Obsandgyne Tables 200pages 156l5f

TYPES OF ABORTION FEATURES History à Mild vaginal bleeding. à No abdominal pain or mild abdominal pain 2. Examination à Good general condition. à The cervix is closed à The uterus is usually the correct size for date 3. U/S which is essential for the diagnosis Showed the presence of fetal heart activity

THREATENED ABORTION

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INEVITABLE ABORTION

1. History  Heavy vaginal bleeding.  with no age of products conception (inevitable)  with age of products of conception (incomplete abortion)  Severe lower abdominal pain which follows the bleeding 2. Examinations  Poor general condition.  The cervix is dilating and products of conception may thru the os  The uterus may be the correct size for date (inevitable abortion) or small for date (incomplete abortion) 3. U/S à Fetal heart activity may or may not present in inevitable abortion or retained products of conception (RPOC) in incomplete abortion 1. History  Heavy vaginal bleeding à which has been stopped.  Lower abdominal pain which follows the bleeding à which has been stopped.

INCOMPLETE ABORTION

COMPLETE ABORTION

MANAGEMENT 1. Reassurance If fetal heart activity is present, > 90% of cases will be progressed satisfactorily 2. Advice: Decrease physical activity, avoid intercourse 3. Hormones i.e. Progesterone & hCG to pregnancy, (no proven value) 4. Anti- D: Adequate dose of anti-D should be given to all Rh –ve, non-immunised patients, whose husbands are Rh +ve 5. ANC as high risk patients Coz liable to late pregnancy complications such as APH and preterm labour. 1. CBC , blood grouping , XM 2 units of blood 2. Resuscitation à large IV line, fluids & blood transfusion 3. Oxytoxic drugs à Ergometrine 0.5 mg IM + Oxytocin infusion (20-40 units in 500 cc saline) 4. Evacuation & curettage. 5. Post-abortion management.

1. Evacuation & curettage in the presence of RPOC. 2. Post-abortion management.

MISSED ABORTION

ANEMBRYONI C PREGNANCY (BLIGHTED OVUM)

2. Examination: The cervix is closed 3. U/S : Showed empty uterine cavity or PROP 1. Most are diagnosed accidentally 1. CBC , blood grouping, XM 2 units of blood during routine U/S in early pregnancy. 2. Platelets count: to exclude the risk of DIC In some cases there may be a history NB : DIC does not occur before 5 weeks of missed abortion or of: IUFD and if occurred will be of mild grade  Episodes of mild vaginal bleeding 3. Options of treatment  Conservative treatment: à if left alone spontaneous  Regression of early symptoms of expulsion will occur pregnancy.  Surgical evacuation of the uterus; by D & C: Indicated in 1 st  Stop of fetal movements after 20 trimester missed abortion weeks gestation.  Medical termination of pregnancy: by Misoprostol (PGE1) 2. Examination: The uterus may be small for date Cytotec: Indicated in 1st & 2nd trimesters missed abortions. 3. U/S (essential for dx) diagnosed if  Cytotec vaginal ( is the best) or oral tab. 200 μg, 2 tab/ 3 two ultrasound (T/V or T/A) at least hrs/ up to 5 doses daily, which can be repeated next day if 7days apart showed an embryo of >7 there is no response in the first day wks gestation (CRL >6mm in  Subsequent surgical evacuation is needed in cases of diameter and gestational sac >20 RPOC mm in diameter) with no evidence of  Main side effects of cytotec: Nausea, vomit & fever. heart activity. 3. Post-abortion management.  It is due to an early death and resorption of the embryo with the persistence of the placental tissue  It is diagnosed if two ultrasound (T/V or T/A) at least 7 days apart showed after 7 weeks of gestation i.e. gestational sac >20mm, an empty gestational sac with no fetal echoes seen.  It is treated in a similar way to missed abortion.

SEPTIC ABORTION

Def: Incomplete abortion complicated by infection of the uterine contents. May be due to criminal interference. Features : Poor general condition  Features of incomplete abortion: Severe vaginal bleeding with age of product of conception, with/without hx of evacuation.  Features of pelvic infection: Pyrexia , tachycardia , general malaise , lower ab pain, pelvic tenderness & purulent vaginal discharge. Bacteriology : Mixed infection  The commonest organisms are : 1. Gram -ve: E.coli , strep & staph 2. Anaerobics: Bacteroides  Rarely Cl. tetani - potentially lethal if not treated adequately. Types :  Mild à the infection is confined to decidua : 80%  Moderate àthe infection extended to myometrium15%  Severe àthe infection extended to pelvis + Endotoxic shock + DIC 5%

1. Investigations :  CBC, blood grouping, XM 2 units of blood.  Cervical swabs (not vaginal) for culture and sensitivity  Coagulation profile , serum electrolytes & blood culture if pyrexia > 38.5 2. Antibiotics: IV Cephalosporin + IV Metronidazole 3. Surgical evacuation of uterus à usually 12 hrs after antibiotic therapy (until reasonable tissue levels of antibiotics achieved) 4. Post-abortion management.

RECURREN T ABORTION

Definition: 3 or more consecutive spontaneous abortions  It may presented clinically as any of other types of abortions . Types :  Primary: All pregnancies have ended in loss  Secondary: One pregnancy or more has proceeded to viability (>24 weeks gestation) with all others ending in loss. Incidence: Occurs in about 1% of women of reproductive age . Causes • Idiopathic recurrent abortion, in about 50%, in which no cause can be found . • The known causes include the followings : 1. Chromosomal disorders:  Fetal chromosomal abnormalities & structural abnormalities  Parental balanced translocation 2. Anatomical disorders:  Cervical incompetence: →congenital and aquired  Uterine causes: → submucous fibroids, uterine anomalies & Asherman’s syndrome 3. Medical disorders:  Endocrine disorders : diabetes , thyroid disorders , PCOS & corpus luteum insufficiency.  Immunological disorders: Anticardiolipin syndrome & SLE.  Thrombophilia: congenital deficiency of Protein C&S and antithrombin III, & presence of factor V Leiden.  Infections  ToRCH - CMV may be a cause of recurrent

Diagnosis : 1. History :  Previous abortions : gestational age and place of abortions & fetal abnormalities.  Medical history : DM , thyroid disorders, PCOS, autoimmune diseases & thrombophilia. 2. Examination :  General : weight, thyroid & hair distribution  Pelvic: cervix (length & dilatation) and uterine size. 3. investigations : A. Investigations for medical disorders:  Blood grouping & indirect Coomb’s test in Rh –ve women  Endocrinal screening: Blood sugar , TFT & LH /FSH ratio  Immunological screening: Anti anticardiolipin antibodies & lupus inhibitor.  Thrombophilia screening: Protein C & S, antithrombin III levels, factor V leiden, APTT and PT.  Infection screening  High vaginal & cervical swabs  ToRCH profile (which scientifically is unnecessary) B. Investigations for anatomical disorders:  TV/US: fibroids, cervical incompetence & PCOS.  Hysteroscopy or HSG, fibroids, cervical incompetence, uterine anomalies & Asherman's syndrome C. Investigations for chromosomal disorders:  Parental karyotyping: Parental balanced

abortion, but ToRH are not causes of recurrent abortion.  Genital tract infection e.g Bacterial vaginosis  Rh – isoimmunization

translocation.  Fetal karyotyping: Fetal chromosomal anomalies.

Management Idiopathic Recurrent Abortion In the Presence of Cause With and good antenatal care , the chance of Treat the cause successful spontaneous pregnancy is about 60-70%  Endocrine disorders  : from husband, family & obstetric • Control DM and thyroid disorders before staff. pregnancy  Advice : stop smoking & alcohol intake, • Ovulation induction drugs , ovarian drilling or IVF in PCOS. decrease physical activity • Progesterone or hCG in corpus luteum  Tender loving care insufficiency .  Drug therapy  In anti-cardiolipin syndrome: • Progesterone & hCG: start from the luteal • Low dose aspirin ( 75 mg/day ) & prednisilone phase & up to 12 weeks. ( 20-30 mg / day), starting when pregnancy is • Low dose aspirin ( 75 mg/day ) start from diagnosed till 37 weeks. the diagnosis of pregnancy & up to 37 • These drugs are not teratogenic. weeks  In thrombophilia: • LMWH (20-40 mg/day) start from the Low dose aspirin ( 75 mg/day) starting when diagnosis of fetal heart activity & up to 37 pregnancy is diagnosed and low molecular weight ws heparin ie LMWH ( 20-40 mg/day) starting when fetal heart activity diagnosed & to continue both till 37 weeks .  In uterine disorders • Cervical cerclage in cervical incompetence, best time at the 14 weeks of pregnancy. • Myomectomy in submucus fibroid, excision of uterine septum in septate & subseptate uterus & adhesolysis in Asherman's syndrome.  In infection:: treatment of the genital tract

infection.  In Rh isoimmunization: Repeated intrauterine transfusion  In parental balanced translocation • Explain the risk of fetal chromosomal disorders ( about 30% ) • Encourage to try again or adoption.

COMPLICATIONS OF ABORTION 1. Haemorrhage . 2. Complication related to surgical evacuation ie E&C and D&C. – Uterine perforation- which may lead to rupture uterus in the subsequent pregnancy. – Cervical tear & excessive cervical dilatation – which may lead to cervical incompetence. – Infection – may lead to infertility & Asherman's syndrome. – Excessive curettage – which may lead to Adenomyosis 3. Rh- iso immunisation à if the anti –D is not given or if the dose is inadequate . 4. Psychological trauma.

POST-ABORTION MANAGEMENT In cases of incomplete, inevitable, complete, missed & septic abortions 1. : from the husband, family& obstetric staff 2. Anti D – to all Rh –ve, nonimmunised patients, whose husbands are Rh+ve 3. Counseling & explanation: A. Contraception (Hormonal, IUCD, Barrier) Should start immediately after abortion if the patient choose to wait , because ovulation can occur 14 days after abortion and so pregnancy can occur before the expected next period . B. When can try again : Best to wait for 3 months before trying again . This time allow to regulate cycles and to know the LMP, to give folic acid, and to allow the patient to be in the best shape (physically and emotionally) for the next pregnancy C. Why has it happened In the fiIn the majority of cases there is no obvious cause In the first trimester abortion, the most common cause is fetal chromosomal abnormality. D. Can it happen again As the commonest cause is the fetal chromosomal abnormality which is not a recurrent cause, so the chance of successful pregnancy next time in the absence of obvious cause is very high even after 2 or 3 abortions E. Not to feel guilty à as it is extremely unlikely that anything the patient did can cause abortion No evidence that intercourse in early pregnancy is harmful No evidence that bed rest will prevent it ..

MISCARRIAGE (ABORTION) Def: Expulsion or extraction of products of conception before fetal viability i.e. before 24 weeks of gestation. Incidence :  Is the commonest gynaecological & obstetric disorder  About 15% of clinically recognized pregnancies end in abortion (this rise to 30% if unrecognized pregnancies are included).  Most abortions occur between 8 and 12 weeks of pregnancy. ETIOLOGY 1st Trimester Abortion 2nd Trimester Abortion 1. Fetal chromosomal abnormalities - particularly trisomy, triploidy & monosomy 1. Multiple pregnancy - is the commonest cause of abortion 2. Cervical incompetence (congenital & - 50– 70 % of the first trimester abortions are due to chromosomal abnormalities acquired ) - the incidence of these abnormalities increased with the increase in the maternal 3. Uterine anomalies and submucous age fibroid 2. Anembryonic pregnancy - Blighted ovum 4. Genital tract infection and PROM 3. Multiple pregnancy 4. Parental balanced translocation 5. Infections: genital tract infection , systemic infection with pyrexia & ToRCH syndrome 6. Endocrine disorders : Diabetes, thyroid disorders , PCOS & corpus luteum insufficiency 7. Uterine disorders: Uterine anomalies , submucus fibroid & Asherman’s syndrome 8. Thrombophilia: Congenital deficiency of protein C & S, & anti-thrombin III 9. Immunological disorders : Anticardiolipin syndrome and SLE 10. Cigarette smoking, anaesthetic agents & chemical agents. 11. Psychological disorders

LABOR PAIN 1ST STAGE  Uterine contractions which cause myometrial ischemia. The pain felt Through hypogastric plexuses, pre aortic plexuses to spinal cord through (T10-L1)  Cervical dilatation. Felt through nerve entering to sacral root.  At this stage this pain is visceral pain, diffuse, poorly localized, in lower abdomen radiated to the back.

SOURCES OF PAIN 2ND STAGE 1-Uterine contractions 2-Stretching of the vulval orifice 3-Pressure on the pelvic floor 2+3 felt through pudendal nerve (S2,3,4) mainly ilioinguinal, genitofemoral, posterior femoral cutaneous nerve. This pain is somatic pain.

3RD STAGE Is usually well tolerated with spontaneous placental delivery. Analgesia may be necessary for manual extraction.

PATHWAYS OF PAIN DURING LABOR  The body of uterus and cervix are supplied by autonomic nervous system (T10-L1) through Hypogastric and Preaortic plexuses.  Vulva, perineum are supplied by:-somatic nerve, -Pudendal N S2-S4 -Genitofemoral N L1-L2 -Post. Femoral coetaneous N S1S3.

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NON-PHARMALOGICAL METHOD Psychoprophylaxis (Lamaze method): Emphasized relaxation coupled with a variety of patterned breathing techniques. Emotional . Massage. Warm water baths. Transcutaneous Electrical Nerve Stimulation (TENS). (works on blocking pain fibers in the posterior ganglia of the spinal cord). Hypnosis. Acupuncture.

No definitive evidence.

ANALGESIA IN LABOR PHARMACOLOGICAL METHOD Best Analgesics those that provide rapid onset, with Minimal to No impact on: Progression of Labor, Maternal Vital Signs, Fetal Vital Signs, Maternal ages, and Uterine contractions INTRATHECAL ANALGESIA INHALATIONAL ANALGESIA Provide better analgesia than o More effective than opioids and is widely used. parenteral opioids: o Most commonly used mixture is Entonox (an  Provide rapid onset of relief. equal mixture of NO & Oxygen).  Can have a long duration of o Provides quick with short duration of effect. action. o Not suitable for prolonged use from early labor,  Typically cause no degree of so most suitable is late in labor or while awaiting motor blockade. epidural analgesia.  Routinely cause no effect on o Adverse effects include nausea & light the fetus. headedness. Problems with Intrathecal Opiods. o It is removed from the body unchanged via the  Pruritus (60-100%). lungs, and does not accumulate under normal conditions, explaining the rapid offset.  Nausea (25-60%). o Not suitable for prolonged use from early  Urinary retention (10-35%). labor(bcoz hyperventilation may result in hypocapnea , tetany , fetal hypoxia, so most suitable is late in labor or while awaiting epidural analgesia.

ANALGESIA IN LABOR PHARMACOLOGICAL METHOD PARENTERAL NARCOTICS Easy istered. Work best in early first stage, when pain is primarily visceral and less intense. Cross placental barrier and so it affects fetus. Narcotics can be given IV, IM or by Continuous infusion, in what is called PCA. Naloxone is a narcotic antagonist, that is injected into the umbilical vein in Opioids toxicity cases PETHIDINE FENTANYL BUTORPHANOL One of the most widely used  Synthetic, more potent than other  Synthetic analgesic. systemic opioids for labor analgesia. opioids, so caution is necessary to  40 times more potent than Work best in early 1st stage when avoid serious respiratory Pethidine. depression. pain is visceral.  Duration 2-4 hours.  Rapid onset , Short action. T1/2(2-4 hour)  It antagonizes the narcotic effects of  Continuous pulse oximetry Usually given IM Pethidine, and therefore not given monitoring and close nursing Quick placental transfer together. surveillance are also needed.  Causes drowsiness and dizziness. Pethidine does not inhibit uterine  Side effect : nausea ,vomiting  Less nausea and vomiting. contraction so has less adverse ,constipation ,drowsiness ,confusion.  Less respiratory depression. effects on baby.  Most serious side effect: delayed Diamorphine is better analgesic maternal gastric emptying (the than pethidine but greater danger to the mother when she respiratory depressant effect on require GA in the presence of full newborn so we don’t use it stomach under GA regurgitation and pulmonary aspiration can occur) tt by: no solid food during labor , antiemetic ,H2 blocker.     

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INTRODUCTION Anesthesia versus analgesia : An analgesic drug such as aspirin may relieve pain but the person who takes aspirin still feels other physical sensation such as pressure , heat ,cold and vibration , in contrast anesthetic drugs blocks all these physical sensation

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ANESTHESIA IN LABOR A] GENERAL INTRODUCTION GA isn’t used in vaginal delivery. GA Used in C/S in certain circumstances.  Extreme emergency situations .  Any contraindication for regional anesthesia e.g infection at needle insertion site, prior back surgery, increase intracranial pressure, etc.  Unexpected prolonged surgery.

ANESTHESIA BENEFITS OF GENERAL  Help the obstetrician to deliver the baby in fetal distress.  Situations where minutes may count for the fetus e.g. ruptured uterus, placental abruption, umbilical cord prolapse.  Situations where rapid induction maybe needed for maternal safety e.g. uncontrolled hemorrhage as in cases of: placenta previa, trauma, placental abruption, ruptured vessels.

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INTRODUCTION Def: Introduction of a local anesthetic into the subarachnoid space. A short procedure time. Rapid onset of the block, and limited duration of action. High success rate. Used very late in labor.

ANESTHESIA IN LABOR B] REGIONAL ANESTHESIA SPINAL ANESTHESIA INDICATION CONTRAINDICATION (1) Operations below  Patient refusal, umbilicus uncooperative patients (2) Any operation in perineum  Hypovolemia or genitalia  Clotting disorders (3) All possible operation on  Septicemia the leg except amputation  Anatomical deformities in (4) Very important to notice the patient back that spinal anesthesia is  Neurological disease indicated for older patient  Inadequate resuscitative with systemic disease . drug and equipments

INTRODUCTION Most effective form of labor pain relief, used in the first and second stages of labor. No direct effect on fetus & doesn’t cross placenta. Injected into the epidural space between L2L3 or L3-L4 interspace. A test dose is given to confirm the catheter position, if no unwanted signs is observed after 5 min of injection, a loading dose can be istered. Analgesia for the pain of labor and vaginal delivery necessitates a block from the T10 to the S5 dermatomes. For cesarean delivery, a block extending from the T4 to the S1 dermatomes is

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EPIDURAL ANESTHESIA INDICATION  Pain.  Prolonged labor.  Maternal hypertensive disorder.  When there is high risk of operative intervention.  High risk fetus group.

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CONTRAINDICATION Patient refusal. Coagulopathy disorders.

COMPLICATION Hypotension, bradycardia if block reachs T2-T4. Post spinal headache (postural) Urinary retention Failure of technique . Epidural or subarachnoid hematoma Spinal cord trauma or infection Rarely, convulsions and blindness

COMPLICATIONS MATERNAL IMMEDIATE  Hypotension  Complete motor and sensory paralysis.  LA-induced convulsions, uncommon but serious.  LA-induced cardiac arrest. DELAYED  Postural puncture headache.  Backache; there is good evidence that epidural does not cause backache.  Urinary retention; To avoid this a catheter is placed early.  Tingling in hands or fingers.  Epidural abscesses; extremely rare.

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desired. The spread of the anesthetic depends upon the location of the catheter tip; the dose, concentration, and volume of anesthetic agent used, and whether the mother is head-down, horizontal, or head-up.

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Local or systemic infection. Hypovolemia.

FETAL No direct adverse effect on fetus. Fetal distress can occur if maternal hypotension occurred.

SPINAL ANESTHESIA ADVANTAGE  Faster, Technically easier  More reliable - Defined endpoint, Minimal chance of patchy block  Denser block  Lower drug exposure for mother and fetus  No chance of systemic toxicity

EPIDURAL ANESTHESIA ADVANTAGE  Can tailor duration to need  Lower chance of postdural puncture headache  Beneficial in patients with cardiac and hypertensive disorders

DISADVANTAGE  Limited duration  Higher chance of postdural puncture headache

DISADVANTAGE  Slower onset  Higher risk of systemic toxicity  Risk of high spinal  Risk of "patchy block” ANESTHESIA IN LABOR C] LOCAL ANESTHESIA

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PARACERVICAL BLOCK INTRODUCTION Def: Bilateral transvaginal local anestethetic injection to block the frankho’s ganglion lateral to cervix. Provides satisfactory pain relief during the first stage of labor. Anesthetic agent is injected into the cervix laterally at 3 and 9 o'clock. Has a short duration of action, so paracervical block may have to be repeated during labor. Because the pudendal nerves are not blocked, another analgesic procedure may be needed. Usually, we use:  Lidocaine

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COMPLICATION Fetal bradycardia (lasts up to 30 min) Results from decreased placental perfusion, due to the druginduced vasoconstriction and therefore should not be used in situations of potential fetal compromise.

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PUDENDAL BLOCK Def: Bilateral transvaginal LA injection to block the pudendal nerve as it through the ischial spine (originate from S3-S4), Relatively safe and simple method of providing analgesia for spontaneous delivery. The successful pudendal block will allow pinching of the lower vagina and posterior vulva bilaterally without pain. Pudendal block usually does not provide adequate analgesia when delivery requires extensive obstetrical manipulation. Complications: Intravascular injection,

 Chloroprocaine, 5 to 10 ml of a 1% solution. (Bupivacaine is contraindicated because of ↑ risk of cardiotoxicity.)

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hematoma, and rarely infection.

ANEMIA IN PREGNANCY PHYSIOLOGICAL CHANGES IN PREGNANCY ANEMIA Progressive increase in plasma volume up till 32-34  Lower Hb normal values: weeks, (50%).  Non-Pregnant 11.5-12 g/dl Progressive increase in Red Cell mass, although the  Pregnant, change with gestation, but generally 10.5 pregnancy, (25%). g/dl. Maximum physiological anaemia occur at 32-34 weeks  Clinical features: gestation.  Mostly detected on routine testing. MCV, MCHC stay constant, i.e. dilutional anaemia.  Tiredness. Progressive fall in platelet count, Low platelets only if  Lethargy. Platelets are <100 or pathologically reduced count. 5 Dizziness. 10% will be 100-150*109/l  Fainting. There is 2-3 fold increase in Iron requirements in pregnancy Hypercoagulable state. IRON DEFICIENCY ANEMIA FOLATE DEFICIENCY ANEMIA The commonest in Anemia results if  Second commonest in pregnancy.  Stores are depleted. pregnancy.  The normal dietary Folate intake is Increased demand by the  Iron intake is poor. inadequate to prevent developing fetus, leads to  Absorption is poor. megaloblastic changes in the bone increased absorption and marrow in 25% of pregnant ladies.  Utilisation is reduced. increased mobilisation from  Demand is increased:  Prevalence varies according to : stores.  Social class.  Multiple gestations. IDA is more common in  Nutritional status.  Chronic blood loss. multiple pregnancies.  Factors increasing the risk of FDA:  Haemolysis. Blood loss at delivery will  Anticonvulsant therapy.  A lot of patients start pregnancy with further increase maternal  Haemolytic anaemia. already depleted stores. anaemia, so it is not only a  Thalassemia.  Menorrhagia.

problem confined to pregnancy period.

 Inadequate diet.  Previous recent pregnancies  Conception while breast feeding.

 Hereditary spherocytosis.

DIAGNOSIS IRON DEFICIENCY ANEMIA  As it is the commonest, it is always presumed to be the diagnosis, but should always be confirmed.  Changes in the indices as follows:  MCV reduced.  MCH, MCHC reduced.  Serum iron fall, <12mmol/l (normally falls in pregnancy).  Total iron binding capacity increased, saturation <15% indicate anaemia.  Serum ferritin, fall.

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INTRODUCTION Incidence 1/250 deliveries 20-30% of APH Majority present as painless vaginal bleeding by 30 weeks of gestation 20% bleeding and abdominal pain Incidental discovery

FOLATE DEFICIENCY ANEMIA  MCV increased.  Megaloblastic changes in the bone marrow.  Reduced serum and red cell folate.

MANAGEMENT  Routine iron supplement, as demand is rarely met by normal iron intake.  Oral supplementation is not without side effects:  Constipation.  Taste.  Diarrhoea.  Nausia and vomiting.  Alternate routes are available:  IM.  IV.  The maximum rate of rise in Hb is around 1g/dl/week.  Severe anaemia diagnosed in the later stages of pregnancy may need transfusion.  Preconception advice for all women is to take folate supplement of 0.4mg/day to reduce the risk of NTD, this will increase to 5mg/day in cases of previous NTD baby, or in case of intake of anti-folate medications

PLACENTA PREVIA PREDISPOSING FACTORS CLASSIFICATION Multiparity Related to internal os. Increased maternal  Minor age Grade I, Low lying Previous placenta placenta previa, recurrence Grade II anterior, rate 4-8% marginal Multiple gestation  Major Previous cesarean Grade II posterior section Grade III, partial Uterine anomalies Grade IV, central, complete.

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PRESENTATION Painless vaginal bleeding, more severe with major degrees Recurrent bouts of bleeding may be from early pregnancy Malpresentation and high presenting part Uterus is soft and not tender Fetus is usually alive and

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MATERNAL RISK Maternal mortality 0.1% mainly from hemorrhage PPH Anesthesia Sepsis Air embolism ?? DIC, late occurring, late

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FETAL RISK High perinatal mortality *** prematurity*** IUGR in 15-20% Congenital malformations doubled Umblical cord complication Malpresentation

*Expectant Management  Keep in hosp esp in major degree  Steroids  Correct anemia ? Blood transfusion  Cross-matched blood should be available all the time  Assess fetal well-being INTRODUCTION Premature separation of the placenta (before delivery of the fetus) Incidence: 0.5-1.5%

DIAGNOSIS Ultrasonography *Abdominal 95% accurate *Vaginal usually for post placenta difficult to define by abdominal ultrasound (done in hosp) * Double set up examination rarely needed in patients not actively bleeding

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well More serious for mother than fetus MANAGEMENT Proper assessment of maternal condition and resuscitation In severe bleeding, emergency cesarean delivery irrespective of gestational age If bleeding after 36-37 weeks, deliver. If bleeding not severe and early pregnancy, expectant management, attempting to reach fetal maturity (36-38 wks) without risking maternal health

*Delivery  Delivery is by cesarean section  ?? Anterior marginal placenta with lower margin >2cm from the internal os (by USS) may be delivered vaginally  Observe for PPH  Prophylaxis for Rh isoimmunization

PLACENTA ABRUPTION PREDISPOSING FACTORS CLASSIFICATION  Hypertension, mostly PET, in Grade 0. Asymptomatic, small retroplacental clot pregnancy after delivery  Previous placental abruption, recurrence rate after one episode 8Grade 1. *External vaginal 17%, after two episodes 25%

CLINICAL FEATURES  Vaginal bleeding, variable amount, no bleeding in concealed  Abdominal pain, discomfort and backache

CLINICAL PRESENTATION Concealed 25-30% Revealed 65-80% Other: Mild Moderate Severe abruption

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Trauma Polyhydromnios Premature rupture of memb. Short cord Smoking High parity and low social class Idiopathic MANAGEMENT

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Ressuscitation, IV canula, IV crystalloid Cross match blood and FFP Assessment of mother, put fixed catheter, CBC, KFT, Urine for protein, and coagulation profile Assessment of fetal wellbeing, CTG Definitive treatment by delivery, assess for labour, do ARM and syntocinon infusion. Any fetal distress or deterioration of maternal condition deliver by C/S DIC, packed RBC and FFP Observe for PPH Observe urine output, risk of renal tubular or cortical necrosis

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bleeding *Uterine tetany and tenderness may be present *No signs of maternal shock *No evidence of fetal distress Grade 2. *External vaginal bleeding may or may not be present. *Uterine tender and tetany *No signs of maternal shock. *Signs of fetal distress present. Grade 3. &External bleeding may or may not be present. *Marked uterine tetany. *Persistent abdominal pain. *Maternal shock. *Fetal death or distress. *Coagulopathy in 30%

ANTEPARTUM HEMORRHAGE Vaginal bleeding after age of viability

in 65% of cases  Uterine tetany and tenderness over placental site, more in concealed  Normal lie and presentation  High incidence of fetal distress and fetal death. Fetus is dead in 25-35% of cases at ission (perinatal mortality 4.467%)  Blood pressure may be normal or elevated, protein urea (IUGR present in 80% of cases delivered after 36 weeks of gestation)  Over distended uterus, rigid, difficult to feel fetal parts in concealed hemorrhage  Evidence of skin ecchymosis in 13% of cases usually those itted with fetal death

Blood loss is a major cause of maternal death Incidence 4% CAUSES o Placenta previa 20-30% o Abruptio placentae 15-20% o Unclassified 50% – Marginal separation – Show – Local causes – Vasa previa – Unknown cause

60% 20% 6% 0.05%

*Vasa Previa: Fetal bleeding presented as acute fetal distress after membranes ruptured GENITAL PROLAPSE: APPROACH HISTORY PROFILE

Name, Age, Gravida, Para, Occupation, Ethnic C/C: LUMP / SOMETHING PROTRUDYING THRU INTROITUS / COMING DOWN BELOW HPI Lump analysis: Duration. Present always/goes back in?  by long standing, at end of the day.  by lying dow Impact on social & sexual life Associated sx: Back pain – uterine prolapsed Urinary sx, can’t empty bladder, must reduce digitally – Cystocele/urethrocele Constip, Incomplete evacuation, must reduce digitally Ulcer, blood stain, purulent vaginal discharge – Risk factors

DDx: Congenital Gatner’s cyst

Childbirth – Multiparity? Vaginal delivery? Long labor?

Inclusion dermoid cyst

Menopause

Urethral diverticulum

 Intra-ab pressure – Obese, Chronic cough, constip,

Large cervical / endometrial polyp

Pelvic surgery Gynea Hx: Menopause, HRT, Pelvic surgeries

Chronic uterine

Past Hx: Chronic cough (COPD, Asthma, Pneumonia, CF), Constipation, Previous surgeries Social Hx: Smoking EXAM Pelvic Exam Inspection – Vulva with cough & straining – Demonstrate prolapse ± incontinence Speculum Rectal Exam – to differentiate rectocele (finger goes thru) & enterocele (finger goes high up)

– Rectocele Procidentia

mass

INVESTIGATIONS MSU – analysis & culture Renal US & IVU – in procidentia & severe cystocele, to R/O hydroureter & hydronephrosis Cystometry – to R/O urge incontinence

PUERPERAL PYREXIA Elevated temperature of more than 38.2ºC for a whole day within the first 10days postpartum. History Introduction Permission Complete patient profile: GA, GravidaPara, Address, Occupation, Blood group Chief Complain Analysis of chief complaint: Duration, onset, documented/not R/O Endometritis: Offensive vaginal discharge, Ab pain R/O Mastitis: Lactating or not, Abnormal breast discharge R/O UTI: Urinary sx, Nausea, vomit, chills, rigors R/O Wound infxn: Wound pus, bleeding from site R/O URTI: Cough, SOB R/O DVT: Leg swelling or redness R/O Bacterial vaginosis: Vaginal discharge during pregnancy Intrapartum Hx: Vaginal delivery/CS? Elective or emergency CS? Induction of labor? Instrumental delivery? PROM? Hx of blood transfusion? Urine catheterization? Hx of pregnancy: Anemic? Bacterial vaginosis during pregnancy? Hx of the same problem in previous pregnancies? PMH/PSH Drug Hx. Family Hx. Social Hx.

Physical Examination: Introduction Permission Privacy. Lighting. Hygiene. General Exam: -

Cannula site (superficial thrombophlebitis)

-

Catheter (uti)

-

Signs of anemia (anemia per se is risk factor)

-

Vital signs

Breast Exam (mastitis) Chest Exam (urti) Thyroid Exam Abdominal Exam: -

Uterine tenderness (endometritis)

-

Uterine subinvolution (endometritis)

-

Inspection of wound (wound infxn)

Pelvic Exam: -

Cervix is open (endometritis)

-

Offensive vaginal discharge (endometritis)

Lower Limb Exam -

Leg circumference (dvt)

-

Doppler (dvt)

URINARY INCONTINENCE APPROACH

HISTORY Age, Parity Analysis of Incontinence: Duration, frequency, amount Precipitating factors 3Ps: Position, Protection, Problem Progression Urinary Diary Association Irritative sx (Freq, Urgency, Nocturia) – urge Obstructive sx (Poor stream, Incomplete void, Straining) – overflow Recurrent UTI – urge Past Obs Hx: Mode of Delivery. Instrumental?, Prolonged 2 nd stage? Baby birth W8. Past Gynea Hx: Sx of Prolapse, Pelvic surgery, Hx of malignancy, Hx of radiotherapy PHYSICAL EXAM General Look Abdominal Exam Respiratory Exam Neurological exam – Mental status, Gait, Lower extremity, Perineal sensation & reflexes. Pelvic Exam Pelvic floor muscle tone Stress test - >90% diagnostic for stress inc Cotton swab @ Q-tip test INVESTIGATIONS 1. Urine analysis & culture 2. Urodynamic studies a. Non-invasive methods:

i. ii. iii. iv.

3. 4. 5. 6. 7.

Uroflowmetry Volume-frequency chart Ultrasound: Residual Volume, Urethral cyst, Diverticulation of urethra EMG by surface electrodes

b. Invasive methods i. Cystometry ii. Urethral Pressure Profilometry iii. RV by Catheter iv. EMG by needle electrodes Ultrasound VCU IVU. Indication: Hematuria, Neuropathic bladder, Uterovaginal fistula. Cystourethroscopy. Indication: Reduced bladder capacity, Short hx (<2yrs) of urgency & frequency, Persistent UTI, High suspicion of tumors or stone. MRI

UROFLOWMETRY Normal flow curve: Bell shaped Normal flow rate >15ml/sec Normal voidal volume >150ml CYSTOMETRY Indications 1. Previous unsuccessful continency surgery 2. Mixed incontinence 3. Voiding disorder 4. Neuropathic bladder

Normal Values Residual Volume >50ml 1st Desire to Void: 150-200ml Bladder Capacity: 400-600ml Detrusor Pressure (Filling phase): <15cmH20 Detrusor Pressure (Voiding phase): 4070cmH20 No leakage when coughing

MANAGEMENT A. CONSERVATIVE Success rate 40-60%. Mainstay in Stress Inc. Stop smoking, alcohol, caffeine. Kegel exercise. Intravaginal device to bladder neck & urethra. B. MEDICAL Mild-Moderate Stress Incontinence Alpha-Agonist Pseudoephedrine Phenylpropanolamine

Urge Incontinence Anticholinergic Drugs Oxybutynin chloride Tolterodine TCA: Imipramine

C. SURGICAL [Stress Incontinence] Colposuspension

Tension-free Vaginal Tape (TVT)

PRE-INVASIVE & INVASIVE CERVICAL DISEASE Dysplasia “lesion in which part of the epithelium is replaced by cells showing varying degrees of atypia” Cervical Intraepithelial Neoplasia (CIN): 



Intraepithelial dysplastic atypia occurring within the metaplastic epithelium of the transformation zone.

Bethesda system ASCUS: Atypical squamous cells of undetermined significance  

LSIL: Low grade squamous intraepithelia l lesion

HSIL:High grade squamous intraepithelia l lesion

Cancer: Squamous cell carcinoma

Original Squamocolumnar Junction(OSCJ): The junction in fetal life between the Stratified SE of the vaginal and ectocervix, and the CE of the end cervical canal. New Squamocolumnar Junction (NSCJ): The upper margin of

Dysplasia / CIN System



Mild dysplasia

Mod.dyspla sia

Severe dysplasia

CIN 1

CIN 2

CIN 3

  





CI S

Canc er

Cervical neoplasia originates within the TZ. Low Risk HPV types (6 and 11), are associated lowgrade cervical lesions (condylomata acuminata, and CIN1). High Risk HPV types (16, 18, 31,33,or 35), are associated with high-grade cervical lesion (CIN2,3) and cervical cancer. HPV 16 is the type universally detected with greatest frequency in high grade lesion and cervical cancer, 50% of SCC, 30% of Aden carcinoma, and in over 80% of preinvasive lesions At least 35%of patients with CIN3 will develop invasive cancer within 10years, whereas lower grades may spontaneously regress.

Screening of asymptomatic women

the squamous metaplasia zone determined by the colposcopy Transformation Zone (TZ): The area lying between the OSCJ and the NSCJ

Risk factors for Cervical Cancer 1. Persistent HPV infection with high risk types 2. Young age at first coitus(20yr) 3. Multiple sexual partners 4. Sexual partner with multiple sexual partners 5. Young age at first pregnancy 6. High parity 7. Lower socioeconomic status 8. Smoking 9. Oral contraceptives use 10.Genital warts 11.Exogenous/endogenous immunosuppression

Papanicolaou Smear  

  

Both the end cervical canal and the ectocervix should be sampled when taking the Pap smear In US , the ACOG has recommended that all women, once they have become sexually active, should undergo an annual Pap smear, then 2-5 years following two or three normal Pap smears In Australia, once sexually active till the age of 65 year, routine smear every 2 years The false negative rate for Pap smear for high grade lesions is 20% New technologies (Thin prep, AutoCyte PREP) are automated liquid based slide preparation systems to decrease the false negative rate

Colposcopy 

 1. 2.

3. 4. 5. 6.

The colposcope is a stereoscopic binocular microscope of low magnification, usually 10x to 40x. Indications for colposcopy: Abnormal cervical smear Abnormal findings on adjunctive screening tests such as HPV testing and cervicography, particularly in cases of ASCUS If the cervix is clinically abnormal or suspicious on naked eye examination Abnormal or unexplained IMb or PCB Persistent vaginal discharge Personal history of in utero DES exposure, vulvar or vaginal neoplasia

BEFORE Colposcopy • A complete medical history and general examination should be performed • A clinical and speculum examination of the cervix, vagina and vulva should be performed • A 3% to 5%acetic acid solution is liberally applied to the cervix using soaked swap -The abnormal findings are acetowhite epithelium and abnormal vascular patterns (mosaicism and punctuation) • Lugol’s iodine application to the cervix is called shiller’s test -Normal ectocervix and vaginal squamous epithelium contains glycogen and stains mahogany-brown • -Normal columnar and squamous metaplasia and neoplastic epithelium do not contain

glycogen, and appear mustard yellow • Satisfactory Colposcopic Examination: If the new SCJ and the entire TZ are seen Evaluation of a patient with an abnormal Pap smear Any patient with a grossly abnormal cervix should have a punch biopsy performed regardless of the results of Pap smear • Patients with ASCUS found in their smear may have a repeat smear in 6 months or HPV testing • About 6-10% of patients with an ASCUS smear will have highgrade CIN on colposcopy, 90% of these can be detected by HPV testing for high-risk types • The colposcopic hallmark of CIN is an area of sharply delineated acetowhite epitheilum, or/and abnormal vascular pattern: punctuation and mosaicism



If colposcopic examination is satisfactory, punch biopsy from the suspicious area with end cervical curettage specimen • Diagnostic cone biopsy of the cervix is indicated if: 1. colposcopic examination is unsatisfactory 2. Endocervical curettings show a high-grade lesion 3. Pap smear shows a high-grade lesion that is not confirmed on punch biopsy 4. Pap smear indicates Adenocarcinoma in situ 5. Microinvasion is present on punch biopsy

• Micro invasive carcinoma: extremely irregular puncate and mosaic patterns are found

Treatment of intraepithelial neoplasia CIN  

Low grade lesions (CIN1) repeat smear in 6 month interval until normal then back to the normal screening program High grade lesions (CIN 2,3):

4. Electrocoagulation, Requires general anesthesia, cervical stenosis may occur, success rates up to 97%.

1. Loop Excision of The Transformation Zone (LLETZ),relatively cheap, it can be performed on an outpatient basis under local anesthesia, and tissue is obtained for histologic evaluation.

5. Cervical conization: (cold knife or laser) -mainly diagnostic but it may be used for treatment, cure rates are as high as with hysterectomy for high grade lesions.

2. LASER, destruction of the TZ by CO2 laser, ablation can be performed as an outpatient procedure with local anaesthesia, expensive.

-Major complications: Bleeding, infection, cervical stenosis and incompetence.

3. Cryosurgery, relatively painless outpatient procedure without anaesthesia, cheap, high failure rate for large lesions, copious vaginal discharge for several weeks.

• Simple hysterectomy is rarely necessary, it may be applicable when sterilization is desired in a patient with CIN III or when there is concomitant uterine or adnexal disease.

CERVICAL CANCER    



Worldwide, cervical cancer is the most common cause of death from cancer in women. In developed countries, regular screening with Pap smear has markedly decreased the incidence of the disease. In US, cervical cancer now ranks only eleventh among cancers in women. The mean age for cervical cancer is 51.4 years, with the number of patients fairly evenly divided between the age groups 30 to 39 and 60 to 69 years The most common type is SCC up to 80%, adenocarcinoma and adenosquamous for 20% to 25%, other cell types are rare.

Symptoms

Physical findings

1. Abnormal vaginal bleeding is the most common presenting symptom. 2. Postcoital bleeding in sexually active women, IMB, and PMB 3. Asymptomatic until quite advanced in women who are not sexually active (unlike endometrial cancer who bleed early) 4. Persistent vaginal discharge, pelvic pain, leg swelling, and urinary frequency are usually seen with advanced disease 5. Vesico-vaginal/recto-vaginal symptoms

1. Usually normal general examination 2. In advanced disease, enlarged inguinal or supraclavicular lymph nodes, edema of the legs, ascites, pleural effusion or hepatomegaly. 3. The Pap smear may be normal in up to 50% of cases (falsenegative rate) 4. Pelvic examination in early disease may be normal, especially if the lesion is endocervical. 5. Visible disease may be, ulcerative, exophytic ornecrotic

CERVICAL CANCER Pattern of spread

Investigations

1.Direct invasion into the cervical stroma, corpus, vagina, and parametrium

1. 2. 3. 4. 5. 6.

2. Lymphatic permeation and metastasis

CBC, LFT, KFT Chest X-ray Pelvic-abdominal CT Scan Biopsy of the lesion Cystoscopy and proctoscopy for clinical staging PET Scan (positron-emission tomography) new technique has the potential more accurately to delineate the extent of disease at the primary site and in lymph nodes.

3. Hematogenous dissemination Treatment Stage IA ( Micro invasive carcinoma)

Stage 1B

Radiation Therapy

• A preoperative diagnosis can be made only on the basis of a cone biopsy of the cervix

May be treated by either radical hysterectomy and bilateral pelvic lymphadenectomy or radiation therapy.



Stage 1A1 :

• The results of treatment by either method are similar.



• Total abdominal / vaginal hysterectomy • Cone biopsy alone may suffice if the patient desires to preserve her fertility, as long as the cone margins are free of disease and the endocervical curetting are

• The advantages of surgery is that the ovaries may be spared in young women, surgical staging may be carried out, and chronic radiation therapy may be avoided. • Radical Hysterectomy: Removal of the uterus along with the adjacent portions of





For patients with stage 1b2, most centers use primary chemo radiation, using weekly cisplatin as the radiation sensitizer Therapy usually begins with external radiation to shrink the central tumor and subsequent intracavitary therapy. External radiotherapy may also be used postoperatively for patients with lymph node mets, or inadequate surgical margins The addition of chemotherapy to radiotherapy has been shown to improve survival.

the vagina, cardinal ligaments , uterosacral ligaments, and bladder pillars.



• Modified radical hysterectomy and pelvic lymph node dissection.

• The most common complication of Rad/Hys is bladder dysfunction, 1% to 2% have permanent dysfunction.



• If childbearing is desired, largecone biopsy or radical trachelectomy and pelvic lymph node dissection may be offered

• The most serious complication of Rad/Hys is ureteric fistula or stricture, which occurs in 1% to 2% of cases



negative. Stage 1A2:

• Lower limb lymphodema, 15% to 20% due to pelvic lymphadenectomy

CERVICAL CANCER Complications of radiotherapy Acute

Chronic



Stage IIa with minimal involvement of the vaginal fornix, radical surgery or chemo radiation may be employed. Stage IIa to stage IVa: Pelvic chemo radiation is the treatment of choice Stage IVb Palliative radiotherapy or palliative chemotherapy

1. Acute cystitis: hematuria, urgency and frequency. 2. Proctosigmoiditis: manifested as tenesmus , diarrhea, and age of blood and mucus in the stool 3. Enteritis: manifested by nausea, vomiting, diarrhea, and colicky abdominal pain 4. Bone marrow depression

 Radiation Enteropathy: 1. Proctosigmoiditis: pelvic pain, tenesmus, diarrhea, and rectal bleeding 2. Ulceration: manifested by rectal bleeding and tenesmus 3. Rectovaginal fistula: manifested by age of stool through the vagina 4. Rectum or sigmoid stenosis manifested by progressive



Vaginal vault necrosis: associated with severe pain and tenderness of the vaginal vault and a profuse discharge.  Urologic Injuries: 1. Hemorrhagic cystitis which may need frequent blood transfusion and urinary diversion 2. Vesicovaginal fistula manifested by the constant

large bowel obstruction

leakage of urine demonstrable by cystoscopy

5. Small bowel injury usually present with cramping

3. Ureterovaginal fistula which is manifested by

abdominal pain and vomiting with alternating diarrhea

constant leakage of urine and is demonstrable by IVU

and constipation

4. Ureteric stenosis which is manifested by progressive hydronephrosis.

Recurrent or Metastatic Disease

Prognosis



 



Chemotherapy: the effectiveness is limited, the most active drug is the cisplatin Pelvic exenteration: Reserved for patients who have central recurrence following irradiation.



Prognosis is directly related to clinical stage With higher stage , the frequency of nodal mets escalate, and the 5-year survival rate diminishes. Adenocarcinoma and adenosquamous carcinoma have a





• • • •

• • •

• • •

Total exenteration involves removal of the pelvic viscera, including the uterus, tubes, ovaries, bladder and rectum Radiotherapy if the initial disease treated with surgery alone

somewhat lower 5-year survival rate than do SCC, stage for stage

PHYSIOLOGICAL CHANGES IN COAGULATION & FIBRINOLOYTICS SYSTEMS IN PREGNANCY Coagulation system : Increase in levels of coagulation factors, – The result of these changes is hypercoagulable mainly fibrinogen and factor VII, VIII, IX and X – from the state in pregnancy beginning of the second trimester. – The benefit of these changes is protection of Fibrinolytic system : Inhibition of the system, due to increase in mother from severe haemorrhage after delivery the levels of plasminogen inhibitors. – The risk of these changes is the increased risk of Platelet count : No change thromboembolism Anticoagulant system : ↓ levels of anti-thrombin III, no change in the levels of protein C & S DISSEMINATED INTRAVASCULAR COAGULOPATHY MAIN CAUSES IN DIAGNOSIS MANAGEMENT PREGNANCY Placental abruption • Clinical observation • Insertion of at least 2 large infusion lines – Preeclampsia & – Vaginal bleeding, oozing from Send at least 20ml of blood for cross-matching eclampsia venepuncture sites & surgical incisions. & coagulation profile, and request at least 6 units of blood & 4 units of FFP. Endotoxic shock – – History of any of the above risk factors. • Correct hypovolaemia – by fluids & whole septic abortion, • Whole blood clotting time – prolonged blood chorioamnionitis ( Normal 5-10 minutes) and puerperal • Correct coagulation disorder – by FFP • Coagulation profile : sepsis NB:- platelet transfusion only indicated in – Platelet count – reduced (Normal Amniotic fluid presence of active bleeding if platelet count is 150,000 – 350,000) embolism – Fibrinogen level – reduced ( Normal 2-4 less than 50,000 , and if no active bleeding, if platelet count less than 20,000. Prolonged shock gm/L) • Empty the uterus as rapidly as possible – by Prolonged retention – APTT – prolonged (Normal 35-43 delivery or D&C. of dead fetus – seconds) NB- DIC is always a 2ry phenomenon to an missed abortion or – PT – prolonged (Normal 10-14 seconds) underlying stimulus, and is usually self-limiting if IUFD for >5 weeks – TT – prolonged (Normal 10 seconds)

–

FDPs levels – increased

the stimulus producing it is removed – therefore the uterus should be emptied as rapidly as possible

THROMBOEMBOLISM RISK FACTORS • Pregnancy – hypercoagulate state . • Maternal age > 35 years. • Parity > 4 • Obesity > 80 kg. • Caesarean section, particularly emergency C.S • Previous history of thromboembolism *the risk of recurrence of thromboembolism is 12%, & the majority occur after delivery . • Prolonged hospital stay. • Family history of thromboembolism. • Thrombophilia ie. Congenital deficiency of antithrombin III, protein C or protein S, & presence of factor V leiden. • Anti – cardiolipin syndrome or presence of lupus inhibitor • Cardiac disease – such as valvular prosthesis or atrial fibrillation. • Sickle cell disease. • Gross varicose veins. • Blood groups other than O • Suppression of lactation with estrogen

DIAGNOSIS DVT PE 1- Sx: Pain & swelling in the leg *There may be (50%) or may be not (50%) prior clinical evidence of DVT. 2- Signs: ↑ temp of the leg, tender calf 1. Sx: Sudden onset of dyspnoea, muscles, a difference of >2cm in the chest pain, cough & haemoptysis, circumference at identical sites of legs, and sudden collapse in massive PE and +ve Homan's sign. *in 50% of patients there are no clinical 2. Signs: Cyanosis, rapid breathing & jugular veins distention. symptoms & signs referable to the 3. Investigations: limbs & pulmonary embolism may be  CXR: May be helpful ie. the 1st indication of thromboembolism Consolidation, infarction & . elevated hemidiaphragm on *Over 80% of DVT are left-sided. affected side, but can be totally 3-Investigations : normal. I. Doppler U/S – Noninvasive, safe,  ECG: Usually normal except when accurate in 95%, more accurate if the embolus is large. DVT above the knee due to absence of collaterals than if DVT  Respiratory alkalosis and low below the knee due to presence of Pco2 - due to hypoxia → collaterals. hyperventilation with blowing off II. Ascending venography – of CO2 and respiratory alkalosis. Contraindicated in the 1st  Ventilation & perfusion lung scan trimester, and maybe indicated  Pulmonary angiography. after that if Doppler U/S is not informative.

ANTICOAGULANTS HMWH HEPARIN @ High molecular weight heparin  Rarely used ( if LMWH is not available ).  Given by I.V route. The therapeutic dose is 10,000 units bolus dose , followed by 24,000 units / day, given via infusion pump.  Monitored therapeutic dose (1mg/kg/day 2x/day) by APTT; should be 2 times of control.  Monitor maintenance (40mg/ml 1x/day) & prophylactic (20-40mg/ml 1x/day) dose by plasma heparin level; should be 0.2-0.4 units/ml.  The action of therapeutic heparin is inhibition of thrombin & factors IX, X, XI & XII.  Heparin DON'T cross the placental barrier & so can be used safely during pregnancy  The side effect is bleeding.  If bleeding occur, stop the treatment, and in practice this is enough. Rarely if bleeding not stopped, give specific antidote ie. Protamine sulphate. The advantages of heparin – compared to warfarin - are:1. Does not cross the placenta 2. Small dose prophylaxis- no haemorrhagic hazard 3. Easily and rapidly reversed as heparin disappears from the circulation in 6 hours. The disadvantages:1. Osteoporosis if given for more than 6 months 2. Thrombocytopenia. LMWH HEPARIN Low molecular weight heparin (LMWH) e.g Enoxaparin sodium (Clexane).  The preferred type used now.  Given by S.C route. The therapeutic dose is 2 mg/kg/day, given in two divided doses.

ORAL WARFARIN The dose is 2.5-5 mg/twice daily Monitored by International Normalized Ratio ie. INR (which should be around 2 ) & by PT (which should be 2-2.5 times of control.) MOA: Inhibition of the synthesis of Vit-K dependent factors: II, VII, IX & X. Disadvantages of warfarin are: 1. Bleeding 2. Teratogenic - if given in 1st trimester during the period of organogenesis coz warfarin cross the placenta: chondrodysplasia punctata, cerebral haemorrhage, calcification & microcephaly. 3. Fetal & Neonatal cerebral haemorrhage if given after 36 weeks. 4. Effect not easily or rapidly reversed as warfarin disappears from the circulation in 3 days.  In case of bleeding, antidote is FFP. *Neither heparin nor warfarin are excreted in breast milk, so that they are safe to be used during lactation.

MEDICAL TREATMENT OF THROMBOEMBOLISM ACUTE PHASE Therapeutic dose of heparin. Either LMWH or HMWH. LMWH’s duration of acute phase therapy 2 – 3 months. LMWH (Clexane) HMWH The therapeutic dose is 2 mg/kg/day, given in two The therapeutic dose is 10,000 units bolus dose, followed by divided doses 24,000 units / day, given via infusion pump. LONG TERM THERAPY Either LMWH (S/C) heparin or Oral Warfarin - If thromboembolism occurs during pregnancy – the best after acute phase therapy for 2-3 months, is to give S/C heparin in the maintenance dose for the rest of pregnancy ( in order to avoid side effects of warfarin during pregnancy) & for 12 weeks postpartum of either S/C heparin or warfarin. - If thromboembolism occurs after delivery – S/C heparin in therapeutic dose for 4 weeks, then either S/C heparin in maintenance dose or oral warfarin , for 3 months. HEPARIN WARFARIN Given by SC route. The best is LMWH, if not available, HMWH. Given orally. Dose of LMWH (Clexane) 40mg/ 1x/day. HMWH 5000IU 2x/day. Dose is 2.5-5mg 2x/day Monitored by plasma heparin level; should be between 0.2-0.4 units/ml. *Monitoring of maintenance or prophylactic dose of SC heparin by APTT is of no value, coz maintenance & prophylactic dose doesn’t ↓ level of coagulation factors & so doesn’t cause prolongation of clotting time.

1. 2. 3. 4.

COUNSELING AFTER AN ATTACK OF THROMBOEMBO DURING PREGNANCY Explain the risk of recurrence in future pregnancies– which is about 12 % Explain the need for prophylactic anticoagulatnts in future pregnancies Avoid the use of combined contraceptive pill. Consider screening for thrombophilia – in absence of other risk factors POLICY OF PROPHYLAXIS

No hx. Did c-section. With 1 risk factor. 1 hx of DVT No risk factor.

Delivery

1wk postpartum

Delivery 1 hx of DVT. Other risk factor (e.g. itted to hospital)

ission

Delivery

6wk postpartum

6wks postpartum

Hx of 2DVT or 1PE or anticardiolipin or lupus inhibitors presence or cardiac Pregnant Delivery 2months indication for prophylactic postpartum anticoagulants (eg AF, valvular prosthesis) *The policy of prophylactic anticoagulant during pregnancy in previous history of pulmonary embolism or DVT or thrombophilia is by LMWH – once daily throughout pregnancy up to 12 hours before delivery . *The policy of prophylactic anticoagulant during pregnancy in cardiac indication : warfarin in the 1st trimester & up to 36 weeks and then by HMWH, I.V, 6000 units/6hrs up to 12 hours before delivery. *S/C heparin is not effective in prevention of cardiac thrombosis, and so warfarin given in the 1st trimester in spite of it’s known teratogenic effects.

CLASSIFICATION

DIABETES IN PREGNANCY DIABETOGENIC DEFINITIONS

PRESENTATION

Diabetes mellitus type I --insulin dependent (Ketosisprone) • Diabetes mellitus type II--non-insulin dependent (Ketosis-resistant) • Impaired Glucose Tolerance and Gestational Diabetes (IGT) SCREENING Why. • 30% have none of the Above risk factors • Not all DM, IGT, have persistent glucosuria • 50% of pregnant women have glucosuria at some time •

MATERNAL • Obstetric: Polyhydramnios, pre-eclampsia (10-15%) • Diabetic Emergencies: Hypoglycaemia, Ketoacidosis, Diabetic coma • Vascular & End-Organs: Renal, Ophthalmic, Peripheral vascular • Neurologic: Peripheral neuropathy GI disturbance

EFFECTS OF PREGNANCY Insulin resistance Increased lipolysis Altered maternal gluconeogenesis

• • •

• • • • • • • •

DM= Fasting venous glucose concentration > 8.0 mmol/l and 2 hrs (75 gm load ) > 11.0 mmol/l (or) one of the above + Symptoms • IGT = Fasting < 8.00 mmol/l, but 2 hr (75 gm load) = (9.0-10.9) •

-Symptoms -Risk factors (hx & examination) -Blood tests-screening

RISK FACTORS Age > 30 Family history of DM Past history of: Diabetes in a previous pregnancy, Unexplained IUFD, Neonatal death, Congenital abnormalities, Recurrent abortions, Large babies > 90 th centile Obesity HTN in multipara Polyhydramnios Recurrent infections: Urinary, Fungal Significant Glycosuria

COMPLICATIONS FETAL (1) Macrosomia & Traumatic delivery (30% in seemingly controlled) (2) Delayed organ maturity (RDS) 6 times (3) Congenital malformations:  Cardiovascular: Transposition of great vessels, VSD, ASD, Aortic coarctation  Central Nervous system: Anencephaly, Holoprosencephaly, Encephalocele  Skeletal & spinal - Caudal regression  Genitourinary - Renal agenesis, ureteral dupliction  Gastrointestinal - anal atresia ** Note: when a two-vessel cord is found, suspect a high incidence of

NEONATAL Hypoglycaem ia RDS Hypocalcaem ia Polycythaemi a

•

Infections: Urinary

congenital anomalies (4) Intrauterine fetal Death advanced DM)

(5) Growth restriction (in

MANAGEMENT • •

Start in preconception time Specific during pregnancy SPECIFIC

CONTROL

Diet: 16 x Wt. (pounds ) + 300 = CALORIES Carbohydrates 60% Fat 20% Protein 20% Insulin: – Regiment A * 3 times sol.-with meals + lnt. Evening Or - Regiment B * 2 types (short & intermediate) Twice Daily Dose (daily) = wt. (kg) x 0.6 first x 0.7 second x 0.8 third 2/3 in A.M. 2/3 1nt + 1/3 short 1/3 in P.M. 1/2 1nt + ½ short.

Control : • Fasting < 5.0 mmol/1 • 2 hrs P.P. < 7.0 mmol/1 • Adjustment when necessary • Glycosylated Hb A1c (retrospective) < 6 Fetal well being: • AFP 16-18 wks • Detailed scan 19-20 wks • Biophysical assay from 28 wks • Fetal wt. & growth two weekly (3rd) Delivery: - Timing depends on: (Around 38 wks) • Maternal factors • Biochemical control • Fetal status - Method --- LSCS in any medical or obstetric complication. **Insulin dose adjusted on hourly basis with caloric requirements intravenously.

DRUGS IN PREGNANCY Epidemiology

Maternal Pharmacokinetics

Fetal pharmacokinetics

Placental pharmacokinetics

 In pregnancy, it is estimated that each woman takes 1-3 drugs beside vitamin supplements or iron

 Changes in body fluid volume.  Changes in CVS parameters.  Changes in

 Plasma binding proteins differ from maternal so free fractions of basic drugs are elevated.  Liver expresses

 Blood flow through the placenta (maternal side) increases during gestation (50 ml/min at 10 weeks of pregnancy to 600 ml/min at 38 weeks)

 About 1/3 of women in the UK take drugs at least once during pregnancy.  Only 6% take a drug during the first trimester.  There has been a considerable reduction in drugs used in pregnancy since the mid-1960s >>> Self-istered drugs from 64% to 9%

pulmonary functions.  Alteration in gastric activity.  Changes in serum binding protein concentrations.  Alteration in kidney function

Drug transfer  Most drugs have a molecular weight below 1000 Daltons.  Drugs less than 100o Daltons cross the placenta(less than 600 Daltons cross easily)  Main determinant of the drug concentration in the Embryo/Fetus is the mother’s blood concentration.  Other factors:  >Lipid solubility and protein binding.  > Degree of ionization at physiologic pH.  >placental blood flow and surface area available for transfer.

metabolizing enzymes, but capacity less than the mother.  Drugs transferred across the placenta undergo 1st hepatic effect through the fetal liver.  Fetal kidneys are still immature.  Fetal urine enters amniotic fluid which may be swallowed by the fetus.

 Compounds that alter blood flow alter maternal drug disposition and placental transfer.  Placental metabolism (dealkylation, hydroxylation, demethylation) affects drugs transfer across the placenta.  At term, the surface area of the placenta is at its maximum and nearly all substances can reach the fetus.

The processes that govern the age of a drug into milk are similar to placental condition:  Maternal serum concentration is the main determinant.  The milk pH is slightly acidic in comparison to serum pH; so weak bases could become trapped in milk ( ion trapping ).

Teratogenesis  It is defined as structural or functional (e.g. renal failure) dysgenesis of the fetal organs.  Typical manifestations include:  >congenital malformations with varying severity.  >IUGR.  >Carcinogenesis.  >fetal demise.  In human, the critical time for druginduced congenital malformations is in the first trimester.  Drug-induced toxicity can occur at any time during gestation.

Type of effects on the fetus:

Barker hypothesis:

 Teratogenecity- readily detected at, or shortly after, birth (thalidomide).  Long term latency- ( DES- increased risk of vaginal adenocarcinoma after puberty, or abnormalities in testicular function and semen production).  Impaired intellectual or social development (exposure to phenobarbitone alters programming of brain)  Predisposition to metabolic diseases (Barker hypothesis: low birth weight is associated with increased risk of diabetes, hypertension and heart disease in adulthood). Malformations

 The thrifty phenotype hypothesis says that reduced fetal growth is strongly associated with a number of chronic conditions later in life. This increased susceptibility results from adaptations made by the fetus in an environment limited in its supply of nutrients. These chronic conditions include coronary heart disease, stroke, diabetes, and hypertension

 The overall incidence of:  > Major congenital malformations is around (2-3)%  >minor malformations is 9%  It has been estimated that:  >25% are due to genetic or chromosomal abnormalities  >10% due to environmental causes including drugs.  >65% of unknown etiology.  The part played by drugs is probably small.

 The critical time for drug-induced congenital malformations is usually the period of organogenesis  >>about 20 to 55 days after conception.  >>about 34 to 69 days (5-10 weeks) after the first day of the last menstrual period.  Interference in this process causes a teratogenic effect.  If a drug is given after this time it will not produce a major anatomical defect, but more of a functional one.

Organogenesis

Pregnancy Risk Categories The drugs are classified according to their risk factor category, and the definitions for each category are used by the Food and Drug istration (FDA) Category A •

•

1)

2) 3) 4)

Controlled studies in women fail to demonstrate a risk to the fetus in the first trimester, there is no evidence of a risk in later trimesters, and a remote possibility of fetal harm The only few medications classified as category A are: Each of the vitamins when used in the recommended doses (RDA) Levothyroxine Antiemetic doxylamine Electrolytes potassium citrate, potassium chloride, and potassium

Category B •

•

•

Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and wellcontrolled studies in pregnant women OR Animal studies have shown an adverse effect, but adequate and wellcontrolled studies in pregnant women have failed to demonstrate a risk to the fetus in any trimester The classical example is paracetamol

Category C •

•

Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks These drugs should only be given if the potential benefit justifies the potential risk to the fetus

Category D •

•

•

There is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks The benefits from use in pregnant women may be acceptable, as if the drug is needed in a lifethreatening situation or for serious diseases for which safer drugs are ineffective or cannot be used Examples include ACE inhibitors and diazepam

Category X •

•

• •

Studies in animals or humans have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit These drugs are contraindicated in women who are or may become pregnant! NEVER EVER PRESCRIBE THEM!! Examples include statins and misoprostol

gluconate

Diethylstilbesterol (DES)

Vitamin A analogues

Synthetic nonsteroidal estrogen that was first synthesized in 1938, and currently it is classified as Category X drug • It was prescribed during 1940-1970 to prevent miscarriages in high risk pregnancies by increasing the level of estrogen and progesterone synthesis by the placenta • In 1971, it was discovered that women between 16-20 years old developed vaginal adenocarcinoma, that was linked to their intrauterine fetal exposure • Approximately 1 in 1000 pregnancies were exposed, and 75% of which resulted in girls with vaginal and cervical carcinomas as well as uterine anomalies • Male offspring had abnormal genitalia and sperm defects Thalidomide •

• • • •

•

• • • • •

•

The most common is isotretinoin, used for the treatment of acne Classified as category X The teratogenic effects of retinoids on animals were known for years before their clinical use The critical exposure time is between 3-5 weeks of pregnancy Contraceptive measures are of at least one month before, during treatment, and no pregnancy for 2 years after a course of the drug Fetal abnormalities have not been associated with topical retinoids but it is advised to avoid their use in pregnancy

• • •

•

Teratogenic effects are seen in up to 25% of babies 50% of affected children have an IQ below 85 It was approximately recorded that between 1982 and 1987: o 900-1300 malformed children o 700-1000 spontaneous abortions o 5000-7000 elective abortions The embryopathy includes: o CNS defects o Craniofacial defects o Cardiovascular defects o Thymic defects o Miscellaneous defects

It is no longer used as an antiemetic It was used in the past by pregnant women in the 1 st trimester when they start having nausea and vomiting The mechanism of action is thought to be partly due to antiangiogenesis Fetal exposure caused high rates of abnormalities (20-30%) that include: o Severe limb shortening defects (phocomelia) o Loss of hearing, facial paralysis, anotia, microtia o Renal malformations o Congenital heart disease It is now used for other diseases, such as drug-resistant multiple myeloma, cutaneous lupus erythematosis, erythema nodosum leprosum, Behcet’s disease, and Kaposi sarcoma (care must be needed if the patient is a woman in reproductive age or likes to become pregnant)

Antibiotics

Class of Medication

Category B

Category C

Antibiotics

Azithromycin Gentamycin Aztreonam Bacitracin Cephalosporin Chloramphenicol s Clarithromycin Clavulanate Dapsone Clindamycin Erythromycin Ethambutol ImipenemMeropenem ciliastatin Metronidazole Isoniazid Nitrofurantoin Linezolid Penicillins Pyrazinamide Polymyxin B Quinolones** Sulbactam Rifampin Tazobactam Spectinomycin Vancomycin Sulfonamides Trimethoprim

Category D

• •

Quinine Streptomycin Tetracyclines

** Although in category C, give concern for fluoroquinoloneinduced fetal cartilage damage, as most obstetricians avoid their use in pregnancy

• • • •

They are the most commonly prescribed drugs in pregnancy The safest being Penicillins (B) and Cephalosporins (B) Trimethoprim (C) is a theoretical teratogen as it is a folic acid antagonist Aminoglycosides can cause ototoxicity (e.g., gentamyicn (C) and streptomycin (D)) Erythromycin (C) is probably safe, but not used from the start Tetracyclines (D): – Safe during the first 18 weeks of pregnancy – Minimal effect on bone but after 24 weeks of gestation, discoloration of the teeth and enamel hypoplasia occur – Maternal hepatotoxicity in the form of acute fatty liver, leading to death in some cases where pregnant women were treated with large doses – Pregnancy is not terminated if the women was found to take them

   



Trimethoprim (C/D) is a theoretical teratogen as it is a folic acid antagonist The aminoglycosides(D) can cause ototoxicity Erythromycin (C) is probably safe Metronidazole (B) o Is a teratogen in animals but there is no evidence of teratogenicity in humans and its benefit in serious anaerobic sepsis probably outweighs any risks Ciprofloxacin (C) o Results indicate that may affect ts, so caution and suggest the need for more studies



Chloramphenicol (C) o Should be avoided in late pregnancy and during labour because of the potential for the “grey syndrome” in the newborn infant Nitrofurantoin (B) o May be istered in pregnancy, but should be avoided near term; may predispose fetal hemolytic anemia Vancomycin (B) o Possible fetal ototoxic effect and should be avoided unless benefit outweighs potential risk





Antifungals 



Griseofulvin (C) o Is a known teratogen in laboratory animals o Has ben demonstrated to cross the human placenta o Is contraindicated during pregnancy o Pregnancy should be avoided for 1 month after treatment o Men should not attempt to father children within 6 months of treatment Ketoconazole (C) o Inhibits placental microsomal aromatase and cytochrome P450 o Should be avoided during pregnancy as there is not enough information to confirm its safety





Triazoles-fluconazole and itraconazole (C) o If treatment of these conditions is clinically indicated, other safer antifungal agents should be used Terbinafine (B) o Approved for the treatment of onchomycosis and it is estimated that 4 million patients worldwide have been treated with oral terbinafine o Avoid as the adverse-effects profile of oral terbinafine in pregnancy is limited

There is no obstacle in giving topical antifungal agents, but systemic oral medications are avoided

Class of Medication

Category B

Category C

Antifungals

Amphotericin B Clotrimazole

Caspofungi Ketoconazole n Nystatin Fluconazole Terconazole Griseofulvin

Antimalarial agents 



Atovaquone/Proguanil (C) o No fetal harm in pregnant rats and rabbits o Proguanil is considered to be the least toxic o Women taking the drug either alone or in combination should be supplemented with FA o Should be used with caution in the first trimester



Chloroquine (C) o At high doses, it is embryo toxic and teratogenic in rats o Chloroquine should not be withheld during pregnancy because the risk of comlications from malarial infection in pregnancy is increased o Safe to be breastfeed (C) Hydroxychloroquine, Mefloquine, Primaquine, Pyrimethamine, Dapsone, D.Halofantrine

Antiviral drugs 



Acyclovir (B) o Not fond to be teratogenic in pregnant mice, rats and rabbits o Probably safe in pregnancy and breastfeeding Amantidine (C) o Dose-related teratogenicity in rats at doses equivalent to the human dose o No fetal harm was observed in pregnant rabbits o Birth defects have been observed in humans but the data are very limited





Anti-retroviral agents o Amprenavir (C), Indinavir (C), Nelfinavir (B/C), Ritonavir (B/C) and Saquinavir (B/C) are protease inhibitors used for the treatment of HIV infection o No evidence of teratogenicity has been observed in animals (exceptions of Indinavir) o Benefit outweigh risks Zidovudine (for HIV positive) category C, must be given for the pregnant woman if she is HIV+ve

o

Avoid during lactation

Anticoagulants Warfarin (D) • •

•

•

It is contraindicated in pregnancy, as it crosses the placenta and may cause bleeding in the fetus Its use in pregnancy is commonly associated in with spontaneous abortions, stillbirth, neonatal death, and preterm birth Coumarins (such as warfarin) are also teratogens; the incidence of birth defects in infants exposed to warfarin in utero appears to be around 5%, although higher figures (up to 30%) have been reported in some studies Warfarin istration in the second and third trimesters is much less commonly associated with birth defects, and when they do occur, are different from fetal warfarin syndrome. The most common congenital abnormalities associated with warfarin use in late pregnancy

Fetal Warfarin Syndrome (FWS) • •

•

Aka dysmorphism due to warfarin, warfarin embryopathy, or DiSala syndrome It occurs when warfarin (or another 4-hydroxycoumarin derivative) is given during the first trimester—particularly between the sixth and ninth weeks of pregnancy Associated conditions include: o Hypoplasia of nasal bridge o laryngomalacia o Pectus carinatum o Congenital heart defects o Ventriculomegaly o Agenesis of the corpus callosum o Stippled epiphyses o Telebrachydactyly

   

•

Associated with nasal hypoplasia and chondrodysplasia in the first trimester CNS abnormalities in later pregnancy High incicence of hemorrhagic complications toward the end of pregnancy Neonatal hemorrhage is difficult to prevent because of the immature enzymes in fetal liver and low stores of vitamin K Recent study doses >5mg had significantly more fetal complications independent of the maternal INR

are central nervous system disorders, including spasticity, seizures, and eye defects

o

Growth retardation

Anticoagulants Heparin (UFH & LMWH) (B) Fast-acting anticoagulant with a high binding affinity for antithrombin III Used in the prophylaxis and treatment of VTE and PE associated with pregnancy, which brings very high mortality to the women if left untreated • Safe during pregnancy as it doesn’t cross the placenta • The most significant side effect is heparin-induced thrombocytopenia, in addition to elevation of aminotransferase, hyperkalemia, and osteoporosis in chronic use  Does not cross the placenta but may cause maternal osteoporosis and HIT Cytotoxic drugs Anticonvulsants • •







Cyclophosphamide (D) and chlorambucil (D), are teratogenic and contraindicated in pregnancy Methotrexate (X) should be discontinued at least 3 months prior to conception and FA (5mg) given preconceptually Azathioprine (D) o Current evidence indicates that maternal use is not associated wth an increased risk of impaired fetal immunity, IUGR,

 o o o o o

Class of Medication

Category B Category C

Category D

Anticonvulsants

Magnesium Ethosuxamide sulfate Gabapentin Lamotrigine Levetiracetam Oxcarbazepine Topiramate Zonisamide

Carbamazepine Clonazepam Diazepam Phenytoin Primidone Valproic acid

All the anticonvulsants cross the placenta, and the four principal anti-epileptic drugs are of category D, and so, most of them are teratogenic Background risk = 3% Untreated epileptic = 4% 1 drug = 7% 2 or more drugs = 15% Val + Carb + Phenytoin = 50%



prematurity and congenital abnormalities o Conflicting information regarding breastfeeding Cyclosporin (D) o Benefits outweighs risk, so use with caution



 

It is allowable to prescribe one drug, as an optimal treatment needed to stop the fits rather than the required drug levels, as having a fit is more dangerous to the mother and baby than the teratogenic effect. So, this is a classical example of outweighing the benefits over the risks of teratoegenesis , which the mother must be aware of Folate has to be given to prevent neural tube defects (5mg/day)

Anti-inflammatory drugs •

• • •

Aspirin and NSAIDS do not produce structural defects but may increase the risk of neonatal hemorrhage (they are considered in category C, but when used in large doses or for prolonged duration, they will be in category D) NSAIDS may also lead to oligohydraminos via effects on the fetal kidney Some are prescribed in early pregnancy in patients with history of antiphospholipid syndrome, recurrent miscarriages, or babies with IUGR They are usually avoided in the last trimester as they may cause premature closure of the ductus arteriosus, with consequent neonatal primary hypertension

Cardiovascular drugs





COX-2 inhibitors o Fetal COX-2 inhibitors can be resposible for neonatal chronic renal failure o Mternal uage should be avoided untl further studies confirm the safety of this group of drugs Colchicine (D) o Given around conception may result in an increased frequency of trisomy 21 by causing chromosomal non-dysjnction o Fetal karyotyping is recommended o It is recommended that colchicine ingestion by either parent be discontinued 3 months before conception

Class of Medication

Category B

Category C

Cardiovascular drugs

Methyldopa Acetazolamide Hydrochlorothiazid Calcium-channel e blockers Clonidine Digoxin Esmolol Flecainide Hydralazine Isosorbides

Category D Labetalol Metoprolol Minoxidil Nitroglycerin Nitroprusside Prazosin Propanolol Terazosin

ACE inhibitors Amiodarone ARBs Spironolactone Atenolol

Cardiovascular drugs •

•

•

If the treatment of hypertension is required before 28 weeks, Methyldopa (B) should be the first drug of choice There is concern for use of betablockers in the 2nd and 3rd trimesters given reports of intrauterine growth restrictions, although labetalol has the most safety data of the class Calcium channel blockers mainly





Beta-adrenergic antagonists (C) o Safety in pregnancy is not so well established o Guidelines of the ISSHP do not recommend the use of oral betaadrenergic antagonists for mild hypertension in pregnancy Angiotension converting enzyme inhibitors (D) o Have been associated with a. Prolonged renal failure and

 

Calcium channel blocker (C) o Safe to use, caution with MgSO2 Spironolactone (D) o Anti-androgenic effects were observed in exposed male animal fetuses in one study o Is contraindicated in pregnancy

•

used for severe pre-eclamptic toxemia (PET) Spironolactone , amiodarone, and ACE inhibitors never prescribed! o

hypotension in the newborn b. Decreased skull ossification , hypocalvaria, and renal tubular dysgenesis c. IUGR, oligohydromnios, PDA Is not thought to produce structural malformations, so it is acceptable to cease treatment early in pregnancy and not necessarily preconception



Amiodarone (D) o Can reach the fetus by transplacental age and induce fetal hypothyroidism o Non-verbal Learning Disability Syndrome o Should be avoided during the 1st trimester of pregnancy

Endocrine drugs • • •

Insulin is preferred over oral hypoglycemic agents Many women are taking progesterons in the 2nd trimester Corticosteroids are relatively safe, but they are not prescribed, even if the woman is breast-feeding

Class of Medication

Category B Category C

Category D

Category X

Hormones

Acarbose Adrenal Desmopressi hormones n Calcitonin Insulin Glipizide Metformin Glyburide Somatostatin Melatonin Troglitazone Repaglinide Vasopressin Rosiglitazone Micronized Tolbutamide Progestero ne

Methimazole Propylthiouracil Tamoxifen Hydroxyprogest -erone

Danazol Estrogens Iodide131 Leuprolide Mifepristone Testosterone

Endocrine drugs 

Oral hypoglycemic drugs o Suphonylureas (D) have been reported as direct cause of neonatal hypoglycemia o There is no firm evidence that these drugs are teratogenic



Corticosteroids (C) o Do not appear to give rise to any serious problems o Transient suppression of the fetal HPAA has been reported o May affect growth later in life



Progestogens (D) o Can masculinize the female fetus o No evidence this occurs with the small amount in the CO



Danazol (X) o Reports suggest virilization of the external genitalia of female fetuses o Should be avoided in pregnancy

•

Cases of neonatal withdrawal syndrome (usually selflimited) have been described in infants chronically exposed to benzodiazepines in utero If used in pregnancy, those benzodiazepines with a better and longer safety record, such as diazepam or chlordiazepoxide, are recommended over potentially more harmful benzodiazepines, such as alprazolam or triazolam Using the lowest effective dose for the shortest period of time minimizes the risks to the unborn child

Tranquilizers & antidepressants 

•

In the United States, the FDA has categorized benzodiazepines into categories D or X due to potential harm to the fetus, SSRIs into category C, and Lithium into D that is not commonly used Their use by expectant mothers shortly before the delivery may result in a floppy infant syndrome, with the newborns suffering from hypotonia, hypothermia, lethargy, and breathing and feeding difficulties

Class of medication

Category B

Antidepressants/ Buproprion antipsychotics/ Buspirone anxiolytics Zolpidem

Bronchial Asthma

•

•

Category C Aripiprazole Chlorpromazi ne Clozapine Haloperidol Olanzapine Quetiapine Risperidone

Category D SSRIs TCAs Thioridazine Ziprasidone

Category X

Alprazolam Other Chlordiazepoxide BDZ Clonazepam Diazepam Lithium Lorazepam Midazolam Oxazepam

Treat as non-pregnant, despite of the side effects of drugs, as an asthma attack (status asthmaticus) can be very serious to the mother and baby In general, respiratory drugs are either into category B or C, and so are relatively safe during pregnancy

•

•

Class of Medication

Category B

Category C

Respiratory drugs

Acetylcysteine Budesonide Cromolyn sodium Ipratropium Montelukast Zafirlukast

Albuterol Corticosteroids (inhaled) Dextromethorphan Guaifenesin Salmeterol Theophylline

Summary The decision to use any potentially harmful drug in pregnancy should be made on a case-by-case basis There should be thorough counseling with the patient  Each case is an individualized case! Before prescribing any drug, consideration must be given to any harmful effects on the fetus. However, no harm must come to the mother or the baby because a disease is inadequately treated To minimize the fetal risks, the lowest effective dose should be used It is not a shame that you don’t know exactly the possible side effects, search for them! To prevent any misinformation about the teratogenicity of certain drugs Keep always up-to-date with the drugs information, especially through the teratogen-information service

• • • • • •

MENORRHAGIA   

It is the most common gynecological case seen in the clinic. It is the most common cause of anemia in developed countries. And the 2nd common cause of iron deficiency anemia after poor diet in the developing countries. – Subjective: Prolonged or heavy Regular menstrual bleeding. – Objective: menstrual blood loss more than 80 ml (more accurate), but not used in practice , just in researches)  Thyroid: hypothyroidism. * Normal menstrual blood loss range from 20 - 80 ml with average of 35 ml.  Coagulation disorder: ITP, VWD, leukemia...  Advanced liver diseases.  Drugs: Warfarin, Heparin, Aspirin, Tamoxifen, and

SYSTEMIC PATHOLOGY (5%)

CAUSES OF MENORRHAGIA PELVIC PATHOLOGIC (35%)

DYSFUNCTIONAL UTERINE BLEEDING (60%)

Fibroid (submucosal). Endometriosis. Adenomyosis. Chronic PID. Copper releasing IUCD. Endometrial hyperplasia and malignancy.  Ovarian tumors; Estrogen producing.      

DYSFUNCTIONAL UTERINE BLEEDING FACTORS OF BLEEDING AMONG MENSES ETIOLOGY 1- PG E2 and PG F2α. 1. Endometrial dysfunction (Ovulatory DUB): 2- Fibrinolytic system. - PG’s imbalance (dec PGF2a : inc PGE2 ratio). 3- Blood Vessels of the endometrium. - Increased fibrinolytic activity.  The most important is prostaglandin release and - Ineffective contraction of myometrial vessels. 2. Hypothalamic – Pituitary – Ovarian hormonal Fibrinolytic system à any disturbance in them à axis: (Anovulatory DUB) bleeding. - Most common age at presentation is less than  Disturbance in prostaglandin release such as if 20 and more than 40. PGE2 increased (it is a vasodilator) will lead to bleeding and increased PG F2α which will cause spasmodic or primary dysmenorrhea. Also, if too much fibrinolytic system activityà menorrhagia. HISTORY PHYSICAL EXAM INVESTIGATION - Complaint: Assess the amount of blood - General examination: - CBC: Hb and platelets. loss. General condition (does she - Pelvic ultrasound: Uterus; size, shape, - Associated Gynecological problem: look pale or not?), Vitals, masses, and endometrial thickness. Adnexia Congestive dysmenorrhea, deep Weight, Thyroid, Lymph - Cervical smear. dyspareunia, chronic pelvic pain, pressure nodes (axillary and - Office biopsy: Pipelle, Novak… symptoms, and vaginal discharge. inguinal), Breast, Abdomen - Hysteroscopy and endometrial biopsy: - Gynecological & Menstrual Hx: Last cx (Pelviabdominal mass/ Mandatory smear, previous gynae surgery, ascites). for women older than 40 years. contraception, IMB, and PCB. - Pelvic examination: - Others, according to the suspected problem. - Medical Hx: Thyroid symptoms, Speculum examination, Hematological disorders… Bimanual examination. - Medications: The previous 4 drugs. - Previous investigations and treatment. DEFINITION Menorrhagia in the absence of organic (pelvic, systemic) pathology. Is a diagnosis of exclusion.

TREATMENT LESS THAN 20 YEARS OLD Menorrhagia is a common cause of Gyn clinic visit in teenager, mainly due to DUB. (delayed maturation of HPO axis) Treatment is simple and for short duration (few months) till the hormonal axis becomes mature. Lines of management: a) Reassurance and explanation. b) Correction of anemia if present. c) Medical treatment. NON-HORMONAL HORMONAL ANTIANTIPROGESTOGENS COMBINED O DANAZOL GnRH ANALOG PROSTAGLANDIN FIBRINOLYTICS Most commonly Tranexamic acid: Norethisterone - 1tab daily for - It is an androgen - 3.75mg IM used. - 3 capsule daily, and 21 days, from analogue (17-α– monthly, for 4 from day 1 to day Medoxyprogest day 5. ethinyl months. Mefenamic acid 5 of the cycle. erone acetate. - ↓ menstrual testosterone). - ↓ Menstrual (Ponstan): - ↓ menstrual - Most common blood loss by - Also blood loss by 80- Is the most blood loss by 50%. drug used for 50%. antiestrogentic & 100%. common drug - Main S/E: nausea DUB. - Less antiprogestrogenic. - Depression of the used by and vomiting, ~ - 5 mg twice daily, commonly used - Depression of the HPO- axis; adolescent 25% of patients from day 5 to day due to its side HPO- axis and has a Menopausalsx. female; for stop it because of 25 of the cycle. effects. direct suppressive - Major risk: dysmenorrhea as these side effects. - ↓ menstrual - Minor S/E: effect on Osteoporosis if well. - Rarely, it may blood loss by Nausea, endometrium. used more than 6 - 3 capsules daily, cause cerebral 25%. vomiting, - ↓ menstrual blood months. from day 1 to day thrombosis, so it is - No serious S/E. headache, loss by 80 – 100%. 5 of the cycle. contraindicated in - Safe to use. - S/E: *Although, these irritability, ↑ in - ↓ menstrual patient with risk Hoarseness of drugs are weight... blood loss by factors for voice. extremely - Major side 25%. thromboembolism. Hirsutism and effective, but they effects: HT, -S/E: gastritis, acne. are no more used thromboembolis gastric ulcer. nowadays due to ↑ muscle mass. m, their serious side cardiovascular… Cliteromegaly. effects. Breast atrophy. Hypooestrogenic

Menopausal sx.

BETWEEN 20 & 40 YEARS OF AGE Two lines of management: A] Medical: same as for the teenagers. B] Levonorgestrol releasing IUCD (Mirena) à they desire contraception; very effective. - 20 mcg of levonorgestrol daily. - It decreases menstrual blood loss by 80–90 %. - ~30% of women are amenorrhoeic after one year of insertion. - It decreases the incidence of PID. - Doesn’t increase risk of ectopic pregnancy. - Side effects: breakthrough bleeding & spotting for the first 3-6 months after insertion.

ABOVE THE AGE OF 40 Three lines of management: A] Medical: Same, not O. B] Mirena: Safely used. C] Surgery: 1) Endometrial resection and ablation: - Day case surgery under GA. - Short stay in hospital, rapid recovery. - Cure rate of 70–80%. - Risk of recurrence 20–30%; Risk of endometrial cancer exists. 2) Hysterectomy: Is the best, 100% cure rate. No recurrence of the problem.

POSTCOITAL BLEEDING Def: Bleeding during or after coitus. “Cervical Ectropion” The cause is almost always cervical:It is normal, physiological, it is not an ulcer. - Cervical ectropion, the commonest cause. - Occurs in high estrogenic state: Pregnancy or CO s. - Cervical ulcer, cervicitis. - The estrogen will cause overgrowth of the columnar - Cervical polyps. epithelium of the endocervix into ectocervix à postcoital - Cervical cancer. bleeding. » How to diagnose? - C/C: PCB and excessive mucoid secretions. - History - In menopause, there will be inversion (the stratified layer - Examination: General and pelvic, speculum. of the ectocervix will move inwards). » Treatment: Should be directed toward the cause; Pap - During pregnancy; Conservative treatment, after delivery smear is mandatory before treatment. it usually improves spontaneously. - If on CO, stop it, reassess again.

INTRODUCTION

ECTOPIC PREGNANCY CAUSES

COMPLICATION

Def: Pregnancy that is implanted outside the uterine cavity The incidence nowadays is triple the previously stated as 0.3%

• • • •

SITES Tubes 95%, Rt. > L - 55% ampulla - 25% Isthmic Cervix, Rud. Horn Ovaries Peritoneal – Abdominal

PRESENTATIONS - Silent –On routine examination or laparotomy - Acute (often rupture) - Subacute (Variable presentations DDX • Threatened miscarriage • Corpus luteum cyst: Amenorrhea, Unilateral pain, Spotting, No Pregnancy sx, Negative HCG, If ruptured – Same treatment. • PID: Bilateral, No amenorrhea or pregnancy sx, Signs of infection (50%)

Any delay in ovum age until implantation stage. • Tubal abnormalities: Diverticulae, False ages, Endosalpingitis • ART • Endocrine disorders: Delayed ovulation, Estrogen/Progesterone Ratio. • Contraceptive failure: Minipill (46%), IUCD(4-9%), Tubal surgery (lig., constr.) • Prior history (10-20% Recurrence) • Pathology: PID, Endometriosis • Others

-Tubal abortion - absorption in tube - Incomplete tubal abortion - Tubal blood mole - Tubal rupture - intraperitoneal bleeding - Broad ligaments MANAGEMENT - I.V. line (wide bore) - Blood, Hb, group, cross- matching - Once diagnosed → laparatomy laparoscopy • Expression • Salpingostomy • Salpingectomy

DIAGNOSIS SYMPTOMS INVESTIGATIONS Amenorrhea (6-10 wks) - Pregnancy test Symptoms of pregnancy • Serum βhCG correlates well with trophoblastCell Abdominal pain (99%): mass. Generalised (45%), Unilateral • Ectopic rarely ruptures when cell mass is small or (35%), Shoulder tip (25%) βhCG levels are low. Abnormal uterine bleeding (75%) • In normal pregnancy values, serum βhCG > 1500 Any form mlu/mL, must see gestational sac Syncopal sx (35%) • In normal pregnancy, hCG Values doubles every Adnexal tenderness (96%) 2.2 days. It doesn’t occur in ectopic pregnancy. Adnexal mass (90%) - Blood Hb, grouping Uterine size: Normal (70%) - Transvaginal Ultrasound: - 6 to 8 wks 25% • Intrauterine sac: - Pseudo sac (10-20%) D&C curettings: -Proliferative, - True sac (Yolk sac F. secretory Poles) - Arias-stella • Adnexial mass (90%): - Sac with fetus or no phenomenon fetus - Echogenic mass (DDx. C.L) • Fluids in P.O.D: - in 80% of Ruptured ectopics

•

- In 20% of normal pregnancy ** If Gest sac > 20 mm or (5-6 wk), must see yolk sac & fetal pole. if not seen, suspect either ectopic or blighted ovum - Laparoscopy

Acute appendicitis

No sx of pregnancy • UTI

ENDOMETRIAL CARCINOMA Malignant lesions of the body of uterus  

Body of uterus composed of 3 layers (endometrium, myometrium, serosa) Myometrium o Smooth muscle o Malignant: Leiomyosarcoma



Endometrium o Glands + Stroma o Glands: Adenocarcinoma o Stroma: Endometrial stromal sarcoma o Glands + Stroma: Uterine carcinomsarcoma/MMMR (mixed malignant Mullerian tumor)

ENDOMETRIAL ADENOCARCINOMA  





Disease of menopause Peak incidence 61.75% in postmenopausal women There is marked geographical and racial variation in the incidence, very common in western countries Most common

Etiology

Pathology



Estrogen-dependent neoplasia

Estrogen-independent neoplasia





 



Normally, endometrium is exposed to estrogen in the 1st half of the menstrual cycle and progesterone in the 2nd half Estrogen is bad, Progesterone is protective When endometrium exposed to estrogen and not opposed by Progesterone, will lead to endometrial hyperplasia and carcinoma CO & progesterone have

   

Younger, perimenopausal women History of chronic estrogen exposure Tumors initially endometrial hyperplasia, progress to carcinoma Well differentiated Favourable prognosis

 

Not associated with endometrial hyperplasia Older, postmenopausal, thin women Less differentiated



gynecological cancer in the US (obesity), rare in Japan and China Emigrant Japanese in America gained similar rates to those of Americans. So, there’s geographical and racial factors



protective effect against endometrial CA This can happen in: 1. Obesity (peripheral conversion of androgens into estrogen) 2. Nulliparous (unovulation) 3. Estrogen HRT 4. Estrogen secreting ovarian tumor 5. Familial: HNPCC Lynch Syndrome (ovarian, colon, endometrial cancer)

   

Most common type of endometrial cancer: Endometrioid adenocarcinoma (80%) Other types: mucinous ca, clear cell ca, squamous ca, papillary serous ca Squamous cell in adenocarcinoma:adenosqumous ca Small group of endometrial ca resembles ovarian ca: Papillary serous & clear cell ca o Elderly (>70), thin o Not estrogen related o Advanced stage at presentation

Commonest is the 1st type (estrogen related)

ENDOMETRIAL ADENOCARCINOMA

ENDOMETRIAL SARCOMA

Spread

Diagnosis



  

 

Direct invasion Lymphatic Blood (rarely)

Presentation 

Postmenopausal bleeding o Only in 10% o 85%: atrophic dermatitis o All PMB should do biopsy

Cervical smear Transvaginal U/S o Endometrial thickness of postmenopausal women is <4mm o If >4mm, do biopsy  Biopsy: by hysteroscopy/D&C  If staging confirmed carcinoma, do staging investigation: CBC, KFT, LFT, CXR, pelvic MRI Prognosis

Rare, very aggressive  Pain & bleeding  2 year suvival LEIMYOSARCOMA     

Most arise from normal endometrium May arise from fibroid transformation Abnormal bleeding, pelvic pain Should be suspected in rapidly enlarge fibroid/ lesions keep enlarging after menopause Diagnosis made after hysterectomy by



Premenopausal: IMB, irregular periods  Pain (late presentation, tumor has invaded locally compressing pelvic plexus and nerves) Physical signs    

Rarely suggest diagnosis Uterine enlargement Palpable LN (groin, supraclavicular) Vaginal nodule (in advanced stage)

   

Stage Grade Myometrial invasion Age o Young: endmetriod type (good px) o Elderly: serous (bad px)



histological examination Adjuvant raditherapy and chemotherapy is questionable, not much benefit

Staging Stage 1: confined to body of uterus Stage 2: involvement of cervix Stage 3: ovaries & tubes Stage 4: Metastasis

Treatment Stage 1 &2 (no bad prognostic factor): Hysterectomy + BSO +/- N dissection Stage 1 & 2 (with bad prognostic factor): adjuvant chemotherapy Stage 3 & 4 (dissemination): combination radiotherapy, chemotherapy, hormonal therapy  Endmetrial ca usually present in early stage  5 year survival rate is 70% ENDOMETRIOSIS Def: Presence of endometrial glands and stroma outside the endometrial cavity and walls.

Deposits proliferate during the menstrual cycle, break down & bleed, causing local inflammatory reaction. Fibrosis & distortion of the tissue affected with dense scarring. Benign. EPIDEMIOLOGY OVERVIEW SITES More commonly in the dependant • Disease of reproductive age • Hormone dependant part of the pelvis group • Responds to estrogen – Ovaries (2/3 of women) • Affect 5-15% of women • Regress after menopause, oopherectomy – Broad ligament • Diagnosed in 20-30% of and during pregnancy – Peritoneal surface of Cul-de-sac women investigated for ETIOLOGY and uterosacral ligaments infertility • Unknown – Rectovaginal septum • More in women whose first • Theories – Rectosigmoid colon degree relative have the – Retrograde menstruation – Distant and laparatomy scars disease – Coelomic epithelium transformation • Often diagnosed incidentally – Lymphatic and vascular spread • High social class women in – Genetic and immunologic factors their thirties and infertile! • Can be diagnosed in any type of women and all age groups PATHOLOGY HISTOPATHOLOGY • Gross • Active endometrial glands and stroma – Hemorrhagic vesicle Free • Blood filled cystic lesions – Papule and later nodule • Fibrosis with glands only no stroma Enclosed • Adhesion formation – White nodules or flattened fibrotic scar Healed  Ovarian endometrioma is an enclosed hemorrhagic cyst of variable sizes

SYMPTOMS • According to site • No relation between extent of the disease and severity of the symptoms • Often discovered incidentally FEMALE Dysmenorrhea, Lower abdominal and pelvic pain, Dyspareunia, Accident to endometriotic cyst, REPRODUCTIVE Low back pain, Infertility, Menstrual irregularity TRACT URINARY TRACT Cyclical haematuria / dysuria, Ureteric obstruction GIT Dyschezia, Cyclical rectal bleeding, Intestinal obstruction SURGICAL SCAR & Cyclical pain and bleeding UMBILICUS LUNGS Cyclical haemoptysis, Haemopneumothorax CLNICAL FINDINGS INVESTIGATIONS DDx DIAGNOSIS • Often Negative • Ca 125 often • All causes of chronic pelvic • Direct visualization of the elevated pain lesion • Suggested by – Laparascopy – Thickening and nodularity • Ultrasonography for • Acute conditions – Laparatomy of uterosacral L. ovarian cyst – Ectopic pregnancy – Tenderness in POD • MRI – Acute PID • Histopathology to confirm – Ovarian mass/ masses – Complicated ovarian cyst the diagnosis – Fixed retroverted uterus – Acute appendicitis and – Tender nodule in the other surgical cervix, umbilicus or scar emergencies

TREATMENT NSAIDS PSEUDOPREGNANCY

- Combined O continuous - Cyclical ?? of limited value Side effect - Synthetic progestogens: Medroxyprogesterone acetate and dydrogesterone high doses continuous Side effect - Levonorgestrel-releasing system reduces dysmenorrhoea and regress POD implants PSEUDO– Danazol androgen derivative 6-9 months MENOPAUSE – Gestrinone, androgen derivative Both drugs have androgenic side effects – GnRH agonists - Menopausal symptoms, Osteoporosis ? Add back therapy SURGERY CONSERVATIVE Young patient, women seeking pregnancy, cysts >3cm in diameter Surgical excision, Laser HYSTERECTOMY & Radical/Definitive surgery BSO FACTORS TO CHOOSE TREATMENT ENDOMETRIOSIS & INFERTILITY • Certainty of diagnosis • Ovarian function • Severity of symptoms • Tubal function • Extent of the disease • Coital function • Fertility • Sperm function • Age • Early pregnancy failure • Damage to other organs

ADENOMYOSIS Endometrial glands deep within the myometrium Unknown etiology Different type of patient and presentation RISK FACTORS TREATMENT Multiparous women • Induce amenorrhea - sx recur once treatment is stopped. Late thirties or early forties • Hysterectomy is the only definitive treatment Severe spasmodic dysmenorrhea Menorrhagia Bulky uterus Diagnosis often histological on examination of hysterectomy sample • • •

• • • • • •

FETAL GROWTH ASSESSMENT Obstetric Care Objective

Fetal growth

The normal fetal growth pattern



Decrease the maternal and perinatal morbidity and mortality



 How to achieve these objectives 1. Early confirmation of dates 2. Detection of congenital malformations 3. Detecting fetal hypoxia 4. Detecting abnormal fetal growth Small for gestational age  

Fetal growth is dependent on genetic, placental and maternal factors. Fetal growth restriction is the second leading cause of perinatal morbidity and mortality.

Small for gestational age is defined as a fetal birth weight below the 10th centile for the stated gestational age. The incidence of SGA fetuses is 5-10%

1/3 of the eventual birth is reached by 28 weeks ,½ by 31 weeks , 2/3 by 34 weeks

Constitutionally Small Fetus 

Unfortunately, it can be concluded that a fetus is constitutionally small only after pathologic processes have been excluded.  Therefore, identification of a constitutionally small infant is usually made in retrospect, after the infant is born Why is the fetus constitutionally small?  1. 2. 3. 4. 5. 6.

Determinants of fetal growth are multifactorial : Race Geographical area Sex (M>F) Maternal age Maternal weight and height Socioeconomic status

Assesing fetal growth 1.History

2.Examination

1. Mother’s age 2. Accuracy of LMP date 3. Infections during pregnancy 4. Multiple pregnancy

General examination Obstetric examination Uterine fundal ht

Uterus size

5. Antenatal care and visits 6. Supplements 7. Past obs. History 8. Past medical history 9. Drug history 10.Family history 11.Socioeconomic history

 

Obtaining serial uterine fundal height measurements. The “Mcdonalds rule” in pregnancy is a rough determination of fetal age in weeks

 

Evaluating the size of the uterus by pelvic examination in the first trimester and subsequent antenatal visits Uterine size = Misleading in: Full bladder, obesity, deep masses, uterine fibroids &multiple pregnancy

Assesing fetal growth 3.Investigation: U/S Uses of US

Diagnosis and Confirmation of Viability

Determination of GA and assessment of fetal size and growth

1. Diagnosis and confirmation of viability in early pregnancy 2. Determination of gestational age and assessment of fetal size 3. Intrauterine or Ectopic pregnancy. 4. Multiple pregnancy 5. Diagnosis of fetal abnormalities 6. Placental localization 7. Assessment of fetal wellbeing

Detection of :

a. b. c. d.

Crown-Rump length Biparietal diameter Head circumference Abdominal circumference e. Femoral length

» Gestational sac (4-5 wks) » Yolk sac (5 wks) » Embryo (5-6 wks) » Visible heart beat (6 wks).

» Up to 13 wks : - Crown-Rump Length (CRL) » from 16 to 24 wks : - Head circumference (HC) - Biparietal Diameter (BPD) - Femur length (FL)

a.Crown-Rump Length (CRL)    

From Crown to Coccyx (Rump) (longitudinal axis). Accurate up to 14 wks (1st TM). It is the most accurate parameter. Provides accuracy of +/- 5 days from the GA.

3.Investigation: U/S b. Bi-parietal Diameter (BPD)    

The transverse width of the head at its widest (the distance between the parietal bones eminence of the skull). Accurate up to 16-24 wks. Provides accuracy of +/- 7 days. It is affected by the shape of the head.



Not affected by the shape of the head.

c.Head circumference (HC)

3.Investigation: U/S d. Femur length (FL)  

e.Abdominal circumference (AC)

Better than BPD in accuracy and timing. Accurate only when the image shows two blunted ends of the femur.

» It is the most accurate single predictor of fetal weight.

 

IUGR Is .. Failure of the fetus to achieve its growth potential True or False? 

All SGA infants are IUGR False 

All IUGR infants are SGA

It is made at the widest points in the abdomen. It is the most accurate single predictor of fetal weight.

IUGR and SGA

Incidence    

3 - 10 % of all pregnancies. 20 % of stillborns are growth retarded. 9 - 27 % have anatomic and/or genetic abnormalities. Perinatal mortality is 8 - 10 times higher for these fetuses.

False Classification of IUGR

Maternal causes



Physiological

Pathological

Multiple pregnancy

1. Decrease Uteroplacental blood flow:

 



Symmetrical growth restriction: fetus whose entire body is proportionally small. Incidence : 20 % Asymmetrical growth restriction: Decrease in subcutaneous fat and abdominal circumference with relative sparing of head circumference and femur length. Incidence : 80 %

- Short stature - Younger or older age (<15 and >45) - Low socioeconomic class - Primiparity - Grand multiparity - Low pregnancy weight - Previous h/o preterm IUGR baby



Pre eclampsia / eclampsia  chronic renovascular disease  Chronic hypertension 2. Maternal malnutrition 3. Maternal hypoxemia - Hemoglobinopathies - High altitudes 4. Drugs - Cigarettes, alcohol, heroin, cocaine - Teratogens, antimetabolites and therapeutic agents such as trimethadione, warfarin, phenytoin - Chronic illness ( DM, renal failure, cyanotic heart disease

etc.)

Fetal causes Physiological

Placental Causes Pathological



Placental insufficiency ( most

- Genetic Factors: - Race, ethnicity, nationality - sex (male weigh 150 -200 gm more female ) - parity (primiparous, weigh less than subsequent siblings)



Genetic disorders (Achondroplasia, Russell - silver syn.)  Chromosomal anomalies: - Chromosomal deletions - trisomies 13,18 & 21  Congenital malformations: eg: Anencephaly, GI atresia, potter’s syndrome, and pancreatic agenesis.

 o o o o 

imp in 3rd trimester) Anatomic problems: Multiple infarcts Aberrant cord insertions Umbilical vascular thrombosis & hemangiomas Premature placental separation Small Placenta

 Fetal Cardiovascular anomalies Congenital Infections:mainly TORCH infections.  Inborn error of metabolism: - Transient neonatal diabetes - Galactosemia - PKU Diagnosis of IUGR  History  Physical examination  Investigations U/S









Abdominal circumference is the single most effective parameter for predicting fetal weight because it’s reduced in both symmetrical & Asymmetrical IUGR . In the presence of normal head and femur measurements, abdominal circumference (AC) measurements of less than 2 standard deviations below

 

Asymmetrical growth restriction: BPD is normal in the 3rd trimester , whereas ratio of HC/AC is abnormal . Symmetrical growth restriction : HC/AC may be normal . amniotic fluid volumes ( oligohydramnios is associated with IUGR) . Umbilical artery & fetal artery dopplar assessments : increased resistance is associated with a greater risk of IUGR as pregnancy progresses.

the mean appear to be a reasonable cut off to consider a fetus asymmetric.

Complications of IUGR Antenatal Complications

Intrapartum complications:

Neonatal complications



  

1- related to hypoxia and acidosis:

   

Metabolic changes (acidosis,…..). Oligohydramnios (80%) Abnormal fetal heart patterns. Abnormal Doppler studies. Intra uterine fetal death.



Abnormal CTG. Fetal death. Meconium stained liquor. Increased incidence of instrumental and caesarean deliveries.

a- meconium aspiration. b- persistent fetal circulation. c- hypoxic ischemic encephalopathy

2- metabolic:

3- related to the etiology:

ahypoglycemia

a- chromosomal abn.

bhypocalcaemia chypothermia dhyperviscocity

b- infection. c- congenital anomalies.

syndrome Management Principles Pre-pregnancy

During pregnancy (Ante-partum)

Mode of delivery



 





Modify lifestyle habits. Detect and treat medical disorders.



 

Regular antenatal care. Serial fetal growth assessment. Serial fetal wellbeing assessment 1-Biophysical profile 2-Computerized CTG 3-Umblical artery Doppler Timing of delivery. Mode of delivery.

Time & Mode of delivery governed by:

Cesarean delivery without a trial of labor: 1. in the presence of evidence of fetal distress

 maternal age  past obs. History  gestational age  fetal well being  status of cervix  availability of direct  monitoring during labor. Ex: scalp PH sampling.

2. for traditional obstetrical indications for cesarean delivery  Induction of labor continuous heart rate monitoring and scalp pH monitoring optimize success of vaginal delivery

FIBROIDS 





Fibroids(Leiomyomas ) are wellcircumscribed benign uterine tumors Arise from the overgrowth of smooth muscle and CT in the uterus They are monoclonal

Frequency

Race

Age

Anatomy











It is the commonest tumor of the female genital tract Being present in at least 20% of women over the age of 35



Leiomyomas occur more commonly in black women than white women, with a black-to-white ratio of 3-9:1 In Caucasian, but not black women it is associated with



Leiomyom as occur most commonly in women older than 30 years But they may occur



Mostly occur in the fundus and body of the uterus; only 3% occur in the cervix They may be solitary, multipe or diffuse o 95% are intramural o Subserosal/ exophytic, they can become pedunculated

proliferation of smooth muscle cells which also contains some fibrous CT elements



The peak age of incidence of symptoms is between 35-45 years

nulliparity or relative infertility

in F of any age

o

Hormonal effects

Mortality/Morbidity

Infertility







Growth may be related to estrogen stimulation o Both estrogen and progestin receptors are present in fibroids o Elevated estrogens levels my cause fibroid enlargement. During the 1st trimester of pregnancy, 15-30% of fibroids may enlarge then shrink I puerperium. Some fibroids may decrease in size during pregnancy o Fibroids may shrink after menopause. Some regrowth may occur with hormonal therapy

Clinical details

Malignant change to become a sarcoma o The true incidence of malignant transformation is difficult to determine because leiomyomas are common, whereas malignant leiomyosarcomas are rare and can arise de novo o The incidence of malignant degeneration is less than 1.0% and has been estimated to be as low as 0.2%

o

May occur as a result of o Narrowing of the isthmic portion of the fallopian tube o Or as a result of interference with implantation, especially interference caused by submucosal fibroids

Rarely, they may occur in the broad ligament Submucosal/ subendometrial fibroids are the least common. They can present as fibroid polyp

Complications during pregnancy 1. Spontaneous miscarriage 2. IUGR 3. Pre-term labour 4. Uterine dyskinesia/ inertia during labour 5. Obstruction of the birth canal 6. PPH 7. Hydronephrosis

 Most women with fibroids are asymptomatic  Only 10-20% of pt require txt  Symptoms of fibroids are related to the (location, size and the # of the tumors)  Symptoms may include the following 1.Bleeding 2.Pressure

3.Pain







Menorrhagia o Increased amount & duration of flow o Is the most common symptom May result in severe anemia and can be life threatening, although this is rare o Usually results from the erosion of a submucosal fibroid into the endometrial cavity Rarely, dilated veins on the surface of a subserosal pedunculated fibroid can cause sudden massive intraperitoneal bleeding

1. On bladder o Frequency, urgency +/incontinence 2. On the colon o Constipation o Difficult defecation o Rectal pain 3. Abdominal cramping results from pressure on the small bowel 4. Generalized pelvic &/ lower abdominal discomfort may be present

Women may experience abdominal cramping  Pain usually is felt during menstruation  Less often, pain occurs intermenstrually 4.Others  

Rare causes of secondary polycythemia, cured with hysterectomy are reported Infertility and/or complications of pregnancy may occur. Submucosal fibroids may affect fertility

Complicated fibroids 1. 2. 3. 4.

Torsion of the pedicle Hemorrhage Infection (usually at the tip of the fibroid polyp) Hyaline degeneration: o present to some degree in most moderate to large fibroids o It becomes painful, enlarged and soft 5. Cystic degeneration

6. Red degeneration (necrobiosis) o Occur typically in pregnancy o Is due to infarction of the center of the tumor during midpregnancy o Characteristically, the fibroid suddenly enlarges and is painful & tender o It can be mistaken with PA/ acute abdominal emergency o In pregnancy it is treated conservatively 7. Calcification o Usually seen in post-menopausal and/or pedunculated fibroid

8. Malignant change

Investigations

U/S appearance

Treatment

 



1. Conservative o The tumor is small and asymptomatic in pregnancy o Near menopause and asymptomatic 2. Medical (LHRH analogues), short term o Contra-indication for surgery o Adjunct to surgery in a large fibroids 3. Surgery o Symptomatic fibroids o Rapidly growing fibroids o Diagnosis is in doubt o Likely to complicate future pregnancy 4. Embolization



U/S is the preferred method In some pt, MRI provides additional information The role of CT is limited o Calcifications may be more visible on CT scans than on conventional radiographs because of the superior contrast differentiation with CT

    



The most frequent is that of a concentric, solid, hypoechoic mas This appearance results from the prevailing muscle These solid masses absorb sound waves and, therefore, cause a variable amount of acoustic shadowing Variable degree of echogenicity, depending on the amount of fibrous tissue and/or calcification Fibroids may have anechoic components resulting from necrosis Fibroids in the lower uterine segment may obstruct the uterine canal, causing fluid to accumulate in the endometrial canal The echogenic endometrial striae may be displaced by a fibroid. Calcifications are hyperechoic, with sharp acoustic

 Hysterectomy is the definitive txt  Myomectomy in women who are subfertile/ those who refuse hysterectomy

shadowing. Diffuse leiomyomatosis GENITAL PROLAPSE Genital prolapse is the downward descent of the uterus and /or the vagina towards or through the introitus Occurr in about 10-30% of multiparous women and in 2% of nulliparous women . TYPES PELVIC ETIOLOGY & PATHOPHYSIO PREVENTION UTERINE VAGINAL UTERUS Weakening of and damage to the Genital ing structures of the pelvic prolapse is a  1st degree:  Cystocele: Prolapse i) Transverse @ organs: preventable Cardinal @ Descent of the of the upper 2/3 of 1. Childbirth: (most imp) disease cervix within the anterior vaginal Mackenrodt’s Increasing parity, prolonged labour, 1. Prevention cervical the vagina. wall and the bearing down before full cervical during ligaments.  2nd degree: bladder. dilatation and difficult instrumental childbirth: ii) Uterosacral Descent of the  Urethrocele: deliveries. Good labor ligaments cervix thru the Prolapse of the 2. Chronic elevation in intramanagement, iii) Pubocervical introitus. lowest 1/3 of the abdominal pressure: Obesity, postnatal pelvic ligaments  3rd degree anterior vaginal smoking, chronic cough, chronic floor exercises, wall and the (Procidentia): constip, heavy lifting at work, abd family planning. Don’t give urethra. Descent of the masses and ascites . 2. Avoiding ↑ cervix and the  Rectocele: Prolapse to the 3. Menopause: Weakness of the pelvic uterus, ie broad whole uterus of the posterior intra-abd due to ↓ collagen and ligaments, round through the vaginal wall and pressure weakness of the connective tissue ligaments and the introitus. the rectum. Obesity , 4. Pelvic surgery : levator ani  Enterocele: True smoking,  Abd / vaginal hysterectomy → chronic cough hernia of the pouch muscles Vault prolapse and chronic of Douglas through VAGINA



the posterior vaginal fornix - may contain bowel or omentum. Vault prolapse: Inversion of the vaginal apex which occur after abdominal or vaginal hysterectomy.

Pelvic floor muscles (the levator ani muscles “mainly” and the superficial and deep transverse perineal muscles) and by the pelvic floor fascia.

 Composuspension → Rectocele and enterocele. 5. Congenital prolapsed - congenital ↓ amount of collagen and weakness of connective tissue of the pelvic . For the prolapse in 2% of nulliparous women . 6. Racial variation . Common in Caucasian women , less common in Asians , and rare in Blacks . Variation in the amount of collagen and connective tissue in the pelvic .

constipation 3. Prevention postmenopa usal: Balanced diet, exercise, calcium & by the increased use of HRT.

DIAGNOSIS EXAMINATION DDx: - Inspection of the vulva with cough and  Anterior straining – demonstrate severe prolapse and vaginal wall  A feeling of something coming down below or a lump may demonstrate stress incontinence prolapse: (provided the bladder is full) within the vagina or protruding from the introitus DDx: Congenital - Speculum examination –either dorsal Gartner’s cyst, worse at the end of the day, ↑ on standing and position (Bivalve) or left lateral position inclusion dermoid coughing, and ↓ by lying down. (Sims). cyst & urethral - Other sx, depends on the organ which prolapsed into - Rectal examination - differentiate between diverticulum. the vagina. rectocele (finger goes thru it) from  Uterine  Uterine prolapse: Low backache - central, worse at enterocele (finger goes high up) . prolapse: the end of the day, ↑ on standing and ↓ by lying DDx: large down. INVESTIGATIONS: cervical or  Cystocele: Urinary sx, pt has to reduce the cystocele - MSU for analysis and culture. endometrial to empty her bladder. - Renal ultrasound and IVU in cases of polyp & chronic  Rectocele: Constipation, incomplete rectal procidentia and severe cystocele to exclude uterine inversion evacuation and the patient has to reduce the hydroureter & hydronephrosis. rectocele digitally to empty her rectum. - Cystometry in cases of incontinence, to exclude urge incontinence  Procidentia: Ulcer, blood stained or purulent vaginal discharge. Coital problems - uncomfortable or difficult intercourse – in uterine and vaginal prolapse. MANAGEMENT CONSERVATIVE TREATMENT: PESSARY INDICATIONS TYPES SIDE EFFECTS & THEIR MANAGEMENT - Patient unfit for surgery . Vaginal infection and discharge, ulceration and bleeding.  Ring pessary – - Patient refuses surgery . commonly used - During pregnancy and after delivery . Precautions: pessary. - During waiting time for surgery.  Shelf pessary – Use silicon pessary. - As a therapeutic test to confirm that Change the pessary yearly or earlier if infection or rarely used HISTORY Sx depends on the site, type & degree of the prolapsed.

surgery may help.

ulceration occurred. Use of vaginal estrogen cream in menopausal patients.

SURGICAL TREATMENT PRE-OPERATIVE ASSESSMENT TYPE OF SURGERY Aims of surgery: Correct prolapse, maintain Depends on: 1. Type of prolapsed, 2. Age and parity UTERINE VAGINAL continence and preserve coital function. i. Vaginal hysterectomy –the i) Cystocele & Success of the surgery depends on: preferred operation in Urethrocele: 1. Preoperative preparation of the patient such as uterine prolapsed. For young Anterior reduce weight in obese, stop smoking and colporrhaphy. treatment of chronic cough. (Gynaecologist can’t do patients who complete the family and in menopausal ii) Rectocele: his part unless the patient fulfills hers). patients. Posterior 2. Postoperative care colpoperineorrhaphy POST-OPERATIVE CARE ii. Manchester (Fothergill) . Immediate postoperative care : operation. iii) Enterocele:  Vaginal pack – remove within 24h. Indicated in young patients Resection of  Foley’s catheter - remove after 1- 2 days. who not complete the enterocele sac.  Prophylactic antibiotics: Metronidazole and family. iv) Vault prolapsed: cephalosporin Consisted of : Abdominal Instructions after discharge - to minimize recurrence 1. Partial amputation of sacrocolpopexy.  Avoiding intercourse for 6 wks. the cervix  Gradual return to normal activities over 2 2. Shortening of the months. transverse cervical  Avoiding smoking, obesity, constipation and ligaments and suturing lifting of heavy objects. them to the front of cervical  Elective C.S. in the subsequent pregnancy. stump. RECURRENT PROLAPSE

of the patient LEFORT - Rarely indicated in elderly and frail patients who are unfit for vaginal hysterectomy or pelvic floor repair. - Rectangular strips of vaginal epithelium are removed from the anterior and posterior vaginal walls in order to obtain a partial closure of the

• •

Recurrence occur in about 20-25% Even with expert surgery and good postoperative care, recurrence can occur, esp in the presence of obesity, smoking and constipation.

3. Anterior and posterior repair.

vagina.

iii. Sacrohysteropexy In patients who complete the family and wish to conserve the uterus

GESTATIONAL DIABETES MELLITUS (GDM) Classification

White’s Classification





Diabetes mellitus type I --- insulin dependent (Ketosis-prone)  Diabetes mellitus type II--- noninsulin dependent (Ketosisresistant)  Impaired Glucose Tolerance and Gestational Diabetes (IGT) Diabetogenic Effects of Pregnancy   

Insulin resistance Increased lipolysis Altered maternal



DM= Fasting venous glucose concentration > 8.0 mmol/l and 2 hrs (75 gm load ) > 11.0 mmol/l (or) one of the above + Symptoms IGT = Fasting < 8.00 mmol/l, but 2 hr (75 gm load) = (9.0-10.9)

How do diabetic pt present   

Symptoms Risk factors ( history & examination) Blood tests--screening

Screening   

30% have none of the Above risk factors Not all DM, IGT, have persistent glucosuria 50% of pregnant women have glucosuria at some time

WHO recommended modified GTT ( 75 gm load) Impaired glucose tolerance

Fasting

Normal

6.0-7.9

Hours 2

6.0 >

And

Or

9.0-10.9

9.0>

gluconeogenesis

Risk Factors DM, IGT, must be suspected in Pregnant women with 1. Age > 30 2. Family history of DM 3. Past history of: - Diabetes in a previous pregnancy

4. 5. 6. 7.

Obesity Hypertension in multipara Polyhydramnios Recurrent infections:Urinary, Fungal 8. Significant Glycosuria

- Unexplained I.U.F.D., Neonatal death - Congenital abnormalities - Recurrent abortions - Large babies > 90th centile Risk factors

Complications

Complications Maternal • Obstetric - Polyhydramnios - pre-eclampsia (1015%) Diabetic Emergencies - Hypoglycaemia •

- Ketoacidosis

Fetal Neurol ogic - Peripheral neuropathy •

Gastrointestinal disturbance •

Infecti ons

(1) Macrosomia & Traumatic delivery

Central Nervous system

(30% in seemingly controlled)

- Anencephaly

** Note: when a two-vessel cord is found, suspect a high incidence of congenital anomalies

Holoprosencephaly

(4) Intrauterine fetal Death

(2) Delayed organ maturity (RDS) 6x (3) Congenital malformations:

- Encephalocele Skeletal & spinal

(5) Growth restriction (in advanced DM)

- Diabetic coma Vascular & End-Organs -Renal •

- Ophthalmic

- Urinary

Cardiovascular :    

Transposition of great vessels Ventricular septal defect Aortic coarctation Artial septal defect

-Caudal regression Genitourinary - Renal agenesis - ureteral dupliction Gastrointestinal

- Peripheral vascular

- anal atresia Complications (Neonatal)

Principles of management:

  

• Start in preconception time • Specific during pregnancy Specific

Hypoglycaemia RDS Hypocalcaemia

Control



Polycythaemia

Diet:

Control :

16 x Wt. (pounds ) + 300 = CALORIES

• • • • Fetal

Carbohydrates

60%

Fat

20%

Protein

20%

Insulin: – Regiment A + lnt. Evening

* 3 times sol.-with meals

Fasting < 5.0 mmol/1 2 hrs P.P. < 7.0 mmol/1 Adjustment when necessary Glycosylated Hb A1c (retrospective) < 6 well being:

• AFP 16-18 wks • Detailed scan 19-20 wks • Biophysical assay from 28 wks • Fetal wt. & growth two weekly (3rd) Delivery: - Timing depends on: (Around 38 wks)

Or - Regiment B intermediate)

* 2 types (short &

Twice Daily Dose (daily) = wt. (kg) x 0.6 first x 0.7 second

• Maternal factors • Biochemical control • Fetal status - Method --- LSCS in any medical or obstetric complication. **Insulin dose adjusted on hourly basis with caloric requirements intravenously.

x 0.8 third 2/3 in A.M.

2/3 1nt + 1/3 short

1/3 in P.M.

1/2 1nt + ½ short.

GESTATIONAL TROPHOBLASTIC NEOPLASIA

Classification of GTN BENIGN Hydatidiform mole 1. Complete mole 2. Partial mole

Genetics of GTN MALIGNANT

 Complete mole: the majority of HM are complete moles and have a 46XX karyotype, both X chromosomes are 1. Invasive mole paternally derived, result from fertilization of an empty 2. Choriocarcinoma ovum by a haploid sperm 3. Placental-site  Partial mole: the karyotype is usually a triploid, often trophoblastic tumor 69XXY, the remaining lesions are 69XXX or 69XYY  Choriocarcinoma: usually aneuploidy or polyploidy typical for anaplastic carcinoma HYDATIFORM MOLE (HM)

Clinical features

Diagnosis

Complete  Vaginal bleeding: the most common presenting symptom, occurs in 97%of cases  Excessive uterine size: large for date is one of the classic signs, occurs in 50% of cases  Toxemia: PET is observed in 27%, usually develops early in the pregnancy  Hyperemesis Gravidarum: Occurs in 25% of cases

Partial  Hyperthyroidism: clinically evident hyperthyroidism is observed in 7%  Trophoblastic Embolization: respiratory distress develops in approximately 2%  Theca lutein ovarian cysts: prominent cysts >6cm develop in 50% of cases  Lower abdominal pain, expulsion of vesicles

 Patients with Partial HM usually do not have the clinical features of complete HM  In general, these patients present with signs and symptoms of incomplete or missed abortion  The diagnosis may be made only after histologic review of the curetting

 Ultrasonography is a reliable and sensitive technique of Complete HM, “Snow storm” pattern  Serum B-HCG higher than normal pregnancy values  Chest film  Blood tests: FBC, BGRH, Coagulation profile, LFT, KFT

HYDATIFORM MOLE (HM) FEATURES

PARTIAL HM

COMPLETE HM

Karyotype

Most commonly 69,XXX

Most commonly 46,XX or 46,XY

Or 69,XXY PATHOLOGY Fetus



-

Amnion, fetal RBC’s



-

Villous edema

Variable, focal

Diffuse

Trophoblastic proliferation

Focal, slight to moderate

Diffuse, slight to severe

Diagnosis

Missed abortion

Molar gestation

Uterine size

Small for date

50% large for date

Theca lutein cysts

Rare

15-25%

Post molar malignant

<5%

9-20%

CLINICAL PRESENTATION

Follow up  The B-HCG radioimmunoassay is the most reliable assay available for the management of patients with GTN  Following molar evacuation or hysterectomy , patients should be followed by weekly determination of B-HCG levels until these are normal for 3 consecutive weeks and the by monthly determination until the levels are normal for 6 consecutive months CONTRACEPTION  Encourage to use effective contraception during the entire interval of follow-up.  Intrauterine device should not be inserted until the patient achieves a normal B-hCG level  If the patient does not desire surgical sterilization, the choice is either hormonal contraception or barrier methods

sequela

Treatment SUCTION CURETTAGE

HYSTERECTOMY

PROPHYLACTIC CHEMOTHERAPY

The preferred method of evacuation , regardless of uterine size in patients who desire to preserve fertility, it involves the following steps:

 If the patient desires surgical sterilization, a hysterectomy may be performed with mole in situ. The ovaries may be preserved even though theca lutein cysts are present

 Controversial  Not indicated in patients with molar pregnancy because 90% have spontaneous remissions  may be useful in the management of high-risk complete HM, especially when hormonal follow-up is unavailable or unreliable

1. Oxytocin infusion- in the OR before the procedure 2. Cervical dilatation then Suction curettage followed by gentle sharp curettage 3. The specimens on suction and sharp curettage should be submitted separately for pathology

MALIGNANT GTN Non-metastatic disease

Metastatic disease

FIGO staging

 Locally invasive GTN develops in 15% of patients after evacuation of a complete mole and infrequently after other gestations  The trophoblastic tumor may perforate through the myometrium, causing intraperitoneal bleeding, or erode into uterine vessels, causing hemorrhage  After molar evacuation, persistent GTN may exhibit features of either HM or choriocarcinoma  After nonmolar pregnancy , persistent GTN always has the features of choriocarcinoma

 Metastatic GTN occurs in 4% of patients after evacuation of a complete mole and infrequent after other pregnancies  Metastasis is usually associated with choriocarcinoma  Trophoblastic tumor perfused by a network of fragile hemorrhagic vessels  Symptoms of mets may result from spontaneous bleeding at metastatic sites Relative incidence of common metastatic sites

REVISED FIGO SCORING SYSTEM

Lung s

80%

Liver

10%

Vagin a

30%

5%

Pelvi s

20%

Brain

10%

Bowe l, kidne y, splee n Other

5%

FIGO Score 4

0

Age (years)

<39

>39

HM

Abortion

Antecedent pregnancy pregnancy

1

2

Term

Interval from index Pregnancy(months) >12

<4

4-6

7-12

Pretreatment hCG level (mIU/ml) 100,000 >100,000 Largest tumor size Metastatic site Brain, liver Number of mets 8 >8 Previous failed chemo drug 2 or more

<1000

1000-10,000

3-4cm lung, vagina 0

>10,000-

5 spleen, kidney

GI

1-4

4single

The total score for a patient is obtained by adding the

individual scoresfor each prognostic factor Total score 0-6= low risk, 7 or more =high risk , FIGO STAGING FOR GTN Stage I: patients with persistently elevated hGC levels and tumor confined to the uterine corpus Stage II: Patients with metastasis to the vagina or pelvis Stage III: patients with pulmonary metastasis with or without uterine, vaginal.or pelvic involvement Stage IV: Patients with advanced disease and involvement of the brain, liver, kidneys, or GIT Diagnostic evaluation 1. 2. 3. 4.

A complete history and examination Measurement of the serum hCG value Hepatic, thyroid and renal function tests Complete blood count

Metastatic work-up 1. 2. 3. 4.

A chest X-Ray CT scan of the abdomen and pelvis CT or MRI scan of the head Measurement of CSF hCG level if any metastatic disease is present and the head CT is negative 5. Selective angiography of abdominal and pelvic organs if indicated MALIGNANT GTN

Diagnosis of post HM trophoblastic neoplasia

1. Plateau of hCG lasts for four measurement over a period of 3 weeks or longer, i.e for days 1, 7,14 and 21 2. A rise in hCG level for three weekly consecutive measurements or longer, over a period of at least two weeks or more, i.e on day 1,7and 14 3. Histological diagnosis of choriocarcinoma  When hCG level remains elevated for 6months or more Management Nonmetastatic (Stage I)

Stage II and III

Stage IV

 Chemotherapy: Single agent chemotherapy is the preferred treatment in patients with stage I disease who desire to retain fertility  Hysterectomy Plus Chemotherapy: if the patient no longer wishes to preserve fertility, hysterectomy with adjuvant single agent chemotherapy Protocol for treatment of stage I GTN

 Low risk patients are treated with primary single-agent chemotherapy, and the High risk patients are managed with primary combination chemotherapy Protocol for treatment of stage II and III GTN

 All patients with stage IV disease should be treated with primary combination chemotherapy and the selective use of radiation therapy and surgery Protocol for treatment of stage IV GTN

 Initial : MTX-FA; if resistant, switch to Act-D or hysterectomy with adjuvant chemotherapy  Resistant: Combination chemotherapy or hysterectomy with adjuvant chemo, local uterine resection  Follow-up hCG: Weekly until normal for 3 wk, then monthly until normal for 12 mo  Contraception: 12 consecutive mo of normal hCG values  Effective contraception during the entire interval of hormonal follow-up

LOW RISK:  Initial: MTX-FA; if resistant , switch to Act-D  Resistant to both: Combination chemotherapy High risk  Initial: Combination chemotherapy  Resistant: Second-line combination chemotherapy Follow up and contraception are the same as in stage I

Initial:  Brain Combination chemotherapy, Whole-head irradiation  Craniotomy to manage complications  Liver Resection to manage complications Resistant: Second-line combination chemotherapy, Hepatic arterial infusion  Follow-up hCG Weekly until normal for 3wk, then monthly until normal for 24mo  Contraception Until there have been 24 consecutive mo of normal hCG

MALIGNANT GTN (Treatment-Chemotherapy) Single agent

Combination

1. Methotrexate : Usually given as a daily dose for 5 consecutive days or every other day for 8 days, alternating with folinic acid rescue (associated with less bone marrow, GIT, and liver toxicity ) 2. Actinomycin D: Given for 5 consecutive days or every other week as a single dose

EMA-CO Regimen for patients with GTN Course 1(EMA) Day 1 Etoposide, Actinomycin D and Methotrexate Day 2 Etoposide, Actinomycin D and Folinic acid 24hr after start of MTX Course 2 (CO) Day 8 Vincristine and Cyclophosphamide

MAC III : Methotrexate-FA, Act-D, and Cyclophosphamide Duration of treatment :  Serum hCG is measured weekly after each course of chemotherapy  Adequate response is defined as a falling the hCG level by 1log after a course of chemotherapy  Single and Combination chemotherapy should be given as often as toxicity permits until the patient achieves three consecutive normal hCG levels  After normal hCG levels are attained, at least two additional courses of chemotherapy are undertaken to reduce the risk of relapse Secondary Tumors: Leukemia, colon cancer, melanoma and breast cancer Fertility outcome: No evidence that patients with GTN followed by chemotherapy have an adverse pregnancy outcome With each subsequent pregnancy : Pelvic USS in 1st trimester to confirm normal gestation, histological review of the placenta, hCG measurement 6 weeks after completion of the pregnancy to exclude occult GTN

CHORIOCARCINOMA  Highly malignant tumor with a predisposition to

PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT)  PSTT is a very rare and unique form of GTN, represent a

haematogenous spread  Follows HM in 3-7% of cases  The organs most frequently affected by mets are, lung, lower genital tract, brain, liver ,kidney and GIT  Some cases manifested by intraperitoneal bleeding seconday to rupture liver or ruptured theca lutein cyst  Patients with pulmonary mets may present with haemoptysis or resp failure  CNS mets presents with neurologic signs resulting from spontaneous bleeding  50% of cases follow HM  Treatment with EMA_CO

GESTATIONAL HTN BP reading ≥ 140/90 mmHg for the first time after 20 weeks of pregnancy • No proteinuria • BP returns to normal within 12 weeks postpartum (if the BP elevation persists, the woman is diagnosed as having chronic hypertension) • Final dx is only

 

   

neoplastic transformation of intermediate trophoblastic cells PSTT can occur after a normal pregnancy, abortion, term delivery, ectopic pregnancy or molar pregnancy Characterized by low B-hCG levels, expression of HPL is incerased on histologic section and as well as in the serum Diagnosis is confirmed by dilatation and curettage and hysterectomy Most cases are confined to the uterus but mets has been reported Surgery is the primary treatment of choice Good prognosis is anticipated in cases localized to the uterus, with distant mets or delayed treatment the outcome is dismal

HYPERTENSIVE DISORDERS IN PREGNANCY-INDUCED HTN PRE-ECLAMPSIA ECLAMPSIA Mild pre-eclampsia CNS • BP ≥ 140/90 mmHg after involvement 20 weeks’ gestation with the • Proteinuria ≥ 1+ by urine occurrence of dipstick or a total protein convulsions that level ≥ 300 mg/24 hours cannot be - Pre-eclampsia can develop attributed to before the 20 week of other causes gestation in hydatidiform mole and in the presence of lupus anticoagulant Severe pre-eclampsia • BP ≥ 160 mmHg systolic

PREGNANCY PREGNANCY-AGGRAVATED HTN Development of PE or eclampsia in pre-existing hypertension detected by a further increase of > 30 mmHg in SBP or >15 mmHg in DBP or New onset proteinuria of >300 mg/24 hours in hypertensive women but with no proteinuria before 20 weeks gestation or A sudden increase in

CHRONIC HTN WITH PREGNANCY Hypertension is present before pregnancy or detected before 20 weeks Or Hypertension first diagnosed after 20 weeks gestation and persisted after 12 weeks postpartum

made postpartum • May even be associated with an increased birth weight

or 110 mmHg diastolic • Proteinuria ≥ 2+ by urine dipstick or a total protein level of 2 gm/24 hours

proteinuria or a drop in platelet count to <100,000/mm3 with HTN and proteinuria before 20wk gestation

PREDISPOSING FACTORS 􀂃 Age: PG<20, all women > 35 􀂃 Parity: PG have double incidence 􀂃 Lower socio-economic status 􀂃 Genetic predisposition: Recessive trait 􀂃 Obstetric complications: multiple and molar pregnancy, fetal hemolytic diseases (hydrops fetalis), polyhydramnios 􀂃 Existing medical conditions: chr BP, ren D, DM, SLE, antiphospholipid AS. 􀂃 Previous PE. The recurrence rate for PE with the same male partner is ~ 20%, and usually becomes apparent at later gestation than in the first pregnancy 􀂃 Obesity: 4.3% for a women with a body mass index <19.8 kg/m2 to 13.3% for those > 35 kg/m2

FACTORS THAT ↓ PET Prolonged exposure to paternal Ag Smoking, but if PE occurs then perinatal mortality triples Placenta previa

PRE-ECLAMPSIA CAUSE (UNKNOWN)

THEORIES (I) Defective trophoblastic invasion of the spiral arteries (II) Immunologic factor (III) Increased pressor responses (IV) Prostaglandins imbalance (V) Genetic predisposition (VI) Inflammatory factors Ischemia could be due to: - Underlying vascular changes (HTN/ Failure of physio chgs of spiral arteries) - Increased myometrial resistance of the myometrial vessels, which could be related to a heightened myometrial tension produced by the large fetus in a primiparous women, by twins, or by polyhydramnios The poorly perfused trophoblast release “factor X” which enters maternal circulation and causes endothelial dysfunction → Imbalance between different classes of locally

PATHOPHYSIOLOGY VASOSPASM Excess Decreased production/ production/sensiti sensitivity to vity to vasoconstrictors vasodilators 􀂃 Angiotensin II 􀂃 Prostacyclin 􀂃 Serotonin 􀂃 Nitric oxide 􀂃 Endothelin INTRAVASCULAR COAGULATION 􀂃 Platelet activation 􀂃 Thrombocytopenia 􀂃 Reduced production of anti-thrombin III PLASMA VOLUME CONTRACTION Redistribution of fluid from the intravascular to interstitial fluid spaces so that total ECF volume remains unaltered

ORGAN HYPOPERFUSION 􀂃 Kidney: ↓ GFR, proteinuria, hyperuricaemia, oliguria 􀂃 Liver: ↑ SGOT, ↑ SGPT, epigastric pain 􀂃 Brain: visual scotomata due to occipital lobe ischemia, headache, convulsions (eclampsia) 􀂃 Placenta: IUGR, placental

Stimulation of the maternal immune system by the early conceptus → Produce blocking Ab to antigenic sites on the placenta, thus preventing the rejection of the fetus and placenta. Hypoimmune response results in damage of the placenta and subsequent PE. PE less common in previously stimulated immunity conditions as: Previous pregnancy, Consanguineous marriages, Increased

PRE-ECLAMPSIA DIAGNOSIS INDICATIONS OF SEVERITY OF INDICATIONS TO TERMINATE PREGNANCY PRE-ECLAMPSIA IN PRE-ECLAMPSIA HISTORY INVESTIGATION 􀂃 Presence of symptoms MATERNAL FACTORS FETAL FACTORS Persistent headache or 􀂃 Personal hx 􀂃 Completed 37 weeks 􀂃 Obvious IUGR 􀂃 CBC: ↑ PCV and other cerebral or visual 􀂃 Past hx 􀂃 Abnormal liver/ renal 􀂃 thrombocytopenia disturbances 􀂃 Menstrual hx functions Oligohydramnios 􀂃 SGOT, SGPT: - Persistent epigastric pain 􀂃 Obstetric hx 􀂃 Severe preeclampsia/ , IUFD Elevated liver enzymes 􀂃 Complaints and eclampsia regardless of 􀂃 Presence of 􀂃 Creatinine clearance, 􀂃 Diastolic BP ≥ 110 mmHg 􀂃 Proteinuria of 2+ or more by hx of present the gestational age congenital fetal serum creatinine, uric urine dipstick or a total protein pregnancy • In selected cases of malformations acid, total protein in level of ≥2 gm/liter in a 24-hour severe PET, where the incompatible urine, and blood urea: urine sampling expertise and with life impaired PHYSICAL EXAM 􀂃 Abnormal lab findings equipment are available, 􀂃 Coagulation profile: 􀂃 Hypertension 􀂃 Obvious fetal growth expectant management PT, PTT, clot. and 􀂃 Edema restriction may be undertaken for bleed. time → in DIC. 􀂃 Obstetric exam 􀂃 Neurological effects: fetal indications Fibrinogen and FDP to • Scotomata, hyperreflexia diagnose DIC • Eclamptic convulsions 􀂃 Fetal Surveillance MANAGEMENT CONVULSION ANTIHYPERTENSIV TIMING OF DELIVERY FLUIDS END-ORGAN COMPLICATIONS PROPHYLAXIS ES Magnesium sulphate 􀂃 Hydralazine 􀂃 Once the dx of Carefu 􀂃 Consumption coagulopathy: ister (MgSO4) 􀂃 Nifedipine severe preeclampsia l. platelets/FFP only if clinical bleeding. Blocks neuromuscular 􀂃 Labetalol has been Colloid 􀂃 Intracranial hemorrhage:Severe conduction through 􀂃 Sodium established, s. headache in the post partum with pre~ or blocking the release of nitroprusside termination of eclampsia. CT scan acetylcholine at NMJ. pregnancy becomes Rx: Combined obstetric and neuro in 3° Toxicity: Neurotoxicity mandatory after hosp (Loss of patellar reflex) , patient stabilization 􀂃 Sub capsular hematoma:Severe Resp depression (RR 􀂃 Mode of delivery epigastric pain+hepatomegaly. US. <12/min), Cardiac toxicity depends upon Rx:Correct coagulopathy. If liver rupture, (cardiac arrest) whether: The woman transfusion + liver surgery. 􀂃 Antidote: Calcium is in labor, The 􀂃 HELLP syndrome: Abnormal vascular

gluconate

progress of labor, The cervix is fit for induction.

tone, vasospasm and coagulation defects. Rx:Delivery regardless GA. Steroids. Platelets only if <20k/ml. Csection in platelets >50k/ml.

CLINICAL FEATURES 􀂃 Premonitory phase 􀂃 Tonic phase 􀂃 Clonic phase 􀂃 Coma

ECLAMPSIA MANAGEMENT EMERGENCY TREATMENT MONITORING DURING HOSPITAL STAY 1. Clear airway ages 􀂃 Close observation: 2. Apply an oxygen mask • Every 30 minutes assess pulse, BP and respiratory rate 3. Protect the patient from harm during • Maintain a fluid balance chart monitoring fluid intake seizures and urinary output 4. Control convulsions with MgSO4 􀂃 Limit IV fluid istration unless excessive blood loss 5. Control high BP to avoid fatal 􀂃 If convulsions occur despite MgSO4 therapy: complications • CT scan should be performed 6. Deliver fetus 􀂃 If severe respiratory insufficiency occurs: 7. Avoid diuretics and hyperosmotic • ICU ission and ventilation agents • Measuring blood gases and blood pH levels 8. Close observation

HISTORY 􀂃 Past history: • Hypertension treated before pregnancy with various antihypertensive medication • Renal problems 􀂃 Obstetric history: • Hypertension during previous pregnancies • Previous superimposed pre-eclampsia • Previous IUFD, IUGR and abortions 􀂃 Family history of hypertension

CHRONIC HYPERTENSION DIAGNOSIS EXAM 􀂃 Hypertension: Presenting before 20 weeks’ gestation 􀂃 Cardiac enlargement: May be present 􀂃 Edema: Occurs when preeclampsia or heart failure occurs as a complication of hypertension

INVESTIGATIONS 􀂃 Urine analysis: Proteinuria indicates occurrence of superimposed preeclampsia 􀂃 Renal function: Serum creatinine, uric acid and BUN 􀂃 Fundus examination: Changes indicating chronic hypertension

MANAGEMENT ANTIHYPERTENSIVE THERAPY - Antihypertensive therapy recommended when SBP > 160-170 and DBP > 105-110, as such treatment decreases the maternal cerebral and cardiovascular complications. - In acute control of severe HTN, the objective of therapy is a gradual reduction of blood pressure to a level of about 140150 / 90-100 mmHg BP should be assessed every 15 minutes initially, once the blood pressure is stabilized the interval can be lengthened to 30 minutes - Lowering the blood pressure rapidly over minutes → abrupt and profound ↓ in BP → ↓ cardiac output to the uterus with possible fetal hypoxia. Continuous fetal heart rate monitoring should be performed during initial therapy to detect such effect and allow early remedial action HYDRALAZINE (Vasodilator), NIFEDIPINE (Ca Channel Blocker), LABETOLOL (Beta-blocker) - most commonly used. 􀂃 Labetalol should be avoided in asthma. Atenolol, ACE inhibitor, ARB and diuretics should be avoided 􀂃 Diuretics are not recommended 􀂃 Angiotensin converting enzyme inhibitors are contraindicated with pregnancy 􀂃 • • •

Termination if: Fetal maturity reached Fetal distress and severe IUGR Additional complications occur (severe preeclampsia, abruptio placentae)

INDICATION When delivery is safer to mother & fetus than continuation of pregnancy. 1. Postdate 2. Pre-eclampsia 3. PROM 4. Chorioamnionitis 5. IUGR 6. IUFD 7. Fetal anomalies 8. DM 9. Abruptio placenta 10. Rh isoimmunication

INDUCTION OF LABOR Indicated in 10-20% CONTRAINDICATION ABSOLUTE RELATIVE 1. Placenta previa 1. Severe pre2. Previous 2C/S, previous 1 due to eclampsia recurrent cause, previous classical 2. Breech C/S presentation. 3. Abnormal antenatal CTG 3. Multiple pregnancy 4. Transverse/oblique lie 4. Grand multipara 5. Absolute contracted pelvis 5. Polydroamnios 6. Active genital herpes infection. 6. Presenting part 7. Tumor occupies pelvis above pelvic inlet. 8. Cervical carcinoma 9. Successful pelvic floor repair & successful surgical rx of stress incontinence.

Bishop Score: Assess cervical condition & station of the head, in 13. BISHOP SCORE 0 Cervical dilatation Closed Cervical length >2cm Cervical consistency Firm Cervical position Station of the head

Posterio r -3

Bishop score <7 – unfavorable cervix. Bishop score 7 or more – favorable cervix

COMPLICATION 1. Hyperstimulation → fetal distress & uterine rupture. 2. Failed induction → increased incidence of C/S. 3. Prolonged labour → instrumental delivery & PPH. 4. More painful → more analgesia 5. Prematurity 6. Infection

order to choose the best method for induction. Total score 1 1-2cm 2-1cm Mediu m Centra l -2

2 3-4cm 1-0.5cm Soft

3 >5cm <0.5cm

Anterior -1-0

Below ischial spine

METHOD OF INDUCTION Not reach effective contractions Bish op <7

Vaginal Prostaglandin

Bish op >=7

Artificial Rupture of Membrane

Oxytocin

Indicated if effective uterine contractions not obtained after 1-2 h  ↑ PG release from fetal of AROM. memb & decidua, & by Complications: mechanical descent of 1. Uterine hyperstimulation → Uterine fetal head rupture & Fetal Distress  ↑ oxytocin from 2. Hypotension if given IV bolus dose. 3. Neonatal jaundice – if total oxytocin posterior pituitary >20 units. (Ferguson reflex) 4. Water intoxication – if total amt of Complications: Cord fluids >1.5L → confusion, convulsion, prolapsed, placental coma, death. abruption, infection. How given: Start 2mU/min, double the dose every 30min. Never exceed 32mU/min (multipara) & 64mU/min (primipara). *Effective uterine contractions: 3-4 contractions, each lasting 50-60seconds in When 10minutes. effective contractions reach, keep lowest effective dose. 

PGE2 (Prostin) – most commonly used. PGE1 (Misoprostol)  Vaginal PGE2 pessory 3mg or Intracervical PGE1 gel 0.5mg  Dose can be repeated every 4-6h for a max dose of 3doses in 24h.  Main complication: Uterine hyperstimulation → Uterine rupture & Fetal Distress.  If cervix remains unfavorable despite max dose of PG (3doses/24h), re-evaluate pt & if there’s no urgent indication for

Induces labor by

MANAGEMENT OF PATIENTS FOR INDUCTION OF LABOR BEFORE INDUCTION DURING INDUCTION 1. Counseling & explanation. 1. Good selection of method of induction (Bishop score) 2. Hx – Assess GA & R/O contraindications of induction. 2. Proper dose of PG or Oxytocin. 3. Obstetrics exam – Assess lie, presentation, 3. Monitoring of labor – Fetal wellbeing, uterine activity, progress engagement. of labor & maternal wellbeing. 4. Vaginal exam: Assess Bishop score & pelvic 4. Adequate pain relief – Best epidural adequacy. 5. Ultrasound: Assess fetal age, wellbeing, amt of liquor & placental site. 6. CTG: Assess fetal wellbeing. TREATMENT OF HYPERSTIMULATION & FETAL DISTRESS >7.25 → Continue vaginal delivery Fetal distress 7.2-7.25 → Repeat pH after 30min Stop oxytocin. <7.2 → Emergency c-section Give oxygen by mask. Lateral decubitus. Rapid infusion normal saline. Uterine Persist hyperstimulation

Fetal scalp Fetal distress persist blood sampling

Terbutaline Hyperstimulation persist 0.25mg bolus IV

Emergenc y Csection

PROLONGED PREGNANCY Post-date pregnancy: Continuation of pregnancy beyond 40 completed weeks Post-term pregnancy: Continuation of pregnancy beyond 42 completed weeks Incidence 5-10% pregnancies. ETIOLOGY Majority of cause – no underlying cause i.e. physiological continuation of the pregnancy. Extremely rare cases may be due to anencephaly, fetal adrenal hypoplasia or to placental sulphatase enzyme deficiency. RISKS A] Placental insufficiency & hypoxia which leads to: 1. Increased perinatal mortality (PNM) 2. Meconium aspiration syndrome 3. Oligohydroamnios & cord compression B] Increased fetal weight & ossification of skull with decreased moulding, which leads to: 1. Prolonged labour and failure to progress which leads to ↑ incidence of C/S. 2. Shoulder dystocia – with its neonatal & maternal risks. a) Maternal risks – vaginal & cervical lacerations & rupture uterus b) Neonatal risks: neonatal asphyxia & death, cervical cord injury, brachial plexus injury (erb’s palsy in C5&C6, klumpk’s palsy in C8&T1, phrenic nerve injury in C4), clavicular & humeral fractures. MANAGEMENT BEFORE DELIVERY DELIVERY 1. Counseling & explanation: explain risks on the fetus. 1. In uncomplicated postdate pregnancy, pt should be 2. Hx – for accurate assessment of GA and to exclude C/I for delivered at 41wks + 3-7days. induction. 2. Method of delivery either induction of labour (method of 3. Obstetric exam: Assess lie, presentation & engagement. induction depends on Bishop score) or by C/S if there is C/I 4. Vaginal exam: Assess Bishop score & pelvic adequacy. for induction. 5. Ultrasound: at 40.41 & 42 wks, to assess amt of liquor, 3. If delivery by induction of labour, a senior obstetrician fetal wellbeing & w8. should attend delivery due to risk of shoulder dystocia and a 6. CTG: every 3days after 40wks, to assess fetal wellbeing. pediatrician should attend due to risk of meconium aspiration. ASSESSMENT OF GA

ANTENATAL METHODS 1. First day of LMP – reliable in 50% of pregnancies. 2. Ultrasound – best is CRL between 7-13wks, then BPD & FL between 1326wks & then BPD & FL after 26wks. 3. Clinical – onset of early pregnancy sx, early bimanual exam, quickening & serial fundal height. INFERTILITY INTRODUCTION Def: Involuntary failure to conceive within 12 months of commencing regular unprotected intercourse. (Old definition within 24 months) • Primary Infertility: No previous pregnancy • Secondary Infertility: With previous pregnancy ( whatever the outcome)

POSTNATAL METHODS 1. Dubowitz score – include an assessment of the physical & neurological features of the newborn. 2. Farr score – which include an assessment of the physical features of the newborn.

PHYSIOLOGY Conception requires : • Oocyte, sperm, at optimal stage • Needs transportation • A receptive place for implantation • Intact Male and Female reproductive systems

Incidence: • 10-15% of married couples • About 75% of couples conceive by 12 months, • About 85% of couples conceive by 24 months.

•

• • • • • •

POSSIBLE CAUSES OF INFERTILITY FEMALE MALE Ovulatory failure factor: (anovulation) Coital factor: (psychological or High centres - hypothalamic-pituitary axis organic) Thyroid Spermatogenesis problem: Adrenal Azospermia, oligospermia Ovarian - PCO(20%), premature failure( >30IU/L) Ductus problem: Azospermia due Genetic & Chromosomal to obstruction (infection) Tubal factor: PID,T.B Uterine factor: Asherman’s, congenital anomaly. Cervical factor: infection, immunological Endometriosis: Coital factor: aparunia, dysparunia, vaginismus Psychosomatic: ? Neurohormones

IDIOPATHIC About 15-30% of Infertility. It is a definition by exclusion, and that depends on the standard investigations used. (Ovulatory, Tubal, Male)

INFERTILITY WORK UP HISTORY EXAM Male: Age, history of mumps, occupation, drugs, chemical, • Male: exam.vas deference -size of testicles , irradiation, hernia operations, varicocele varicocele, endocrine stigmata • Female: Age, menstrual cycle (regularity) - previous pregnancies, • Female: B.P - Thyroid - galactorrhoea – Abortions and TOP, galactorrhoea - 1°/2° - contraceptions , hirsutism. Abdominal and pelvic exam Hirsutism. genitalia (External & Internal) • Both: Coital history:- S.T.D - past med & surgical hx, smoking and taking drugs SPECIAL INVESTIGATIONS OVULATION CERVICAL FACTOR TUBAL & UTERINE MALE FACTOR OTHERS FACTORS 1. B.B.T.chart: - Cx score (amount, (CILIA, FERTILIZATION, Semen analysis: by CBC Biphasic an increase spinnbarkeit, ferning, os) TRANSPORT) coitus interruptus or Urine analysis of 0.5C, progesterone - Cervical mucus alteration: - Tubal insufflation masturbation after S.T.D – effect thin-clear-watery–elastic (Rubin’s test) obsolete abstinence of 3-5 days Chlamydia 2. Cx mucus (subjective) nowadays delivered within 2 hours Rubella titer alteration: - Elasticity (spinnbarkeit) - Hysterosalpingogram: to lab. TFT Mittelschmerz pain - Fernning (arborization or using radioopaque water Skull x ray 3. Hormonal assay: crystallization) of NaCl due soluble, no G.A Normal values: by WHO CT Scan S. progesterone d21 to unopposed action of - Laparascopy + criteria X ray chest. (20-30nmol/L), estrogen Methylene blue dye test: Volume: >2ml S. prolactin - P.C.T:(post coital test): under G.A, checks for liquification in 20- 30 <20ng/ml positive if: more than 5-10 endometriosis and D&C minutes S. FSH and LH first sperm in (H.P.F) alive in the same sitting Density: >20-250 Mil/ml days of period forward progressive motility (when done in luteal Motility: > 50% forward 4. Endometrial biopsy after 6-12 hours of sexual phase) motility within 2 h. -d 21- secretory intercourse at time of - Hysteroscopy - in Morpho: > 30% normal endometrium. i.e.T.B ovulation. Repeat 3 times if Ashemann’s synd. forms 5. U.S.S - monitoring Negative (wrong timing, congenital anomaly to of follicles 18-22 mm, cervical hostility due ? visualize the uterine Seminal fluid 90% of d12=12mm antibodies, severe oligo or cavity (using CO2 or ejaculate: 2\3 from 6. Laparascopy azospermia) glyceine solution) seminal vesicles laparatomy - Cross hostility test - Hy-co-sy (fructose), 1\3 from •

incidental findings 7. LH peak (LH home kits): 26h later ovulation occur 8. Pregnancy

(Kremer test) if P.C.T is (hysterosalpingoprostate (zinc & acid ph.) negative contrast-sonagraphy) In azospermia + - Antisperm antibody titre using Echovist oligospermia: hormonal and MAR ( mixed FSH,LH, prolactin & agglutination reaction) karyotyping INFERTILITY MANAGEMENT INDUCTION OF OVULATION TUBAL FACTORS CERVICAL FACTOR A] Fertility agents: • Selective • improve cervical score: Treat • Oral agents: 90% induce ovulation, but 60% pregnancy Hysterosalpingogra infection, Cryocautery, -In cases of hyperprolactinaemia : m Estrogen Bromocriptine (ergot alkaloids, dopamine agonist) • Surgery: • immunological - ? Lisuride 1x1 microsurgery: after corticosteroids for the male Cabergoline(Dostinex) 1mg weekly falloposcopy: during the luteal phase of -Clomiphene citrate (clomid): 50mg _ 200mg _ (d2 - d6), for 6 • Salpingolysis, female ,Male use of condom cycles. It is oral cyclical, synthetic, nonsteroidal, weak for 6 months salpingostomy, estrogen with antiestrogenic activity excision & • SIUI and SIVF -Tamoxifen : 10-40mg (d2 - d6) for 6 cycles, in PCO reanastom. (success -Cyclofenil : 200mgb.d for 10 days from 10-40%) In PCOS :metformin (oral insulin sensitizers) • Uterine anomalies: Side effects: ovarian cysts, twins 5%, hair loss, GIT, rarely Myomectomy for hyperstimulation syndrome (OHSS) fibroids Metroplasy in certain • Injectable agents cases Gonadotrophin therapy: urinary extracts, now recombinant • I.V.F program - HMG: (FSH+LH) (Humegon-pergonal) injections 1-3 ENDOMETRIOSIS MALE FACTOR

ampules daily or every other day till follicular maturation, about 5-10 injections - FSH: only (metrodin) in P.C.O - H.C.G: (pregnyl,profasi) - 5000 - 10000 unit after follicular maturation to release oocyte - L.H.R.H-a: - ( Busserlin-Zoladex-superfact-Decapeptyl ) continuous (nasal or s.c. 4-6 times daily or depot IM) to deplete endogenous FSH,LH - L.H.R.H-a: - pulsatile infusion every 90 minutes, 15ug - L.H.R.H.antagonist Side effects: multiple pregnancy 25% - hyperstimulation syndrome (if severe) -ascitis, large ovarian cysts, hydrothorax, thromboembolic disease, multiorgan failure • B- Surgical: Ovarian drilling, wedge resection(obsolete) Options of treatment: Oral fertility agents → Injectables → SIUI,SIVF

• • •

Danazol, LHRH a treatment (medical) Conservative surgery: I.V.F. program

 Treatment directed towards cause.  Advice: stop smoking and alcohol, avoid tight underwear, take regular cold baths, improvements in coital practice.  Psychological therapy: for sexual dysfunction  In severe oligospermia and azoospermia, check for karyotype (Klinefelter’s syndrome, testicular atrophy)  hMG for hypothalamiituitary failure.  Bromocriptine for hyperprolactinemia.  Surgical treatment in vasectomy reversal.  Varicocele ligation in varicocele.  ART: SIUI,ICSI (by TESE or MESA)

ARTIFICIAL INSEMINATION 

Artificial insemination (AI)  AIH: intravaginal, intracervical and pericervical, intrauterine, intraperitoneal  AIH(DI)  IUI and SIUI  The mostly used nowadays: is SIUI (stimulated intrauterine insemination: - Proper selection of the cases - Controlled ovarian stimulation - Preparation of semen - Timing of insemination

ASSISTED REPRODUCTION TECHNIQUES (ART) IVF + ET (EMBRYO VARIANTS OF IVF TRANSFER)  Up to 35% could o G.I.F.T: Gamete intra fallopian transfer (indicated: unexplained benefit from infertile infertility, oligospermia, couples endometriosis. (C.I.tubal damage)  Candidates: Tubal factor , endometriosis o Procedure: Laparascopy at ovulation retrieve oocycte mix with prepared , oligospermia semen - deposit both in tube ,unexplained infertility o Z.I.F.T  It is expensive, requires sophisticated o SUZI subzonal injection lab. facilities, highly o ICSI intracytoplasmic sperm injection skilled medical, o PESA percutaneous epididymal sperm nursing, scientific and aspiration tech. personnel o MESA o TESE OUTCOMES OF IVF PREGNANCIES 25% risk of miscarriage 2-5% risk of ectopics, heterotropic pregnancy 25% risk of multiple pregnancy Increase risk of prematurity, low birth wt, Cs

RESULTS OF IVF  

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E.T (1) - 10% chance of single pregnancy E.T (3) - 25-30% chance of single pregnancy. 5% twins, 1%triplets Efficiency: 25-35% for each cycle - Take home baby 15-20% According to the infertility factor and the centre

RISKS OF IVF Psychological trauma if failed (OHSS) ovarian hyperstimulation syndrome Multiple pregnancy

INSTRUMENTS 1) Sims Speculum. Uses: for visualising fistulae (abnormal holes or connections) and prolapse (protrusion) of the rectum orbladder into the vagina

Uses: Pelvic exams.

2) Bivalve speculum To take Pap smear. To take cone & punch biopsy.

3) Curette Dilation & curettage. Evacuation & curettage.

GLANDS: ADENOCARCINOMA ENDOMETRIU M

STROMA: ENDOMETRIAL STROMAL GLANDS + STROMA: MMT LEIOMYOSARCOMA

MYOMETRIUM OTHERS INTRODUCTION  Peak incidence is at age of 61 years  75% occur in postmenopausal women  Only 5% occur before age of 40  There is marked geographical and racial variation in the incidence

ENDOMETRIAL ETIOLOGY Excessive unopposed estrogen stimulation of the endometrium Increase Obesity, Nulliparity, Late menopause, PCO, Estogensecreting ovarian tumors, Unopposed estrogen therapy, Family history of breast, ovary, colon, endometrial tumors, DM Decrease OC, Progesterone

CARCINOMA CLINICAL PRESENTATION  PMB  Intermenstrual bleeding/irregular periods  Heavy regular periods  Watery discharge/offensive  Pain ENDOMETRIAL BIOPSY SHOULD BE DONE IN ALL PATIENTS WITH PMB

PATHOLOGY  Growth is usually adenocarcinoma  Adeno-acanthoma/ adenosquamous tumors  Serous papillary/

DIAGNOSIS  Always investigate PMB, continuous or irregular bleeding before assuming benign cause for the bleeding  Cervical smear  TVS

PROGNOSIS  Stage  Grade  Myometrial invasion  Age  Tumor size Assessment of these

PHYSICAL FINDINGS  Rarely suggest the diagnosis  Uterine enlargement  Palpable lymph node in the groin. Supraclavicle.  Vaginal nodule

TREATMENT  Low risk stage I: TAH, BSO  High risk: postoperative radiotherapy  Stage II: TAH,BSO+ radiotherapy/radical hysterectomy

clear cell  Grade 1 → grade 3  Spread: Direct invasion, Lymphatic, Blood

 Endometrial biopsy  Hysteroscopy +curettage  If confirmed, CBC,KFT,URINE, MRI.CXR

factors require laparotomy and histology (surgical pathological staging)

 Stage III /IV: individualized .rarely surgery usually chemo, radiotherapy and hormonal  Follow up  Recurrence usually within 2 years (70%)  Overall 5 year survival is 60%

FIGO STAGING Stage 1 Confined to the body of uterus Stage 2 Involvement of cervix Stage 3 Extension into adnexae,vagina or positive L.N Stage4 Distant mets

ENDOMETRIAL SARCOMA  Endometrial stromal sarcoma  Malignant mixed mullerian tumors (carcinosarcoma)  More in black. Previous pelvic irradiation  Present with bleeding and pain  Poor prognosis

LEIOMYOSARCOMA 5-10% May arise from transformation of fibromyoma (0.2%) Mostly arise from normal myometrium Peak incidence is 10 years older than fibromyoma Present with abnormal bleeding and pelvic pain and wt loss Should be suspected in rapidly enlarging fibroids In 80%,diagnosis is made after hysterectomy Ideally should be treated by TAH, BSO, washing and full staging  Adjuvant radiotherapy or chemotherapy?       

BASIC CONCEPTS

PRESENTATION Part of the fetus occupying the lower segment of the uterus Cephalic (Head, 95%), Breech (Buttocks, 3-4%), Shoulder, Cord, Compound. Malpresentation is any presentation other than cephalic. LIE Relation of longitudinal axis of fetus to the mother’s longitudinal axis Longitudinal (99%) Transverse Oblique

STATION Relation between the lowest bony part of the presenting part to the imaginary line between two ischial spines -3, -2, -1, 0, +1, +2, +3 [if above line: -ve, if below line: +ve] Assessed through vaginal exam. ENGAGEMENT age of the widest diameter of the presenting part through the pelvic inlet. If <2 fingers needed to palpate fetal head in pelvic grip: Engaged. *Pelvic inlet: Upper border of symphysis pubis (ant), sacral promontory (post), ileopectineal line of iliac crest (lateral).

POSITION Relation between the dominator (bony landmark of the fetus) to the internal pelvis. 8: Anteriorly (left, right, direct), Posteriorly (left, right, direct), Transverse (left, right) Most common: Left occipito-anterior. Malposition is any position other than occipito anterior. *Bony landmarks: Vertex: Occipital Face: Mental Brow: Frontal Shoulder: Scapula Breech: Sacrum

FETAL ATTITUDE Relation of fetus parts to each other Well-flexed (normally), Extended

BREECH PRESENTATION DEFINITION CAUSES DIAGNOSIS Buttocks occupying Maternal Causes: Nulliparity, Old age, Fibroid, Hx: Subcostal pain (coz fetal head) lower segment of Polyhydroamnios, oligohydroamnios, Bicornuate Abd exam: Leopold maneuver –solid ballotable uterus. / septate uterus, Hx of breech, Uterine/pelvis rounded mass in fundus; soft irregular mass in Commonest tumors. pelvis. malpresentation. Fetal Causes: Prematurity, IUGR, Large babies, Vaginal exam: 2 ischial tuberosities & tip of Commonest cause is Multiple gestations, Fetal abnormalities, sacrum. prematurity. Congenital anomalies, Short umbilical cord, US: Confirm dx, look placental site, uterine Cephalo-pelvic disproportion. abnormality, # of babies, liquor amount, estimate fetal weight. TYPES FRANK @ EXTENDED COMPLETE FOOTLING Hips flexed, knees Feet present beside Hip & knee extended in extended. buttocks. Both hips & one or both sides. Primigravida. knees flexed. Preterm singleton. Multipara. A] EXTERNAL CEPHALIC VERSION (ECV) NOTES METHOD CONTRAINDICATIONS COMPLICATION S Done at term Prep her as if to do C-section – NPO, cannula, conduct in Absolute: HTN, PET, Previous Labor, PROM, (>37th wks) OT, ultrasound, CTG. 2 C-sections, Multiple Placental coz may revert Rotate the baby by direction of his nose until it becomes gestation with 1st twin abruption, to breech, or cephalic. breech, Abnormal CTG, HSV, Cord induce labor. Repeat CTG. Previa, Pt refusal. compression & Success rate If Rh-ve mother, give antiD coz risk of fetomaternal Relative: IUGR, prolapsed, 60%. hemorrhage. Polyhydroamnios, Fetal Discharge waiting for spontaneous vaginal delivery. oligohydroamnios, fetal bradycardia. anomaly. B] ASSISTED VAGINAL BREECH DELIVERY C] CAESEREAN SECTION CRITERIA ASSISTANCE Absolute Indications: Prematurity, Footling breech. Normal baby weight 2.5-3.5kg After delivery of buttocks, → 1) Episiotomy Superior to vaginal breech >36wks GA. Good pelvimetry (roomy 2) Keep fetal back anterior delivery. pelvis). Fetal head flexed, Breech type After appearance of scapula → 3) Rotate 90 to Frank or Complete. Experienced deliver anterior shoulder & vice versa. obstetrician. Anethetist (Epidural), No After visible hair line → 4) Either Liverpool

other indications for C-section, Multiparous, Normal labor progress, Uncomplicated pregnancy.

maneuver, or Mauriceau-Smellie-Veit maneuver or forceps delivery.

FACE & BROW PRESENTATIONS FACE Vaginal Exam: Nose, cheeks, mouth. Commonly misdiagnosed as breech. TYPES MENTO-ANTERIOR

Presenting diameter: 9.5cm. MENTOPOSTERIOR

MANAGEMENT If fully dilated → Allow vaginal delivery. If not fully dilated → Can augment labor with oxytocin. COMMON NOTES Never attempt to convert face to vertex. Never apply vacuum. Can use forceps. Can augment with syntocinon. Large episiotomy. If fully dilated → Csection. If not fully dilated → Monitor for conversion into vertex presentation. If fetus dead →

BROW Vaginal exam: Orbital ridges & nose. CAUSES Grand multiparous Neck swelling (cystic hygroma, goiter etc) Anencephaly

SHOULDER PRESENTATION Transverse or oblique lie. Abd Exam: Head in one flank & buttock in another. No vaginal exam till R/O previa. CAUSES Placenta previa, Prematurity, Polyhydroamnios, Multiple pregnancy, Abnormal uterus, Fibroid, Cervical cancer, Contracted pelvis, Relaxed ab wall. MANAGEMENT: C-section

Presenting diameter: 13cm. C-section. Never vaginal delivery.

Presenting diameter: 13cm.

Craniotomy.

DEFINITION Umbilical cord as the presenting part, below any part of the fetus. Coz ill-fitting presenting part into lower segment of uterus → cord can go into space below presenting part mainly when footling breech or AROM.

UMBILICAL CORD PROLAPSE RISK FACTORS CONSEQUENCES Multiparity Cord compression & Prematurity Vasospasm → Cutting Macrosomia blood from fetus → Fetal Breech distress. Polyhydroamnios Outcome depends on GA & duration of compression.

MANAGEMENT Emergency C-section Vaginal delivery only if delivery is imminent (when vaginal quicker than c-section: fully dilated & presenting part very low) While waiting for C-section - Fill bladder with 1L - Push presenting part up - Tredelenburg position

ESSENTIAL HYPERTENSION CLASSIFICATION According to Severity: A] Mild B] Severe (>160/110) According to Complications A] Uncomplicated B] Complicated. Any of the following: Cardiomyopathy; Age >40; Duration of HTN >15yrs; Renal disease; DM,

MATERNAL RISK Superimposed PET. Abruptio. Cerebral hemorrhage Exacerbation of HTN Renal failure Congestive heart failure.

FETAL RISK IUGR. IUFD. Prematurity. PNMM directly related to HTN severity.

CT disease or coarctation of aorta; Previous hx of perinatal loss. MANAGEMENT PRENATAL ANTENATAL DURING LABOR POSTNATAL Assess cause & severity. Mild uncomplicated HTN, stop drugs & Observe BP. Observe BP esp 48h Look for risk factors. observe 3months. If BP stayed mild, Strict fluid control. postpartum. Review drugs. don’t give drugs. Continue AHD if taking Observe for pulm edema. Establish baseline – CBC, If BP >160/110, give drugs. them. Observe for hypertensive urine analysis, 24h urine Observe fetal growth (IUGR/IUFD) Continuous fetal heart encephalopathy. collection test, KFT, Echo, Observe maternal condition. monitoring. Reassess cardiac & renal ECG, CXR. No indication to induce labor before f(x). 41wks. CARDIAC DISEASES Predictors (NYHA Functional Classification) # Risk of Complicates 1% of pregnancies. predictors complications Complications during pregnancy: HF, Cardiac dysf(x) – EF>60 or <40 0 3% arrhythmia, stroke & death. 1 30% Presence of pulm HTN Assessment before pregnancy is essential. 2 60% Presence of cyanosis (low Hb saturation) Can be congenital, rheumatic & ischemic. Presence of aortic or mitral valve stenosis Hx of CHF, arrhythmia or TIA MANAGEMENT PRENATAL ANTENATAL DURING LABOR Classify patients (predictors of Monitor signs & sx of HF. Avoid pain coz pain ↑ EF → acute HF. Avoid complications). Serial Echo. hypotension. Investigations. Serial fetal monitoring. Left lateral position with oxygen mask. Review drugs. Continuous saturation monitoring. Give predictions (safe to go thru Shorten 2nd stage labor (instrumental?). pregnancy?) Prophylactic antibiotics. Careful fluid therapy. Continuous CTG. Continuous ECG.

HYPERTHYROIDISM OVERVIEW MANAGEMENT 95% cases due to Graves. 50% have +ve family hx. Carbimazole & PTU are most commonly used drugs. Clinical picture similar to non-pregnant. Both cross placenta, to a lesser extent does PTU, so even in Most discriminatory features in pregnancy are weight moderate doses may cause fetal hypothyroidism. loss, tremor & lid lag. Both not teratogenic. Thryotoxicosis usually improves in pregnancy as other β blockers used in thyroid crisis. Thyroidectomy rarely autoimmune. indicated in pregnancy. Exacerbations may occur esp in 1st trimester (α subunit Radioiodine contraindicated in pregnancy (also 4months of βhCG resembles TSH) before) & during lactation. Thyrotoxicosis associated with infertility, recurrent Check for neonatal & fetal thyrotoxicosis. pregnancy loss, IUGR, preterm labor, higher PNMM. HYPOTHYROIDISM OVERVIEW MANAGEMENT Commoner than thyrotoxicosis. Associated with other autoimmune like DM & pernicious Thyroxine supplements are the anemia. only replacement therapy. Clinical picture similar to non-pregnant. Crosses placenta but only very Most discriminatory feature are cold intolerance, slow pulse & delayed relax of tendon little amount will reach fetus, so reflexes. fetus not at risk of dev Pregnancy itself has no effect on hypothyroidism. hyperthyroidism. Associated with infertility, miscarriages, anemia, fetal loss, IUGR & PET. Association b/w untreated hypothyroidism & reuced IQ & neurodev delay in offspring. EPILEPSY OVERVIEW MANAGEMENT Most cases are idiopathic and no underlying cause. The lowest effective dose. Try with 1 drug & give full dose of folic 30% familial. acid 5mg. All types of seizures can occur in pregnancy. Try stopping AED, if she is fit free for >2yrs. Most AED are teratogenic. Detailed anomaly scan at around 2owk gestation. In majority of cases, frequency of seizure are not Vit K supplement for the last 4wks of pregnancy for pts taking altered by pregnancy. valproic acid. Risk of seizures are highest in peripertum period. Avoid pain & long course of labor. 5-10% risk of transmitting epilepsy. Major malformations caused by AED are NTD, orofacial defects & The fetus is relatively resistant to short episodes of congenital heart defects. hypoxia. Minor malformations are dysmorphic features, hypertelorism,

hypoplastic nails & digits. MENOPAUSE 

 

occurs secondary to a genetically programmed loss of ovarian follicles Defined as the cessation of menstrual periods menopause occurs at a mean age of 51.4 years in normal women

Epidemiology

The menopausal transition 

  

variation in menstrual cycle length (>7 days different from normal menstrual cycle length, which is 21 to 35 days) ≥2 skipped cycles and an interval of amenorrhea ≥60 days elevated serum FSH concentration Cessation menstrual period (not recognized until after 12 months of amenorrhea).



Perimenopause — "around the menopause," and begins with the menopausal transition and ends 12 months after the last menstrual period  Menopause — Menopause is defined by 12 months of amenorrhea after the final menstrual period. It reflects complete, or near complete, ovarian follicular depletion and absence of ovarian estrogen secretion.  Postmenopause — is defined as (early) the first five years after the final menstrual period. It is characterized by further and complete dampening of ovarian function and accelerated bone loss; many women in this stage continue to have hot flashes. (late) begins five years after the final menstrual period and ends with death Endocrinology

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

Although the average age at menopause is approximately 51 years, for 5 percent of women, it occurs after age 55 (late menopause), and for another 5 percent, between ages 40 to 45 years (early menopause). Menopause occurring prior to age 40 years is considered to be premature ovarian failure

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The age of menopause is reduced by about two years in women who smoke There is also a tendency for women who have never had children and for those with more regular cycles to have an earlier age of menopause Other factors that may be important include: 1. A family history of early menopause 2. A history of type 1 diabetes mellitus 3. The presence of a variant of form galactose-1phosphate uridyl transferase 4. Shorter cycle length during adolescence (which is also a predictor of higher basal FSH).

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Menstrual cycle and hormone patterns begin to change many years prior to menopause. In the late reproductive years, prior to the menopausal transition, menstrual cycles are ovulatory, but follicular phase length begins to shorten. In the early menopausal transition, women begin to experience some menstrual irregularity. During this stage, inhibin B concentrations fall due to a decline in follicular number, and as a result, serum FSH levels begin to rise, with relative preservation of estradiol secretion (normal or high estradiol levels), but with low luteal phase progesterone concentrations . The preservation of estradiol secretion appears to be due to an increase in aromatase activity. In the late menopausal transition, cycle variability increases. High FSH and low estradiol values may be suggestive of menopause, After menopause, when ovarian follicles are depleted, the ovary no longer secretes estradiol. However, it continues to produce and secrete androgens under the continued stimulation of LH

Clinical Manifestations 1.Bleeding patterns

2.Hot flushes

3. Depression and mood changes



Chronic anovulation and Progesterone deficiency in this transition period may lead to long periods of unopposed estrogen exposure and therefore anovulatory bleeding and endometrial hyperplasia.  Oligomenorrhea (irregular cycles) for six or more months, or an episode of heavy dysfunctional bleeding.  Irregular or heavy bleeding during the menopausal transition may be treated with lowdose oral contraceptives or intermittent progestin therapy 4.Sleep disturbance

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A distressing feature of hot flashes is that they are often associated with arousal from sleep. In addition, primary sleep disorders are common in this population, even in the absence of hot flashes.

Clinical Manifestations

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

The most common acute change during menopause is the hot flush, which occurs in up to 75 percent of women in some cultures, but only about 20 percent of these women seek medical attention for treatment of their flashes. As noted above, hot flushes are most common in the late menopausal transition and early postmenopausal periods They are self-limited, usually resolving without treatment within one to five years, although some women will continue to have hot flushes until after age 70. The prevalence of vasomotor symptoms is quite variable across cultures

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Hot flushes typically begin as the sudden sensation of heat centered on the upper chest and face that rapidly becomes generalized. The sensation of heat lasts from two to four minutes, is often associated with profuse perspiration and occasionally palpitations, and is often followed by chills and shivering, and sometimes a feeling of anxiety. Hot flushes usually occur several times per day, although the range may be from only one or two each day to as many as one per hour during the day and night. Hot flashes are particularly common at night.

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However, a significant association between the menopausal transition and risk for depression seems apparent overall. In the largest prospective cohort study to date, the Study of Women's Health Across the Nation (SWAN) reported that women in early perimenopause had a higher rate of mood symptoms (14.9 to 18.4 percent) than premenopausal women (8 to 12 percent) These mood symptoms primarily were irritability, nervousness, and frequent mood changes, but not feeling "blue," and were more common in women with lower educational attainment. Several studies have reported that a prior history of depression or PMS is a strong predictor of depressive recurrence during the menopausal transition .

5.Genitourinary symptoms a.Vaginal dryness

b.Sexual dysfunction

c.Urinary symptoms

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The epithelial lining of the vagina and urethra are very sensitive to estrogen, and estrogen deficiency leads to thinning of the vaginal epithelium. This results in vaginal atrophy (atrophic vaginitis) causing symptoms of vaginal dryness, itching and often, dyspareunia. The prevalence of vaginal dryness was about 47 percent of women On exam, the vagina typically appears pale, with lack of the normal rugae and often has visible blood vessels or petechial hemorrhages. Vaginal pH, which is usually <4.5 in the reproductive years, increases to the 6.0 to 7.5 range in postmenopausal women not taking estrogen. The increase in pH and vaginal atrophy may lead to impaired protection against vaginal and urinary tract infection

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Estrogen deficiency leads to a decrease in blood flow to the vagina and vulva. This decrease is a major cause of decreased vaginal lubrication and sexual dysfunction in menopausal women This neuropathy appears to be completely reversible with estrogen replacement therapy The cervix also can atrophy and become flush with the top of the vaginal vault. The elasticity of the vaginal wall may decrease and the entire vagina can become shorter or narrower.

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Low estrogen production after the menopause results in atrophy of the superficial and intermediate layers of the urethral epithelium with subsequent atrophic urethritis, diminished urethral mucosal seal, loss of compliance, and irritation; these changes predispose to both stress and urge urinary incontinence. The prevalence of incontinence increases with age. It has not been established, however, that the frequency of urinary incontinence increases across the menopausal transition Although data are conflicting, systemic estrogen therapy does not appear to be effective for the treatment of urinary incontinence. Recurrent urinary tract infections are also a problem for many postmenopausal women. In addition to epithelial atrophy, estrogen deficiency can increase vaginal pH and alter the vaginal flora, changes which may predispose to urinary tract infection

6.Others  

Breast pain Breast pain and tenderness are common in the early menopausal transition, but begin to diminish in the late menopausal transition Menstrual migraines — Menstrual migraines are migraine

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Balance — Impaired balance in postmenopausal women may be a central effect of estrogen deficiency .Problems with balance may play a major role in the incidence of forearm fractures in





headaches that cluster around the onset of each menstrual period. In many women, these headaches worsen in frequency and intensity during the menopausal transition . Skin changes — The collagen content of the skin and bones is reduced by estrogen deficiency. Decreased cutaneous collagen may lead to increased aging and wrinkling of the skin. The collagen changes may be minimized with estrogen. t pain — Although the prevalence is not known, some women experience diffuse t pain during the menopausal transition and postmenopausal period

Long-term issues 



women. The incidence of Colles' fractures increases markedly in women at age 50 but remains stable in men up to the age of 80. A mechanism other than osteoporosis must be invoked to explain this observation because osteoporosis occurs gradually. The fracture is usually caused by falling on an outstretched hand. The role of estrogen therapy on falls is discussed elsewhere.

Diagnosis

Bone loss — Bone loss  Menopause is defined clinically as 12 months of begins prior to amenorrhea in a woman over age 45 in the absence menopause. The annual of other biological or physiological causes. rates of loss during  The best approach to diagnosing the menopausal these phases were transition is a longitudinal assessment of menstrual approximately 1.8 to 2.3 cycle history and menopausal symptoms (vasomotor percent in the spine and flushes, mood changes, sleep disturbances). 1.0 to 1.4 percent in the  Differential diagnosis — Hyperthyroidism should hip. Higher body mass always be considered in the differential diagnosis index was associated pregnancy, hyperprolactinemia. with slower bone loss;  Atypical hot flashes and night sweats may be due to ethnicity had no effect. other disorders, such as medications, carcinoid,  Cardiovascular pheochromocytoma, or underlying malignancy. disease  Dementia Summary & recommendations

Hormone Replacement Therapy (HRT) 

Postmenopausal hormone therapy is currently recommended short-term for the management of moderate to severe vasomotor flushes. Long-term use for prevention of disease is no longer recommended Hormone preparations 

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Combined, continuous conjugated estrogens e.g. (0.625 mg) and medroxyprogesteroneacetate (MPA 2.5 mg). Un-opposed estrogens (in

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Most postmenopausal women, with the EXCEPTIONof women with breast cancer or known cardiovascular disease, who have symptoms of vaginal atrophy and/or vasomotor instability are good candidates for estrogen therapy (for the shortest duration possible depending upon symptoms). Vasomotor instability For postmenopausal women with moderate-to-severe vasomotor symptoms (and no history of breast cancer or cardiovascular disease), short-term estrogen therapy as the treatment of choice Urogenital atrophy — With the exception of women with breast cancer, almost all postmenopausal women are candidates for vaginal estrogen. Osteoporosis — We currently do not consider estrogen to be a first-line therapy for osteoporosis. Therefore, the management of women who choose not to or cannot take estrogen is the same as for other postmenopausal women. Cardiovascular disease prevention — Estrogen is NO longer indicated for the prevention of CHD in postmenopausal women. The best means of primary and secondary prevention of cardiovascular disease involves attention to risk factors such as smoking, hypertension, dyslipidemia, and diabetes mellitus

hysterectomised patients )  Oral preparations , local , injectables , vaginal preparations and implants Uses 

Treat short term menopausal symptoms  Disease prevention Disease prevention   

Coronary heart disease Osteoporosis Dementia

Women with POF

Women with breast cancer

Androgen replacement

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



In healthy women with premature ovarian failure, we continue their hormone therapy until their late 40s or age 50 years. At that point, the same discussion of potential risks and benefits of postmenopausal hormone therapy should take place



Although women with breast cancer often experience early menopause due to adjuvant chemotherapy, and may have vasomotor symptoms due to tamoxifen therapy, estrogen therapy should NOT be prescribed. The epidemiologic data and clinical trial data have been inconsistent, but the increased risk of breast cancer recurrence with estrogen therapy in one trial (HABITS), is of great concern. We therefore do not recommend estrogen for women with a personal history of breast cancer.

The known decrease in ovarian androgen production rates and serum androgen concentrations has caused concern that menopause might be associated with a decline in libido. An age-associated decline in sexual desire has been observed in both men and women. However, it is unclear whether the decline in libido in women is age- or menopaelated, since studies in women have not shown a significant correlation between libido and the serum estradiol or testosterone concentration

MULTIPLE GESTATIONS EPIDEMIOLOGY Hellin’s rule: 1 in 80n-1 pregnancies 60% are Dizygotic (dichorionic and diamniotic) 40% are Monozygotic (one in 250 births, constant worldwide) - 10% (dichorionic and diamniotic) - 20% (monochorionic and diamniotic) - 10% (monochorionic and monoamniotic)

DEFINITION & TYPES Any pregnancy in which two or more fetuses exist simultaneously Types  Dizygotic (dichorionic and diamniotic), (fraternal)  Monozygotic 0-72 hr → dichorionic and diamniotic 4-8 d → monochorionic and diamniotic Incidence varies with: Ethnic group (Blacks more), 9-12 days → monochorionic and Maternal age (Older more), Parity (Multi more), monoamniotic >12th day → coned (Siamese) twins, Family Hx, COH, 10 and 20% with CC & hMG res. (Only in 1:70,000 (thorcopagus is the dizygotic twins) commonest) CHORIONICITY UNIQUE COMPLICATIONS WITH IN MONOCHORIONIC DETERMINATION Ultrasound “TWIN-TWIN TRANSFUSION “ACARDIAC TWIN” - 30% of twins will be of SYNDR (TTTS)” different sex One baby will give blood to Two growing fetuses but only - 23% will have monochorionic the other baby through an one heart beating placenta AV anastomosis. Cause: Living cells in the - 27% will have same sex, deformed baby is sustained by dichorionic placentas, but the healthy twin’s circulation. different blood grouping - 20% have same sex, dichorionic placentas, and identical blood grouping that will require HLA or DNA PCR analysis

“FETUS PAPYRACEOUS” Fetus in a multi-gestation pregnancy dies in-utero & then partially/completely absorbed by the mother or twin. @Twin embolization (vanishing) syndrome

PREGNANCY COMPLICATIONS Hyperemesis gravidarum Hypertensive disease, 4x more common than singletons Gestational diabetes Anaemia Hydramnios in 12%, primarily in monozygotic twins Reflux, ab discomfort, back pain, leg swelling, bladder sx and haemorrhoids. APH (PP and Abruptio, as larger placental area and PET) Thromboembolic disease: appropriate prophylaxis

and Rx

PRESENTATIONS Four principal combinations of presentations Cephalic/cephalic 60% Cephalic/breech 20% Breech/cephalic 10% Breech/breech 10% First two, many obstetricians will allow vaginal delivery with the same contraindications as for singleton pregnancies The same applies for trial of vaginal delivery in the presence of a previous lower segment Caesarean Section Complication Abortion (12-12wk) Premature labor (2432wk) IUGR Fetal defects

Singleto n 1% 1%

Dichor ~ 2% 5%

5% 1%

10% 2%

Anesthetic: Epidural

SECONDARY PRIMARY

Labour management: IV line, Delivery in theatre, Twin CTG machine 2 resuscitation trolleys, 2 obstetricians, 2 paediatricians, Inform SCBU PPH: IV line, Blood grouped and saved, Oxytocin infusion following delivery

20% 8% FOLLICULAR CYST ANC: Consultant-led team. More CORPUS LUTEAL CYST GRANULOSA-THECA LUTEAL POLYCYSTIC ENDOMETRIOTIC CYST

EPITHELIA L OVARIAN NEOPLAS

LABOR MANAGEMENT

DIAGNOSIS OF MULTIPLE PREGNANCIES Size and hormones Diagnosis of multiple gestations History, examination (4cm larger than x1) and investigations

Monochor ~ 12% 10%

DEATH OF ONE FETUS IN A TWIN NON-NEOPLASTIC PREGNANCY. FUNCTIONAL CYST Dichorionic – Preterm labor Monochorionic – Hypotension → Death / Handicap of the other. Doesn’t lead to DIC as readily as singleton.

INDICATIONS FOR ELECTIVE CSECTION - Malpresentation of the first twin - Second twin larger than the first - Evidence of IUGR in one or both twins - Monochorionic twins - History of fertility treatment

BENIGN BORDERLIN E MALIGNANT

MUCINOU S SEROUS ENDOMETRIOI

CLEAR CELL (MESONEPHROI GERM CORD GRANULOSA-THECA NON-CELL D) CELL (GONADAL STROMAL) DERMOID CYST BRENNET TUMORS SOLIDSAC DYSGERMINO GESTATIONAL FIBROMA (MEIG’S ANDROGEN SECRETING TUMOR MALIGNANT YOLK

FOLLICULAR CYST - Usually less than 5 cm - Benign and asymptomatic - Thin wall, contain clear fluid - Rescan in 4 weeks - If enlarge or symptomatic, consider surgery

-

OVARIAN NEOPLASM NON-NEOPLASTIC FUNCTIONAL CYST CORPUS LUTEAL CYST GRANULOSA-THECA LUTEIN CYST Excessive bleeding into corpus - in molar pregnancy or part luteum of hyperstimulation Cyst filled with blood syndrome - Due to excessive Delayed period + pain gonadotrophin Usually the following period is heavy

POLYCYSTIC OVARY ENDOMETRIOTIC CYST

PRIMARY OVARIAN TUMORS A] EPITHELIAL - Benign - Borderline:  Epithelial tumors with no invasion of basement membrane  15% of epithelial tumors, mostly serous and stage 1 (70-85%).  10 year survival is 95%. Late recurrence.  Extensive histological sectioning is essential to exclude invasion. - Malignant MUCINOUS SEROUS ENDOMETRIOD - Large tumors. - Most common - Few cases arise in Multilocular filled with endometriosis - Contain clear fluid mucin - 30% coexist with - Often bilateral. - If ruptured → primary endometrial Around age of pseudomyxoma cancer menopause peritonei - Malignant type is the commonest ovarian cancer

BRENNER - Usually benign.occur in reproductive life - May be associated with endometrial hyperplasia - May coexist with mucinous cystadenoma

CLEAR CELL @MESONEPHROID - Associated with endometriosis in 25% - Worst prognosis

OVARIAN NEOPLASM PRIMARY OVARIAN TUMORS B] GERM CELL TUMORS BENIGN DERMOID CYST @ BENIGN CYSTIC TERATOMA - 25% of all ovarian neoplasm - Contain tissue derived from two or more germ cell layers - Unilocular cyst. May contain teeth, bone , cartilage, nerves, hair, thyroid,.. Tissues - Almost always benign. Malignant changes may occur in any component - Occur at any age. Peak is 20-30 years. - Bilateral in 20%

MALIGNANT Rare. 3% of ovarian cancers SOLID TERATOMA Peak incidence in second decade

NONGESTATIONAL CHORIOCARCINO MA - Secrete HCG - May be component of solid teratoma

YOLK SAC @ ENDODERMAL SINUS - Highly malignant. Affect young age - Partly solid. Secrete alpha fetoprotein

DYSGERMINOMA

- Most common. Highly malignant - Usually spread by lymphatics - Very radiosensitive - Occur in young women. May arise in gonadal dysgenesis

C] GERM CORD @ GONADAL STROMAL @ SEX CORD TUMORS GRANULOSA THECA CELL TUMOR ANDROGEN-SECRETING TUMORS FIBROMA - Moderate to large size - Androblastoma - Solid tumor - Solid, as enlarge may have cystic - Sertoli-leydig - May be associated with meigs’ spaces - Gynandroblastoma syndrome - Yellow tinge on cut surface Cause virilization - Tend to have long pedicle - Thecoma is benign, but granulosa is malignant - Occur at any age .50% postmenopausal - Secrete estrogen - Usually stage 1. Late recurrence SECONDARY @ METASTATIC OVARIAN TUMORS  Always bilateral. From mucin secreting tumors, stomach and colon (Krukenberg tumors)  May be secondary to breast

INTRODUCTION - Wide variety of tumors - 25% of female genital tract tumors - In U.K, the most common pelvic cancer - Worst prognosis of all female genital tract cancers - Life time risk is 1% - Spread by local spread, lymphatic and rarely by blood

MALIGNANT EPITHELIAL OVARIAN TUMORS ETIOLOGY PRESENTATION PHYSICAL FINDINGS Risk Factors:  Silent disease – 75% Benign: Nulliparity, Family - Usually mobile. unless large or present at advanced history, Fertility complicated stage drugs - Dermoid cyst anterior to bladder  Symptoms of Protective Factors: • Malignant: abdominal Number of - Bilateral involvement pregnancies, OC, - Ascites  Symptoms of distant Tubal ligation. - Hard deposit in pelvis metastases - Leg edema  General malaise, - Signs of bowel obstruction of ureteric weight loss obstr  Hormonal production

COMPLICATION  Torsion - common with dermoid/fibroma - Severe abdominal pain/vomitting  Rupture  Haemorrhage  Impaction  infection

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OVARIAN TUMOR IN PREGNANCY Found incidentally Corpus luteal/dermoid 2% are malignant If discover early and persist , surgery around 16 weeks If complicated, operate immediately

FIGO STAGING Stage Growth limited to one or both ovaries 1 Stage Growth limited to one or both ovaries with 2 pelvic extension Stage Tumor involving one/both ovaries with 3 peritoneal implants outside pelvis/positive retroperitoneal or inguinal nodes.

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INVESTIGATION Uss /CT scan Tumor markers( ca125,CEA, HCG,alpha FP Urea and electrolyte LFT Chest X ray Ascitic tap Calculate risk malignancy index.

RISK MALIGNANCY INDEX  CA 125 estimation  Menopausal status pre menopausal score = 1 post menopausal score= 3  Ultrasound score Multi locular, solid areas, bilateral, ascitis, intra ab mets. if 0 or 1 score = 1 if 2-5 score= 3 RMI = CA125 x M x U

Stage 4

Growth involving one or both ovaries with distant mets.

PRIMARY - Primary cytoreduction - TAH, BSO, OMETECTOMY, WASHINGS, BOWEL SURGERY - Optimal debulking: less than 2 cm residual tumors - Staging once histology is available - If confined to ovary and young age, conservative surgery CHEMOTHERAPY Indication – stage 1c and above • Platinium based - Taxol - 6 cycles at 3 weekly intervals - Monitoring: examination CA125 FBC, U&E

MALIGNANT EPITHELIAL OVARIAN TUMORS MANAGEMENT SURGICAL INTERVAL DEBULKING SECOND LOOK SURGERY - Alternative to primary surgery - Assess response to medically unfit chemotherapy large ascitis - Plan future severe malnutrition management - 3 cycles of chemotherapy –surgery – 3 - Only in research more cycles of chemotherapy context. - Aim : to improve patient condition less extensive surgery to achieve optimal debulking - May improve survival FOLLOW UP How aggressive?. Three monthly for one year then six monthly then yearly History, examination and CA125 Imaging if recurrence is suspected clinically or by CA125

PALLIATIVE SURGERY - Removal of intestinal obstruction - Survival is very poor - Quality of life considerations

SCREENING Life time risk is 1% 5% of tumors are genetic History of breast cancer increases risk by factor of 2 History of ca ovary increases the risk by factor of 3 One first degree relative affected: risk 2.7% 2 first degree relatives affected : risk is 13%  If BRCA1 mutation carrier : risk is 50%  Problems : - no pre-cancerous stage - unknown natural course  TVS AND CA125 ON YEARLY BASIS  ONGOING STUDY TO EVALUATE THIS.

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Endometritis Salpingitis Oophoritis Parametritis Peritonitis DDx UTI Early pregnancy complication, Ectopic pregnancy Appendicitis, diverticulitis Complicated ovarian tumor Other causes of lower ab pain

COMPLICATIONS Tuboovarian abscess, polymicrobial, 50% bilateral  Tubal damage, infertility and future ectopic.  Fitz-Hugh-Curtis syndr  Reinfection is 25% 

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PELVIC INFLAMMATORY DISEASE PATHOLOGY EPIDEMIOLOGY CLINICAL FEATURES  Incidence variable o Lower ab pain and o Non specific, lack Infection ascend to tenderness sensitivity and 10-13%, the uterus resulting in o Deep dysparunea specificity underestimated, endometritis with increasing o Abnormal vaginal or o Positive predictive plasma cell infiltration  Age, teens value of clinical cervical discharge Tubes, mucosal diagnosis is 65-90%  Sexual activity, o Cervical excitation inflammation with as compared to early coitus, and adnexal swelling, redness and laparoscopy multiple partners, tenderness deciliation, polymorph o Excess of WBC in often proceeded by o Fever >38°C infiltration of the the vagina present STD (chlamydia, GC) o Adnexal mass in submucosa, exudate in lower genital with 2ndary invasion fills the lumen, 20% of cases tract infection also with anaerobes adhesions and spread o Raised ESR, WBC, o Endometrial biopsy to the serosal surface,  Contraception CRP not recommended pus from the fimbria Pills? Protective o Excess of as routine Ovaries and Leukocytes in the IUCD Cu releasing↑ investigation formation of tubovagina risk ovarian abscess or o General symptoms Barrier protective mass depend on severity  Parity 75% are nulliparous INVESTIGATIONS TREATMENT CBC, CRP, Urine Mild cases : Ambulatory Severe cases: it! IV cephalosporin + Antibiotic metro till 24 h, analysis and culture Doxycycline 2x/day/14d Indications to it: improvement → oral HVS, Endocervical + metronidazole Surgical emergency doxycycline and swab 2x/day/5d cannot be excluded, metronidazole USS, adnexal mass or (if GC suspected add Clinically severe abscess ciprofloxocine single disease, Tuboovarian Clindamycine Laparoscopy if there dose) abscess, PID in Ofloxocine+ is doubt about pregnancy, Lack of metronidazole diagnosis or no Or response to oral Clindamycine improvement after Ofloxocine + therapy, Intolerance to 24-48 hours of proper



Chronic PID, adhesions, pelvic pain, dysparunea, dysmenorrhea

treatment  BhCG

metronidazole

oral therapy

ive therapy

NOTES *TUBERCULOSIS POSTPARTUM HEMORRHAGE Def1: Any blood loss >500mL (vaginal) and >1000mL (caesarian) following  Patients notofimproving on antibiotic  Rare delivery. (Blood loss estimation inaccurate) Def2: 10%therapy drop ofshould PCV. (Depends on timing of test after onset) have laparoscopy  Often secondary to pulmonary Def3: Any bleeding which result in the signs & sx of hemodynamic instability. (Blood loss response differ from ppl – esp  IUCD may be left in situ in women TB anemia, PET, cardiac diseases, dehydration) with mild PID butHEMOSTATIC should be MECH  May present as pelvi- RISK FACTORS INCIDENCE TYPE removed in sever cases abdominal The leading At term, the estimated blood flow to  Primary (Early) PPH:  mass Previous PPH  Laceration  Tuboovarian abscess may be  Systemic symptoms, cause of the uterus 500-800mL/min. 10-15% Excessive blood loss  Abruptiomenstrual  Instrumental maternal drainedof Cardiac output. abdominally, within 24h of delivery disturbance, amenorrhoea, delivery  Retained mortality. lapaporoscopic Natural hemostatic mech: (esp 1st 6h). infertility or USS guided  LGA placenta Occur in 4% of 1) Contraction & retraction of  Secondary  (Late) aspiration on pelvic collection Treated by antituberculous Failure to  HTN disorders deliveries. myometrial fibers PPH: Excessive blood progress  Induction & drugs and surgery 2) Hypercoagulable state in late loss between 24hduring 2nd Augmentation of pregnancy 6wks postpartum stage labor 3) Integrity of the genital tract (esp 2nd wk)  Placenta accreta ETIOLOGY Bleeding mostly from endometrial spiral arterial arterioles & decidual veins that supplied & drain intervillous spaces of placenta. Causes of primary PPH: 1) Tone; 2) Trauma; 3) Tissue; 4) Thrombosis; 5) Uterine Inversion TONE (ATONY, 75-80%) TRAUMA TISSUE THROMBOSIS UTERINE INVERSION Failure of contraction & retraction of Vascular beds in - Retention of Preexistent: ITP, Just after 2nd stage myometrial muscle fibers. genital tract are part of TTP. of labor, due to Predisposing factors: engorged during placenta. Acquired: uterine atony, cervix 1) Uterus overdistention – Multiple pregnancy. 50% cases of 1- Abruptio (Leak is open & placenta gestation, LGA, Polyhydroamnios. 1) Laceration in 2ndary PPH. AF) attached. 2) Prolonged labor → fatigue. cervix & vagina – 2- HELLP (low Plt) Inexperienced doc 3) Drugs – Halogen anest, nitrate, NSAID, spontaneous/ - Incomplete 3- Sepsis → DIC exert fundal

MgSO4, Nifedipine. 4) Placenta previa - ↓content of musculature of the wall. 5) Bacterial toxins – chorioamnionitis, endometritis & septicemia. 6) Fibroid esp intramural. 7) Grand multipara >5 8) Precipitous labor 9) Abruptio esp concealed coz interstitial bleeding. CLINICAL MANIFESTATION Heavy vaginal bleeding ↓ BP ↑ HR ↓ RBC count (Hct) Swelling & pain in tissues in the vaginal & perineal area.

instrumental/ manipulation of fetus/ LGA/ precipitous labor. 2) Uterine rupture → intraperitoneal bleeding. 3) Hematoma – perineal, vaginal or broad ligament hematoma. COMPLICATION

4- Dilutional coagulaopathy 5- Amniotic fluid embolism – intravascular infusion of small amt of AF.

pressure while pull umbilical cord before complete placental separation. Inversion → Traction of peritoneal structure → Vasovagal response → Vasodilation → Hypovolemic shock.

DDx OF CAUSES

Hx: Ask risk factors of uterine atony & coagulopathy. Exam: Soft boggy & large uterus with profuse vaginal bleeding?  Atony.  Bright red bleeding b4 separation of placenta? Trauma.  Abdominal / vaginal mass increasing in size? Hematoma.  Bleeding severe, bright red, no clots but uterus contracts well? Coagulopathy. Cupping of fundus or non-palpable fundus? Uterine inversion. Fever & tenderness? Endomyometritis. If no cause identified → Manual exploration of genital tract. MANAGEMENT OF PRIMARY POSTPARTUM HEMORRHAGE Identification of those at risk of PPH. Start prophylactic measures during labor to minimize maternal mortality. 1. CBC – Hb & Plt (correct anemia if present). 2. Blood typing & Ab screening (Xmatch 2-6units blood) 3. Insert large bore IV line. ROUTES OF MANAGEMENT RESUSCITATION EVALUATE SURGICAL PROGNOSIS Oxygen by mask. Monitor pulse, BP, 1. Laparotomy to drain Depends on 2 large bore IV lines. Central venous line. Urine output, free blood & inspect any cause of PPH, Draw blood – CBC, coagulation screen, urea, creatinine, blood gases, level injury & repair. duration, electrolyte. of consciousness. 2. Uterine artery ligation amount of Immediate fluid replacement with NS or RL. Order regular CBS 3. Internal iliac (inferior blood loss & 

Anemia Hypotension & hypovolumic shock Renal failure Risks of blood transf Surgery complications & sepsis Sheehan syndr Venous thrombosis & embolic effects (coz of surgery, bed rest & hypercoagulable state)

separation of accreta or precreta.

Transfuse RBC as available & appropriate. counts & hypogastric) artery effectiveness FFP if abnormal coagulation test results & sites oozing. coagulation tests ligation. of rx. Cryoprecipitate if abnormal coagulation tests not to guide blood 4. Total hysterectomy Prompt dx & corrected with FFP. component 5. Selective arterial rx. Plt concentrates if plt count <50x10/L & bleeding therapy. embolization continues. MANAGEMENT OF UNDERLYING CAUSE TONE TRAUMA TISSUE COAGULOPATHY Assess uterine size & tone. Cervical & vaginal Removed even if bleeding stopped Confirm by risk factors & Bimanual – express clots, lacerations → absorbable with use of uretrotonics. abnormal coagulation stimulate uterine continuous stitch. Diffcult without GA. test. contractions. Large lower genital tract, Resuscitate adequately. Manual FFP: 1U=1g fibrinogen Empty bladder. unstable broad lig & explore. Cryoprecipitate:VIII, XiII & Uterine artery ligation, retroperitoneal hematoma Vaginal hand in situ to ↓ fibrinogen. selective arterial → incision, drain, ligation, discomfort, infxn, trauma. Plt concentrate: 1u ↑ 20embolization or subtotal/ packing. Adherent? Curettage. 25k plt. total hysterectomy. Uterus rupture → sub/TAH. Packed RBC: 1U ↑ 1g/dL Uterotonic drugs.

SECONDARY POSTPARTUM HEMORRHAGE ETIOLOGY RISK FACTORS Retained products of conception (RPOC) – C-section most common cause of 2ndary PPH Prolonged ROM Infection – often 2ndary to RPOC. 1-3% after Prolonged labor with multiple exams. spontaneous vaginal delivery. Most common Manual removal of placenta cause of postnatal morbidity between day2Mother’s age at extremes 10. Low socioeco status Maternal anemia placental site - ↑amt of bleeding. Lacerations – includes episiotomy Trauma – Rupture of vulval hematoma Internal fetal monitoring Extent of bleeding less than Pre-existing uterine disease – Fibroids Severe meconium staining in liquor primary PPH. Others (rare) – Blood disorders, Carcinoma of Prolonged surgery cervix. ASSESSMENT INVESTIGATIONS MANAGEMENT Dx obtained clinically. Crossmatch 2-4units of blood if Mainstays: Bed rest & IV antibiotic [Hx: Crampy ab pain? age of bits of placenta? marked bleeding. therapy. Sx of infxn. Duration of labor. Smooth? Coagulation profile as indicated. Curettage not performed outinely Instrumental? Placenta complete? Complication?] Speculum exam – check status (risk of uterus perforation) Exam: Check temp, HR, BP. of cervical os & obtain No oxytocin. Assess uterine size. Larger than appropriate? endocervical swab. Gentle digital evacuation of uterus Assess clinical signs of blood loss. Estimate total US – may be used if RPOC under GA performed with antibiotic blood loss. suspected. Blood clots may coverage. Establish IV line as indicated. resemble RPOC. Iron supplement if Hb low. Oxygen via face mask as indicated. CBC OVERVIEW Commonly presents as prolonged or excessive bleeding once woman has returned home after 24h-6wks postpartum. Most commonly at 2nd wk. 2ndary to sloughing of eschar on

DYSPLASIA Def: Lesion in which part of the epithelium is replaced by cells showing varying degree of atypia.

PREINVASIVE CERVICAL DISEASE Cervical Intraepithelial Neoplasia (CIN) BETHESDA SYSTEM System Intraepithelial dysplastic atypia occurring ACSUS LSIL HSIL CANCER within the metaplastic epithelium of the transformation zone. Mild Moder8 Severe CIN Cancer OSCJ – Original squamocolumnar junction.

dysplasia

dysplasi a CIN 2

dysplas ia CIN 3

NSCJ – New squamocolumnar junction TZ – Transfomation zone – area between OSCJ & NSCJ. CIN 1 OVERVIEW RISK FACTORS Cervical neoplasia originates within TZ.  Persistent HPV infxn of high risk types. Low risk HPV (types 6 & 11) are associated with low-grade  Young age at first coitus cervical lesions (condyloma acuminata and CIN1)  Multiple sexual partners. Sex partner with multiple sex High risk HPV (type 16, 18, 31, 33 or 35) associated with partners. high-grade cervical lesion (CIN2,3 and Cancer).  Young age at first pregnancy. HPV type 16 is the type universally detected with the  Multiparity. greatest frequency in high grade lesion & cervical ca. 50%  Low socioeco status SCC, 30% adenoca, & >80% preinvasive lesions. AT least 35% pt with CIN3 will dev invasive ca within 10yrs ,  Smoking & O  Genital warts whereas lower grades may spontaneously regress.  Exogenous / endogenous immunosuppresion SCREENING PAP SMEAR COLPOSCOPY Before Colposcopy Both the end Stereoscopic binocular microscope of low Complete hx and general exam. cervical canal and magnification, usually 10x to 40x. • A clinical and speculum examination of the cervix, the ectocervix vagina should be sampled Indications for colposcopy: and vulva. when taking the Pap - Abnormal cervical smear • A 3% to 5%acetic acid solution is liberally applied to smear - Abnormal findings on adjunctive the • The false negative screening tests (HPV testing and cervix using soaked swap rate for Pap smear cervicography) - The abnormal findings are acetowhite epithelium & for high grade -If the cervix is clinically abnormal or abnormal vascular patterns (mosaicism and lesions is 20% suspicious on naked eye exam. punctuation) • New automated - Unexplained IMB or PCB • Lugol’s iodine application to the cervix is called liquid based slide - Persistent vaginal discharge shiller’s test preparation systems - Personal history of in utero DES exposure, -Normal ectocervix and vaginal squamous epithelium to decrease the false vulvar or vaginal neoplasia. contains glycogen and stains mahogany-brown negative rate • Normal columnar and squamous metaplasia and neoplastic epithelium do not contain glycogen, and appear mustard yellow • Satisfactory Colposcopic Examination: If the new SCJ & entire TZ are seen.

EVALUATION FOR ABNORMAL PAP SMEAR  Any patient with a grossly abnormal cervix should have a punch biopsy performed regardless of the results of Pap smear • Patients with ASCUS found in their smear may have a repeat smear in 6 months or HPV testing • About 6-10% of patients with an ASCUS smear will have high-grade CIN on colposcopy, 90% of these can be detected by HPV testing for high-risk types • The colposcopic hallmark of CIN is an area of sharply delineated acetowhite epitheilum, or/and abnormal vascular pattern: punctuation and mosaicism • Micro invasive carcinoma: extremely irregular puncate and mosaic patterns are found.  If colposcopic examination is satisfactory, punch biopsy from the suspicious area with end cervical curettage specimen. • Diagnostic cone biopsy of the cervix is indicated if: - colposcopic examination is unsatisfactory - Endocervical curettings show a high-grade lesion - Pap smear shows a high-grade lesion that is not confirmed on punch biopsy - Pap smear indicates Aden carcinoma in situ - Microinvasion is present on punch biopsy TREATMENT OF ABNORMAL INTRAEPITHELIAL NEOPLASIA CIN  Low Grade Lesions (CIN1) - Repeat smear in 6 month interval until normal then back to the normal screening program.  High grade lesions (CIN 2,3): 1. Loop Excision of The Transformation Zone (LLETZ), relatively cheap, it can be performed on an outpatient basis under local anesthesia, and tissue is obtained for histologic evaluation. 2. LASER, destruction of the TZ by CO2 laser, ablation can be performed as an outpatient procedure with local anaesthesia, expensive. 3. Cryosurgery, relatively painless outpatient procedure without anaesthesia, cheap, high failure rate for large lesions, copious vaginal discharge for several weeks. 4. Electrocoagulation, Requires general anesthesia, cervical stenosis may occur, success rates up to 97%. 5. Cervical conization: (cold knife or laser) -mainly diagnostic but it may be used for treatment, cure rates are as high as with hysterectomy for high grade lesions. -Major complications: Bleeding, infection, cervical stenosis and incompetence. • Simple hysterectomy is rarely necessary, it may be applicable when sterilization is desired in a patient with CIN III or when there is concomitant uterine or adnexal disease.

CERVICAL CANCER INTRODUCTION SYMPTOMS FINDINGS INVESTIGATIONS Worldwide, cervical ca is the most Abnormal vaginal bleeding is Usually normal general CBC, LFT, KFT common cause of cancer death in the most common exam. CXR, Pelviwomen. presenting sx. In advanced disease, abdominal CT Mean age for cervical ca is 51.4yrs, Postcoital bleeding in enlarged inguinal or Bx of lesion with the number of pt evenly divided sexually active women, IMB, supraclavicular LN, edema of Cystoscopy & between age groups 30-39 and 60-69. PMB. the legs, ascites, pleural proctoscopy for Most common type is SCC (80%), Asymptomatic until quite effusion, hepatomegaly. clinical staging. adenocarcinoma & adenoquamous advanced in women who are Pap smear may be normal in PET scan to for 20-25%, others are rare. not sexually active. up to 50% of cases (false delineate the Persistent vaginal discharge, negative) extent of disease PATTERN OF SPREAD pelvic pain, leg swelling & Pelvic exam in early disease at the primary site 1. Direct invasion into cervical stroma, urinary frequency are may be normal, esp if lesion and in LN. corpus, vagina and parametrium. usually seen in advanced is endocervical. 2. Lympathic permeation & mets. disease. Visible disease may be 3. Hematogenous dissemination. Vesico-vaginal & ulcerative, exophytc or rectovaginal sx. necrotic. TREATMENT Stage IA IA1 – Total abdominal / vaginal hysterectomy. - Cone bx alone may suffice if pt wants to preserve fertility, as long as cone margins free from disease & endocervical curetting -ve. IA2 – Modified radical hysterectomy and pelvic LN dissection. - If wants childbearing, large cone biopsy or radical trachelectomy & pelvic LN dissection are offered. Stage IB a) Radical Hysterectomy & Bilateral pelvic lymphadenectomy – Removes uterus, adjacent portions of vagina, cardinal ligaments, uterosacral ligaments & bladder pillars. Spares ovaries, can surgically stage, prevent chronic radiation. Most common complication: Bladder dysfunction, 1-2% permanent. Most serious complication: ureteric fistula or stricture 1-2%. Lower limb lymphoedema 15-20%. b) Radiation Therapy – Begins by external radiation to shrink central tumor & cavitary lesion. Also done postop for pt with LN mets, or inadequate surgical margins. Addition of chemo to radiotherapy improves survival. Stage II IIA with minimal involvement of vaginal fornix - Radical surgery or chemo radiation. IIA – IVA – Pelvic chemo is the rx of choice. Stage Palliative radio or chemotherapy. IVB Recurre Chemotherapy – Limited effectiveness. Most active drug is cisplastin. nt or Pelvic exenteration – Removal of pelvic viscera (uterus, tubes, ovaries, bladder, rectum) - For pt who have

Mets

central recurrence following irradiation. Radiotherapy if initial disease treated by surgery only. PROGNOSIS Directly related to clinical staging. With higher stage, nodal mets escalate, & 5yr survival diminishes. COMPLICATIONS OF RADIOTHERAPY    

ACUTE Acute cystitis – Hematuria, urgency, frequency. Proctosigmoiditis – Tenesmus, diarrhea, age of blood & mucus in stool. Enteritis – Nausea, vomit, diarrhea, colicky ab pain. BM depression.

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CHRONIC Radiation enteropathy: Proctosigmoiditis (pelvic pain, tenesmus, diarrhea, rectal bleeding), ulceration (rectal bleeding & tenesmus), rectovaginal fistula (stool thru vagina), Rectum or sigmoid stenosis (progressive large bowel obstr), Small bowel injury (cramping ab pain, vomit, diarrhea) Vaginal vault necrosis - Severe pain in vaginal vault & profuse discharge. Urologic injury: Hemorrhagic cystitis, Vesicovaginal & Ureterovaginal fistula (constant urine leakage), Ureteric stenosis (hydronephrosis)

PREMATURE RUPTURE OF MEMBRANE (PROM) Definitions

Etiology

Clinical presentation

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Premature rupture (PROM) denotes spontaneous rupture of fetal membranes before the onset of labor. This can occur at term (PROM) or preterm (PPROM). Preterm premature rupture of membrane (PPROM): +\- Uterine contraction( preterm labor ? )

*It has been suggested that the term preterm PROM (PPROM) should be used to define those patients who are preterm with ruptured membranes, whether or not they have contractions.

Ascending Infection (vaginal \ cervical) Abnormal membrane (deficient collagen and minerals è weakness)  Incompetent cervix  Nutritional deficiencies of copper, ascorbic acid.  Smoking  Consider causes of preterm labor a. multiple gestation. b. Low socioeconomic class. c. Ethnicity…..etc

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Sudden Gush of clear vaginal fluid Rule out : o Episodic urinary incontinence o Leucorrhea o loss of the mucus plug symptoms suggestive of Chorioamnionitis ?

Method of diagnosis (Investigations)  Never do a digital vaginal exam on a patient who is not in labor, whether preterm or term 1. Sterile Speculum exam  Direct visualization of liquor ‫ ؛‬Pooling  High Vaginal Swab (HVS) à assess Chorioamnionitis  Nitrazine  Ferning Sterile , not only to prevent infection but bcoz you may take the swab from the speculum and get a false positive Dx of PPROM involves first examining the abdomen (assess the lie , position , ease of examination àmay indicate oligohydramnios )

Bcoz we may face a case that we suspect PPROM but we don’t see the liquor ex. : Severe oligohydramnios à will appear in the abdominal exam (small for GA on fundal height …etc ) Fetal head closing the cervix à manipulate the head and see if liquor comes out There’s No rupture of membranes à think about other DDx for the Gush of fluid (U. incontinence , leucorrhea ,loss of the cervical mucous plug )

Method of diagnosis (Investigations) 1. Sterile Speculum exam Direct visualization of liquor

Nitrazine blue test

False Positives Cervical mucus Blood Vaginal infection (BV) Semen

Fern like

e positive Cervical mucus Blood Urine

Fern and Nitrazine Tests 1. Insert speculum for sample collection, avoid the use of lubricant. 2. Collect vaginal secretion from the posterior vaginal pool with two cotton sterile swabs. Do not touch the mucus plug in the cervix. Do not contaminate the specimen with saline/koh. 3. After collection, immediately rub the swab against a glass slide, creating a very thin smear, do not apply a coverslip. 4. Allow slide to dry for 5-10 minutes. Fals 5. Using a microscope, examine the dried smear under 10X power without a cover slip. 6. If present, saline in the amniotic fluid crystallizes to form a fern-like pattern.

1.Tear off a 2-3 cm piece of Nitrazine paper. 2.Apply fluid collected from the vaginal pool directly to the paper. 3.A blue color change is consistent with amniotic fluid pH of 7-7.5. The Nitrazine paper container includes a chart of color change and pH. 2.U/S 

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assess gestational age , fetal growth and wellbeing Assess amniotic fluid volume. rule out fetal anomalies

Saline

Complications

Chorioamnionitis

1. Depends on fetal age, duration and liquor volume lift 2. Prolonged PPROM 􀂃 Chorioamnionitis development and neonatal infections 3. Prematurity related complications (RDS , PDA , IVH , NEC, ROP , BPD , …) 4. Oligohydramnios : if >24 weeks may lead to pulmonary hypoplasia 5. Positional hypoplasia. Suspect Chorioamnionitis 􀂃 maternal fever and Uterine tenderness in a confirmed case of PROM and without UTI or URI Management : Vaginal cultures , IV Antibiotics and prompt delivery (not necessarily CS)

Suspect Chorioamnionitis in the presence of any change (rather than absolute values) of: 1. Pulse rate 2. Temperature more than 38 (unexplained) 3. Tense or tender uterus 4. Color or smell of vaginal secretions * 5. Fetal heart rate. Management : take Vaginal gram stain and cultures , give IV Antibiotics

Deep infection , (in the uterus which is in the abdominal cavity , not exposed to the omentum or other defense mechanisms and the immune system ) So it could put the mother and the fetus at risk of sepsis …

if gram stain positive prompt delivery (not necessarily CS) REGARDLESS of Gestational Age

Any change of maternal HR , Temp , Tense tender uterus

WBC CRP may be high or low , so don’t count on them as well as the vaginal discharge ( may not be present) Management 

the main principle of the management would be conservative balancing between prematurity and infection (Unless there’s indications to terminate preg)

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Main risk is prematurity

First look if we have any indication to terminate the pregnancy : 1.Chorioamnionitis 2.Severe oligohydramnios 3.Congenital anomalies

it and give

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Antibiotic use is recommended (Erythromycin and Metronidazole) but it may not prevent fetal infection* also may mask Chorioamnionitis.

…… ?

PRETERM BIRTH 

A birth that occurs before 37

Significance

Pathogenesis

Tocolytics : short term use only Steroids: Betamethasone

Blood doesn’t reach the fetal lung so we may face cases of congenital pneumonia despite Abx use

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completed weeks of gestation. Subclassifications of PTB are variably and inconsistently defined as: Late preterm = 34 to 36 weeks

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Moderately preterm = 32 to 34 weeks Very preterm = <32 weeks Extremely preterm = <28 weeks 

PTB can also be defined by birth weight (BW): Low birth weight (LBW) — BW less than 2500 g

•

Taken together with its sequelae, PTB is by far the leading cause of infant mortality in the United States. PTB is also a major determinant of shortand long-term morbidity in infants and children. INCIDENCE — In the United States, 12.8 percent of births in 2006 occurred preterm and 3.66 percent were less than 34 weeks of gestation

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Approximately 70 to 80 percent of PTBs occur spontaneously. preterm labor (PTL) s for 40 to 50 percent of all PTBs and preterm premature rupture of membranes (PPROM) s for 20 to 30 percent. The remaining 20 to 30 percent of PTBs are due to intervention for maternal or fetal problems

Clinical and laboratory evidence suggest that a number of pathogenic processes can lead to a final common pathway that results in preterm labor and delivery.

The four primary processes are: 1. Activation of the maternal or fetal hypothalamiituitary-adrenal axis 2. Infection 3. Decidual hemorrhage 4. Pathological uterine distention

Very low birth weight (VLBW) — BW less than 1500 g Extremely low birth weight (ELBW) — BW less than 1000 g RISK FACTOR, CLINICAL MANIFESTATIONS AND DIAGNOSIS FACTORS • • •

PTL is one of the most common reasons for hospitalization of pregnant women. In one systematic review, approximately 30 percent of preterm labors spontaneously resolved. Signs and symptoms of early PTL include

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Uterine contractions are a normal finding at all stages of pregnancy, thereby adding to the challenge of distinguishing true from false labor. The frequency of contractions increases with gestational age, the number of fetuses, and at night. The diagnosis of PTL is generally based upon clinical criteria of regular painful uterine contractions accompanied by cervical

menstrual-like cramping, constant low back ache, mild uterine contractions at infrequent and/or irregular intervals, and bloody show. However, these signs and symptoms are nonspecific and often noted in women whose pregnancies go to term. •

Initial evaluation of women with suspected PTL should determine: 1. The presence and frequency of uterine contractions 2. Whether there is uterine bleeding 3. Whether the fetal membranes have ruptured 4. Gestational age 5. Fetal well-being

Physical examination •

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The uterus is examined to assess firmness, tenderness, fetal size, and fetal position. A sterile speculum examination is performed to rule out ruptured membranes, to visually examine the vagina and cervix Obtain specimens for laboratory testing . A digital examination to assess cervical dilatation and effacement is performed after placenta previa and PPROM have been excluded

dilation and/or effacement. Specific criteria, which were initially developed to select subjects in research settings, include persistent uterine contractions (four every 20 minutes or eight every 60 minutes) with documented cervical change or cervical effacement of at least 80 percent, or cervical dilatation greater than 2 cm. Digital cervical examination has limited reproducibility between examiners, especially when changes are not pronounced; therefore, some centers evaluate the cervix via transvaginal ultrasound to confirm the diagnosis A short cervix has been variously defined as a cervical length less than 2.0 cm, 2.5 cm, or 3.0 cm. Lab tests •

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Urine culture, since bacteriuria and pyelonephritis are associated with PTB. Rectovaginal group B streptococcal culture, to determine need for antibiotic prophylaxis. Tests for gonorrhea and chlamydia. Testing for gonorrhea and chlamydia may be omitted if previously performed, the results were negative, and the patient is not at high risk of acquiring sexually transmitted infections.

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Fetal fibronectin (fFN),a swab for fFN on all symptomatic patients considered at high risk for PTB. Perform transvaginal sonographic measurement of cervical length. We only send the swab to the laboratory for FFN determination if the cervical length is 20 to 30 mm Given the link between cocaine use and placental abruption, perform drug testing in patients with risk factors for drug abuse

TRIAGE BASED UPON CERVICAL LENGTH

MANAGEMENT OF WOMEN WITH PRETERM LABOR

 Cervical length >30 mm — These women are at low risk of PTB,  Regardless of fFN result. Discharge the patients home after an observational period of four to six hours during which confirm fetal well-being  Exclude the presence of an acute precipitating event (eg, an abruption or overt infection),  Follow-up in one to two weeks  Cervical length 20 to 30 mm — PTB is more likely in women with cervices 20 to 30 mm than in women with longer cervices, but most women in this group do not deliver preterm. Therefore, send the swab for fFN testing in this subgroup of women. If the test is positive (level greater than 50 ng/mL), then actively manage the pregnancy to prevent morbidity associated with PTB.  Cervical length <20 mm .These women are at high risk of PTB regardless of fFN result. Therefore, we do not send their swabs for fFN testing to the laboratory and actively manage them to prevent morbidity associated with PTB.

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Hospitalize women diagnosed with PTL at less than 34 weeks of gestation and initiate the following treatments: Antenatal glucocorticoids to reduce neonatal morbidity and mortality associated with PTB Appropriate antibiotics for GBS chemoprophylaxis Tocolytic drugs for up to 48 hours to delay delivery so that glucocorticoids given to the mother can achieve their maximum effect. Appropriate antibiotics to women with positive urine culture results or positive tests for gonorrhea or chlamydia.

MANAGEMENT OF ASYMPTOMATIC WOMEN AT HIGH RISK OF PTB • • • •

Interventions to prevent PTB generally have not been successful, with some exceptions (eg, supplemental progesterone). Women with risk factors for PTB are sometimes followed with serial ultrasound measurement of cervical length. A cervical length ≥35 mm is generally considered normal and reassuring; as cervical length decreases below 35 mm, the risk of PTB increases We manage asymptomatic patients at high risk of PTB similar to the way we manage symptomatic patients, but with a higher cervical length threshold for intervention. This minimizes overtreatment of high risk asymptomatic patients and undertreatment of symptomatic patients. Surveillance with serial cervical length measurements is begun at 22 weeks. Cervical length ≥35 mm - The risk of PTB is low. See these patients in routine follow-up in one to two weeks.

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Cervical length 25 to 34 mm - obtain a fFN concentration. If the test is positive (level greater than 50 ng/mL), then actively manage the pregnancy to prevent morbidity associated with PTB. Cervical length <25 mm - The risk of PTB is increased. We actively manage the pregnancy to prevent morbidity associated with PTB, as described above.

PREMATURE RUPTURE OF MEMBRANE (PROM) •

Refers to

Etiology & RF

Outcome

membrane rupture before the onset of uterine contractions; preterm PROM (PPROM) is the term used when the pregnancy is less than 37 completed weeks of gestation. PPROM occurs in 3 percent of pregnancies and is responsible for, or associated with, approximately onethird of preterm births. In management of PPROM, Points of contention include: •

1. Expectant management versus intervention 2. Use of tocolytics 3. Duration of istration of antibiotic prophylaxis 4. Timing of istration of antenatal glucocorticoids 5. Methods of testing for maternal/fetal infection 6. Timing of delivery.

The pathogenesis of PPROM is not completely understood. There are multiple etiologies, mechanical and physiological, that probably share a final common pathway leading to membrane rupture. • Risk factors for PPROM are similar to those for preterm labor A history of PPROM in a previous pregnancy Genital tract infection Antepartum bleeding Cigarette smoking have a particularly strong association with PPROM Although a small randomized trial suggested vitamin C supplementation might lower the risk of PPROM , a larger randomized trial in which both vitamin C and E were given refuted this finding and suggested the risk of PPROM may actually be increased with antioxidant supplementation . •

1. 2. 3. 4. 5.

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Approximately one-third of women with PPROM develop potentially serious infections, such as intraamniotic infection (chorioamnionitis), endometritis, or septicemia. Endometritis is more common after cesarean than vaginal delivery. The fetus and neonate are at greater risk of PPROM-related morbidity and mortality than the mother. The majority of pregnancies with PPROM deliver preterm and within one week of membrane rupture.

•

Preterm infants are especially vulnerable to a variety of problems, such as hyaline membrane disease, intraventricular hemorrhage, periventricular leukomalacia and other neurologic sequelae, infection (eg, sepsis, pneumonia, meningitis), and necrotizing enterocolitis. The rates of these morbidities vary with gestational age and are higher in the setting of chorioamnionitis

•

PPROM is also associated with increased risks of abruptio placentae and prolapse of the umbilical cord. Fetal malpresentation is common, given the preterm gestational age and the frequent occurrence of reduced amniotic fluid volume. The risk of cord prolapse is especially high (11 percent in one study) in the setting of both nonvertex fetal presentation and PPROM. Early, severe, prolonged oligohydramnios can be associated with pulmonary hypoplasia, facial deformation, and orthopedic abnormalities. Such complications are most likely when membrane rupture occurs at less than 23 weeks of gestation.

RF for Pre-term birth

1. Stress Single women, Low socioeconomic status, Anxiety, Depression, Life events (divorce, separation, death)Abdominal surgery during pregnancy 2. Occupational fatigue Upright posture, Use of industrial machines, Physical exertion, Mental or environmental stress 3. Excessive or impaired uterine distention Multiple gestationPolyhydramniosUterine anomalyUterine leiomyomaDiethylstilbestrol 4. Cervical factors History of second trimester abortionHistory of cervical surgeryPremature cervical dilatation or effacement Clinical Manifestation & Dx

5. Infection Sexually transmitted infections, Pyelonephritis, appendicitis, pneumonia, Systemic infection, Bacteriuria, Periodontal disease 6. Placental pathology Placenta previa, Abruption, Vaginal bleeding 7. Miscellaneous Previous preterm delivery, Substance abuse, SmokingMaternal age (<18 or >40), AfricanAmerican race, Poor nutrition and low body mass index, Inadequate prenatal care, Anemia (hemoglobin <10 g/dL)Excessive uterine contractility, Low level of educational achievement, Genotype 8. Fetal factors Congenital anomaly, Growth restriction

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History — The classic clinical presentation of PPROM is a sudden "gush" of clear or pale yellow fluid from the vagina. However, many women describe intermittent or constant leaking of small amounts of fluid or just a sensation of wetness within the vagina or on the perineum. A clinical history suggestive of PPROM should be confirmed by visual inspection or laboratory tests to exclude other causes of vaginal/perineal wetness, such as urinary incontinence, vaginal discharge, and perspiration. Physical examination — The best method of confirming the diagnosis of PPROM is direct observation of amniotic fluid coming out of the cervical canal or pooling in the vaginal fornix. If amniotic fluid is not immediately visible, the woman can be asked to push on her fundus, Valsalva, or cough to provoke leakage of amniotic fluid from the cervical os. Digital examination should be avoided because it may decrease the latency period (ie, time from rupture of membranes to delivery) and increase the risk of intrauterine infection Nitrazine and fern tests — If PROM is not obvious after visual inspection, the diagnosis can be confirmed by testing the pH of the vaginal fluid, which is easily accomplished with nitrazine paper. Amniotic fluid usually has a pH range of 7.0 to 7.3 compared to the normally acidic vaginal pH of 3.8 to4. False-negative and false-positive nitrazine tests results occur in up to 5 percent of cases.

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False negative tests results can occur when leaking is intermittent or the amniotic fluid is diluted by other vaginal fluids. False positive results can be due to the presence of alkaline fluids in the vagina, such as blood, seminal fluid, or soap. In addition, the pH of urine can be elevated to near 8.0 if infected with Proteus species. In the United Kingdom, an absorbent pad (AmnioSense) that changes color at pH > 5.2 is used as a panty liner and marketed to pregnant women. In a study of 157 pregnant women, the sensitivity and specificity of this device for diagnosis of membrane rupture were 98 and 65 percent, respectively Ultrasonography — Ultrasound examination may be of value in the diagnosis of PPROM. Fifty to 70 percent of women with PPROM have low amniotic fluid volume on initial sonography . A mild reduction of amniotic fluid volume may have many etiologies. On the other hand, the finding of anhydramnios or severe oligohydramnios, combined with a characteristic history, is highly suggestive of rupture of membranes, although renal agenesis, obstructive uropathy, or severe utero-placental insufficiency also can cause marked reductions in amniotic fluid volume. Instillation of indigo carmine —One-half hour later, the tampon is removed and examined for blue staining, which indicates leakage of amniotic fluid.

Management

Initial evaluation

The management of pregnancies complicated by PPROM is based upon consideration of several factors, which are assessed upon presentation Gestational age

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Expeditious delivery of women with PPROM is indicated if intrauterine infection, abruptio placentae, repetitive

1. 2. 3. 4.

Availability of neonatal intensive care FHR decelerations, or a high risk of cord Presence or absence of maternal/fetal infection prolapse is present or suspected Presence or absence of labor • In each of these conditions, fetal wellFetal presentation (Breech and transverse lies are unstable and may being can deteriorate with expectant increase the risk for cord prolapse) management, and there are no 5. Fetal heart rate (FHR) tracing pattern therapeutic interventions available other 6. Likelihood of fetal lung maturity than delivery. 7. Cervical status (by visual, not digital, inspection unless induction is planned or the woman is in labor) Our simplified algorithm for management of other women with PPROM is shown in the • • • • • •

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Antenatal glucocorticoids Antibiotics Treatment of overt infections Tocolysis Hospitalization Tissue sealants (A variety of tissue sealants (eg, fibrin glue, gelatin sponge) have shown some success in stopping leakage in case reports. Neither the safety nor the efficacy of these sealants has been established ). Supplemental progesterone (There is no evidence that istration of supplemental progesterone has any beneficial effects in women with PPROM )

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Maternal surveillance Fetal surveillance Timing of delivery Gestational age <34 weeks — In general, prematurity is the greatest risk to the fetus with PPROM. As discussed above, we ister a course of antenatal glucocorticoids, prophylactic antibiotics for seven days, and tocolytics for 48 hours, as indicated. Gestational age greater than 34 weeks Method of delivery — Cesarean delivery is performed for standard indications; otherwise labor is induced. Favorable Cervix vs Unfavorable cervix

PRETERM LABOUR MANAGEMENT Principles of management

Tocolytic agents

Contraindications to Tocolysis

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Initial assessment must be done to ascertain cervical length and dilatation and the station and nature of the presenting part.* Identify treatable causes (such as a urinary tract or vaginal infection) Should be placed in the lateral decubitus position, monitored for the presence & frequency of uterine activity & cervical changes.. High vaginal swab.(B strep, Ureaplasma, Mycoplasma,Gardnerella vaginalis)* Blood sugar, CBC, serum electrolytes level, urinalysis, and urine culture and sensitivity.

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Ultrasound (dates, cause, growth).  Rest and fluids will improve 50 % of cases. HOW? By the inhibition of the ADH released from the post pitutary gland from the same site where oxytocin is released..

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Used to reduce and stop uterine Contraction .  We use them for 48-72 hours *.. 1)corticosteroids work

1. 2. 3. 4. 5. 6.

2)in cases we don’t have good NICU facilities until we transfer the pt. to another hospital.

1. 2.

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It is acceptable to ister antibiotics *to patients who are in preterm labor (a 7-day course of ampicillin and/or erythromycin).. **allergyà use clindamycin or vancomycin .. To prevent the progression of a silent infection to clinical amnionitis

Tocolytic therapyà if the patient doesn’t respond to bed rest & hydration

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Tocolytics are routinely used at less than 34 weeks gestation if there are no contraindications to treatment. Treatment is individualized from 34-37 weeks.

Severe PET Severe APH IUGR Chorioamnionitis Fetal anomalies Cardiac disorders, Arrhythmias. 7. Thyrotoxicosis. Tocolytic agents Magnesium sulfate Calcium channel blocker (nifedipine) 3. Sympathomimetic agents (ritodrine, terbutaline) 4. Prostaglandin inhibitors (indomethacin) 5. Atosiban

TOCOLYTIC AGENTS

β. Sympathomimetic agents  

Action

Side effects

Notes

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Decrease intracellular Ca

1. Fetal and maternal tachycardia. 2. Hypotension. 3. Rarely chest pain. 4. Hyperglycemia. 5. Hyperkalemia. 6. Right heart failure

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Dose control by maternal response and pulse

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Competes with Ca+2 for entry into the cell à decrease free intracellular Ca

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Higher doses are required (1 gm 4 hourly orally) compared to eclampsia Useful in selected cases such as diabetes, heart diseases Strict serum levels should be observed It is used as an intravenous medication to halt premature labour..

Ritodrine hydrochloride Salbutamol

MgSO4

respiratory depression and cardiac conduction defect.

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Atosiban

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Oxytocin antagonist

PG synthetase inhibitors

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It prevents conversion of arachidonic acid into

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 If prolonged use: a. Oligohydramnios.

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PG

Indomethacin Aspirin Flufenamic acid

Ca channel blockers

b. Premature closure of ductus arteriosus(May lead to neonatal PHTN & CF) c. Platelet dysfynction.

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nifedipine inhibit slow inward of calcium ions  Nifedipine during the second phase of action potential of uterine smooth muscle cell. Is tocolytic therapy effective? • • • •

Has minimal side effect : a. b. c. d.

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Headache Flushing hypotension tachycardia

Animal studies showed fetal acidosis

Failed to decrease preterm incidence in large population studies. It did prolong gestation, decreased RDS , improved neonatal survival & increased birth weight. Use after 34 weeks is limited. All agents delayed labour by 72 hours in 80% of treated patients

Role of Glucocorticoids

Surfactant

Lung maturity

L/S ratio

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Reduces the mortality, RDS & IVH ..  It`s recommended use up to 34 weeks.  Dose consists of : **2 doses of 12 mg of betamethasone(Developmen t of CNS), IM 24 hours apart or ** 4 doses of 6 mg of dexamethasone, IM, 12 hours apart.  SO ,It has both

Phospholipids i. Phosphotidyl – lecithin ii. Phosphotidylinositol iii. Phosphotidylglycerol  Proteins  Carbohydrate  Salts and neutral lipids  It is produced by pneumocytes type II (proliferates at 24 weeks and function by

Fetal lungs are mature if: 1)Phosphatidylglycerol is present in amniotic fluid or 2) Lecithin– sphingomyelin (L/S) ratio is > 2

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>2 indicates lung maturity. Lecithin increases from 35 weeks onward while sphyngomyline remains constant after 35 weeks Measured by liquid chromatography. 2% of infant with L/S>2 develop RDS Blood and meconium may reduce the L/S ratio but has no effect on PG detection.

prophylactic and therapeutic use.

34 week)

PRETERM BIRTH ETIOLOGY CLINICAL FEATURES 1) Infection – mostly subclinical 1. Cramping lower ab pain infxn of choriodecidual space that starts irregular & with 2) Overdistension of uterus – time ↑ in freq & intensity & polyhydromnios, multiple becomes more regular. pregnancy 2. Low back ache 3) Vascular (placental 3. Bloody vaginal discharge abnormalities) 4) Intercurrent illness –  Extremely preterm: 24pyelonephritis, pneumonia. By 27th wk either direct spread or indirect chemical triggers eg endotoxins. 5) Cervical weakness 6) Idiopathic – esp in mild preterm births 7) Iatrogenic MANAGEMENT INVESTIGATIONS 1. it at least 24h 1. Sterile speculum exam – amniotic fluid pooling 2. According to GA 2. Transvaginal USS – asses cervical dilation. <34wks – antenatal steroids (given in 2 doses 12h apart) Normal cervix ~3.5cm in length. 3. Prophylactic antibiotics (erythromycin until culture indicates 3. Vaginal swab for GBS otherwise) 4. Urinalysis & culture (UTI main cause of preterm 4. Tocolytics – for 48h until steroids works or till transfer to a hosp labor) with good NICU facility 6. fetal fibronectin (fFN) When to ask? - cervical length >3.5cm& not in labor – no need - cervical length <2n5cm & in labor – no need - 2.5 < cervical length < 3.5cm – need fFN CLASSIFICATION GESTATIONAL AGE BIRTH WEIGHT Mild preterm Low birth weight:  Late preterm: 34-36th wk <2.5kg Very low birth weight:  Moderate preterm: 32<1.5kg 33rd wk Extremely low birth  Very preterm: 28-31st wk Weight: <1kg

“Braxton-Hicks contraction” @ False Labor @ Practice Contractions - Sporadic uterine contractions that start around 6 weeks, to aid body in its preparation in birth. Infrequent, irregular, only mild cramping.

(Preterm labor ↑ progressively & becomes more intense & regular with time)

PREMATURE RUPTURE OF MEMBRANE Amniorrhexis (spontaneous rupture of membranes) before the onset of uterine contractions. Preterm PROM (PPROM) – preterm (<37 wks) with ruptured membrane, with or without contractions. RISK FACTOR HX & PE LAB TESTS CONSIDERATIONS o Hx of previous Hx: Vaginal loss of fluid Pulm Management depends a R/O episodic urinary incontinence, leukorrhea or maturation lot to GA at time of memb PPROM loss of cervical mucus plug. studies. rupture. o Vaginal & cervical PE: Pooling of amniotic fluid in posterior vaginal Gram stain & Also quantity of remaining infxn culture. amniotic fluid. o Antepartum bleeding fornix. Confirm by: o Cigarette smoking 1) NItrazine paper (alkali → blue) Amniotic fluid index (AFI): have a particularly 2) Microscopic exam (ferning) Vertical axis of amniotic strong association Sterile vaginal speculum. fluid present in four with PPROM *No digital vaginal exam!! quadrants. Abnormal is o Abnormal memb USS: R/O fetal anomalies, assess GA & amniotic <5cm. physiology fluid volume. o Incompetent cervix o Nutritional deficiencies MANAGEMENT GA <24 wks (Pre24wks > GA > 36wks (Preterm PROM) GA 36wks or viable PROM) more (PROM) Risk of dev of A] Conservative Expectant Management - To continue pregnancy until the lung profile is Induce labor pulmonary mature. Diagnose chorioamnionitis at an early stage to minimize fetal & maternal risks. after 6-12h hypoplasia – due “Chorioamnionitis” – Maternal temp >38°C with no other sites of infxn, fetal tachy, if no to fetal crowding tender uterus, uterine irritability on NST. Presence of bacteria by Gram/culture. spontaneous with thoracic Ampicillin/erythromycin prolongs interval of delivery in pt with PPROM. contractions

compression, restriction of fetal breathing and disturbances of pulm fluid production & flow. Positional skeletal abnormality eg talipes equinovarus.

When diagnosed, ampicillin + gentamycin after taken enough cultures. Then induce labor. C-section if cervix unfavorable, fetal involvement or presence of active genital herpes. B] Tocolytic Therapy – To gain time for pulm maturation. Unsuccessful if with infection. C] Cortisteroids Use - Given to pt with PPROM only up to 32 wks GA. D] Outpatient Management Can consider after inpatient observ for 2-3d without any evidence of infxn. Rules of eligibility: Pt reliable, fully informed of risks, prepared to participate in her own care. Fetus vertex. Cervix closed. Restrict physical activity. No coitus. Monitor temp at least 4x/d. Rush to hosp if >37.8°C. Seen weekly to measure temp, NST after 28wk, evaluate baseline fetal heart rate & AFI. Contraindicated in oligohydramnios.

occur.

PROLONGED PREGNANCY Definitions

RISKS

Post date pregnancy: continuation of pregnancy beyond 40 completed weeks

Placental insufficiency and hypoxia

Increased fetal wt, ossification of skull & decreased moulding

Post term pregnancy: continuation of pregnancy beyond 42 completed weeks

1. Increased perinatal mortality: Doubled for each week after 42 weeks 2. Meconium aspiration syndrome 3. Oligohydromnios 4. Cord compression

1. Prolonged labour and failure to progress: increase incidence of C/S 2. Shoulder dystocia:  Maternal risks: vaginal & cervical lacerations & rupture uterus  Neonatal risks: i. Neonatal asphyxia & death ii. Cervical cord injury iii. Brachial plexus injury: Phrenic N. injury (C4 injury), Erb’s palsy (C5&C6 injury), Klumpk’s palsy (C8 & T1) iv. Clavicular & humeral fractures

Incidence 5-10% of pregnancies Aetiology  

In majority of cases there is no underlying cause (it’s a physiological continuation of pregnancy) Extremely rare, due to i. Anencephaly ii. Fetal adrenal hypoplasia

iii.

Placental sulphatase enzyme deficiency

How to manage pt in Post-date & Post-term pregnancy

Assesment of GA:

Before delivery

During delivery

A.Antenatal methods

1. Counselling and explanation  Explain the risk of post-date and post term on the fetus 2. History  For accurate assessment of GA  To exclude contraindications for induction 3. Obs exam  To assess lie, presentation and engagement 4. Vaginal exam  To assess Bishop score and pelvic adequacy 5. U/S (at 40, 41 and 42 weeks)  To assess amount of liquor, fetal wellbeing and wt 6. CTG (every 3 days after 40 weeks)  To assess fetal wellbeing

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1. 1st day LMP (reliable in 50% of pregnancy)

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Uncomplicated post-date pregnancy: deliver at 40+3-7 days Method of delivery: a. Induction of labour (depends on Bishop score) b. C/S if there’s contraindication for induction If delivery by induction of labour, senior obs(risk of shoulder dystocia) and paed(risk of meconium aspiration) should attend the delivery.

2. U/S: CRL (7-13 weeks), BPD & FL (1326 weeks & >26 weeks) 3.Clinical: i. ii. iii. iv.

early pregnancy symptoms early bimanual exam quickening serial fundal ht

B.Postnatal methods 1. Dubowit score: assessment of physical and neurological features of the newborn

2. Farr score: assessment of physical features of the newborn

PUERPERIUM PHYSIOLOGIC CHANGES DURING PUEPERIUM The period following delivery of the baby and placenta to about 6-8 weeks postpartum. During that the reproductive organs and the maternal physiology return toward the non-pregnant status. LOCAL UTERUS

Uterine involution.  Structure - autolysis of excess muscle fibers - obliteration & thrombosis of blood vessels, then degeneration & transformation into elastic tissue - separation of the decidua  Weight - reduced (1kg after delivery  70-100g end of puerperium)  Size - after delivery the length of the uterus is 20 cm and felt at the level of umbilicus - after one week it is midway between umbilicus and symphysis pubis - after 2 weeks it is at the level of symphysis - by the end of the 6th week it is 7.5 cm long  Uterine ligaments - are involuted Subinvolution predisposes to prolapse and retroversion. Endometrial lining rapidly regenerates, so that by the 7th day the endometrial glands will be evident. By the 16th day, the endometrium is restored throughout the uterus, except at the placental site. The contractions of the arterial smooth muscle and compression of the vessels by contraction of the myometrium result in homeostasis. The size of the placental bed decreases by half, and the changes in the placental bed result in the quantity and quality of the lochia that is experienced.

“Lochia” Bloodstained uterine discharge that is composed of cervical mucous, vaginal transudate, and products of necrosis and sloughing of the superficial layer of the decidua - Lochia rubra (red): consists mainly of blood and decidua. It lasts for 5 days. - Lochia serosa (pale): due to relative  in RBCs and predominance of leukocytes. It lasts for 5 days. - Lochia alba (white): consists mainly of leukocytes and mucus. It lasts for 5 days. - Persistence of red lochia means subinvolution. - Offensive lochia means infection. - In severe infection with septicaemia, lochia is scanty and not offensive - The period of time the lochia can last varies, although it averages approximately 5 weeks. - Often, women experience an increase in the amount of bleeding at 7-14 days secondary to the sloughing of the eschar on the placental site.

CERVIX The cervix begins to rapidly revert to a non-pregnant state (less elastic, more firm) but it never returns to the nulliparous state. By the end of the first week, the external os is closed to the extent that a finger could not be easily introduced. By the end of the second week the internal os should be closed. VAGINA In the first few days the streched vagina is smooth & edematous, but by the end of the third week rugae begin to appear, but never completely return to its prepregnant size

PUERPERIUM PHYSIOLOGIC CHANGES DURING PUEPERIUM LOCAL OVARIES PERINEUM The resumption of normal The perineum has been stretched and function by the ovaries is highly traumatized, and sometimes torn or cut, during variable and is greatly influenced the process of labor and delivery. The swollen and by breastfeeding the infant. engorged vulva rapidly resolves, and swelling and The woman who breastfeeds her engorgement are completely gone within 1-2 infant has a longer period of weeks. amenorrhea and anovulation Most of the muscle tone is regained by 6 weeks, than the mother who chooses to with more improvement over the following few bottle-feed. months. The muscle tone may or may not return to Mother who does not breastfeed normal, depending on the extent of injury may ovulate as early as 27 days after delivery. ABDOMINAL WALL Most women have a menstrual The abdominal wall remains soft and poorly toned period by 12 weeks; the mean for many weeks. The return to a prepregnant state time to first menses is 7-9 weeks. depends greatly on exercise

WEIGHT Decreased due to - evacuation of uterine content. - more fluids loss through urine and sweat

TEMPERATURE A reactionary increase may occur following difficult delivery, but it does not exceed 38˚C and drops within 24 hrs. A slight rise may occur in the 3rd day due to breast engorgement.

PHYSIOLOGIC CHANGES DURING PUERPERIUM GENERAL BREAST BOWEL BLOOD Changes that prepare the mother for Tendency to Increase breastfeeding occur throughout constipate coagulability of pregnancy: Causes : blood continue - Lactogenesis is triggered initially - Atony of bowel during the first 2 by the delivery of placenta - Laxity of ab and weeks despite of - Falling level of Estrogen and perineum decrease in a Progesterone - Anaroxia number of - Continue presence of PRL - Loss of fluids coagulation factor - If mother is not lactating, the - Fear of evacuation: This may increase Pain from stretched incidence of PE Prolactin level  and return to perineum, prolapse and DVT. normal within 2-3 weeks Hb concentration - Colostrum secreted during the first hemorrhoid, or anal fissure tends to fall in the 3 days first 2-3 days URINE “Colustrum” - yellowish, high protein concentration (IgA), protects against Increase in urine production by the 2nd4th day infection, replaced by milk at the Retention of urine is not uncommon 3rd-4th day postpartum Causes: - Atony of bladder neck - Engorgement of the breast - Laxity of ab - Large and painful breast - Compression of urethra by vulval edema But, suckling relieve the discomfort or hematoma Suckling  PRL (milk secretion) + Oxytoxin (milk ejection)

CARDIOVASCULAR - Immediately following delivery, there is marked increase in peripheral vascular resistance due to the removal of the low-pressure uteroplacental circulatory shunt - The cardiac output and plasma volume gradually return to normal during the first two weeks of puerperium - Pulse is normal but may increase if there is infection or hemorrhage

PATHOLOGIC CHANGES DURING PUERPERIUM POST PARTUM HEMORRHAGE PSYCHOLOGICAL It is an excessive (>500 mL at vaginal and >1000 mL at POSTPARTUM BLUES cesarean) blood loss after delivery.  Complicates 50% of deliveries  First 24 hà primary  Mild, transient, self-limited disorder.  Up to 6 weeksà secondary  Mood swings, with change in appetite and sleep.  First 2 weeks after delivery, often resolves by postpartum day 10.  No pharmacotherapy is indicated. PRIMARY SECONDARY POSTPARTUM DEPRESSION Causes: Causes: - Complicates 5% of pregnancies 1) Uterine atony 1) Retained products of - Sx: Sadness, fatigue, changes in sleeping and eating Risk Factors: conception patterns, reduced libido, crying episodes, anxiety, and chorioaminionitis, multiple Management: irritability. gestations, macrosomic Heavy bleedingàIV infusion - Usually in the first few months, and may last up to several fetus, fibroid. months or even a year. and X-match of blood. Rx: Massage and bimanual - Treatment is recommended for 9-12 months beyond Syntocinon (synthetic compression, then remission of symptoms. oxytocin). oxytocin infusion, POSTPARTUM PSYCHOSIS Examination under ergometrin, prostaglandin F2 anesthesia.  Rare but serious. If bleeding persists despite Evacuation of the uterus.  Sx: Restless agitation, confusion, delusions, hallucination, uterine contraction, suspect Antibiotics given if placental thoughts of self harm. 2) Genital tract trauma tissue is found, even without  Rarely presents before the 3rd postpartum day but Cervical and vaginal evidence of overt infection. usually does so before 4 weeks. lacerations If blood loss is not excessive,  Recovery occurs over 4-6 weeks. use pelvic US to exclude  Patient should be referred urgently to a psychatrist and retained products. will usually require ission to a psychiatric unit. 2) Endometritis Pathophysiology 3) Bleeding disorders  Poorly understood, but may be due to rapid changes in estrogen, progesrtone and prolactin in postpartum patients.  Stress - Responsibilities of child rearing  Postpartum thyroid dysfunction (psychiatric disorders).  Seen in higher rates in patients with history of

depression or other mental illnesses.

PATHOLOGIC ENDOCRINE SHEEHAN’S SYNDROME Anterior pituitary gland enlarges during pregnancy due to an increase in the size and the number of prolactin secreting cells If significant hemorrhage occur during the peripartum period, ischemic necrosis of the gland will happen. Full clinical picture apparent after 95% destruction 1)  PRL  Failed lactation 2)  FSH & LH  Anovulation & 2ndary amenorrhea 3) Hypothyroidism  Brady, cold intolerance, constip 4)  ACTH  Hypotension &  weight Rx: Replacement therapy -cortisone & thyroxine for life. -HMG for induction of ovulation if pregnancy is desired. POSTPARTUM THYROIDITIS Transient destructive inflammation of Thyroid gland occuring within the 1st year after delivery. Believed to result from modif to the immune system necessary in pregnancy. 2phases: 1) Thyrotoxicosis 2) Hypothyroidism The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism. POSTPARTUM GRAVE’S DISEASE  Less common than PPT.  Similar to Grave’s disease in other settings.  Autoimmune Ab against TSH receptors 

CHANGES DURING PUERPERIUM NEURO – OBSTETRIC PALSY BLADDER PROBLEMS One or both of the lower *Urinary retention, voiding difficulty, limbs may develop signs & and bladder over-distension are sx of motor and/or sensory common. neuropathy following *The baby's exit may have traumatized delivery. it leading to temporary paralysis. Causes: *Loss of bladder sensation due to 1- Compression or regional anesthesia. stretching of the *Swelling and pain in the perineal area. lumbosacral plexus as it *Psychological (fear) factors crosses the sacroiliac t during decent of the fetal Over-distention will lead to : head. 1. Dampen bladder sensation, render it 2- Herniation of the hypo-contractile and lead to fibrous lumbosacral discs (L4/L5) replacement of smooth muscle. may also occur in the 2. Over flow incontinence. exaggerated lithotomy position and during It's important to urinate within 6-8h of instrumental delivery. delivery. This  rate of UTI and prevent any Features: Sciatic pain, damage and bleeding that can happen unilateral foot drop, when bladder gets overly full. hypoaesthesia, muscle If the female didn’t urinate during this wasting. period, we insert a catheter. -Most cases resolve spontaneously in a matter of days or weeks, or managed orthopaedically. URINARY INCONTINENCE Vaginal delivery strongly implicated in the development of stress incontinence.

Excess production of thyroid hormones.  Needs treatment, like any other grave’s disease.

- Delivery weakens muscles around the bladder and pelvis, which makes it harder to control when urine starts. - Hormonal changes

PATHOLOGIC CHANGES DURING PUERPERIUM BOWEL FUNCTION DISORDERS THROMBOEMBOLISM PUERPERAL PYREXIA CONSTIPATION * The risk of thromboembolic Def: Temperature of 38C or higher on disease rises 5 fold during It is a common problem during puerperium any two of the first 10 days pregnancy periods. postpartum, exclusive of the first 24h * The majority of deaths occur in There are three main causes: measured orally by a standard the puerperium and are more technique 1. Interruption of normal diet, dehydration common after caesarean section. during labor. * If DVT or pulmonary embolism is 2. Fear of evacuation due to pain from Causes of pyrexia: suspected, a full anticoagulant sutured perineum, prolapsed hemorrhoid, * Genital tract infection; upper tract therapy should be commenced & a (bulky tender uterus) , or perineal anal fissures. bilateral venogram or lung scan 3. Atony of intestinal, abdominal, perineal infection only should be carried out within 24 – muscles. * UTI. 48 hours. Management: * Breast infections e.g. mastitis. *Adequate fluid intake and increase in fiber * Resp tract infection - more common intake. after anesthesia. *Stool softener (laxatives) if necessary. * Thrombophlebitis and deep vein Laxatives: lactulose, ispaghula thrombosis. ANAL INCONTINENCE & FECAL URGENCY * Wound infections; Anemia. Incontinence of stool and flatus are frequent * Non-puerperal related causes e.g. complications of childbirth. appendicitis. Anal incontinence is associated with: - Anal sphincter damage especially operative delivery. - Following repair of third or fourth degree tear. - Stool impaction. - Dev of the anovaginal or rectovaginal fistula. - Pelvic floor dysfunction

PUERPERAL INFECTIONS Infections are among the most prominent puerperal complications. Fever remains the hallmark of puerperal infection, and the patient with fever can be assumed to have genital infection until proven otherwise. ENDOMETRITIS MASTITIS URINARY TRACT INFECTION Def: Infection of the endometrium or Def: Inflammation of the mammary gland 2-4 % of women dev UTI decidua, with extension into the Could be : postpartum. myometrium and parametrial tissues. - Congestive mastitis (breast engorgement). Causes: Bladder and the lower Usually develops on the 2nd or 3rd - Infectious mastitis urinary tract remains postpartum. Both are more common in Primigravidas. hypotonic, Catheterization, Birth Etiology: PROM > 24 hours, Cesarean Infectious mastitis and breast abscess are trauma, Conduction anesthesia, section, Chorioamnionitis, Excessive uncommon complications of the breastfeeding. Frequent pelvic exam. number of digital pelvic exam, Almost certainly occur as a result of trauma to Commonest m/o: E.coli and Prolonged labor > 12 hour, Low the nipple and the subsequent introduction of Proteus spp. socioeconomic status, Toxemia, the Organisms from the infant’s nostrils. intrauterine monitoring devices, PreMost common m/o: Staph aureus. Sign & sx: Dysuria, Frequency, existing vaginitis and cervicitis. Loin pain if pyelonephritis, Bacteriological findings: Anaerobic Rx: isolation. Cease breast feeding from Systemic sx, May be strep, Gram negative coliforms, affected breast. Expression of milk. Culture & asymptomatic and recognized Bacteroid spp., Aerobic strep, sensitivity. Flucloxacillin commenced while on routine mid-stream urine Chlamydia and Mycoplasma (difficult to awaiting sensitivity result. 10% with breast (MSU) sample. culture) abcess need surgical incision & drainage. (performed on all patients who INFECTIOUS CONGESTIVE DDx: UTI, Acute pyelonephritis, Lower have been catheterized in Usually occur on the genital tract infection, Wound infection, 1 wk or more after labor) nd rd delivery. 2 or 3 postpartum Atelectasis, Pneumonia, Exam: Raised temperature, Usually one breast is day. Thrombophlebitis, Mastitis, Supra-pubic and/or renal angle involved. Breast swollen, Appendicitis. tenderness. Tender, redness, tender, tense and Management: Investigation: MSU, White cell swollen and hot. warm. it, Evacuation of retained products count, Nitrites and leucocytes Temp may be mildly of conception under antibiotics cover, Pt is febrile and on dipstick. appears ill. elevated. Parenteral broad-spectrum antibiotics,

usually stopped once the patient is afebrile for 24-48 hours, tolerating a regular diet, and ambulating without difficulty.

Purulent discharge may be present.

Axillary adenopathy can be seen.

Rx: Broad-spectrum antibiotics until the results of culture and sensitivity are known, then be specific. Bed rest. High fluid, light solid diet.

PUERPERIUM Definition

Physiological changes during puerperium

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Local changes

General changes

1. 2. 3. 4.

1. Weight 2. Temperatu re 3. Bowel habit

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The period following delivery of the baby and placenta to about 6-8 weeks postpartum. During that the reproductive organs and the maternal physiology return toward the non-pregnant status Family

Uterus Cervix Vagina Ovaries

5. Perineum 6. Abdominal wall 7. Breast

4. Blood 5. Urine 6. CVS

Local physiological changes 1.Uterine Involution Structure Autolysis , enzymatic digestion of the cytoplasm  obliteration & thrombosis of blood vessels, then degeneration & transformation into elastic tissue.  separation of the decidua  Weight - reduced from 1000gm -after delivery- into 70-100gm by the end of puerperium 

 Size  after delivery the length of the

 Within 2 to 3 days postpartum, the remaining decidua become differentiated into two layers: 1. Superficial layer → becomes necrotic → sloughs off as vaginal discharge = lochia 2. Basal layer (adjacent to the myometrium) → becomes new endometrium 

The endometrial lining rapidly regenerates, so that by the 7th

Lochia Lochia is the bloodstained uterine discharge that is composed of cervical mucous, vaginal transudate, and products of necrosis and sloughing of the superficial layer of the decidua - Lochia rubra (red): consists mainly of blood and decidua. It lasts for 5 days. - Lochia serosa (pale): due to relative decrease in RBCs and predominance of leukocytes. It

uterus is 20 cm and felt at the level of umbilicus.  after one week it is midway between umbilicus and symphysis pubis.  after 2 weeks it is at the level of symphysis.  by the end of the 6th week it is 7.5 cm long  Uterine ligaments - are involuted and subinvolution predisposes to prolapse and retroversion

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day the endometrial glands will be evident. By the 16th day, the endometrium is restored throughout the uterus, except at the placental site. The contractions of the arterial smooth muscle and compression of the vessels by contraction of the myometrium result in homeostasis. The size of the placental bed decreases by half.

lasts for 5 days. - Lochia alba (white): consists mainly of leukocytes and mucus. It lasts for 5 days. 

Persistence of red lochia means subinvolution (arrested involtion)  Offensive lochia means infection , it may be accompanied by pyrexia and tender uterus. - In severe infection with septicaemia, lochia is scanty and not offensive.  

The period of time the lochia can last varies, although it averages approximately 5 weeks Often, women experience an increase in the amount of bleeding at 7-14 days secondary to the sloughing of the eschar on the placental site

Local physiological changes 2.Cervical changes

4.Ovaries

5.Perineum

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The cervix begins to rapidly revert to a non-pregnant state (less elastic, more firm) but it never returns to the nulliparous state.  Before childbirth, the os is a small, regular, oval opening. After childbirth, the orifice is a transverse slit.  The external os of the cervix contracts slowly and is narrowed by the end of the first week to the extent that a finger could not be easily introduced.  By the end of the second week the internal os should be closed. 3.Vaginal changes In the first few days the streched vagina is smooth & edematous, but by the end of the third week rugae begin to appear, but never completely return to its prepregnant size.

The resumption of normal function by the ovaries is highly variable and is greatly influenced by breastfeeding the infant. The woman who breastfeeds her infant has a longer period of amenorrhea and anovulation than the mother who chooses to bottle-feed. The mother who does not breastfeed may ovulate as early as 27 days after delivery. Most women have a menstrual period by 12 weeks; the mean time to first menses is 7-9 weeks

In the breastfeeding woman, the resumption of menses is highly variable and depends on a number of factors, including how much and how often the baby is fed and whether the baby's food is supplemented with formula. The delay in the return to normal ovarian function in the lactating mother is caused by the suppression of ovulation due to the elevation in prolactin. Half to three fourths of women who breastfeed return to periods within 36 weeks of delivery. The lactational amenorrhea method is 98% effective for up to 6 months if:   

The mother is not menstruating The mother is nursing > 2 to 3 times per night, and ≥ every 4 hours during the day without other supplementation. The baby is < 6 months old

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The perineum has been stretched and traumatized, and sometimes torn or cut, during the process of labor and delivery. The swollen and engorged vulva rapidly resolves, and swelling and engorgement are completely gone within 1-2 weeks.  Most of the muscle tone is regained by 6 weeks, with more improvement over the following few months. The muscle tone may or may not return to normal, depending on the extent of injury 6.Abdominal wall The abdominal wall remains soft and poorly toned for many weeks. The return to a prepregnant state depends greatly on exercise

General physiological changes 1.Weight

2.Temperature

3.Breast changes

Decreased due to

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The changes to the breast that prepare the mother for breastfeeding occur throughout pregnancy

- evacuation of uterine content. - more fluids loss through urine and sweat. 4.Bowel changes There’s tendency to constipate Causes : 1. Atony of the intestine 2. Laxity of abdomen and perineum 3. Aneroxia 4. Loss of fluids 5. Fear of evacuation; pain from stretched perineum,prolapse hemorrhoid, or anal fissure

A reactionary increase may occur following difficult delivery, but it does not exceed 38˚C and drops within 24 hours  A slight rise may occur in the 3rd day due to breast engorgement 5.Urine

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Increase in urine production by the 2nd-4th day  Retention of urine is not uncommon  Causes: 1. Atony of bladder neck 2. Laxity of abdomen 3. Compression of urethra by vulval edema or hematoma

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Lactogenesis is triggered initially by the delivery of placenta At delivery, the abrupt, large decrease in progesterone and estrogen levels leads to increased production of alpha-lactalbumin → stimulates lactose synthase→ increased milk lactose Continue presence of Prolactin If the mother is not lactating, the Prolactin level decreases and return to normal within 2-3 weeks.

6.Blood changes

7.Cardiovascular changes

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Leukocytosis occurs during and after labor up to

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Colostrum yellow-colored liquid secreted by the breasts that contains minerals, protein, fat, antibodies, complement, macrophages, lymphocytes, lysozymes, lactoferrin, and lactoperoxidase. It is secreted during the first 35 days.  Engorgement of the breast with milk is common on days 2 to 3 postpartum  Often painful  Often accompanied by transient temperature elevation  suckling relieve the discomfort. Suckling oxytocin ME cell contraction and milk expulsion.

Immedietely following delivery, there is marked increase

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30,000/μL Increase coagulability of blood continue during the first 2 weeks despite of decrease in a number of coagulation factor This may increase incidence of PE and DVT Hemoglobin concentration tends to fall in the first 2-3 days

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in peripheral vascular resistance due to the removal of the low-pressure utero-placental circulatory shunt The cardiac output and plasma volume gradually return to normal during the first two weeks of puerperium Pulse is normal but may increase if there is infection or hemorrhage

Management 1. Observation  Pulse, T, BP  Breast, lochia, urine output, bowel motion 2. Rest and Exercise  Rest in bed for 2 days after uncomplicated vaginal delivery  Complicated/ operation needs a few days longer  Movement in and outside the bed are advised to minimized the risk of DVT

Problems in the puerperium 3. Diet  Food rich in proteins, vitamins, mineral and fluid 4. Care of the breast  Wash the nipple and areola with warm water and soap before and after each feed 5. Local Aseptic  The vulva and perinuem are washed with antiseptic lotion after each micturation and defecation  Then, use sterile vulval pad  Add local antibiotic if perineal stitch is present

6. Care of the bladder 1. Patient is encouraged to micturate frequently 2. If retention present, catheter is applied under aseptic condition 7. Care of the bowel  Uptake of vegetables are highly advisable to prevent constipation  Sufficient fluid intake and the use of glycerine suppositories if needed

1. Postpartum hemorrhage. 2. Neurological Problems. 3. Psychological problems. 4. Endocrine problems. 5. Miscellaneous problems. 6. Puerperal Pyrexia & Sepsis. 7. Infections. 8. Pelvic septic thrombophlibitis. 9. Thromboembolism

POST-PARTUM HEMORRHAGE 

It is an excessive blood loss after delivery First 24 h=primary

Primary PPH

Secondary PPH

Management

1.Uterine atony

3.Retained products of conception

1. Heavy bleeding, IV infusion and X-match of blood. 2. Syntocinon (synthetic oxytocin). 3. Examination under anesthesia. 4. Evacuation of the uterus. 5. Antibiotics given if placental tissue is found, even without evidence of overt infection

-R.F: chorioaminionitis, multiple gestations, 1. macrosomic fetus, fibroid.2. -Trt: massage and bimanual compression, 3. then oxytocin infusion, ergometrin, prostaglandin F2α

Up to 6 weeks=secondary >500 mL at vaginal delivery and >1000 mL at cesarean delivery.

2. Genital tract trauma

-if blood loss is not excesive, -Associated more with secondary PPH. -use pelvic US to exclude retained products. 4.Others Endometritis , bleeding disorders.

-cervical and vaginal lacerations.

PSYCHOLOGICAL PROBLEMS Postpartum Blues

Postpartum Depression.

Postpartum Psychosis

Pathophysiology

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Complicates 50% of deliveries Mild, transient, self-limited disorder. Mood swings, with

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complicates 8-15% of pregnancies symptoms include sadness, fatigue, changes in sleeping and eating patterns, reduced libido, crying episodes, anxiety, and irritability. usually in the first few months, and

Rare but serious. Symptoms include restless agitation, confusion, delusions, hallucination, thoughts of self harm.

Poorly undertood, but may be due to rapid changes in estrogen, progesterone and prolactin in postpartum patients.

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change in appetite and sleep. First week after delivery. often resolves by postpartum day 10. No pharmacotherapy is indicated.

may last up to several months or even a year. TREATMENT

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Pharmacologic intervention is typically required:

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1. 2. 3. 4.

Antidepressants Anxiolytic agents Electroconvulsive therapy Mother should be co-managed with a psychiatrist

Rarely presents before the 3d postpartum day but usually does so before 4 weeks. Recovery occurs over 46 weeks The patient should be referred urgently to a psychatrist and will usually reqiure ission to a psychatric unit.

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Stress Responsibilities of child rearing Postpartum thyroid dysfunction (psychiatric disorders). These psychological disorders are seen in higher rates in patients with history of depression or other mental illneses.

ENDOCRINE DISORDERS Sheehan’s syndrome

Postpartum Thyroiditis

Postpartum Grave’s disease

Anterior Pituitary gland enlarges during pregnancy due to an increase in the size and the number of prolactin secreting cells

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If significant hemorrhage occur during the peripartum period ischemic necrosis of the gland will happen. The full picture is seen with destruction of 95% of the gland 1.Decreased prolactin: causes Failed Lactation (commonly the first symptom). 2. Decreased FSH & LH: causes anovulation & secondary amenorrhea 3. Hypothyroidism: causes bradycardia , cold intolerance, constipation, …… 4. Decreased ACTH: causes hypotension & loss of weight

Transient destructive inflammation of Thyroid gland occuring within the 1st year after delivery.  it is believed to result from the modifications to the immune system necessary in pregnancy  2 phases 1. Thyrotoxicosis. 2. Hypothyroidism. 

The process is normally selflimiting, but when conventional antibodies are found there is a high chance of this proceeding to

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Less common than PPT. Similar to Grave’s disease in other settings. Autoimmune antibodies against TSH receptors leading to excess production of thyroid hormones . Needs treatment, like any other grave’s disease.

Treatment

permanent hypothyroidism.

REPLACEMENT THERAPY -cortisone & thyroxine for life. -HMG for induction of ovulation IF pregnancy is desired.

NEUROLOGICAL PROBLEMS

BLADDER FUNCTION PROBLEMS

BOWEL FUNCTION DISORDER

Thromboembolism

Obstetric palsy

Bladder problems

Constipation

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Condition by which one or both of the lower limbs may develop signs & symptoms of motor and/or sensory neuropathy following delivery.

Urinary retention, voiding difficulty, and bladder overdistension are common.

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-May be due to: 1- compression or stretching of the lumbosacral plexus as it crosses the sacroiliac t during decent of the fetal head. 2 -Herniation of the lumbosacral discs (L4/L5)

*The baby's exit may have traumatized it leading to temporary paralysis. *loss of bladder sensation due to regional anesthesia. *Swelling and pain in the perineal area. *psychological (fear) factors Over-distention will lead to : 1. dampen bladder sensation, render it hypo-contractile and

It is a common problem during puerperium periods.  There are three main causes: 1. Interruption of normal diet, dehydration during labor. 2. Fear of evacuation due to pain from sutured perineum, prolapsed hemorrhoid, anal fissures. 3. Atony of intestinal, abdominal, perineal muscles.  Management: 1. adequate fluid intake and increase in fiber intake. 2. stool softener (laxatives) if necessary. 3. Laxatives:lactulose, ispaghula Anal incontinence and fecal urgency

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The risk of thromboembolic disease rises 5 fold during pregnancy The majority of deaths occur in the puerperium and are more common after caesarean section. If DVT or pulmonary embolism is suspected, a full anticoagulant therapy should be commenced & a bilateral venogram or lung scan should be carried out within 24 – 48 hours

may also occur in the exaggerated lithotomy position and during instrumental delivery. Features include: -sciatic pain. -unilateral foot drop. -hypoaesthesia. -muscle wasting. -Most cases resolve spontaneously in a matter of days or weeks, or Managed orthopaedically.

lead to fibrous replacement of smooth muscle.

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2. Over flow incontinence.It's important to urinate within (6) to (8) hours of delivery.

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This decrease rate of UTI and prevent any damage and bleeding that can happen when your bladder gets overly full. If the female didn’t urinate during this period, we insert a catheter. Urinary incontinence

1. 2. 3. 4. 5.

Incontinence of stool and flatus are frequent complications of childbirth. Anal incontinence is associated with: Anal sphincter damage especially operative delivery. following repair of third or fourth degree tear. Stool impaction. Development of the anovaginal or rectovaginal fistula. Pelvic floor dysfunction

Vaginal delivery strongly implicated in the development of stress incontinence. *Delivery weakened muscles around the bladder and pelvis, which make it harder to control when urine starts. *Hormonal changes

Puerperal pyrexia

PUERPERAL INFECTIONS

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puerperal pyrexia is defined as a temperature of 38℃ or higher on any two of the first 10 days postpartum, exclusive of the first 24h measured orally by a standard technique causes e.g. appendicitis.

 Causes 1. genital tract infection; upper tract (bulky tender uterus) , or perineal infection only 2. urinary tract infection. 3. Breast infections e.g. mastitis. 4. respiratory tract infection - this is more common after anesthesia. 5. thrombophlebitis and deep vein thrombosis. 6. wound infections ; Anemia.  non-puerperal related

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Infections are among the most prominent puerperal complications . Fever remains the hallmark of puerperal infection , and the patient with fever can be assumed to have genital infection until proven otherwise. 1. Endometritis 2. Mastitis 3. UTI

PUERPERAL INFECTIONS 1.Endometritis 

Endometritis is an infection of the endometrium or decidua, with extension into the myometrium and parametrial tissues .  Usually develops on the 2nd or 3rd postpartum day . Etiology 1. 2. 3. 4. 5. 6. 7. 8. 9.

PROM > 24 hours Cesarean section Chorioamnionitis Excessive number of digital pelvic examination Prolonged labor > 12 hour Low socioeconomic status . Toxemia . intrauterine monitoring devices . pre-existing vaginitis and

Sign & symptoms

Differential diagnosis

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1. Urinary tract infection. 2. Acute pyelonephritis. 3. Lower genital tract infection. 4. Wound infection. 5. Atelectasis. 6. Pneumonia. 7. Thrombophlebitis. 8. Mastitis. 9. Appendicitis Management

Body temp. >38c in two occasion 6h apart or once >38.5  Lower abdominal pain  Change in Lochia : more profuse, Foul smelling or purulent  Leukocytosis which may be difficult to interrupt because of the physiological leukocytosis seen postpartum Investigations (Bact.findings) Anaerobic streptococci .

1. it to hospital. 2. Evacuation of retained products of conception under antibiotics cover. 3. Parenteral broad-spectrum antibiotics, usually stopped once the patient is afebrile for 24-48 hours, tolerating a regular diet, and ambulating

cervicitis

1. 2. 3. 4.

Gram negative coliforms Bacteroid spp. Aerobic streptococci Chlamydia and Mycoplasma (difficult to culture)

without difficulty.

PUERPERAL INFECTIONS 2.Mastitis

3.Urinary tract infection

Definition

Incidence

Examination

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Approximately 2-4 % of women develop UTI postpartum .  During and Following delivery: 1. the bladder and the lower urinary tract remains somewhat hypotonic . 2. Catheterization . 3. Birth trauma . 4. Conduction anesthesia 5. Frequent pelvic examination  The commonest organisms are E.coli and proteus spp. Sign & Symptoms

-Raised temperature.

1. 2. 3. 4.

1. Broad-spectrum antibiotics until the results of culture and sensitivity are known, then be specific . 2. Bed rest . 3. High fluid, light solid diet .

Inflammation of the mammary gland Could be : a. Congestive mastitis ( breast engorgement). b. Infectious mastitis  Both are more common in Primigravidas  Infectious mastitis and breast abscess are uncommon complications of the breastfeeding . Treatment 1. isolation of the mother & baby 2. ceasing breast feeding from affected breast. 3. Expression of milk either manually or by electric pump. 4. microbiological culture & sensitivity of a sample of milk. 5. flucloxacillin can be commenced while awaiting sensitivity result.

Dysuria. Frequency of micturition. Loin pain if pyelonephritis occurs. Systemic symptoms such as pyrexia and tachycardia. 5. May be asymptomatic and recognized on routine mid-stream

-Supra-pubic and/or renal angle tenderness . Investigation -MSU. -White cell count. -Nitrites and leucocytes on dipstick. Management

6. 10% of woman with mastitis develop breast abcess which need surgical incision & drainage under general anesthesia.

urine (MSU) sample. 6. (This should be performed on all patients who have been catheterized in labor)

RHESUS ISOIMMUNIZATION FETOMATERNAL HEMORRHAGE Leakage of Rh+ve fetal cells in Rh-ve maternal circulation during pregnancy Examples: Spontaneous abortion, Induced abortion, APH, E.C.V, Cordocentesis, CVS, amniocentesis, Severe preeclampsia, Ectopic pregnancy, Caesarean section, Manual removal of placenta, Silent feto-

1- If ABO is incompatible: RBC easily destroyed, so not reaching enough immunological component to cause antibody response and reaction 2- If ABO is compatible: Rh +ve fetal cells à remain in circulation (life span) until removed by R.E.S à destroyed à liberating Ag (D) à isoimmunization.

Mild Cases: Fetal RBC destruction from IgG anti D à anaemia It takes time: à compensating hemopoiesis à excess of 1st pregnancybilirubin. is almost always not unconjugated affected: Severe Cases: 1% duringdestruction labour or 3rd stageRBC à severe Excessive of fetal 10% 6 months after delivery anemia à Tissue Hypoxia à Cardiac / circulatory and15% the 2nd pregnancy failure à by Generalized edema à Heart Failure à Ascites -àIntrauterine Fetal Death With excessive unconjugated bilirubin >310-350 mol/L à es BBB à kernicterus à permanent neuro and mental disorders. FETAL & NEONATAL EFFECTS - Haemolytic anaemia of newborn Hb 14-18g/dl - Icterus gravis neonatorum Hb 10-14g/dl - Hydrops fetalis (Erythroblastosis fetalis)

Factors Affect Dev of Rhesus antibodies: 1- Inborn ability to respond 2- Protection if ABO incompatible1\10 3- Strength of Rh Ag stimulus (CDe=R1) 4- Volume of leaking feta blood (0.25ml) IgM (7 days) doesn’t cross placenta, then IgG 21 days crosses placenta)

INTRODUCTION Rhesus factor: Agglutinogen (C,D,E) mainly D C,D,E dominant antigen d,e recessive antigen - Rh +ve about 85% (homozygous DD35% or heterozygous Dd 50%‚

MANAGEMENT A) Prophylaxis 1- Prevention of Rhesus isoimmunization: Anti D (RhoD IgG) Standard dose for >20w, and ½ standard dose for <20weeks. Given within 72h of the incident. SD: I.M. injection: 500 iu = 100 ugm (UK) - neutralize 5ml (4ml + 1ml) = 100fetal cells SD in USA 300ugm=1500iu - neutralize 15ml

- Rh negative about 15%. Incidence of Rh -ve in far east is about 1% Examples of Rh factor: (CDe=R1) , (Cde=r) (cDE=R2) Other systems: kell-antikell, luther, Duffy, etc . Introduction of foreign protein (Ag) à production of Ab to neutralize the Ag. In ABO and other non Rhincompatibility: It usually causes mild anemia, mainly as there is no intrapartum boosting . In Rhesus isoimmunization: mainly (D), but C,E can produce antibodies. Kleihauer-Betke technique (acid elution test): Measure amount of feto-maternal haemorrhage. If 0.1- 0.25ml of fetal blood leaks (critical volume) this will produce isoimmunization represented by 5 fetal cells in 50 low power microscopic field of peripheral maternal blood. So 1ml is represented by 20 fetal cells

K-B test if large amount of leaking à another SD if mother is Rh -ve, baby Rh +ve with no isoimmunization (checked by indirect or direct coomb’s test) 2- A.P istration of anti D SD at 28w or at 28 and 36w will reduce Rh isoimmunization B) 1- Antibody Screening: for all pregnant women in ANC for irregular antibodies (mainly for Rhesus Negative women) then start at 20w, and every 4 weeks 2- Management following detection of Rh antibodies - Should be treated in specialized centers - Quantitative measures of antibodies + husband genotype - Repeat titration (indirect coomb’s, detecting of antibodies) titer or specific enzymes for antibodies IU - Amniocentesis once necessary - Obstetrical management based on timing of I.U trans-fusion (Now cordocentesis + fetoscopy) versus delivery 3- Amniocentesis: should be performed under ultrasound guidance if titer > 1\16 = 0.5-1 ugm = > 2.5-5 I.U - timing: 1st amniocentesis 10 weeks before previous IUFD - Start from 20-22 weeks, 2-4 weekly or more frequent if needed - Amniotic fluid analysis: spectrophotometry: optical density at the height of optical density deviation at wave length 450 nM.

IU transfusion (cordocentesis, in the past intraperitoneal transfusion) versus delivery of the baby: - Using Lily’s chart - Prediction chart (Queenan curve) - Whitefield’s action line -Alternatively follow up with doppler study for the fetal middle cerebral artery. Prognosis depends on: Obstetric hx, paternal genotype, maternal history (blood

transfusion, antibody titre) amniocentesis results. Delivery: Vaginal versus Cs Intensive plasmaphoresis: when severe cases anticipated, using continous flow cell separator, as early as 12 w Postnatal management: for the neonate - direct coomb’s test, Blood group, Rh type, Hb, bilirubin . - Mild cases: phototherapy, correction of acidosis - Severe cases :exchange transfusion

SMALL FOR GESTATIONAL AGE INTRODUCTION - Fetal growth is dependent on genetic, placental and maternal factors. - Fetal growth restriction is the second leading cause of perinatal morbidity and mortality. ASSESSING FETAL GROWTH HISTORY PHYSICAL EXAM USES OF ULTRASOUND - Mother’s age a) General Exam - Diagnosis and confirmation - Accuracy of LMP b) Obstetrical Exam of viability in early pregnancy date Uterine Fundal Height - Determination of gestational

FETAL VIABILITY Detection of : » Gestational sac (45wks)

- Infections during pregnancy - Multiple pregnancy - ANC and visits, Supplements - Past obs. Hx, Past Med Hx, Drug Hx, Family Hx, Socioeconomic Hx.

- Obtaining serial uterine fundal height age and assessment of fetal measurements. size - The “Mcdonalds rule” in pregnancy is a - Intrauterine or Ectopic rough determination of fetal age in weeks pregnancy. Uterus size: by pelvic examination in the - Multiple pregnancy first trimester and subsequent antenatal - Diagnosis of fetal visits. abnormalities Misleading in: Full bladder, obesity, deep - Placental localization masses, uterine fibroids & multiple - Assessment of fetal wellpregnancy being DETERMINATION OF GA AND ASSESSMENT OF GROWTH UP TO 13TH WEEKS GA FROM 16 – 24 WEEKS GA CROWN-RUMP LENGTH BIPARIETAL DIAMETER HEAD CIRCUMFERENCE FEMUR LENGTH (CRL) (BPD) (HC) (FL)  From Crown to  The transverse width Not affected by the - Better than BPD shape of the head. in accuracy and Coccyx (Rump) of the head at its timing. (longitudinal axis). widest (the distance - Accurate only  Accurate up to 14 between the parietal st when the image bones eminence of wks (1 TM). shows two blunted the skull).  It is the most ends of the femur.  Accurate up to16-24 accurate wks. parameter.  Accuracy of +/- 7  Accuracy of +/- 5 days. days from the GA.  It is affected by the shape of the head.

» Yolk sac (5wks) » Embryo (5-6wks) » Visible heart beat (6wks).

ABDOMINAL CIRCUMFERENCE (AC)  Made at the widest points in the abdomen.  Most accurate single predictor of fetal weight.

SMALL FOR GESTATIONAL AGE (SGA) Small for gestational age is defined as a fetal birth weight below the 10 th centile for the stated gestational age. The incidence of SGA fetuses is 5-10% CONSTITUTIONAL (70%) SGA

PREMATURITY (10%) INTRAUTERINE GROWTH RESTRICTION (20%)

SYMMETRICAL IUGR (20%) ASYMMETRICAL IUGR (80%)

A] CONSTITUTIONALLY SMALL FETUS  Unfortunately, it can be concluded that a fetus is constitutionally small only after pathologic processes have been excluded.  Therefore, identification of a constitutionally small infant is usually made in retrospect, after the infant is born. Causes (Multifactorial): Race, Geographical area, Sex (M>F), Maternal age, Maternal weight and height, Socioeconomic status

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B] INTRA-UTERINE GROWTH RESTRICTION Failure of the fetus to achieve its growth potential INCIDENCE TYPES 3 - 10 % of all pregnancies. • Symmetrical growth restriction: fetus whose entire body is proportionally small. (20%) 20 % of stillborns are growth retarded. • Asymmetrical growth restriction: Decrease in subcutaneous fat and 9 - 27 % have anatomic and/or genetic abdominal circumference with relative sparing of head circumference abnormalities. and femur length. (80%) Perinatal mortality is 8 - 10 times higher for these fetuses. CAUSES OF IUGR MATERNAL MATERNAL FETAL FETAL PATHOLOGICAL PLACENTAL CAUSES PHYSIOLOGICAL PATHOLOGICAL CAUSES PHYSIOLOGICAL CAUSES CAUSE CAUSES Multiple pregnancy • ↓ Uteroplacental • Genetic disorders • Placental  Genetic Factors: blood flow: (Achondroplasia, insufficiency Short stature  Race, ethnicity, - PET/eclampsia Russell silver synd) (most imp in 3rd Younger or older nationality trimester) • Chromosomal age (<15 and >45) - chronic renovascular  sex (male weigh anomalies: • Anatomic Low socioeconomic disease 150 -200 gm - Chronic HTN Chromosomal deletions problems: class more than • Maternal malnutrition Trisomies 13,18 & 21 Multiple infarcts Primiparity female) Aberrant cord • Maternal hypoxemia • Congenital Grand multiparity  Parity insertions Hemoglobinopathies malformations: Low pregnancy (primiparous, - Umbilical - High altitudes Ex: Anencephaly, GI weight weigh less than vascular thrombosis atresia, Potter’s • Drugs Previous h/o subsequent & hemangiomas syndrome, and preterm IUGR baby - Cigarettes, alcohol, siblings) - Premature pancreatic agenesis. heroin, cocaine placental separation - Teratogens, • Fetal Cardiovascular - Small Placenta antimetabolites and anomalies therapeutic agents such • Congenital Infxn: as trimethadione, mainly TORCH. warfarin, phenytoin. • Inborn error of • Chronic illness (DM, metabolism: renal failure, cyanotic - Transient neonatal heart disease etc.) diabetes

- Galactosemia - PKU DIAGNOSIS • History, Physical examination, Investigations • Ultrasound • Abdominal circumference is the single most effective parameter for predicting fetal weight because it’s reduced in both symmetrical & Asymmetrical IUGR . In the presence of normal head and femur measurements, abdominal circumference (AC) measurements of less than 2 standard deviations below the mean appear to be a reasonable cutoff to consider a fetus asymmetric. COMPLICATIONS ANTENATAL NEONATAL • Metabolic changes 1- Related to hypoxia and acidosis: (acidosis etc). a- Meconium aspiration. • Oligohydramnios b- Persistent fetal (80%) circulation. • Abnormal fetal c- Hypoxic ischemic heart patterns. encephalopathy. • Abnormal Doppler 2- Metabolic: Hypoglycemia, studies. HypoCa, Hypothermia, • IUFD Hyperviscocity syndrome INTRAPARTUM 3- Related to the etiology: • Abnormal CTG. a- Chromosomal • Fetal death. abnormalities. • Meconium stained b- Infection. liquor. c- Congenital anomalies. • ↑ incidence of instrumental and caesarean deliveries.

Asymmetrical growth restriction : BPD is normal in the 3rd trimester , whereas ratio of HC/AC is abnormal . • Symmetrical growth restriction : HC/AC may be normal . • Amniotic fluid volumes ( oligohydramnios is associated with IUGR) . Umbilical artery & fetal artery dopplar assessments : increased resistance is associated with a greater risk of IUGR as pregnancy progresses. •

PRE-PREGNANCY Modify lifestyle habits. • Detect and treat medical disorders. •

• • •

• •

MANAGEMENT ANTEPARTUM Regular antenatal care. Serial fetal growth assessment. Serial fetal wellbeing assessment 1- Biophysical profile 2- Computerized CTG 3- Umbilical artery Doppler Timing of delivery. Mode of delivery.

Time & Mode of delivery governed by: Maternal age, Past obs. History, GA, Fetal well being, Status of cervix, Availability of direct monitoring during labor (Ex: scalp PH sampling). Mode of Delivery  Cesarean delivery without a trial of labor: 1. in the presence of evidence of fetal distress 2. for traditional obstetrical indications for cesarean delivery

 Induction of labor Continuous heart rate monitoring and scalp pH monitoring optimize success of vaginal delivery SHOULDER DYSTOCIA Risk Factors 1. Fetal macrosomia 2. Maternal DM 3. Others: - Antepartum: Obesity, Multiparity, Post-term gestations, Short stature, Previous hx of macrosomia, Previous hx of shoulder dystocia - Intrapartum: Labor induction, epidural analgesia, Prolonged labor, Operative vaginal delivery

Def: Difficult delivery of the shoulder. Arrest of normal labor after the delivery of the head by the impaction of anterior shoulder against symphysis pubis. Posterior shoulder may also be obstructed by sacral promontory. Complications Fetal risks - Asphyxia - Birth trauma: Brachial plexus injuries (Erb’s & Klumpke’s), Frx humerus & clavicle - Death

Maternal risks Genital tract trauma  risk of PPH Uterine rupture

Clinical Manifestations Fetal shoulder fails to deliver after delivery of fetal head despite routine maneuvers. Impaction of fetal shoulder behind pubic symphysis. “Turtle sign”: Retraction of fetal head into perineum after its delivery and before the shoulders can be delivered.

Pregnancies at Risk Cannot accurately predict (50% without risk factors) ACOG recommends CS for EFW ≥5kg in nonDM mothers and ≥4.5kg in DM mothers.

HELPER

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HUMAN H: Call for Help.PAPILLOMAVIRUS (HPV) OVERVIEW PREVALENCE & TRANSMISSION CLINICAL PRESENTATION  Mostly asymptomatic; no visible There are about 200 HPV genotypes, 30 • Common viral STI with an E: Evaluate for Episiotomy to 40 types of HPV are typically estimated 20 million infected lesions (latent infection). transmitted through sexual and persons in the US and 5 million  Characterized by readily visible Midline episiotomy. infect the anogenital region. new cases every year. "warty" growths (condylomata F(x): Facilitates delivery of posterior The most clinically evident results of • About 75% of sexually active acuminata) on the vulva, infection with human papillomavirus shoulder. adults will be infected sometime in vagina, cervix, urethra, and L: Legs @ (HPV) are condyloma acuminata orMcRobert’s their Maneuvre life. perianal area, that can be pruritic genital warts. • Transmission HPV canlegs. occur Hyperflexion, abduction & external rotation of of maternal or cause bleeding. Majority of genital warts are caused by even when there are no visible  HPV infection usually clears F(x): Straightens maternal lordosis, remove sacral promontory as HPV types 6 and 11 which have little lesions (latent). spontaneously within 2 years, but obstr, open pelvis to max dimension, pelvic inlet into plane oncogenic potential. • During pregnancy, condylomata recurrences are common. to maxmay expulsive force. HPV types 16 and 18 mayperpendicular cause flat increase in number and size, Suprapubic Pressure @ Mazzanti Technique from warts and have beenP:linked with the however, transmission dev of cervical ca. Direct suprapubic pressure mother tofetal infant is very rare. against anterior DIAGNOSIS TREATMENT shoulder to dislodge from under symphysis pubis.  Clinical exam  Provider-applied topical therapies include: podophyllin resin 10% to  Biopsy of the lesion (uncertain of 25% in tincture of benzoin and trichloroacetic acid (TCA) or E:lesions Enter @ Rubin Maneuvres bichloracetic acid (BCA) 80% to 90%. diagnosis or for that are & Wood-Corkscrew  Patient-applied topical therapies include: podofilox solution or gel and unresponsive to therapy) Rubin: Digital pressure to the posterior aspect of anterior shoulder, pushing towards fetal chest. imiquimod cream.  Surgical therapies include: cryotherapy, manual excision, Woods: Digital pressure applied to anterior aspect of posterior shoulder, pushing electrocautery, laser vaporization, and intralesional interferon. towards fetal  back. Reasons for treating visible genital warts are to relieve symptoms (pain and/or bleeding) and sometimes for cosmetic concerns of the R: Release of posterior shoulder @ Jacquemier Maneuvre patient Hand inserted into vagina, and the posterior arm is grasped and pulled resulting delivery in posterior shoulder & displacement of anterior shoulder. Gaskin All-Fours Put patient on all fours (knee-chest position) and repeat maneuvers. Last Resorts: Zavanelli Maneuvre: Replace head back into pelvis & deliver CS. Deliberate fracture of clavicle.

OVERVIEW • STD caused by the HSV type I or type 2.  HSV-1 is most commonly associated with oral lesions (cold sores), but about 30% of primary GH is due to HSV-1. • HSV-2 is the cause of 70% of primary GH and 95% of recurrent GH. • Characterized by repeated eruptions of small, painful blisters on the genitals, around the rectum, or covering adjacent areas of skin (genital ulcer).

HERPES SIMPLEX VIRUS (HSV) PREVALENCE TRANSMISSION  Genital herpes (GH) is the  Virus enters body thru most prevalent STD in the mucosa or microabrasions US. in the skin and follows the  Although only about 5% of sensory nerves to the dorsal spinal ganglion women report a history of where it remains dormant genital herpes infection, until reactivated. as many as 25% to 30%  Transmission occurs have antibodies on serologic testing through intimate genital, (asymptomatic). oral or anal .  Transmission from an  An infected mother can infected male to his transmit the virus to her female partner is more infant during delivery likely than from an resulting in significant fetal infected female to her mortality and morbidity. male partner.

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COMPLICATION Psycho distress. (counseling) Neuro involvement (aseptic meningitis, transverse myelitis or autonomic neuropathy). Herpes keratitis (corneal scarring and blindness). ↑ risk of HIV infection Neonatal herpes (vertical transmission)

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PRIMARY Typically asymptomatic Presents up to 3 weeks after acquisition Begins with flulike symptoms (malaise, myalgias, nausea, diarrhea, and fever). Vulvar burning and pruritus followed by multiple bilateral vesicles that appear next and usually remain intact for 24 to 36 hours before evolving into painful genital ulcers. Inguinal adenopathy, dysuria and acute urinary retention may occur. Require a mean of 10 to 22 days to heal, with no scarring.

DIAGNOSIS  Clinical diagnosis  Viral culture from vesicular fluid (the gold standard; low sensitivity)  DNA PCR assays for HSV (experimental)  A Tzanck smear (cytology)  Type- specific antibodies for HSV-1 and HSV-2 IgG (diagnose the primary infection and the serotype of the causative organism).

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RECURRENT When the virus becomes reactivated and travels down the sensory nerve to the mucoepithelial surface. Can occur as frequent as 16x/yr. Trigger factors include fever, menses, emo stress, or local trauma. Usually occur in the same area, unilateral, may be less painful than those of the first episode but can still be uncomfortable. Systemic sx are uncommon with recurrences. By the 7-9th day, most lesions are healed without scarring. TREATMENT The goals of treatment for GH are sx relief, acceleration of lesion healing, and a ↓ in frequency of recurrences. Antiviral - acyclovir, famciclovir, and valacyclovir are safe and effective for treating primary and episodic outbreaks, and suppressive therapy for patients with chronic disease.

NEONATAL  85% of cases occur during birth, 5% are infected in utero, and10% of cases are acquired postnatally.  Risk of transmission to the newborn is 30-57% in cases where the mother acquired a primary infection in the 3rd trimester of pregnancy, risk of transmission by a mother with existing antibodies for both HSV-1 and HSV-2 is about 1-3%.  Neonatal herpes may take three forms: 1) Disseminated (with the high morbidity and mortality despite appropriate treatment) 2) CNS only (high morbidity, some mortality despite treatment) 3) Skin/Eye/Mouth involvement only (low morbidity and almost no mortality with treatment)

MANAGEMENT FOR NEONATAL HERPES  Acyclovir may be istered orally to pregnant women with mild or moderate outbreaks, but for primary infections or severe recurrent outbreaks, IV therapy should be istered.  At the onset of labor, all women should be questioned carefully about symptoms of genital herpes, and should be examined carefully for herpetic lesions.  Patients with typical prodromal symptoms or active lesions in labor should be delivered by cesarean section.  Preventing is difficult because 70-80% of afflicted

 No treatment completely eradicates virus.  Education and ive counseling.

newborns are born to mothers with no hx of prior infection or signs or sx at or around the time of delivery.

INTRODUCTION o Most common bacterial STI in US. o Obligate intracellular bacteria that grows in vitro only in tissue culture. o Infects columnar epithelium of endocervix, urethra, endometrium, fallopian tubes & rectum. o No vaccine. Antibodies doesn’t protect against reinfection. RISKS For pregnant women: Preterm labor, Chorioamnionitis, Postpartum endometritis. 30% untreated chlamydial cervicitis progress to PID. For infant: Neonatal conjuntivitis & pneumonia

CHLAMYDIA TRACHOMATIS CLINICAL FEATURES Hx : Most (70% women + 50% men) are asymptomatic! o Mucopurulent cervicitis or mucopus o Acute urethritis with dysurea but minimal frequency & urgency & negative urine culture. Examination: Mucopurulent cervical discharge & Cervical Erythema Lab tests o Tissue culture - expensive o Antigen tests o DNA hybridization & nucleic acid amplification tests NAATs (PCR or ligase chain reaction)

SCREENING Selective screening.  All sexually active female <26yrs  All women with risk factors (unmarried, multiple sexual partners, inconsistent use of barrier contraception, previous hx of STI, pregnant) DNA amplification test TREATMENT 1. Presumptive treatment with appropriate antibiotics o Azithromycin 1g orally single dose, or o Doxycycline 100mg 2x/day for a week o Pregnant? Amoxicillin or erythromycin 2. Treat all sexual s within the past 60 days of diagnosis. PDPT. 3. Testing for other STI 4. Abstinence from sexual for 7 days after starting treatment.

GONORRHEA INTRODUCTION SIGNS & SYMPTOMS o Gram negative diplococcus Neisseria o Asymptomatic (Most women, but 5% Gonorrhea men) o Infects cuboidal & columnar o Increased vaginal discharge with epithelium in endocervical & urethral lower ab/pelvic pain. mucosa. o Dysurea with urethral discharge. o Also rectal & nasopharyngeal mucus o Proctitis with rectal bleeding, memb. discharge, pain. o Coinfection with Chlamydia & o Endocervical mucopurulent Trichomonas. discharge & bleeding. o No vaccines. o Mucopurulent urethral discharge. o 15% untreated gonococcal cervical o Pelvic tenderness with cervical infxn progress to PID. excitation. RISKS TREATMENT GUIDELINES To pregnant women: Preterm 1. Treatment with appropriate antibiotics. labor & delivery, 2. Simultaneous treatment for chlamydia chorioamnionitis, postpartum (1g azithromycin in single oral dose) endometritis. 3. Treatment of all sexual s within 60days To infants: Neonatal before diagnosis. conjunctivitis (ophthalmia 4. Abstinence from sexual activity for 7 days. neonatorum). 5. Testing for other STIs. 6. Counselling regarding long-term complications: Chronic pelvic pain, tubal infection, subfertility.

DIAGNOSTIC TESTS o Gram staining: Gram –ve diploccocci in leukocytes. Very sensitive in men. In women, 50% sensitive. o Culture: Thayer-Martin or Transgrow media. Sensitive & specific but takes time. o Nucleic acid amplification tests (NAATs): PCR & LCR. More expensive but rapid & high sensitivity & specificity. o Nucleic acid hybridization tests TREATMENT o Single oral dose of cefixime, or o Single IM dose of ceftriaxone, or o Single IM dose of spectinomycin, or o Single oral dose of ciprofloxacin, or o Single dose of oral (Ampicillin 2g or Amoxycillin 1g) + Probenicid 2g Pregnant? Penicillin & cephalosporin are safe!

o

o o

INTRODUCTION Treponema pallidum, motile anaerobic spirochete. Can be eradicated, yet can reinfect. Spread: STD or Congenital

o o

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SYPHILIS DIAGNOSIS History and physical examination Lab investigations: Blood tests  Non-specific – VDRL, rapid plasma reagin test  Treponema-specific – TPHA, FTAAbs Dark-field microscopy

PRIMARY SYPHILIS o

o

o

1st stage after infxn. Appear 2-3wks after . “Chancre” - Firm, painless, non-itchy ulcers with rolled edges most commonly on vulva, vagina or cervix. Spontaneously disappear.

SECONDARY SYPHILIS o o o

o

2-3 months after Systemic sphirochetemia. Fever, malaise, general adenopathy, maculopapular skin rash “money spots”. Broad exophytic excrescences “condyloma lata” on vulva. Spontaneously disappear.

TREATMENT o Mode of delivery: Vaginal delivery; C-section only for obstetric indications. o STD Prevention: Avoid multiple sexual partners, promote use of barrier contraceptives. o Treatment: Benzathine penicillin (G) in pregnancy o Allergy? Full penicillin dose with oral desensitization regimen under controlled conditions. LATENT TERTIARY SYPHILIS SYPHILIS Absence of sx o Necrotic, ulcerative nodules or physical “gumma” findings. o Sx dependent on which organ affected. CVS: Aortitis, saccular aneurysm CNS: Meningitis, Tabes dorsalis, Dementia, Ataxia MSS: Osteitis

CONGENITAL SYPHILIS Transmission: Transplacental age from mother to fetus during delivery. Or, at birth. Birth outcomes in congenital syphilis: Low birth weight, prematurity, congenital anomaly, miscarriage or death of baby. Early Manifestation (<2 yrs) Late Manifestation (>2 yrs) Non-immune hydrops, “Hutchinson” teeth macerated skin, anemia, “mulberry” molars thrombocytopenia, “saber” shins hepatosplenomegaly. “saddle” nose Fetal death rates high – 8th nerve deafness.

Perinatal mortality rate 50%. Placenta typically large & edematous.

VDRL FTA-Abs Dark field CSF

Primar y + +

Seconda ry + + +

Laten t + + +

Tertiar y + + + + if CNS involve d

VAGINAL DISCHARGE NORMAL VAGINAL DISCHARGE   

Discharge is common to all women and helps vaginas stay healthy by regularly flushing them out and maintaining their pH. A normal vaginal discharge consists of about a teaspoon (4 milliliters) a day that is white or transparent, thick to thin, and odorl This is formed by the normal bacteria and fluids the vaginal cells put off. The discharge can be more noticeable at different times of the month depending on ovulation, menstrual flow, sexual activity and birth control.

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It is not uncommon for the normal discharge to be dark, brown or discolored a day or two following the menstrual period.  The following situations can increase the amount of normal vaginal discharge: 1-Emotional stress 2-Ovulation (the production and release of an egg from your ovary in the middle of your menstrual cycle) 3-Pregnancy 4-Sexual excitement

ABNORMAL VAGINAL DISCHARGE When is vaginal discharge a sign of an infection? Your vaginal discharge might be a sign of an infection if it:

Here are some key ways to determine if your vaginal discharge is normal or if you have cause for concern: Normal

Cause for concern

Colour

Clear or whitish discharge (may be yellowish when dried)

Yellow or greenish discharge, or discharge that suddenly changes color

Scent

Mild scent or none at all

A strong, foul, sometimes "fishy" odor, or a sudden change in odor

Texture

Can vary from "paste" like and somewhat sticky to clear and stretchy, depending on where you

Clumpy or lumpy discharge, with "cottage cheese" like

1-Causes itching 2-Causes swelling 3-Has a bad odor 4-Is green, yellow, or gray in color 5-Looks foamy or like cottage cheese

Volume

ABNORMAL VAGINAL DISCHARGE May be due to:

are in your cycle and whether you are aroused

texture

Can vary from very little to quite a lot (particularly when ovulating or aroused)

Sudden changes in volume, particularly if other symptoms are present

1. Atrophic vaginitis (seen in women who have gone through menopause and have low estrogen levels) 2. Bacterial vaginosis (BV) -Bacteria that normally live in the vagina overgrow, causing a grey discharge and fishy odor that worsen after sexual intercourse. BV is usually not sexually transmitted. 3. Cervical or vaginal cancer (rarely a cause of excess discharge) 4. Chlamydia 5. Desquamative vaginitis and lichen planus 6. Forgotten tampon or foreign body 7. Gonorrhea 8. Other infections and sexually transmitted diseases 9. Trichomoniasis 10. Vaginal yeast infection 11. Allergic reactions,Cervical polyp,Cervicitis, Genital Warts (HPV), Pelvic inflammatory disease

CANDIDAL VAGINITIS common vaginal infection in

Risk factors

Clinical Presentation

the United States. • Etiology   

The etiologic agent is a yeast (fungi) organism, usually Candida albicans. The organism is a common inhabitant of the bowel and perianal region Thirty percent of women may have vaginal colonization and have no symptoms of infection.

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Contraceptive practices (e.g., birth control pills and vaginal spermicides, which influence vaginal pH) Use of systemic steroids, which influence the immune system Use of antibiotics, which alters the microbiology of the vagina; 25% to 70% of women report yeast infections after antibiotic use. Any antibiotic, particularly a broadspectrum agent, may play a causative role. Tight clothing, panty hose, and bathing suits (yeast thrives in a dark, warm, moist environment) Undiagnosed or uncontrolled diabetes mellitus

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Another reason for a refractory monilial infection may be compromised immune status; with recurrent monilial vaginitis, an HIV test is indicated, along with a fasting serum glucose level. There has been a recent increase in the number of infections caused by nonalbicans species. Up to 20% of infections maybe caused by organisms such as Candida tropicalis and Torulopsis glabrata. These organisms may be resistant to standard treatment regimens

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Patients with monilial vaginitis characteristically complain of a thick, white discharge and extreme vulvar pruritus. The vulva may be red and swollen, fissures may occur Symptoms may recur and be most prominent just before menses or in association with intercourse Yeast infections may occur more frequently during pregnancy Patients with infections caused by C. tropicalis and T glabrata may have an atypical presentation. Irritation may be paramount, with little discharge or pruritus.

Diagnosis 

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Diagnosis is made by history, physical examination, and microscopic examination of the vaginal discharge in saline and 10% KOH. On examination, excoriations of the vulva may be noticeable; the vulva

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Infection with C. tropicalis and T glabrata may not be associated with the classic discharge; discharge may be white-gray and thin. #Vaginal pH may be normal or slightly more basic than

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Wet mount microscopic examination reveals hyphae or pseudohyphae with budding yeast in 50% to 70% of women with yeast infections. Cultures are not necessary to make the diagnosis except in some cases of recurrent infections.

and vagina may be erythematous, with patches of adherent cottage cheese-like discharge. Candidal infections of the vulva are characterized by classic satellite lesions.

normal (4.0 to 4.7).

CANDIDAL VAGINITIS Treatment 

Many agents are available for the treatment of vulvovaginal candidiasis. These include topical agents, which may be available over the counter (OTC) or by prescription, and oral agents, which are available by prescription only. 1. Antifungal intravaginal agents are istered as suppositories or creams. These drugs are available in three regimens: a single dose, 3-day course, or 7-day course. Agents include butoconazole, clotrimazole, miconazole, tioconazole, and terconazole. OTC regimens should be used only by women who have been diagnosed with a yeast infection in the past and are experiencing identical symptoms.

Chronic yeast infection 2. Oral Agents: Ketoconazole, Fluconazole Fluconazole is available as a single-dose (150 mg) treatment for uncomplicated vaginal candidiasis. -Ketoconazole is used effectively for the treatment of chronic and recurrent candidiasis; a 5% incidence of hepatotoxicity limits more widespread use. The dosing schedule is 200 mg twice a day for 5 days, then 100 to 200 mg daily for 6 months 3. Boric acid capsules intravaginally, 600 mg for 14 days, may be effective.

(5% of women). In most cases, no exacerbating factor can be found; however, the following possibilities should be considered 1-Failure to complete a full course of therapy. 2-HIV infection. Recalcitrant candidiasis may be a presenting symptom in women with HIV infection. HIV testing should be considered and offered to the patient. 3-Chronic antibiotic therapy. 4-Infection with a resistant organism such as C. tropicalis or T glabrata. 5-Sexual transmission from the male partner. 6-Allergic reaction to partner's semen or a

vaginal spermicide. 7-Diabetes. Patients should have a fasting serum glucose level if they have recurrent infections.

TRICHOMONAS VAGINALIS Trichomonas vaginalis vaginitis (trichomoniasis) is the third most common vaginitis, ing for 25% of cases. Etiology  

trichomonad can be recovered from 70% to 80% of the male partners of the infected patient; therefore, Trichomonas vaginitis is an STD. #This infection is the most prevalent nonviral STD in the United States (Van der Pol, 2005, 2007). Unlike other STDs, its incidence appears to increase with age in some studies. Trichomoniasis is more commonly diagnosed in women because most men are asymptomatic. However, up to 70 percent of male partners of women with vaginal trichomoniasis will have trichomonads in their urinary tract.

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This parasite is usually a marker of high-risk sexual behavior, and co-infection with other sexually transmitted pathogens is common, especially Neisseria gonorrhoeae. Trichomonas vaginalis has predilection for squamous epithelium, and lesions may increase accessibility to other sexually transmitted species. Vertical transmission during birth is possible and may persist for a year.

TRICHOMONAS VAGINALIS Clinical presentation

Diagnosis

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Trichomonas vaginitis is a multifocal infection involving the vaginal epithelium, Skene glands, Bartholin glands, and urethra.  No symptoms may be noted in up to one-half of women with trichomoniasis. However, in those with complaints, vaginal discharge is typically described as foul, thin, and yellow or green. Additionally, dysuria, dyspareunia, vulvar pruritus, and pain may be noted. At times, symptomatology and physical findings are identical to those of acute pelvic inflammatory disease. Laboratory tests 1-The vaginal pH is usually between 5.0 and 7.0.

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2-Saline wet mount of the vaginal discharge reveals numerous leukocytes and the highly motile, flagellated trichomonads (as many as 75% of cases). 3-Cultures are not usually necessary to make the diagnosis. They should be obtained when the diagnosis is suspected but cannot be confirmed by wet mount examination.

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4-Pap smears may be positive in as many as 65% of cases. Positive Pap smears should be confirmed by wet mount examination because of the high false-positive rate.

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Incubation with T vaginalis requires 3 days to 4 weeks, and the vagina, urethra, endocervix, and bladder can be infected, such colonization may persist for months or years in some women. With trichomoniasis, the vulva may be erythematous, edematous, and excoriated. The vagina contains the above-described discharge, and subepithelial hemorrhages or "strawberry spots" may be seen on the vagina and cervix. Trichomoniasis is typically diagnosed by microscopic identification of parasites in a saline preparation of the discharge. Trichomonads are anteriorly flagellated, and therefore mobile, anaerobic protozoa. They are oval and slightly larger than a white blood cell (WBC). Trichomonads become less motile with cooling, and slides should be read within 20 minutes. Inspection of a saline preparation is highly specific, yet sensitivity is not as high as hoped (60 to 70 percent). In addition to microscopy, vaginal pH is often elevated The most sensitive diagnostic technique is culture, which is impractical because special media (Diamond media) is required and few laboratories are equipped. Moreover, nucleic acid amplification tests (NAAT) for trichomonal DNA are sensitive and specific, but not widely available. Alternatively, the OSOM Trichomonas Rapid Test (Genzyme, Cambridge, MA) is an immunochromatographic assay, which has 88 percent sensitivity and 99 percent specificity. It is available for office use, and results are available in 10 minutes (Huppert, 2005). Trichomonads may also be noted on Pap smear screening and sensitivity approximates 60 percent. Women with trichomonal infection should be tested for other sexually transmitted infections. Additionally, sexual (s) should be evaluated or referred for evaluation

TRICHOMONAS VAGINALIS Treatment 

Because Trichomonas is sexually transmitted, both partners require therapy; 25% of women will be reinfected if their partner does not receive treatment. A-Vaginal therapy alone is ineffective because of the multiple sites of infection, and systemic agents are necessary. B-If both partners are treated simultaneously, cure rates of 90% are achieved with treatment with metronidazole. Patients should be warned that a disulfiram-like reaction may occur and that they should abstain from alcohol use during treatment. 1-The preferred regimen is 2g in one dose because of ease of compliance. As many as 10% of patients may experience vomiting. 2-An alternative regimen is 500 mg twice daily for 7 days. C-Resistant cases may require treatment with intravenous metronidazole. Because resistance is rare, other causes, such as noncompliance of the patient or partner, should be considered. D-Metronidazole is contraindicated for use during the first trimester of pregnancy. After this time, it can be used to treat Trichomonas infections. E-Infected patients should be screened for other STDs. BACTERIAL VAGINOSIS Bacterial vaginosis is the

Etiology

Risk factors

most common vaginal infection in the United States today. In the past, bacterial vaginitis was known as nonspecific vaginitis and Gardnerella vaginitis.

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Bacterial vaginosis is a polymicrobial clinical syndrome caused by an overgrowth of a variety of bacterial species, particularly anaerobes, often found normally in the vagina. Organisms most often involved include Bacteroides, Peptostreptococcus, Gardnerella vaginalis, and Mycoplasma hominis. The anaerobic bacteria produce enzymes that break down peptides to amino acids and amines, resulting in compounds associated with the discharge and odor characteristic of this infection.

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This condition is not considered by the Centers for Disease Control and Prevention (CDC) consensus group to be a sexually transmitted disease (STD), and it is seen in women without previous sexual experience. Many risk factors, however, are associated with sexual activity, and an increased risk of acquiring STDs has been reported in affected women 1-Oral sex 2-Douching 3-Black race 4-Cigarette smoking 5-Sex during menses 6-Intrauterine device 7-Early age of sexual intercourse 8-New or multiple sexual partners 9-Sexual activity with other women

BACTERIAL VAGINOSIS Clinical presentation

Diagnosis

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Fifty percent of women with bacterial vaginosis are asymptomatic. In symptomatic patients, the most common presentation is a malodorous, gray discharge.

 Three of the following four criteria must be present: A-The vaginal pH is generally between 5.0 and 5.5. B-Wet mount preparations with saline reveal a CLUE CELL background with minimal or no leukocytes, an abundance of bacteria, and the characteristic clue cells. The clue cells are squamous cells in which coccobacillary bacteria have obscured the sharp borders and cytoplasm. C-Application of 10% KOH to the wet mount specimen produces a fishy odor, indicating a positive WHIFF test. D-A gray, homogenous, malodorous discharge is present

Treatment Therapy is based on the use of agents with anaerobic activity and involves both topical and systemic agents. The combination appears to be 90% effective A-Vaginal preparations: 1-Intravaginal 2% clindamycin cream is used at bedtime for 7 days. 2-Intravaginal metronidazole is applied once a day for 5 days. B-Oral regimens: 1-Metronidazole may be istered two ways: 500 mg twice daily for 7 days or a single, 2-g dose. 2-Clindamycin, 300 mg twice daily for 7 days (may be associated with diarrhea, especially Clostridium difficile) C-Sexual partners should be treated in cases of repeated episodes of bacterial vaginosis. Routine treatment of partners has not been shown to improve cure rates or lower reinfection rates. D-Treatment during pregnancy is critical; data suggest an association of adverse maternal and fetal outcomes with bacterial vaginosis.

1-Clindamycin may be used throughout pregnancy. 2-Metronidazole may be used after the first trimester. E-Patients with recurrences should be screened for STDs

PREVENTION

To help prevent and treat vaginal discharge: 1-Keep your genital area clean and dry. 2-Do not douche. While many women feel cleaner if they douche after menstruation or intercourse, it may actually worsen vaginal discharge because it removes healthy bacteria lining the vagina that are there to protect you from infection. It can also lead to infection in the uterus and fallopian tubes, and is never recommended. 3-Use an over-the-counter yeast infection treatment cream or vaginal suppository, if you know that you have a yeast infection. 4-Eat yogurt with live cultures or take Lactobacillus acidophilus tablets when you are on antibiotics to avoid a yeast infection.

5-Use condoms to avoid catching or spreading sexually transmitted diseases. 6-Avoid using feminine hygiene sprays, fragrances, or powders in the genital area. 7-Avoid wearing extremely tight-fitting pants or shorts, which may cause irritation. 8-Wear cotton underwear or cotton-crotch pantyhose. Avoid underwear made of silk or nylon, because these materials are not very absorbent and restrict air flow. This can increase sweating in the genital area, which can cause irritation. 9-Use pads and not tampons. 10-Keep your blood sugar levels under good control if you have diabetes

If the discharge is caused by a sexually transmitted disease, your sexual partner (or partners) must be treated as well, even if they have no symptoms. Failure of partners to accept treatment can cause the infection to keep coming back and may lead to pelvic inflammatory disease or infertility.

Also call if:

Call your doctor rightaway if:

#Your symptoms worsen or last longer than 1 week despite home care measures.

#Your discharge is associated with fever or pain in your pelvis or abdomen. #You have been exposed to a sexual partner with gonorrhea, chlamydia, or other sexually transmitted disease. #You have increased thirst or appetite, unexplained weight loss, increased urinary frequency, or fatigue –- these may be signs of diabetes

#A child who has not reached puberty has vaginal discharge. #You think that your discharge may be related to a medication. #You are concerned that you may have a sexually transmitted disease or you are unsure of possible exposure.

#You have blisters or other lesions on your vagina or vulva (exterior genitalia). #You have burning with urination or other urinary symptoms -- you may have a urinary tract infection.