a good indicator of normal fetal autonomic function. Loss of reactivity is commonly associated with a fetal sleep cycle but may result from any cause of central nervous system depression, including fetal acidosis.
Results of nonstress tests are classified as reactive or nonreactive. Various definitions of reactivity have been used. Most commonly, the nonstress test is considered reactive, or normal, if there are two or more fetal heart rate accelerations within a 20-minute period, with or without fetal movement discernible by the woman, according to ACOG. The nonreactive stress test lacks sufficient fetal heart rate accelerations over a 40-minute period. The nonstress test of the neurologically healthy preterm fetus is frequently nonreactive--from 24 to 28 weeks of gestation, up to 50 percent of nonstress tests may not be reactive, and from 28 to 32 weeks of gestation, 15 percent of nonstress tests are not reactive.
BIOPHYSICAL PROFILE
The biophysical profile discussed in the ACOG bulletin is a nonstress test plus four observations made by real-time ultrasonography. The five components of the biophysical profile are as follows: (1) nonstress test; (2) fetal breathing movements (one or more episodes of rhythmic fetal breathing movements of 30 seconds or more within 30 minutes); (3) fetal movement (three or more discrete body or limb movements within 30 minutes); (4) fetal tone (one or more episodes of extension of a fetal extremity with return to flexion, or opening or closing of a hand; and (5) determination of the amniotic fluid volume (a single vertical pocket of amniotic fluid exceeding 2 cm is considered evidence of adequate amniotic fluid).
Each of the components is given a score of 2 (normal or present as defined previously) or 0 (abnormal, absent or insufficient). A composite score of 8 or 10 is normal, a score of 6 is equivocal and a score of 4 or less is abnormal. In the presence of oligohydramnios, further evaluation is warranted regardless of the composite score.
MODIFIED BIOPHYSICAL PROFILE
During the late second or third trimester, amniotic fluid reflects fetal urine production. Placental dysfunction may cause diminished fetal renal perfusion, which can lead to oligohydramnios. Therefore, assessment of amniotic fluid volume can be used to evaluate long-term uteroplacental function. This led to the development of the modified biophysical profile.
The modified biophysical profile combines the nonstress test with the amniotic fluid index, which is the sum of measurements of the deepest cord-free amniotic fluid pocket in each of the abdominal quadrants, as an indicator of long-term function of the placenta. An amniotic fluid index of more than 5 cm is thought to be an adequate volume of amniotic fluid. The modified biophysical profile is considered normal if the nonstress test is reactive and the amniotic fluid index is greater than 5 cm and abnormal if the nonstress test is nonreactive or the amniotic fluid index is 5 cm or less.
UMBILICAL ARTERY DOPPLER VELOCIMETRY
Doppler ultrasonography is used to assess the hemodynamic components of vascular impedence. Umbilical artery Doppler flow velocimetry has been adapted as a fetal surveillance technique because it is believed that flow velocity waveforms in the umbilical artery of fetuses with normal growth differ from those of fetuses with growth restriction. The umbilical flow velocity waveform of a normally growing fetus has high-velocity diastolic flow, while in cases of intrauterine growth restriction, the umbilical artery diastolic flow is diminished. With extreme intrauterine growth restriction, the flow may be absent or even reversed. There is a high perinatal mortality rate among such pregnancies.
Indications for Antepartum Fetal Surveillance
The results of antepartum fetal surveillance have not definitively demonstrated improved perinatal outcome. Therefore, all indications for antepartum testing should be considered somewhat relative. Usually, antepartum fetal surveillance is used in pregnancies with a high risk of antepartum fetal death. Some of the conditions in which testing is appropriate include the following:
* Maternal conditions: antiphospholipid syndrome, poorly controlled hyperthyroidism, hemoglobinopathies such as hemoglobin SS, SC or S-thalassemia, cyanotic heart disease, systemic lupus erythematosus, chronic renal disease, type 1 diabetes mellitus and hypertensive disorders.
* Pregnancy-related conditions: pregnancy-induced hypertension, decreased fetal movement, oligohydramnios, polyhydramnios, intrauterine growth restriction, post-term pregnancy, moderate to severe isoimmunization, previous fetal demise (unexplained or recurrent risk) and multiple gestation with significant growth discrepancy.
Recommendations
The following ACOG recommendations are based on limited or inconsistent scientific evidence (Level B):
* Women at high risk for stillbirth should undergo antepartum fetal surveillance using the nonstress test, contraction stress test, biophysical profile or modified biophysical profile.
* Initiation of testing at 32 to 34 weeks of gestation is appropriate for most pregnancies that are at increased risk of stillbirth. In pregnancies with multiple or particularly worrisome high-risk conditions, testing may be initiated as early as 26 to 28 weeks of gestation.
* When the clinical condition that prompted testing persists, a reassuring test should be repeated weekly or, depending on the test used and the presence of certain high-risk conditions, twice weekly until delivery. Any significant deterioration in fetal activity requires fetal reevaluation, regardless of the amount of time that has elapsed since the last test.
* An abnormal nonstress test or modified biophysical profile usually should be further evaluated by a contraction stress test or a full biophysical profile. Subsequent management should then be predicated on the results of the contraction stress test or biophysical profile, the gestational age, the degree of oligohydramnios (if assessed) and the maternal condition.
* Oligohydramnios, defined as no ultrasonographically measurable vertical pocket of amniotic fluid greater than 2 cm or an amniotic fluid index of 5 cm or less, requires (depending on the degree of oligohydramnios, the gestational age and the maternal clinical condition) delivery, or close maternal or fetal surveillance.
* In the absence of obstetric contraindications, delivery of the fetus with an abnormal test result often may be attempted by induction of labor with continuous monitoring of the fetal heart rate and contractions. If repetitive late decelerations are observed, cesarean delivery generally is indicated.
* Recent, normal antepartum fetal test results should not preclude the use of intrapartum fetal monitoring.
* Umbilical artery Doppler velocimetry seems to benefit only pregnancies complicated by intrauterine growth restriction. If used in this setting, decisions regarding timing of delivery should be made using a combination of information from the Doppler ultrasonography and other tests of fetal well-being, along with careful monitoring of maternal status.
* Middle cerebral artery Doppler velocimetry should be considered an investigational approach to antepartum fetal surveillance.

Amniotic Fluid Meconium

Meconium is derived from the Greek mekonion a word for poppy juice or opium

FORMATION AND COMPOSITION OF MECONIUM
-Meconium is first identified in the fetal intestine at approximately 70- 85 days' gestation

-It is composed mainly of water (72- 80%) & bile acids

MECONIUM IN AMNIOTIC FLUID
-The degree of tissue stain with meonium depends on (I) meconium concentrations (2) length of exposure
(3) the nature of the exposed tissues

-Vernix : stains yellow in 12 hours
-Finger nails stain yellow in ; 4-6 hours
-Surfrace staining of the placenta within 1 hour
-Umbilical cord staining after l hour with 5% meconium and at 15 minutes with 1% meconium
-Meconitum in pulmonary macrophages suggests antepartum aspiration

-Meconium have (1) Direct VC effects on umbilical vein due to bile acids
(2) Enhance the ability of amniotic funid to sustain bacterial growth

EFFECTS OF MECONIUM ON PULMONARY MATURITY TESTING

1-Meconium has a variable effect on L/S ratio ,it may interfer with phospholipid fraction and raising
the L/S ratio or it may increase sphingomyelin concentration due to cellular debris so decrease L/S

2-PG determination by immunologic method not affected by meconium

ULTRASONOGRAPHIC DETECTION OF MECONIUM-STAINED AMNIOTIC FLUID

1-A.F.appear echogenic or particulate.
2-Diagnosis of Fetal meconium peritonitis , it is a chemical inflammation of the peritoneum caused by
the escape of sterile meconium through a perforation in the bowel
The potential etiologic mechahisms include:
• Intestinal atresias
• Congenital bowel anomalies
. Volvulus
• Intussusception
• Cystic fibrosis

Diagnosis
• Increased echogenicity of the bowel
• Acoustic shaddowing suggesthlg calcifications
• Polyhydramnios
• Ascites
• Dilated intestinal loops filled with fluid
Amniocentesis to rule out chromosomal abnormalities ,cystic fibrosis and to check fetal lung maturity

THEORIES OF MECONIUM PASSAGE
1-Maturation Theory
-Because it is seldom passed before 34 weeks, its presence in amniotic fluid may reflect gastrointestinal
maturity in late gestation
-Transit time through the fetal small intestine decreases as gestation advances. In the 32-week fetus
transit time to the colon 9 hours compared with 4 .5 hours in the term fetus.
-Immaturity of intrinsic and extrinsic innervation of the bowel may impair the ability of the
premature fetus to pass meconium

2-Theory of Fetal Distress

-Meconium was released when the oxygen saturation of the umbilical vein was below 30 % , it is
passed in response to parasympathetic stirnulation during cord compression
-Amniotic fluid meconium was present more than twice as biophysical profile (BEP) score was
(6 or less) than normal .

3-Role of Intestinal Hormones
-Motilin is an intestinal polypeptide that stimulate motor function in the colonic smooth muscles . Mean
motilin levels in cord venous blood are high in term than in preterm infants. A fourfold inerease in
cord plasma motilin level in term infants with abnormal fetal heart rate.

-The relatinship between meconium passage and motilin may help to explain the passage of' meconium
in the preterm fetus

INCIDENCE, ASSOIATIONS, AND PERINATAL OUTCOME

I -Second-Trimester Passage of Meconium

-Discolored A. fluid is encoutered in approximately 2% of genetic amniocenteses .Perinatal outcome is
favorable in more than 90 % of patients. Most patients with stained fluid had clear fluid at the time of
delivery, indicating the transient nature
-The green -stained or brown - stained second-trimester amniotic fluid usually contains degraded blood
pigments rather than meconium and biochemical testing or spectrophotometric analysis.

II-Third-Trimester Passage of Meconium

-The incidence varies from 2 – 11 %. The management of' the high-risk patient is controversial , the
fetus shomd undergo additional antenatal evaluation if delivery is not imminent.

II-Intrapartum Meconium

-The incidence is between 7% - 22% , it approaches 40 % in post-term gestation
-Risks of perinatal morbidity and mortality, especially when accompanied by abnormal FHR patterns
as decreased baseline variability and f'ewer FHR accelerations.Late decelerations are not necessary
present .

-The relationship to low Apgar scores and acidosis remains controversial.

IV-MECONIUM CONSISTENCY

- Thick meconium is associated with a higher incidence of poor fetal outcome compared with thin
staining.
- Thick meconium is often deseribed as "pea-soup," particulate, viscous, and opaque, in contrast with
watery, translucent, lightly-stained thin meconium.
-"Early" passage of meconium (passed during or before the active phase of' labor) carried a greater risk
than "late" passage (passed during the second stage, after clear fluid had been noted).

-The presence of meconium per se does not imply fetal distress during labor unless other parameters
support such a contention. The most important clinical value of meconium-stained amniotic fluid is
to alert the obstetrician to look further for signs of fetal compromise. The obstetrician should initate
suction of the infant's oropharynx at delivery and the need to alert the pediatric staff

MECONIUM ASPIRATION SYNDROME AND ITS PREVENTION

-This term refers to the presence of meconium below the vocal cords and in the lungs. When amniotic
fluid contains meconium, meconium is found below the vocal cords in approximately one third of
neonates
- Fetal breathing (gasping in particular) is the mechanism by which meconium enters the lungs.
- It develops in 2 - 8% of infants delivered through meconium-stained amniotic fluid .
- In its mild form, it may present with neonatal tachypnea associated with normal pH and low Pco2,
resolying within 2-3 days.
-In its more severe form, the syndrome present as hypoxemia, acidosis, and respiratory failure within
minutes to hours after birth.

-The pathophysiology involve a combination of mechanical Obstruction and Chemical pneumonitis of
the small airways by particulate meconium inhaled at the time of the infant's first breath .
-Pulmonary vascular spasm lead to pulmonary hypertension and right-to-left shunting through the
patent foramen ovale or ductus arteriosus.
-Hypoxia may lead to convulsions, renal failure, DIC, and heart failure .
-The death rate is up to 40% in some studies.

DELEE AND TRACHEAL SUCTIONING

-Suctioning of the fetus immediately after delivery of the head and before delivery of the thorax, with
Selective tracheal intubation and suctioning
-Unfortunately, even the most vigorons suctioning before the first breath does not remove meconium
already aspirated into the lungs before birth

ASPHYXIA, PULMONARY ARTERY HYPERTROPHY, AND MECONIUM
Hypoxia, pulmonary hypertension anal ptrsistent fetal circulation are the hallmarks of MAS.AMNIOINFUSION FOR MECONIUM

-The amnioinfusion experienced a sixfold decrease in the incidence of meconium visualized below the
vocal cords.
-The benefit of amnioinfusion is not related to the meconium per se but, rather, to alleviating umbilical
cord compression and variahle fetal heart decelerations, thereby restoring normal fetal oxygenation

Amniotic fluid embolism

Definition :
It is an unpreventable and unpredictable complication of obstetrics characterized by :
. Acute postpartum hypoxia
. Haemodynamic collapse
. coagulopathy

Incidence :
Bet. 1 : 800 and 1 : 8000
It occur around the time of delivery but has been proposed to occur also after illegal abortion or transabdominal amniocentesis
The route of delivery does not appear to affect the risk of occurrence .

Pathophysiology :
The exact cause is unknown .
It is described as a biphasic process . Initially , profound haemodynamic and oxygenation alteration occur followed by the development of consumptive coagulopathy in 40% of cases .
It was thought that AFE is the result of passage of a large volume of amniotic fluid into the venous circulation to the right side of the heart and pulmonary vasculature, producing pulmonary hypertension , hypoxaemia and death .
More recently, it is suggested to be the result of immune mediated process similar to anaphylactic and septic shock . However the precise mechanism is not yet determined .

Clinical picture :
It was found that :
.70% of cases occurred during labour ( but before delivery ) and
.30% after delivery ( the majority within 5 minutes of delivery ). Several cases occurred during CS without prior labour .
.75% of cases occurred after rupture of membrane.
Signs and symptoms :

A) Cardiovascular :
. Hypotension
. Cardiopulmonary arrest
. Transient hypertension
B) Respiratory :
. pulmonary oedema
. Adult resp. distress syndrome
. Cyanosis
. Dyspnea
. Bronchospasm
. Cough
. Chest pain
C) Haematologic : coagulopathy
D) Uteroplacental - fetal :
. Atony
. Fetal distress
E) Other :
. Seizure
. Headache
N.B.: it was observed that a larger proportion of male fetuses is associated with this disorder .

Diagnosis :
The diagnosis of AFE is usually made on clinical grounds .
Diagnostic criteria suggested by Clark and Coworkers in 1995 are:
1- Acute hypotension or cardiac arrest
2-Acute hypoxia (defined as dyspnea , cyanosis or resp. arrest )
3- Coagulopathy ( defined as laboratory evidence of intravascular coagulation , fibrinolysis , or severe clinical hage in absence of other explanation )
4-Acute signs and symptoms have onset during labour , CS , dilatation and evacuation or within 30 min. postpartum .
5- Absence of any other significant confounding condition or potential explanation for signs and symptoms observed .

Differential diagnosis :
It should be noted that clinical manifestations of this syndrome are variable and all classic criteria may not be present .
Other clinical conditions should be excluded :
1- Septic shock
2- Acute myocardial infarction .
3- Aspiration pneumonia
4- Pulmonary embolism
5- Placental abruption
6- Anaesthetic accident
7- acute puerperal inversion

Investigations :
If the condition is suspected , immediate laboratory and radiographic evaluation :
1) Arterial blood gases to observe hypoxia , hypercarpia and acidosis
2) Complete blood count , blood type and cross match .
3) DIC profile ( platelets ,fibrinogen ,fibrin split products and prothrombin & partial thromboplastin time ) .
4) Chest radiography : usually non specific but in 70% of cases pul. oedema is evident
5) ECG : tachycardia , ST segment and T wave changes or right ventricular strain pattern .
Management :
The management is non specific and supportive
1- O2 administration by face mask or by +ve pressure through endotracheal tube .
2- Pulse oximetry is useful in continuous O2 saturation monitoring .
3- Cardiopulmonary resuscitation if cardiac arrest . If the patient suffers cardiac arrest and does not respond to resuscitative measures in the 1st several minutes , perimortem CS should be performed as soon as possible .
4- Care of the intake and output in cases of pulmonary oedema
5- Fruzemide to improve diuresis
6- Pulmonary artery catheterisation may provide help for patients who are clinically unstable
7- Haemodynamic support to treat hypotension using crystalloids or blood component therapy as indicated .
8- Pressor agents such as dopamine , norepinephrine and ephedrine to maintain B.P.
9- Inotropic support with digoxin should be considered in non hypoxic patient because of common occurrence of left ventricular failure
10- Corticosteroids may be helpful as the syndrome may be immune mediated . Hydrocortisone 500mg IV every 6 hours until the patient responds or expires
11- When coagulopathy occurs blood component therapy
Heparin should not be used in DIC secondary to AFE
12- Electronic fetal monitoring if the fetus is undelivered and of viable age.
13- If the baby is viable, the decision must be made whether to proceed with operative delivery
Prognosis :
* Maternal :
Mortality :
Is as high as 80% ( 60% of deaths usually occur at the time of cardiopulmonary arrest ) .
Morbidity :
. women who survived without experiencing cardiac arrest have a higher rate of normal neurologic outcomes than did those who survived cardiac arrest. Long standing sequlae of AFE include neurologic complications such as partial loss of vision and hemiplegia .
. Acute renal insufficiency occur secondary to hypotension or DIC
* Neonatal :
Neonatal survival is reported most recently as 80% with 50% of those surviving being neurologically intact. The shorter the arrest to delivery interval, the better is the rate of infant survival which shows the importance of proceeding promptly to delivery if after cardiac arrest, initial resuscitative measures are not successful within a few minutes.

laparoscopic management of ovarian cysts / DR. Alaa Mosbah ,M.D OBS & GYN

Laparotomy is favored than laparoscopy in the following conditions :

1.postmenopausal patients

2.family history of ovarian cancer

3.systemic symptoms {weight loss ,bowel obstruction,etc.}

4.abnormal endocrine function {e.g ., excess androgen or estrogen production}

5.ascites

6.sonographic evidence of papillations , thick septae ,solid mass or bilaterality in post menopausal

7.size of ovarian cyst more than 10 cm

8.serum CA-125 >35 u /ml in postmenopausal patients

Principles of laparoscopic management of ovarian cysts :

A.Before surgery :
1-select properly patients by history,age,menopausal status,sonographic appearance,and tumor markers.

2-thoroughly counsel patients regarding risks and complications,surgical experience and skill, and possible need for laparotomy

3-consider mechanical / antibiotic bowel preparation if G.I.T involvement is suspected .

B.At surgery :

1.examine pelvis and abdomen for tumor implants ,bowel adhesions or peritoneal excrescences.

2.obtain washings before commencing resection,particularly in postmenopausal patients

3.try to remove cyst intact and minimize spillage

4.if cyst is opened , examine lining

5.if cyst appears functional,or cant be removed ,always obtain a biopsy of cyst wall

6.enucleate or excise; don’t drain .

7.when in doubt , obtain a frozen section

DR. Alaa Mosbah

laparoscopy

The role of ultrasonography in the diagnosis of endometriosis

OBJECTIVE: to evaluate transvaginal ultrasound scanning as a diagnostic test for the accurate diagnosis of pelvic endometriosis . METHODS: This study was carried out on 250 women during the period from March 2003 through March 2005 .All patients had laparoscopy for infertility and/or chronic pelvic pain. Biopsies were performed on all suspected lesions when possible for histological examination. They underwent TVS within one week before laparoscopy . Ovarian endometriosis has been distinguished from non-ovarian endometriosis involving other pelvic organs. The sensitivity, specificity, predictive values and accuracy of TVS for predicting pelvic endometriosis were assessed. RESULTS: The sensitivity, specificity, PPV, NPV & diagnostic accuracy of TVS for the diagnosis of all pelvic endometriosis were 83.3, 92.2, 86.9, 89.8 and 88.8 % respectively . The sensitivity, specificity, PPV, NPV and diagnostic accuracy of TVS for the diagnosis of ovarian Endometriosis were 96.6, 99.5, 96.6, 99.5 and 99.2% respectively . The sensitivity, specificity, PPV, NPV and diagnostic accuracy of TVS for the diagnosis of nonovarian endometriosis were 77.2, 94.1, 82.2, 92.1, and 89.6 % respectively. The sensitivity, specificity and diagnostic accuracy of TVS for the diagnosis of endometriosis by detection of Thickening of the uterosacral ligaments , mass or nodule in douglas pouch , mass in rectovaginal space , fixed RVF uterus , free blood in douglas pouch , douglas pouch oblitration , mass or nodule in uterovesical pouch and adenomyosis were 75, 91.3 and 86.3 % ; 66.6 , 89.5 and 83.3 % ; 66.6, 96.6 and 93.9 % ; 63.6 , 92.7 and 87.8 % ; 54.5, 85.4 and 80.3 % ; 63.6, 89 and 84.8 %; 36.3, 89 and 80.3 %; 75, 75 and 75 % respectively . CONCLUSION: TVS accurately diagnoses ovarian endometriosis but is less accurate for the diagnosis of nonovarian endometriosis .Also , we found that TVS has a better accuracy in diagnosing rectovaginal septum involvement and uterosacral endometriosis than uterovesical pouch and douglas pouch endometriosis .

Technical Guidelines on Unaided Visual Inspection of the Cervix "Clinical Downstaging"

DEFINITION:
Downstaging for cervical cancer is defined as "the detection of the disease in an earlier, curable stage, in asymptomatic women, using a simple speculum for visual examination of the cervix".
HISTORICAL BACKGROUND:
This strategy was proposed by WHO in 1985, as an alternative approach in the developing countries where a meaningful coverage of all at risk women by cervical cytology would not be possible for decades to come.
It is important to recognise that earlier detection of cancer of the cervix was achieved in a number of developed countries prior to the introduction of cervical cytology screening. The evidence for this is indirect, but relates to data on downstaging of cancer of the cervix and reduction in mortality from the disease, from the historical records in Sweden and Canada. This downstaging arose not from a deliberate policy, but from programmes of public and professional education which made women and their health care providers aware of the symptoms and signs of the disease and its potential curability if detected early. These programmes therefore appeared to be successful of themselves, while also preparing the population for the successful introduction and acceptance of cervical cytology screening.
RATIONALE FOR CLINICAL DOWNSTAGING OF CANCER OF THE CERVIX:
Organised cytology screening is the mainstay of early detection of cervical cancer. Unfortunately in developing countries, where the load of the disease is heavy and the populations are virtually unscreened, nation-wide cytology screening programmes are not possible in fore-seeable future because of paucity of economic and manpower resources.
At present, in the developing countries, 80-85% of women with cervical cancer present to the treatment centres at advanced stages, when treatment no matter how sophisticated, fails to improve survival time. The objective of the "downstaging" approach is to improve the stage distribution of cervical cancer at the time of diagnosis with the aim of improving prognosis. Several pilot studies have proven that upto 50-70% of cases of cervical cancer can be detected on visual examination, not only overt cases but also some cases of CIN.
Though visual screening is a sub-optimal approach in comparison to the cytological screening, it is relevant in areas where there is a heavy load of prevalent cancer and screening by cytology is not yet feasible but adequate treatment facilities are available. Such a strategy is not expected to decrease the incidence of invasive cancer, but would decrease morbidity and mortality from the disease through early detection.
APPROACH TO CLINICAL DIAGNOSIS:
Approaches to visual screening currently being evaluated include;
1. Unaided visual inspection of the cervix, referred to as "Downstaging" by WHO. It involves looking at the cervix during a speculum examination to detect early stage cancer.
2. Unaided visual inspection of the acetic acid treated cervix:
Visual inspection of cervix treated with 3-5% acetic acid could serve as a "helpful supplement" in aiming to detect CIN.
3. Aided visual inspection of the acetic acid treated cervix:
This approach involves the use of a small, lightweight, low-powered (2-4X), monocular telescope to view acetic acid treated tissues. This technique is currently being evaluated in several Asian countries, but its sensitivity, specificity and any advantage that it confers in comparison with unaided visual inspection is yet to be determined.
4. Speculoscopy:
In this method an additional fluorescent light source aids in the detection of white lesions in acetic acid treated cervix. Information regarding its efficacy as a screening tool is limited.
5. Cervicography:
Cervicography involves the inspection, by trained personnel, of photographs of the cervix taken at the time of speculum examination. Its sensitivity and specificity in comparison with cervical cytology has not been established. Special cameras are required and special readers have to be available to assess the photographs.
HEALTH EDUCATION:
Health education is a pre-requisite of any screening programme. Adequate programmes of public and professional education to make them aware of the symptoms and signs of the disease and of its potential curability if detected early, should be organised to accompany, and preferably precede, introduction of the screening programme. This will encourage the women to willingly (voluntarily) join the screening programme, which will go a long way in improving patient compliance. On the other hand the health personnel involved should possess adequate knowledge about the disease to be able to anticipate a woman's worries and questions and be prepared to deal with them in a professional and reassuring manner.
WOMEN TO BE SCREENED:
As for cervical cytological screening, it is important that the age groups examined are those where the incidence of cervical cancer is high. The maximum age range can be considered to be 30-35 years and above.
PERSONNEL NEEDED FOR THE EXAMINATION:
Female primary health care workers should be employed to do the clinical examination. These health workers should be trained for a period of at least one-week, in the gynaecology department of a district hospital, on how to perform a speculum examination of the cervix. By the end of the training they should be well acquainted with the symptoms and signs of the disease and be able to distinguish a clinically normal cervix from a cervix with simple erosion or one with a suspected invasive cancer. They should also be trained on how to take a specimen for culture and a cervical smear for diagnostic purposes. During the training an adequate exposure of the health worker to women with clinically normal and abnormal findings will have to be ensured by the training gynaecologist. Some primary health care workers may already have performed speculum examinations of the cervix as part of family planning programme, however, such workers should still be specially trained to recognise the signs of invasive cervical cancer.
EQUIPMENT REQUIRED:
Visual examination should be preferably performed at the primary health clinics but if need be can be done at woman's residence, provided adequate facilities are available.
Examination table, preferably with stirrups.
Sterile speculae, preferably Cusco's.
Sterile rubber gloves
Source of light, a lamp or a torch.
Stationary.
THE EXAMINATION:
The procedure and the reason for it should be carefully explained to the woman to be examined and she should be made as comfortable as possible.
Privacy of the patient is important female relative or friend maybe of assistance in providing reassurance. Good visualisation of the cervix is essential, therefore adequate light is important.
Speculum should be lubricated with warm water only, prior to insertion.
Woman should not be using any intravaginal medication at the time of the examination.
The examination should not be performed during menstrual period.
REPORTING VISUAL INSPECTION FINDINGS:
Objective of the visual examination is solely, to be able to recognise clinically normal from abnormal cervix and refer abnormal looking cases for further evaluation and diagnosis.
All findings should be carefully recorded in the provided printed forms .
The gross appearance of the cervix should be classified into;
Normal
Abnormal
Suspicious of Malignancy
NORMAL CERVIX:
A normal cervix appears smooth, round, pink, lubricated with clear mucoid secretion and has a central hole the 'external os'. The shape of the external os varies with parity, being round in a nulliparous woman and slit like or cruciate in a multipara. Cervix in postmenopausal women appears atrophic.
ABNORMAL CERVIX:
This category will include all benign looking lesions, such as;
Hypertrophy
Redness or Congestion
Irregular surface
Distortion
Simple erosions (that do not bleed on touch)
Cervical polyps (with smooth surface)
Abnormal discharge (foul smelling, dirty/greenish, white/cheesy, blood stained)
Nabothian follicles
Prolapsed uterus
These appearances usually accompany following clinical conditions;
Infections
Ectopy (Erythroplasias)
Benign tumours
SUSPICIOUS OF MALIGNANCY:
Malignancy should be suspected when there is;
An erosion that bleeds on touch
A growth with an irregular surface
Both of these lesions may be friable and bleed on touch or may be accompanied with an offensive discharge.
FREQUENCY OF EXAMINATION:
For clinical diagnosis there are no data as yet to suggest an appropriate frequency of screening, though different intervals selected according to available resources in different projects may eventually provide guidance. Every two or three year planned examinations would be appropriate in the absence of an abnormality. The women should be advised to return to the clinic if symptoms develop between scheduled examinations.
REFERRAL PROTOCOL:
A woman with normal findings should be called back for a repeat examination after 2 or 3 years, according to the decided policy.
For women with abnormal findings but not suspected to have cervical cancer, a number of clinical conditions may be relevant, including infections. If necessary facilities are available a swab should be taken for culture at the time of examination and sent to the laboratory. The patient should be referred to the Primary Health Clinic for further evaluation and treatment by the physician.
Women suspected to have malignant lesions should be directly referred to the oncology centre for further assessment.
ASSESSMENT AND EVALUATION OF THE PROGRAMME:
In areas where downstaging programmes have been initiated every measure should be taken to assess the efficiency of the staff and evaluate effectiveness of the approach.
The staff of the gynaecology department at the oncology referral centre should make field visits to randomly examine the women already been examined by the Primary Health Care workers to assess false positive and false negative rates of visual inspection. Furthermore, the field staff should be given refresher course when and where possible.
With regards to the evaluation of effectiveness of the programme, it is important to remember that the programme should not be expected to have immediate impact on improving the stage distribution of cases in an area but only after it has been in operation for several years will it be possible to judge its effectiveness.
Thus it is advisable to base evaluation of the programme on the following measures:
SHORT TERM MEASURES:
Change in background knowledge of the target population. Two random sampling surveys should be performed. The first prior to the introduction of the health education campaign and the second, one year after the campaign has been completed.
Proportion of women in the target population screened. For this (as well as some of the other evaluation measures) it will be necessary to procure accurate estimates of the numbers of women in the target population.
Proportion of women screened found to be abnormal.
Proportion of women screened abnormal who attend for diagnosis and therapy.
Utilisation of treatment services and proportion of cases treated by surgery, radiotherapy and palliative care. It is to be expected that the proportion of cases that can only be treated by palliative care will diminish with time, and thus this can also be regarded as an additional long-term evaluation measure.
Rates of detection of CIN (by degree) and invasive cancer.
Determination of the economic costs of the programme.
LONG TERM MEASURES:
Change in stage distribution of invasive cancers. It is unlikely that a stage shift indicative of true effectiveness would be seen in less than three years and possibly would not be seen for five or more. Screening can be expected to bring to light disease that is detectable, but which has not yet been recognised because the symptoms are not intrusive this will increase the apparent incidence in the areas and indeed the stage distribution may shift as such disease is likely to have a better prognosis than disease that presents between screens or that with more severe symptoms.
Change in rate of advanced disease. This, if calculated on an annual basis, should begin to fall with effective programmes after about three to four years, if not before, for a highly effective programme with rapid and almost complete screening of the target population.
Change in mortality from the disease. With an effective programme, mortality from the disease will fall. This effect should be detectable within one or two years of a significant reduction in the rate of advanced disease.

Use of Anti-D Immunoglobulin for Rh Prophylaxis

This guideline should be read in conjunction with the National Institute for Clinical Excellence’s Technology Appraisal Guidance No 41 Guidance on the use of routine antenatal anti-D prophylaxis for RhD-negative women, May 2002.
1. Introduction
The development of anti-D antibodies generally results from fetomaternal haemorrhages (FMH) occurring in RhD negative women who carry an RhD positive fetus. Post-delivery immunoprophylaxis using anti-D Immunoglobulin (anti-D Ig) began in the UK in 1969. The programme has been an astounding success; deaths attributed to RhD alloimmunisation fell from 46/100,000 births before 1969 to 1.6/100,000 in 1990.
Guidelines on Rh immunoprophylaxis were updated in 1976, 19813 and 1991.4 However RhD alloimmunisation continues to occur. There is clear evidence that the 1991 guidelines are not being fully applied. However the most important cause of anti-D antibodies is now immunisation during pregnancy where there has been no overt sensitising event. Late immunisation during a first pregnancy is responsible for 18-27% of cases. Immunisation during a second or subsequent pregnancy probably accounts for a similar proportion of cases, although in this situation it is impossible to distinguish late sensitisation from failure of prophylaxis at the end of the preceding pregnancy.
The current recommendations are taken directly from the updated guidelines drawn up by a joint working group of the British Blood Transfusion Society and the Royal College of Obstetricians and Gynaecologists.
2. Test for the size of fetomaternal haemorrhage
Studies have shown that 99.2-99.3% of women have a FMH less than 4ml at delivery. Up to 50% of larger FMHs occur after normal deliveries. However, the following clinical circumstances are more likely to be associated with large FMH:
traumatic deliveries including caesarean section
manual removal of the placenta
stillbirths and intrauterine deaths
abdominal trauma during the third trimester
twin pregnancies (at delivery)
unexplained hydrops fetalis Tests to estimate the size of the FMH are recommended in many countries including the UK, the USA, Canada, France and Ireland, although not in most European countries. While the Kleihauer acid elution test which detects fetal haemoglobin (HbF) is the test usually undertaken in the UK and Canada, tests which specifically identify RhD positive red cells are used in the USA.
In some European countries (exceptions include the UK, France and Ireland), a standard postnatal dose of 1000-1500iu is used with no requirement for a routine Kleihauer test. Unfortunately, this policy does not take account of the fact that up to 0.3% of women have a FMH greater than 15ml which will not be covered by 1500iu of anti-D Ig. Hence, if the 1500iu dose is implemented without a test to quantitate FMH, over 200 women each year in the UK will receive less protection than they do now. The recommended policy in the UK is to obtain an anticoagulated blood sample as soon as possible (within two hours) after delivery and to undertake a Kleihauer screening test to identify women with a large FMH who need additional anti-D Ig (Grade B recommendation).
Flow cytometry offers an alternative technique for quantifying the size of FMH. It has a number of advantages in that results are more accurate and more reproducible than those from the Kleihauer test and that it detects RhD positive cells, making it particularly helpful in patients with high HbF levels. Not all hospitals will have ready access to a flow cytometer though several Blood Centres offer to estimate FMH. Flow cytometry is probably most effectively employed in those cases where a Kleihauer screening test indicates a large FMH which requires accurate quantitation and follow-up. The rosetting technique1 is a relatively simple serological method which offers another alternative for quantifying FMH of RhD positive red cells greater than 4ml.
3. Anti-D Ig preparations available in the UK
Until 1994, only anti-D Ig prepared from immune plasma donated by unpaid UK volunteer donors, either by the Bio Products Laboratory (BPL) or by the Scottish Protein Fractionation Centre (PFC) was available in the UK. Recently, imported anti-D Ig has been licensed in the UK. It should be noted that imported products may be prepared from plasma collected from paid donors within and outside the EC. The currently available preparations are:
BPL (Intramuscular)
PFC (Intramuscular)
250iu (50mcg)
500iu (100mcg)
2500iu (500mcg)
250iu (50mcg)
500iu ( 100mcg)
5000iu (1000mcg)
IMPORTED
Intramuscular 1250iu (250mcg) "Partobulin" from IMMUNO (licensed in the UK)
Intravenous 600iu (120mcg) or 1500iu (300mcg) from WINRHO (not licensed in the UK)
In view of the theoretical risk of nvCJD posed by UK plasma all anti-D produced by BPL and PFC is now manufactured from US plasma.
4. Administration
Intramuscular anti-D Ig is best given into the deltoid muscle as injections into the gluteal region often only reach the subcutaneous tissues and absorption may be delayed.
For successful immunoprophylaxis, anti-D Ig should be given as soon as possible after the sensitising event but always within 72 hours. If it is not given before 72 hours, every effort should still be made to administer the anti-D Ig, as a dose given within 9-10 days may provide some protection (Grade B recommendation). Women who are already sensitised should not be given anti-D Ig.
Women who have a weak expression of the RhD blood group (Du) do not form anti-D and do not therefore require prophylaxis. It should be noted that anti-D Ig does not protect against the development of other antibodies which can cause haemolytic disease of the newborn.
5. Prophylaxis following abortion
Some RhD negative women require anti-D Ig following abortion; 250iu before 20 weeks' gestation and 500iu thereafter. A test for the size of FMH should be performed when anti-D Ig is given after 20 weeks.
5.1 Therapeutic termination of pregnancy: Anti-D Ig should be given to all non-sensitised RhD negative women having a therapeutic termination of pregnancy, whether by surgical or medical methods, regardless of gestational age (Grade B recommendation).
5.2 Ectopic pregnancy: Anti-D Ig should be given to all non-sensitised RhD negative women who have an ectopic pregnancy (Grade B recommendation).
5.3 Spontaneous miscarriage: Anti-D Ig should be given to all non-sensitised RhD negative women who have a spontaneous complete or incomplete abortion after 12 weeks of pregnancy (Grade B recommendation). Published data on which to base recommendations in earlier miscarriages are scant. There is evidence that significant FMH only occurs after curettage to remove products of conception but does not occur after complete spontaneous miscarriages. Anti-D Ig should therefore be given when there has been an intervention to evacuate the uterus. On the other hand, the risk of immunisation by spontaneous miscarriage before 12 weeks' gestation is negligible when there has been no instrumentation to evacuate the products of conception and anti-D Ig is not required in these circumstances (Grade C recommendation).
5.4 Threatened miscarriage: Anti-D Ig should be given to all non-sensitised RhD negative women with a threatened miscarriage after 12 weeks of pregnancy. Where bleeding continues intermittently after 12 weeks' gestation, anti-D Ig should be given at 6-weekly intervals (Grade C recommendation). Evidence that women are sensitised after uterine bleeding in the first 12 weeks of pregnancy where the fetus is viable and the pregnancy continues is scant though there are very rare examples. Against this background, routine administration of anti-D Ig cannot be recommended. However it may be prudent to administer anti-D Ig where bleeding is heavy or repeated or where there is associated abdominal pain particularly if these events occur as gestation approaches 12 weeks (Grade C recommendation). The period of gestation should be confirmed by ultrasound.
6. Prophylaxis following sensitising events before delivery
Anti-D Ig should be given to all non-sensitised RhD negative women after the following potentially sensitising events during pregnancy:
invasive prenatal diagnosis (amniocentesis, chorion villus sampling, fetal blood sampling)
other intrauterine procedures (e.g. insertion of shunts, embryo reduction)
antepartum haemorrhage
external cephalic version of the fetus
closed abdominal injury
intrauterine death A dose of 250iu is recommended for prophylaxis following sensitising events up to 20 weeks of pregnancy. For all events after 20 weeks, at least 500iu anti-D Ig should be given followed by a test to identify FMH greater than 4ml red cells; additional anti-D Ig should be given as required (Grade B recommendation).
7. Postnatal prophylaxis
At least 500iu of anti-D Ig must be given to every non-sensitised RhD negative woman within 72 hours following the delivery of a RhD positive infant (Grade B recommendation). This includes women with alloantibodies other than anti-D. There is no universal policy regarding the postnatal dose which varies in different countries; 1500iu (300mcg) is the standard dose in the USA, 500-600iu (100-120 mcg) in Canada and 1000-1250iu (200-250mcg) in many European countries except the UK, Ireland and France. The MRC dosage trial showed that 500iu (100mcg) of anti-D Ig given intramuscularly, which is capable of suppressing immunisation by 4-5 ml of RhD positive red cells, was as effective as both 1500iu and 1000iu.
A test to detect FMH greater than 4ml must also be undertaken, so that additional anti-D Ig can be given as appropriate (Grade B recommendation).
Some women who have received anti-D Ig during pregnancy may have detectable anti-D in their blood at delivery. Because it may be difficult or impossible to distinguish between such passive anti-D Ig and weak anti-D resulting from early immunisation, anti-D Ig should be given to any eligible woman with weak anti-D antibody at delivery unless it has been clearly confirmed that she is already sensitised (Grade B recommendation).
8. Routine antenatal prophylaxis
9. Transfusion of RhD positive blood components
9.1 RhD positive platelet transfusions: It should usually be possible to provide RhD negative platelets for women of childbearing age who need a platelet transfusion. Occasionally, if an appropriate product is not available, it may be necessary to use RhD positive platelets. In these circumstances, prophylaxis against possible Rh alloimmunisation by red cells contaminating the platelet product should be given (Grade B recommendation).
Each unit of platelets prepared according to the UK Guidelines from one whole blood donation contains less than 1 X 109 (< 0.1ml rbc). 250iu (50mcg) anti-D Ig should be given following every three adult doses (i.e. derived from up to 18 routine donations) of platelets. Patients who have marked thrombocytopenia should be given the anti-D Ig subcutaneously to avoid the possibility of a haematoma following intramuscular injection.
9.2 Inadvertent transfusion of RhD positive blood: When less than 15ml of RhD positive blood have been transfused to a RhD negative woman capable of childbearing, the appropriate dose of anti-D Ig should be given (Grade B recommendation). When more than 15ml have been transfused, it is preferable to use the larger anti-D Ig IM preparation (2500iu or 5000iu). The dose should be calculated on the basis that 500iu of anti-D Ig will suppress immunisation by 4ml of RhD positive red blood cells (rbc) (Grade B recommendation).
When more than 2 units of RhD positive blood have been transfused, consideration should be given to undertaking an exchange transfusion to reduce the load of RhD positive red blood cells in the circulation and the dose of anti-D Ig required to suppress immunisation. In this situation, the patient should be counselled regarding the implications of both non-intervention (for future pregnancies) and of treatment, including any hazards from receiving donated blood, the exchange procedure itself and of larger doses of anti-D Ig including IV anti-D (Grade C recommendation).
Immediate exchange transfusion will reduce the load of RhD positive rbc (a one-blood-volume exchange will achieve a 65-70% reduction in RhD positive cells; a two-volume exchange 85-90%). Following exchange transfusion, the residual volume of RhD positive red cells should be estimated using flow cytometry or rosetting. Intravenous anti-D Ig is the preparation of choice, achieving adequate plasma levels immediately and being twice as effective microgram (mcg) for mcg as intramuscular anti-D at clearing rbc. The dose to be administered should assume that 500iu of anti-D Ig IV will suppress immunisation by 8-10 ml of fetal rbc. Intravenous anti-D Ig is available for use in the UK on a named patient basis only from WINRHO (Canada). Intramuscular anti-D Ig must not be given intravenously. An appropriate combined dose of intravenous and intramuscular anti-D Ig should be determined in discussion with a specialist in Transfusion Medicine. Follow-up tests for RhD positive rbc should be undertaken every 48 hours and further anti-D Ig given until all RhD positive red cells have been cleared from the circulation. Free anti-D in the patient's serum does not necessarily reflect adequate prophylaxis and anti-D Ig treatment should be continued until RhD positive rbc are no longer detectable.
Passive anti-D Ig given in large doses may be detectable for up to six months or more and tests for immune anti-D may not be conclusive for 9-12 months.
10. Conclusion and summary of recommendation
RhD immunisation continues to occur. In some cases this results from failure to adhere to previously published guidelines on RhD prophylaxis. However the most important cause of anti-D is now immunisation during pregnancy where there has been no overt sensitising event. This problem is not covered by previous guidelines.
The key recommendations of the current guidelines are as follows:
Following delivery, irrespective of the dose of anti-D Ig routinely administered, postnatal prophylaxis must include a screening test to identify women with a large FMH who need additional immunoglobulin (Grade B recommendation).
Anti-D Ig should be given after sensitising events before delivery and after abortion (Grade B recommendation).
Anti-D Ig is no longer necessary in women with threatened miscarriage with a viable fetus and cessation of bleeding before 12 weeks' gestation (Grade C recommendation).
At least 500iu of anti-D Ig should be given to non-sensitised RhD negative women at 28 weeks and 34 weeks of pregnancy according to NICE guidance (Grade A recommendation).

Postpartum hemorrhage - Key points

Postpartum hemorrhage - Key points

1-Postpartum hemorrhage is common problem in obstetrics (approximately 3% to 5% of obstetric patients) and can occur in patients without risk factors for hemorrhage (20% of cases).

2-Active management of the third stage of labor should be used routinely to reduce its incidence. Use of oxytocin after delivery of the anterior shoulder is the most important and effective component of this practice.

3-Oxytocin is more effective than misoprostol for prevention and treatment of uterine atony and has fewer adverse effects.

4-Routine episiotomy should be avoided to decrease blood loss and the risk of anal laceration.

5-Appropriate management of postpartum hemorrhage requires prompt diagnosis and treatment.

6-The Four T's mnemonic can be used to identify and address the four most common causes of postpartum hemorrhage:

a- Tone: uterine atony

b- Trauma: laceration, hematoma, inversion, rupture

c- Tissue: retained tissue or invasive placenta

d- Thrombin: coagulopathy

7-Rapid team-based care minimizes morbidity and mortality associated with postpartum hemorrhage.

8- Massive transfusion protocols allow for rapid and appropriate response to hemorrhages more than 1,500 mL of blood loss.

Prof. Alaa Mosbah

2019

U.S in Obstetrics

Second trimester pregnancy

Drugs & Pregnancy , DR. Alaa Mosbah M.D OBS & GYN

Antibiotics in Pregnancy

Class B: No risk in controlled animal studies
Antifungal Topical Agents
Amphotericin B
Nystatin (Mycostatin)
Terbinafine (Lamisil) - not in Briggs (1998)
Clotrimazole (Mycelex)
Antiparasitic agents
Metronidazole or Flagyl (after first Trimester)
Avoid single dose therapy
Praziquantel - not in Briggs
Permethrin (topical) - not in Briggs (1998)
Anti-Tuberculosis agents
Ethambutol
Didanosine - not in Briggs (1998)
Antiviral agents
Nelfinavir - not in Briggs (1998)
Ritonavir
Saquinavir
Famciclovir
Valacyclovir
Antibiotics
All Cephalosporin Antibiotics (except Moxalactam)
All Erythromycin except Erythromycin Estolate
Azithromycin (Zithromax)
All Penicillin Antibiotics
Clindamycin
Macrodantin (before third trimester)
Sulfa antibiotics (before third trimester)
Class C: Small risk in controlled animal studies
Antifungal agents
Fluconazole (Diflucan)
Griseofulvin
Itraconazole (Sporanox)
Ketoconazole (Nizoral)
Antimalarial agents
Mefloquine (Lariam)
Chloroquine
Primaquine
Antiparasitic agents
Albendazole - not in Briggs (1998)
Ivermectin - not in Briggs (1998)
Mebendazole
Pentamidine
Thiabendazole
Pyrantel
Anti-Tuberculosis agents
Dapsone
Isoniazid (INH)
Pyrazinamide
Rifampin
Antiviral agents
Lamivudine
Stavudine
Zalcitabine
Zidovudine
Delavirdine - not in Briggs (1998)
Nevirapine
Indinavir
Cidofovir
Foscarnet
Ganciclovir
Acyclovir
Amantadine
Rimantadine
Interferon alpha
Antibiotics
Imipenem-Cilastin
All Fluoroquinolone antibiotics
Clarithromycin (Biaxin)
Pediazole - not in Briggs (1998)
Sulfisoxazole - not in Briggs (1998)
Trimethoprim
Vancomycin
Chloramphenicol
Gentamicin
Vaccines
Tetanus Toxoid
Diphtheria toxoid
Polio Vaccine (live and inactivated)
Rabies Vaccine
Class D: Strong evidence of risk to the human fetus
Antiparasitic agents
Metronidazole or Flagyl (First Trimester)
New evidence suggests first trimester safety
Burtin (1995) Am J Obstet Gynecol 172:525-9
Antibiotics
Amikacin (Class D per manufacturer)
Kanamycin
Streptomycin
Tobramycin (Class D per manufacturer)
Sulfa (Third Trimester)
All Tetracycline antibiotics
Doxycycline
Tetracycline
Minocycline
Erythromycin Estolate (llosone)
Due to hepatotoxicity in pregnant women
McCormack (1977) Antimicrob Agents Chemother 12:630
Macrobid and Nitrofurantoin (Third Trimester)
Do not use either of these past 38 weeks
Can cause Hemolytic Anemia in newborns
Related to immature liver and G6PD Deficiency
Vaccines
Yellow Fever Vaccine
Class X: Very high risk to the human fetus
Antimalarial agents
Quinine
Antiviral agents
Ribavirin
Rebetron - not in Briggs (1998)
Vaccines
Measles Vaccine
Mumps Vaccine
Rubella Vaccine
Small Pox Vaccine
TC-83 Venezuelan Equine Encephalitis Vaccine
References
Briggs (1998) Drugs in Pregnancy and Lactation, 5th ed
Larimore (2000) Prim Care 27(1):35-53

Analgesic Medications in Pregnancy

Class A: No risk in controlled human studies
Acetaminophen (Tylenol)
Class B: No risk in controlled animal studies
Narcotics (Class D if prolonged use or high dose)
Nalbuphine (Nubain)
Meperidine (Demerol)
Butorphanol (Stadol)
Fentanyl (Duragesic)
Hydromorphone (Dilaudid)
Methadone (Dolophine)
Morphine Sulfate
Oxycodone (Percocet)
NSAIDs (first or second trimester only)
Ibuprofen (Motrin)
Indomethacin (Indocin)
Ketoprofen (Orudis)
Naproxen (Naprosyn)
Piroxicam (Feldene)
Sulindac (Clinoril)
Class C: Small risk in controlled animal studies
Narcotics (Class D if prolonged use or high dose)
Codeine (Tylenol with codeine)
Hydrocodone (Vicodin)
Tramadol (Ultram)
Propoxyphene (Darvocet)
Barbiturates
Butalbital (Fiorinal)
Class D if prolonged use or high dose
NSAIDs (first or second trimester only)
Aspirin
Etodolac (Lodine)
Ketorolac (Toradol)
Nabumetone (Relafen)
Oxaprozin (Daypro)
Class D: Strong evidence of risk to the human fetus
Aspirin (Third Trimester)
All NSAIDs (Third Trimester)
Prolonged use or high dose of any Narcotic
Prolonged use or high dose Butalbital (Fiorinal)
General Anesthesia - not in Briggs (1998)
Lactation Safe Analgesic Medications
Acetaminophen (Tylenol)
Ibuprofen (Motrin)
References
Briggs (1998) Drugs in Pregnancy and Lactation, 5th ed
Larimore (2000) Prim Care 27(1):35-53

Cardiovascular Medications in Pregnancy

Class B: No risk in controlled animal studies
Anticoagulants
Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Danaparoid (Orgaran)
Heparin
Antihypertensives
Methyldopa (Aldomet)
Acebutolol (first trimester only)
Pindolol (first trimester only)
Antiarrhythmic
Encainide
Sotalol (Betapace) - first trimester only
Diuretics
Torsemide (Demadex) - not in Briggs (1998)
Amiloride
AntiHyperlipidemic
Cholestyramine
Colestipol
Class C: Small risk in controlled animal studies
Antiplatelet Medications
Clopidogrel (Plavix) - not in Briggs (1998)
Dipyridamole (Persantine)
Ticlopidine (Ticlid) - not in Briggs (1998)
Antiarrhythmic
Atropine
Digoxin
Disopyramide (Norpace)
Lidocaine
Procainamide
Quinidine
Amiodarone
Neonatal Hypothyroidism
Intrauterine Growth Retardation
Cardiac disturbance
Antihypertensive
Hydralazine
Diazoxide
Clonidine
Nitroprusside (Nipride)
Prazosin
Reserpine
All Calcium Channel Blockers
Most Beta Blockers (first trimester only)
Metoprolol
Nadolol
Propranolol
Timolol
Esmolol (Class C in all trimesters)
Diuretics
Acetazolamide (Diamox)
Furosemide (Lasix)
Mannitol
Lipid lowering medications
Niacin
Gemfibrozil (Lopid)
Class D: Strong evidence of risk to the human fetus
Anticoagulants
Coumadin (Warfarin)
Dicumarol
Antihypertensive
ACE Inhibitors
Angiotensin II Antagonists
Most Beta Blockers (second and third trimester)
Associated with Intrauterine Growth Retardation
Metoprolol
Nadolol
Propranolol
Timolol
Acebutolol (second and third trimester)
Pindolol (second and third trimester)
Atenolol
Diuretics
Ethacrynic Acid
Triamterene (Class B per manufacturer)
Bumetanide (Bumex)
Hydrochlorothiazide
Spironolactone
Class X: Very high risk to the human fetus
HMG CoA Reductase Inhibitors (Statins)
Fluvastatin
Lovastatin
Pravastatin
Simvastatin
References
Briggs (1998) Drugs in Pregnancy and Lactation, 5th ed
Larimore (2000) Prim Care 27(1):35-53

Endocrine Medications in Pregnancy

Class A: No risk in controlled human studies
Dessicated Thyroid (Armour Thyroid)
Levothyroxine (T4 or Synthroid)
Liothyronine (T3 or Cytomel)
Class B: No risk in controlled animal studies
Acarbose (Precose)
Calcitonin
Insulin
Metformin (Glucophage)
Prednisone
Prednisolone
Class C: Small risk in controlled animal studies
Acetohexamide
Beclomethasone
Betamethasone
Bromocriptine
Chlorpropamide (Diabinase)
Dexamethasone
Glipizide (Glucotrol)
Glyburide (Micronase or DiaBeta)
Triamcinolone
Class D: Strong evidence of risk to the human fetus
Lynestrenol
Medroxyprogesterone
Methimazole
Propylthiouracil (preferred over Methimazole)
Tamoxifen
Tolbutamide (Orinase)
Class X: Very high risk to the human fetus
Clomiphene (Clomid)
Danazol
Diethylstilbesterol (DES)
Estrogens (all)
Iodide I-131
Leuprolide (Leupron)
Norethindrone
Norethynodrel
Norgestrel
Oral Contraceptives
References
Briggs (1998) Drugs in Pregnancy and Lactation, 5th ed
Larimore (2000) Prim Care 27(1):35-53

Hematology Medications in Pregnancy

Class B: No risk in controlled animal studies
Iron Sulfate - Not in Briggs (1998)
Anticoagulants
Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Danaparoid (Orgaran)
Heparin
Class C: Small risk in controlled animal studies
Antiplatelet Medications
Clopidogrel (Plavix) - not in Briggs (1998)
Dipyridamole (Persantine)
Ticlopidine (Ticlid) - not in Briggs (1998)
Chemotherapeutics
Asparaginase
Dacarbazine
Dactinomycin
Interferon alfa
Class D: Strong evidence of risk to the human fetus
Chemotherapeutics
Bleomycin
Cisplatin
Cyclophosphamide
Cytarabine
Daunorubicin
Doxorubicin
Etoposide
Fluorouracil
Hydroxyurea
Melphalan
Mercaptopurine
Methotrexate
Plicamycin
Tamoxifen
Vinblastine
Vincristine
Miscellaneous Agents
EDTA - Not in Briggs (1998)
Penicillamine
Anticoagulants
Coumadin (Warfarin)
Dicumarol
Class X: Very high risk to the human fetus
Leuprolide (Lupron)
Aminopterin
References
Briggs (1998) Drugs in Pregnancy and Lactation, 5th ed
Larimore (2000) Prim Care 27(1):35-53

Respiratory Medications in Pregnancy

Class B: No risk in controlled animal studies
Cromolyn Sodium (Intal)
Ipratropium Bromide (Atrovent)
Terbutaline (Brethine, Brethaire)
Montelukast (Singulair) - not in Briggs (1998)
Nedocromil (Tilade) - not in Briggs (1998)
Zafirlukast (Accolate) - not in Briggs (1998)
Class C: Small risk in controlled animal studies
Albuterol (Proventil, Ventolin)
Beclomethasone (Vanceril, Beclovent)
Most used Inhaled Corticosteroid in pregnancy
Budesonide (Pulmicort) - not in Briggs (1998)
Flunisolide (AeroBid) - not in Briggs (1998)
Fluticasone (Flovent) - not in Briggs (1998)
Inhaled Triamcinolone (Azmacort)
Metaproterenol (Alupent)
Pirbuterol (Maxair) - not in Briggs (1998)
Salmeterol (Serevent) - not in Briggs (1998)
Theophylline
Zileuton (Zyflo) - not in Briggs (1998)
References
Briggs (1998) Drugs in Pregnancy and Lactation, 5th ed
Larimore (2000) Prim Care 27(1):35-53

Simple theme. Theme images by Flashworks. Powered by Blogger.

Professor Alaa Mosbah with Medical Graduates

Thursday, November 14, 2019

Prof. Alaa Mosbah YouTube channel

No comments:

Post a Comment