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USMLE Step 3 (Subject) / Obstetrics (Lesson)

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• Nonstress test (NST) A noninvasive test (CTG) that measures FHR reactivity to fetal movements   Indications: maternal medical conditions (e.g., gestational diabetes, preeclampsia) or fetal conditions (e.g., fetal heart defects, fetal growth restriction) Usually performed in the third trimester (after the 32nd gestational week) A normal NST would show ≥ 2 FHR accelerations.- Reactive nonstress test: if the nonstress test is normal→ High-risk conditions: weekly nonstress tests  → Uncomplicated pregnancy: reassurance and discharge- Non-reactive nonstress test: if the NST is nonreactive (< 2 FHR accelerations)→ Perform vibroacoustic stimulation and record the NST for another 20 minutes→ If the NST is still non-reactive: check the biophysical profile (BPP) or perform contraction stress test
• Contraction stress test (CST) Measures FHR reactivity in response to uterine contractions Such contractions are stimulated with oxytocin administration.
• Biophysical profile (BPP) A noninvasive test that evaluates the risk of antenatal fetal death, usually performed after the 28th gestational week. Measured parameters: each parameter receives a score of either 0 (abnormal) or 2 (normal) points.- Ultrasound exam→ Fetal movement→ Fetal tone→ Fetal breathing→ Amniotic fluid volume→ NST (optional, not always performed) Interpretation:- Total score ≥ 8 points: no signs of fetal compromise at the time of testing → reassurance- Total score ≤ 4 points: potential fetal compromise → delivery is indicated (if pregnancy duration is < 32 0/7 weeks, administer steroids and continue close monitoring)
• Delivery – Definitions Preterm delivery: Delivery at 20 to < 37 weeks. Term delivery: Delivery at 37 to < 42 weeks. Postterm delivery: Delivery at ≥ 42 weeks.
• Gestational diabetes mellitus Definition: Impaired glucose tolerance diagnosed during pregnancy; associated with an increased risk of maternal and fetal morbidity Epidemiology:- Occurs in 5-7% of all pregnancies- Usually in the second and third trimesters (less common in the first trimester) Risk factors:- Gestational diabetes in prior pregnancy- Recurrent pregnancy loss- At least one birth of a child diagnosed with fetal macrosomia Clinical features:- May present with edema; warning signs include polyhydramnios or large-for-gestational age infants (> 90th percentile) Screening and diagnostics:- First and second trimester (the first 24 weeks of pregnancy): the diagnosis of diabetes mellitus and gestational diabetes is confirmed with two independent measurements ≥ 126 mg/dL and 92-125 mg/dL respectively  - Third trimester (at 24-28 weeks)→ Recommended in all pregnancies!→ Initial screening: 50-g, one-hour oral glucose challenge test. Blood glucose level should be < 135 mg/dl.→ Confirmation test: 100-g, three-hour oral glucose tolerance test (oGTT). Blood glucose level should be < 140 mg/dl Treatment:- Dietary modifications and regular exercise (walking)- Strict blood glucose monitoring (4x daily)- Insulin therapy if glycemic control is insufficient with dietary modifications- Metformin and glyburide in patients who refuse insulin therapy- Regular ultrasound to evaluate fetal development- Consider inducing delivery at week 39-40 if glycemic control is poor or if complications occur Complications:- Maternal: → Gestational hypertension→ Preeclampsia, eclampsia, and HELLP syndrome→ Urinary tract infection  - Fetal: Diabetic fetopathy
• Diabetic fetopathy Onset: second and third trimester Pathophysiology: chronic fetal hyperglycemia → fetal hyperinsulinemia + islet cell hyperplasia, insulin-like growth factor, and growth hormones → ↑ metabolic effects and oxygen demand → fetal hypoxemia Effects:- Macrosomia: birth weight > 90th percentile or > 4000-4500 g (due to stimulated growth and adipogenesis) → increased risk of birth injuries (e.g., shoulder dystocia)- Polycythemia  - Neonatal hypoglycemia and other electrolyte imbalances (hypocalcemia, hypomagnesemia)- Respiratory distress (due to insufficient production of pulmonary surfactant)- Hypertrophic cardiomyopathy (polycythemia → redistribution of iron → iron deficiency in cardiac tissue AND hypoxemia → impaired cardiac remodeling)- Polyhydramnios (fetal hyperglycemia → fetal polyuria)
• Stages of labor First stage of labor: period from the onset of labor until complete dilation of the cervix has occurred- Latent phase of labor:→ Occurs during onset of labor (regular contraction) → ends at 6 cm of cervical dilation  → Primipara: < 20 hours→ Multipara: < 14 hours- Active Phase:→ Occurs after the latent phase at ≥ 6 cm of cervical dilation → ends with complete (∼ 10 cm) cervical dilation  → Primipara: ≥ 1.2 cm/hour→ Multipara: ≥ 1.5 cm/hour Second stage of labor: a stage of labor that begins once the cervix is completely dilated and ends with the birth of the infant→ Primipara: < 3 hours→ Multipara: < 2 hours Third stage of labor: stage of labor that begins with the birth of the infant and lasts until the complete expulsion of the placenta→ Duration: 30 minutes
• Abnormal labor Etiology: Abnormalities of the 3 P's of labor- Pelvis: size and shape of the maternal pelvis (e.g., small bony pelvis)- Passenger: size and position of the infant (e.g., fetal macrosomia or abnormal orientation)- Power: strength and frequency of contractions (e.g., dysfunctional contractions) First stage of labor:- Prolonged latent phase→ Diagnosis: poor acceleration phase with a cervical dilation ≤ 6 cm→ > 20 hours in a primipara→ > 14 hours in a multipara→ Management: Rest, hydration, and adequate analgesia. Oxytocin may be considered in well-rested mothers if the other measures have been implemented.- Prolonged active phase→ Etiology: abnormalities of the 3 P's of labor→ Diagnosis: ≥ 6 cm cervical dilation without adequate dilation (< 1 cm/2h)  → Management: Augmentation with oxytocin for hypotonic contractions, analgesia for hypertonic contractions- Arrested active phase→ Etiology: abnormalities of the 3 P's of labor→ Diagnosis: ≥ 6 cm cervical dilation with ruptured membranes and no cervical change for ≥ 4 hours if adequate contractions are present; or no cervical change for > 6 hours if only inadequate contractions are present→ Management: cesarean section Prolonged second stage of labor- Etiology: abnormalities of the 3 P's of labor- Diagnosis: failed delivery of the baby after 3 hours in a primipara and after 2 hours in a multipara (an extra hour may be added if an epidural was administered)- Management→ Augmentation with oxytocin if uterine contractions are inadequate and progress is > 1 cm after 60-90 minutes of pushing→ Trial of forceps or vacuum delivery if the fetal head is engaged AND maternal contractions are adequate→ Cesarean section if the fetal head is not engaged→ Complications of a prolonged second stage are postpartum hemorrhage and a poor neonatal outcome! Prolonged third stage of labor- Etiology: inadequate contractions or retained placenta (e.g., abnormal placental implantation such as placenta increta, placenta percreta, or placenta accreta)- Diagnosis: failed delivery of the placenta after 30 minutes- Management→ Manual removal of the placenta→ Hysterectomy if the above approach fails
• Rupture of membranes Premature rupture of membranes (PROM): rupture of membranes occurring before onset of labor at term- Epidemiology: ∼ 15% of pregnancies- Risk factors: Ascending infection (common), Cigarette smoking, Multiple pregnancy, Previous preterm delivery, Previous PROM- Complications: Umbilical cord prolapse, Placental abruption, Chorioamnionitis Preterm premature rupture of membranes (PPROM): rupture of membranes before onset of uterine contractions AND before 37 weeks' gestation- Epidemiology: occurs in 2-5 % pregnancies- Risk factors: previous PPROM, in addition to PROM risk factors- Complications: Preterm delivery, Pulmonary hypoplasia, Chorioamnionitis, PROM complications Diagnosis:- Sterile speculum examination→ Positive pool: amniotic fluid exiting the cervix and pooling in the vaginal fornix→ Detection of amniotic fluid: during sterile speculum examination  a) Litmus test or nitrazine test: test strips turn blue  b) Positive fern test: fern pattern on glass slide  c) Positive IGF1: IGF1, normally present in amniotic fluid, appears in the cervix if membranes rupture.  - Ultrasound: Oligohydramnios may be present. Management:- Stable patients< 23 weeks→ Expectant management (intervention based on viability of fetus)→ Bed rest, antenatal corticosteroids (to avoid fetal lung hypoplasia or immaturity), antibiotic prophylaxis (to reduce risk of infection with group B Streptococcus and preterm labor), and planned delivery ≥ 34 weeks→ Outcome is usually poor (fetal pulmonary hypoplasia) and termination of pregnancy may be considered.23-33 weeks→ Expectant management  → Bed rest, antenatal corticosteroids (to avoid fetal lung hypoplasia or immaturity), antibiotic prophylaxis (to reduce the risk of infection with GBS and preterm labor), and planned delivery ≥ 34 weeks→ Tocolysis (e.g., with indomethacin, magnesium sulfate) may be used to delay delivery up to 48 hours.  ≥ 34 weeks→ Delivery of the fetus is usually recommended.→ The risks of prematurity are diminished compared to the risk of infection and other complications with expectant management. - Unstable patients: require prompt delivery of the fetus→ Chorioamnionitis (also collect cervical cultures and commence empiric antibiotic therapy prior to delivery)→ Abruptio placentae→ Cord prolapse→ Nonreassuring fetal heart rateTocolysis is contraindicated in advanced labor (cervical dilation > 4cm), chorioamnionitis, nonreassuring fetal signs, abruptio placentae, or risk of cord prolapse!
• Hypertensive pregnancy disorders – Types Gestational hypertension: pregnancy-induced hypertension with onset after 20 weeks gestation  - Defined as a systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg on 2 separate measurements at least 4 hours apart Chronic hypertension: hypertension diagnosed < 20 weeks gestation or before pregnancy Preeclampsia: gestational hypertension with proteinuria, renal insufficiency, thrombocytopenia, evidence of liver damage (e.g., elevated liver enzymes, epigastric pain), pulmonary edema, and/or cerebral edema (headache, visual blurring, vomiting, an altered mental status)- Superimposed preeclampsia: preeclampsia that occurs in a patient with chronic hypertension- HELLP syndrome: a life-threatening form of preeclampsia (HELLP is an acronym: H = hemolysis; EL = elevated liver enzymes; LP = low platelets)   Eclampsia: severe form of preeclampsia with convulsive seizures and/or coma
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• Hypertensive pregnancy disorders Risk factors:- Thrombophilia (e.g., antiphospholipid syndrome)- Obesity (BMI ≥ 30)- Age < 20 or > 40 years- African-American race- Diabetes mellitus or gestational diabetes- Chronic hypertension- Chronic renal disease (e.g., SLE)- Nulliparity  - Previous preeclampsia  - Family history- Multiple gestation (twins)- Chromosomal anomalies or congenital structural anomalies- Hydatidiform moles Clinical features:- Gestational hypertension: Nonspecific symptoms (e.g., morning headaches, fatigue, dizziness) can occur.- Preeclampsia: 90% occur after 34 weeks of gestation- Preeclampsia without severe symptoms:→ Usually asymptomatic→ Nonspecific symptoms may include: Headaches, visual disturbances, RUQ or epigastric pain, rapid development of edema→ Hypertension→ Proteinuria- Preeclampsia with severe symptoms:→ Severe hypertension (systolic ≥ 160 mmHg or diastolic BP ≥ 110 mmHg)→ Proteinuria, oliguria→ Headache→ Visual disturbances (e.g., blurred vision, scotoma)→ RUQ or epigastric pain  → Pulmonary edema→ Cerebral symptoms (e.g., altered mental state, nausea, vomiting, hyperreflexia, clonus)- HELLP syndrome:→ Onset: most commonly > 27 weeks gestation (30% occur postpartum)→ Preeclampsia usually present (∼ 85%) → Nonspecific symptoms: nausea, vomiting, diarrhea→ RUQ pain (liver capsule pain; liver hematoma)→ Rapid clinical deterioration (DIC, pulmonary edema, acute renal failure, stroke, abruptio placentae)- Eclampsia→ Onset: the majority of cases occur in the intrapartum and postpartum period→ Most often associated with severe preeclampsia (but can be associated with mild preeclampsia)→ Eclamptic seizures: generalized tonic-clonic seizures (usually self-limited) Treatment:- Preeclampsia with mild symptoms:→ Hospitalization and delivery indicated if: Pregnancy ≥ 37 0/7 weeks gestation→ In all other cases, continue outpatient monitoring- Preeclampsia with severe symptoms:→ Delivery is indicated if:a) Pregnancy is ≥ 34 0/7 weeks gestationb) Pregnancy is < 34 0/7 weeks gestation with maternal or fetal instability  → Procedure: vaginal delivery should be conducted if possible, but often cesarean delivery is needed for younger gestational age, immature cervix, or poor maternal or fetal condition.→ Expectant management: if pregnancy < 34 weeks and mother and fetus are stable- Eclampsia: Stabilization and delivery- HELLP syndrome: Stabilization and delivery if ≥ 34 weeks gestation or at any gestational age with deteriorating maternal or fetal status (If the fetus is viable, delay labor until 24-48 h after corticosteroid administration)ARDS and cerebral hemorrhage are the most common causes of death.
• Acute fatty liver of pregnancy A rare disease most common in the third trimester characterized by extensive fatty infiltration of the liver, which can result in acute liver failure Pathophysiology: dysfunction of fatty acid β-oxidation Clinical features:- Sudden onset of jaundice- RUQ pain, nausea, and vomiting- Coagulopathy with an increased risk of disseminated intravascular coagulation (DIC) - Hypoalbuminemia → ascites Complications:- Acute liver failure- Acute renal failure- Encephalopathy- Fetal and maternal death (10%) Diagnosis:- Laboratory analysis: → ↑ AST, ↑ALT→ ↑ WBC, ↓ platelets→ Hypoglycemia→ Liver synthesis parameters: ↓↓ clotting factors, ↓↓ Cholinesterase- Imaging: rule out other diagnoses (e.g., liver hematoma)- Therapy: immediate Cesarean (C)-section
• Intrahepatic cholestasis of pregnancy A rare disease most common in the third trimester that presents with pruritus, jaundice, and an elevation in serum bile acid concentrations Epidemiology: Intrahepatic cholestasis occurs in 0.1-0.2% of pregnancies. Clinical features:- Jaundice- Pruritus Complications:- Fetal growth restriction- Increased fetal mortality- Premature labor and increased preterm birth rates - Recurrence in following pregnancies (40-60%) Diagnosis:- ↑ Total serum bile acid levels (cholic acid and chenodeoxycholic acid) > 10 micromol/L- ↑ ALP- ↑ ALT, AST- ↑ direct bilirubin- Hepatitis serology (to rule out viral hepatitis)→ Antismooth muscle and antimitochondrial antibodies (to rule out autoimmune liver disease) Therapy:- First-line medication: ursodeoxycholic acid PO- Cholestyramine PO → may cause a deficiency in fat-soluble vitamins and lead to related adverse effects   Prognosis: fully reversible postpartum
• Hyperemesis gravidarum Severe, persistent nausea and vomiting associated with a > 5% loss of pre-pregnancy weight and ketonuria with no other identifiable cause. Clinical features: nausea, vomiting, physical signs of dehydration, hypersalivation, orthostatic hypotension, malnourishment Diagnosis: Clinical diagnosis- Electrolyte disturbances (hypokalemia and hypochloremic metabolic alkalosis)- Signs of dehydration (e.g., ↑ hematocrit)- Ketonuria Treatment:- Antiemetic therapy (pyridoxine, diphenhydramine)- May require glucocorticoid therapy - IV fluid resuscitation/replacement (see IV fluid therapy)  - Electrolyte and thiamine repletion  
• Postpartum hemorrhage (PPH) Definition:- Blood loss > 500 mL after vaginal birth occurring at any time, either before, during, or after placental delivery- Blood loss > 1000 mL for cesarean section occurring at any time, either before, during, or after placental delivery Etiology:- Uterine atony (most common)- Abnormal placental separation (e.g., retention or incomplete placental detachment)- Maternal injury during birth (spontaneous or iatrogenic)  - Bleeding diathesis Clinical features:- Features of anemia- Features of hypovolemic shock Complications:- Thromboembolism- Sheehan syndrome- Abdominal compartment syndrome
• Uterine atony Failure of the uterus to effectively contract and retract after complete or incomplete delivery of the placenta, which can lead to severe postpartum bleeding from the myometrial vessels Epidemiology: responsible for ∼ 80% of PPH cases Risk factors: overdistention of the uterus- Multiparity- Multiple pregnancy- Post-term pregnancy- Instrumental delivery- Anatomical abnormalities (i.e., fetal, uterine, abnormal placental implantation)- Large for gestational age newborn (e.g., > 4000 g)- Poor myometrial contraction following prolonged or rapid and forceful birth Clinical findings:- Abnormal vaginal bleeding- Soft, enlarged (increased fundal height), boggy ascending uterus Diagnosis: clinical diagnosis Treatment:- Monitoring, adequate large-bore IV access (≥ 16 gauge), and an ice pack  - Fluid therapy (with intravenous crystalloid solutions)- Oxygenation- Uterine massage and external compression: A clenched fist is inserted into the anterior vaginal fornix and exerts pressure on the anterior wall of the uterus. The other hand is positioned externally and presses against the inner fist, located in the uterine body.- Uterotonic agents as needed:1. IV oxytocin (diluted in saline)2. IM carboprost tromethamine (if the patient does not suffer from asthma)3. IM methylergonovine (if no hypertension or arterial disease is present)4. Prostaglandins such as misoprostol (useful when injectable uterotonic agents are unavailable or contraindicated)4. Tranexamic acid: Give when initial therapies fail to stop bleeding; stops fibrinolysis and reduces mortality.  - Last resort: hysterectomy
• Abnormal placental separation Defective decidual layer of the placenta leading to abnormal attachment and separation during postpartum period Epidemiology: placental detachment abnormalities due to anatomical causes occur in 0.2–1% of all pregnancies Risk factors: prior damage to the endometrium- History of uterine surgery (e.g., endometrial ablation, hysteroscopic removal of intrauterine adhesions, dilatation, and curettage)- Prior births by cesarean section- Placenta previa Types:- Placenta accreta (80% of cases): chorionic villi attach to the myometrium (but do not invade or penetrate the myometrium) rather than decidua basalis.  - Placenta increta (15% of cases): chorionic villi invade or penetrate into the myometrium.- Placenta percreta (5% of cases): chorionic villi penetrate the through the myometrium, penetrate the serosa, and in some cases, adjacent organs (e.g., rectum or bladder) Clinical features:- Retained products of conception (RPOC): any placental fragments or membranes that remain within the uterus due to abnormal placental separation in the postpartum period, suggested by:→ Abnormal uterine bleeding or postpartum hemorrhage at the time of attempted manual separation of the placenta→ Fever→ Pelvic or uterine tenderness Treatment:- If the placenta does not separate within 30 minutes after birth or there is evidence of postpartum hemorrhage, the following measures are to be taken:1. General measures:→ Monitoring, adequate large-bore IV access (≥ 16 gauge), and an ice pack  → Volume replacement therapy (with intravenous crystalloid solutions)→ Oxygenation2. Brandt-Andrews maneuver: One hand is placed on the abdomen, securing the uterine fundus and preventing uterine inversion. The other hand applies steady downward traction on the umbilical cord.3. Uterotonic agents→ Oxytocin: if the placenta remains in the uterus despite traction→ Carboprost (Prostaglandin F2-alpha)4. If only partial removal of placenta is suspected: postpartum inspection of the placenta and fetal membranes → sonography to locate the succenturiate placenta5. Manual palpation, followed by dilation and curettage (D&C) or vacuum removal of RPOC under anesthesia/regional anesthesia and high-dose IV administration of uterotonic agents 6. Last resort: hysterectomy in failed attempts for placental detachment, persistent bleeding, and prostaglandinresistance
• Mastitis Epidemiology- Incidence: up to 10% of nursing mothers (particularly 2-4 weeks postpartum) Etiology: Staphylococcus aureus (most common) Clinical features:- Tender, firm, swollen, erythematous breast (generally unilateral)- Pain during breastfeeding- Reduced milk secretion- Flu-like symptoms, malaise, fever, and chills- In some cases, reactive lymphadenopathy Diagnosis: Clinical diagnosis- Breast milk cultures or imaging may be required if there is no response to initial treatment. Treatment:- In nursing mothers, frequent emptying of the breast: Breastfeeding with alternate breasts is recommended every 2-3 hours.  - Analgesics (e.g., ibuprofen)- Cold compresses- Antibiotic treatment→ Oral penicillinase-resistant penicillin or cephalosporin (e.g., dicloxacillin or cephalexin)→ In the case of methicillin-resistant Staphylococcus aureus (MRSA): clindamycin or trimethoprim-sulfamethoxazole (TMP-SMX)  
• Chorioamnionitis Common bacteria: Ureaplasma urealyticum (up to 50% of cases), Mycoplasma hominis (up to 30% of cases), Gardnerella vaginalis, bacteroides, group B Streptococcus, E. coli Risk factors:- Prolonged labor or premature rupture of membranes (PROM)- Pathological bacterial colonization of vaginal tract (e.g., STDs, frequent UTIs)- Iatrogenic: multiple digital vaginal exams, invasive procedures (e.g., amniocentesis) Clinical features:- Fever (> 38 °C or > 100°F)- Tachycardia > 120/min- Uterine tenderness, pelvic pain- Malodorous and purulent amniotic fluid, vaginal discharge- Premature contractions, PROM- Fetal tachycardia > 160/min in cardiotocography Diagnostics: Chorioamnionitis is a clinical diagnosis (fever plus ≥ 1 additional symptom). Tests support or confirm diagnosis if the clinical presentation is ambiguous (e.g., in subclinical chorioamnionitis). Management:- Maternal antibiotic therapy→ Vaginal birth: IV ampicillin plus gentamicin (broad coverage)→ Cesarean birth: IV ampicillin and gentamicin, plus clindamycin (anaerobe coverage to minimize post-cesarean complications, e.g., endometritis)- Delivery→ Swift delivery is generally indicated to minimize both maternal and fetal complications. → Cesarean section is not generally indicated, but is often necessary because of obstetrical complications (e.g., insufficient contractions).
• Intrauterine growth restriction Intrauterine growth restriction (IUGR) is defined as lower than normal fetal growth characterized by an estimated fetal weight below the 10th percentile for a given gestational age. Etiology:- Substance use (e.g., alcohol, cigarettes, cocaine, heroin)- Teratogenic drugs: ACE inhibitors, carbamazepine, phenytoin, warfarin- Placental insufficiency - Placenta previa- Multiple gestations- Placental abruption- Umbilical artery thrombosis/extensive infarction - Uterine malformations (e.g., fibroids)- Fetal factors: Genetic abnormalities (e.g., aneuploidy), cyanotic congenital heart defects, TORCH infections Asymmetrical IUGR is the most common manifestation of IUGR (∼ 70%), has a late onset, and is usually due to maternal systemic disease (e.g., hypertension) that results in placental insufficiency. Symmetrical IUGR is less common (∼ 30%) and is usually due to a genetic disorder (e.g., aneuploidy), congenital heart disease, or early intrauterine TORCH infection that affects the fetus early in gestation. Diagnostics:- Serial ultrasonography→ Decreased fetal growth: fetal weight below the 10th percentile of a given gestational age, as estimated on ultrasound→ Small placenta  → Oligohydramnios- Doppler velocimetry of umbilical artery: reduced or reversed diastolic flow; ↑ systolic/diastolic ratio  - Nonstress test: late decelerations of the fetal heartbeat, bradycardia- Biophysical profile: Oligohydramnios (AFI < 5), absent fetal breathing movements, decreased fetal movement and tone. A score ≤ 4 indicates fetal hypoxia and/or placental insufficiency. In this case, labor should be induced. Treatment:- Treatment of the underlying condition (e.g., treatment of hypertension in pregnancy, gestational diabetes mellitus)- Close monitoring of fetal status and placental development (NST, CST, BPP)- If the infant is close to term, administer steroids and induce labor after 48 hours.- If there are signs of nonreassuring fetal status or deterioration of maternal vital signs (e.g., pre-eclampsia), induce labor or perform immediate cesarean section.
• Placental abruption Etiology:- Predisposing factors: Hypertension (most common cause), preeclampsia/eclampsia- (Abdominal) trauma (up to 10% of cases): car accidents, falls, iatrogenic (e.g., post-amniocentesis)- Sudden decrease in intrauterine pressure  - Previous abruption, chorioamnionitis, prolonged rupture of membranes, short umbilical cord- Maternal age: < 20 years and > 35 years- Alcohol and cigarette consumption, cocaine use Clinical features- Continuous, dark, vaginal bleeding (revealed abruptio placentae)→ In ∼ 20% of cases, the hemorrhage is mainly retroplacental; vaginal bleeding does not occur (concealed abruptio placentae)- Abdominal pain or back pain, uterine tenderness  - Hypertonic contractions (rigid uterus), premature labor- Fetal distress (60% of cases)- Vaginal exam contraindicated: may worsen bleeding!In cases of retroplacental hemorrhage, patients may present with signs of hypovolemic shock without evident vaginal bleeding! Diagnostics: clinical - Ultrasound (transabdominal, transvaginal): only 25% sensitivity!→ Presentation of the placental position and a possible retroplacental hematoma→ Monitoring vital signs of the fetus (heartbeat, fetal movement)→ To rule out placenta previa in unclear cases- Fetal heart rate monitoring- Laboratory tests: CBC, coagulation factors   Management:- Normal fetal findings and a hemodynamically stable mother:→ < 34th week of pregnancy: Fetal lung maturity induction with corticosteroids (e.g., betamethasone), if necessary, tocolysis (e.g., nifedipine, β2-adrenergic agonist). Aim for a normal delivery.→ 34th to 36th weeka) Active uterine contractions present: vaginal delivery  b) No contractions + no signs of fetal distress + bleeding has stopped: expectant management and observation> 36th week: Delivery- In acute symptoms and a live fetus: Emergency cesarean section- In acute symptoms and intrauterine fetal death: Induction of vaginal delivery through pharmacologic uterine contraction inducers and opening of the amniotic sac
• Placenta previa Presence of the placenta in lower uterine segment, which might lead to partial or full obstruction of the neck of the uterus with high risk of hemorrhage (rupture of placental vessels) and birth complications Risk factors:- Maternal age > 35 years, multiparity, short intervals between pregnancies- Previous curettage or cesarean section- Previous placenta previa, previous/recurrent abortion Clinical features:- Sudden, painless, bright red vaginal bleeding  - Usually occurs during the 3rd trimester (before rupture of the membranes), stops spontaneously after 1-2 hours, and recurs during birth- Often causes preterm delivery (∼ 45% of cases)- Soft, nontender uterus- Usually no fetal distress Diagnostics:- Transvaginal ultrasound to assess the position of the placenta  - Digital vaginal examinations are contraindicated in cases of hemorrhage of unknown cause! Approach:- Gestational age < 37 weeks→ No active bleeding AND no evidence of fetal distress: expectant management→ Severe, active bleeding OR evidence of fetal distress: stabilization and emergency cesarian section- Gestational age > 37 weeks: immediate deliveryExpectant management:- Hospitalization and observation for 48 hours- If gestational age is < 34 weeks: fetal lung maturity induction with corticosteroids (e.g., betamethasone)- If gestational age is between 34 and 37 weeks and delivery is likely within 7 days: fetal lung maturity induction with corticosteroids- If mild uterine contractions are present: tocolysis with magnesium sulfate may be performed (especially if the fetus is extremely premature)   Route of delivery:- Lower segment cesarean section is almost always preferred; ideally scheduled at 36-37 weeks gestation  - Induction of labor and/or vaginal delivery may be performed in the operating room if the mother is hemodynamically stable, fetal cardiac status is reassuring, and the placenta lies > 2 cm away from the internal os on ultrasonography
• Uterine rupture Etiology:- Uterine distention→ Delay in labor progression because of fetal malpresentation→ Fetal macrosomia and multiple gestations→ Overdose of oxytocin- Uterine scar/prior uterine surgery (e.g., C-section or myomectomy)  - Traumatic rupture (e.g., iatrogenic or caused by an accident) Clinical features:- Imminent rupture→ Severe abdominal pain→ Increased contractions followed by hyperactive labor→ Bandl ring: muscular ring that can be seen above the belly button due to the powerful contractions of the upper uterine segment  - Uterine rupture→ Severe abdominal pain→ Sudden pause in contractions→ Fetal distress (e.g., deteriorating fetal heart rate)→ Vaginal bleeding→ Hemodynamic instability (as a result of abdominal bleeding)→ Loss of fetal station  → Palpable fetal parts through the rupture Treatment:- Imminent rupture: Immediate IV tocolysis + Emergency C-section- Uterine rupture: Immediate laparotomy with emergency C‑section- Uterine dehiscence: Cesarean delivery before labor begins is recommended to avoid a complete rupture.
• Spontaneous abortion Maternal:- Septate uterus- Uterine leiomyomas- Uterine adhesions- Cervical incompetence- Systemic diseases including diabetes mellitus, hyperthyroidism, hypothyroidism, genetic disorders, infections, hypercoagulability (e.g., antiphospholipid syndrome, which is associated with recurrent miscarriages)- Chromosomal abnormalities account for up to half of all spontaneous abortions- Congenital anomalies- Trauma- Iatrogenic (e.g., amniocentesis or chorionic villus sampling)- Environmental (exposure to toxins such as drugs or maternal smoking during pregnancy) Threatened abortion: - Vaginal bleeding + Fetal activity- Cervical os: closed- Reversible Inevitable abortion:- Vaginal bleeding, and visible/palpable products of conception- Fetal activity may be present.- Cervical os: dilated- Irreversible Missed abortion:- No bleeding- No expulsion of the products of conception- No fetal activity- Cervical os: closed- Irreversible Incomplete abortion:- Vaginal bleeding; products of conception within the cervical canal or uterus- Usually occurs > 12 weeks' gestation- Cercial os: dilated- Irreversible Complete abortion:- Vaginal bleeding; products of conception completely outside of the uterus- Usually occurs < 12 weeks' gestation- Cervical os: closed- Irreversible Treatment:- Threatened abortion: Expectant management (symptoms will resolve or will progress to inevitable, incomplete, or complete abortion).- Other forms: → Expectant management (option for women < 14 weeks gestation): Surgical evacuation is usually recommended if evacuation does not occur after 4 weeks.→ Medical evacuation: Misoprostol is used to induce cervical ripening and expulsion of the products of conception. When available, pretreatment with mifepristone 24 hours prior is recommended.  → Surgical evacuation (dilation and curettage): Preferred method in septic abortion or if there is heavy bleeding or significant maternal disease- Rh(D)-negative women should receive Rh(D)-immune globulin in cases of vaginal bleeding during pregnancy.
• Preeclampsia prevention Definition: New-onset hypertension & proteinuria &/or end-organ damage at >20 weeks gestation High risk:- Prior preeclampsia- Chronic kidney disease- Chronic hypertension- Diabetes mellitus- Multiple gestation- Autoimmune disease Moderate risk- Obesity- Advanced maternal age- Nulliparity Prevention:- Low-dose aspirin at 12 weeks gestation
• Preventing neonatal group B Streptococcus infection Antenatal screening:- Rectovaginal culture at 36-38 weeks gestation Indications for intrapartum prophylaxis:- GBS bacteriuria or GBS urinary tract infection in current pregnancy (regardless of treatment)- GBS-positive rectovaginal culture in current pregnancy- Unknown GBS status PLUS any of the following:→ <37 weeks gestation→ Intrapartum fever→ Rupture of membranes for ≥18 hours→ Prior infant with early-onset neonatal GBS infection  Intrapartum prophylaxis: Intravenous penicillin
• Gestational diabetes mellitus – Complications First trimester:- Congenital heart disease: transposition of the great vessels, ventricular septal defect, truncus arteriosus, tricuspid atresia, patent ductus arteriosus, dextrocardia- Neural tube defects- Small left colon syndrome- Caudal regression syndrome: rare structural anomaly of the caudal region; aplasia or hypoplasia of the sacrum or lumbosacral spine Second and third trimester:- Macrosomia: birth weight > 90th percentile or > 4000-4500 g (due to stimulated growth and adipogenesis) → increased risk of birth injuries (e.g., shoulder dystocia)- Polycythemia  - Neonatal hypoglycemia and other electrolyte imbalances (hypocalcemia, hypomagnesemia)- Respiratory distress (due to insufficient production of pulmonary surfactant)- Hypertrophic cardiomyopathy (polycythemia → redistribution of iron → iron deficiency in cardiac tissue AND hypoxemia → impaired cardiac remodeling)- Polyhydramnios (fetal hyperglycemia → fetal polyuria)
• Preterm labor Gestational age: < 32 weeks- Betamethasone- Tocolytics- Magnesium sulfate- Penicillin if GBS positive or unknown Gestational age: 32 0/7 to 33 6/7 weeks- Betamethasone- Tocolytics- Penicillin if GBS positive or unknown Gestational age: 34 0/7 to 36 6/7 weeks- ± Betamethasone- Penicillin if GBS positive or unknown
• Preterm labor Gestational age: < 32 weeks- Betamethasone- Tocolytics- Magnesium sulfate- Penicillin if GBS positive or unknown Gestational age: 32 0/7 to 33 6/7 weeks- Betamethasone- Tocolytics- Penicillin if GBS positive or unknown Gestational age: 34 0/7 to 36 6/7 weeks- ± Betamethasone- Penicillin if GBS positive or unknown
• Shoulder dystocia An obstetric emergency in which the anterior shoulder of the fetus becomes impacted behind the maternal pubic symphysis during vaginal delivery   Epidemiology: ∼ 0.2-3% of births Risk factors:- History of shoulder dystocia- Fetal macrosomia- Prolonged second stage of labor- Maternal diabetes mellitus- Maternal obesity- Post-term pregnancy Clinical features:- Features of arrested active phase of labor- Turtle sign: the fetal head is partially delivered but retracts against the perineum- Failed restitution of the head Treatment:- The patient should stop bearing down and lie supine with the buttocks on the edge of the bed.- Perform shoulder dystocia maneuvers:→ First-line: McRobert's maneuver→ Any internal maneuvers below may be attempted to next.→ If all above maneuvers fail, attempt the all fours position.→ Last-resort options: Fracture of fetal clavicle, Zavanelli maneuver, Symphysiotomy
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• Medical contraindications to pregnancy - Left ventricular ejection fraction < 40%- NYHA class III-IV heart failure- Prior peripartum cardiomyopathy- Severe obstructive cardiac lesions- Severe pulmonary HTN (Eisenmenger syndrome)- Unstable aortic dilation > 40 mm
• Neonatal breast enlargement Neonatal breast hypertrophy- Bilateral- Firm, disc-like tissue under areolae- ± Galactorrhea- Management: Reassurance Mastitis:- Unilateral- Focal erythema, tenderness, induration- Management: Antibiotics Abscess:- Unilateral- Focal erythema, tenderness- Fluctuance ± purulent discharge- Management: Antibiotics ± drainage
• Routine prenatal laboratory tests Initial prenatal visit:- Rh(D) type, antibody screen- Hemoglobin/hematocrit, MCV- HIV, VDRL/RPR, HBsAg- Rubella & varicella immunity- Pap test (if screening indicated)- Chlamydia PCR- Urine culture- Dipstick for urine protein 24-28 weeks:- Hemoglobin/hematocrit- Antibody screen if Rh(D) negative- 50-g 1-hour GCT 35-37 weeks:- Group B Streptococcus culture
• Neonatal jaundice Phototherapy:- Indications:→ Increase of total serum bilirubin above the threshold for phototherapy (children > 95th percentile on nomogram (e.g., > 15 mg/dL in a 48-hour-old term infant, > 20 mg/dL in 96-hour-old infant))  → For neonates born < 35 weeks gestation, threshold bilirubin levels for treatment are lower because premature infants are at a greater risk of neurotoxicity.  - Contraindication: ↑ direct (conjugated) bilirubin → danger of “bronze baby” syndrome  - Continued until total bilirubin levels < 15 mg/dL Exchange transfusion:- Indications→ Threshold in a 24-hour-old term baby is a total serum bilirubin value > 20 mg/dL  → Inadequate response to phototherapy, or a rapid rise in the total serum bilirubin level (> 1 mg/dL/hour in less than 6 hours)→ Acute bilirubin encephalopathy→ Hemolytic disease, severe anemia
• Polycystic ovary syndrome Clinical features:- Onset typically during adolescence- Menstrual irregularities (primary or secondary amenorrhea, oligomenorrhea)- Difficulties conceiving or infertility- Obesity and possibly other signs of metabolic syndrome- Hirsutism- Androgenic alopecia- Acne vulgaris and oily skin- Acanthosis nigricans: hyperpigmented, velvety plaques (axilla, neck)- Premature adrenarche Diagnostics: Two of the following three criteria1. Hyperandrogenism (clinical or laboratory)2. Oligo- and/or anovulation3. Polycystic ovaries on ultrasound- ↑ Testosterone (both total and free) or free androgen index - ↑ LH (LH:FSH ratio > 2:1)- Estrogen is normal or slightly elevated  - Transvaginal ultrasound: Enlarged ovaries with numerous anechoic cysts, "string of pearls" appearance Evaluate for metabolic disease:- Test for hypertension- Monitor BMI- Assess for insulin resistance or type 2 diabetes mellitus → oral glucose tolerance test- Assess for hyperlipidemia → measure serum lipids and cholesterol Treatment:- First-line: Weight loss- Not trying to conceive: OCPs - Trying to conceive:→ Ovulation induction with clomiphene citrate or letrozole → Ovulation induction with exogenous gonadotropins or laparoscopic ovarian drilling
• Exercise during pregnancy Goal: 30 minutes of moderately intense exercise most days of the week Benefits:- ↓ Gestational diabetes mellitus risk- ↓ Preeclampsia risk- ↓ Cesarean delivery risk  - Shorter postpartum recovery- Weight management Recommended:- Walking/running- Cycling- Yoga  - Swimming- Light-weight strength training   Not recommended:- Scuba diving- Contact sports- Exercise with falling risk  - Skydiving
• Gestational pemphigoid Bullous, pemphigoid-like dermatosis during pregnancy of unknown cause (most likely immunological) Epidemiology: 1:50,000 pregnancies (in the US) Clinical presentation:- Commonly starts in the periumbilical region during the 2nd and 3rd trimester- Intensely pruritic, mostly non-blistering lesions (eczema, urticarial or papular lesions) on extremities and mucous membranes- Grouped vesicles with herpetiform appearance (“gestational herpes”) usually occur as the disease advances. Diagnostics: The diagnosis is confirmed via biopsy and immunofluorescence. Treatment:- High-potency topical steroids- Antihistamines  Prognosis: Usually self-limiting; heals spontaneously after delivery, but associated with complications (e.g., premature labor, increased lifetime risk of autoimmune disease)
• Neonatal soft tissue injuries Caput succedaneum: benign edema of the scalp tissue that extends across the cranial suture lines   Cephalohematoma: subperiosteal hematoma that is limited to cranial suture lines   Subgaleal hemorrhage: bleeding between the periosteum of the skull and the aponeurosis that may extend across the suture lines; associated with a high risk of significant hemorrhage and hemorrhagic shock  
• Cervical insufficiency Painless cervical dilation, in the absence of uterine contractions and/or labor, in the second trimester of pregnancy Etiology: Most cases are idiopathic. Risk factors:- Previous mid-trimester pregnancy loss and/or preterm birth- Previous obstetric or gynecological trauma (e.g., termination of pregnancy, rapid delivery, multiple gestations, or cervical conization)- Cervical connective tissue weakness (e.g., Ehler-Danlos syndrome)- Diethylstilbestrol exposure Clinical features:- Painless cervical dilation with or without prolapsed membranes- Pelvic cramps or backache  - ↑ Volume, changed color (yellow or blood-stained), and/or thinner consistency of vaginal discharge Diagnosis: - Clinical diagnosis typically before 24 weeks' (may be up to 28 weeks') gestationOR - History of ≥ 2 previous mid-trimester pregnancy losses or ≥ 3 preterm births not explained by any other cause, and a transvaginal ultrasound cervical length < 25 mm before 24 weeks' gestation Treatment:- Serial cervical ultrasound monitoring should be commenced in high-risk women (i.e., previous preterm birth) between 16-24 weeks' gestation.  - Cervical cerclage- Vaginal progesterone supplementation: indicated for a short cervical length at < 24 weeks' gestation in the absence of a previous preterm birth- Strict bed rest is not recommended.
• Neonatal polycythemia Definition: Hematocrit > 65% in term infants Causes:- Increased erythropoiesis from intrauterine hypoxia: maternal diabetes, hypertension, or smoking; IUGR- Erythrocyte transfusion: delayed cord clamping; twin-twin transfusion- Genetic/metabolic disease: hypothyroidism or hyperthyroidism; genetic trisomy (13, 18, 21) Clinical presentation:- Asymptomatic (most common)- Ruddy skin- Hypoglycemia, hyperbilirubinemia- Respiratory distress, cyanosis, apnea- Irritability, jitteriness- Abdominal distension Treatment:- Intravenous fluids- Glucose- Partial exchange transfusion
• HIV management during pregnancy Antepartum:- HIV RNA viral load at initial visit, every 2-4 weeks after initiation or change of therapy, monthly until undetectable, then every 3 months- CD4 cell count every 3-6 months- Resistance testing if not previously performed- ART initiation as early as possible- Avoid amniocentesis unless viral load ≤1,000 copies/mL Intrapartum:- Avoid artificial ROM, fetal scalp electrode, operative vaginal delivery- Viral load ≤1,000 copies/mL: ART + vaginal delivery- Viral load >1,000 copies/mL: ART + zidovudine + cesarean delivery Postpartum:- Mother: continue ART- Infant (maternal viral load ≤1,000 copies/mL): zidovudine- Infant (maternal viral load >1,000 copies/mL): multidrug ART
• Postpartum endometritis Definition: inflammation of the endometrium, possibly also including the myometrium and parametrium Etiology: mostly polymicrobial (2-3 ascending organisms, e.g., Gardnerella vaginalis, Staphylococcus epidermidis, group B Streptococcus, and/or Ureaplasma urealyticum, all of which are usually found in the normal vaginal flora.)   Pathophysiology: lochia retention → ideal breeding ground for infection → postpartum endometritis/postpartum endomyometritis → postpartum sepsis Risk factors:- Cesarean section (C-section)  - Prolonged labor- Multiple cervical examinations- Retained products of conception after delivery or abortion- Meconium in amniotic fluid- Low socioeconomic status Clinical findings:- Fever- Lower abdominal pain, uterine tenderness- Chills, malaise- Foul-smelling lochia Diagnostics: primarily clinical; in some cases, the following tests can be used to confirm the diagnosis: Gram stain or wet mount of vaginal discharge- Blood and urine cultures Treatment:- Antibiotic treatment: IV clindamycin and gentamicin- Ampicillin-sulbactam is a reasonable alternative if resistance to clindamycin is a concern.- Uterine curettage to remove retained products of conception.- Hysterectomy in case of life-threatening complications or no response to conservative therapeutic measures.
• Peripartum cardiomyopathy Risk factors - Maternal age > 30- Multiple gestation- Preeclampsia, eclampsia Clinical features:- LVEF < 45%- Onset: 36 weeks gestation - 5 months postpartum - No other cause of heart failure Management:- Deliver based on maternal hemodynamic stability - Standard systolic heart failure regimen- Thromboembolism prophylaxis Recurrence risk:- LVEF <20% at diagnosis- Persistent left ventricular systolic dysfunction
• Indications for specialized RBC treatments Irradiated:- Bone marrow transplant recipients- Acquired or congenital cellular immunodeficiency- Blood components donated by first or second degree relatives Leukoreduced:- Chronically transfused patients- CMV seronegative at-risk patients (e.g., AIDS, transplant patients)- Potential transplant recipients- Previous febrile nonhemolytic transfusion reaction Washed:- IgA deficiency- Complement-dependent autoimmune hemolytic anemia- Continued allergic reations (e.g., hives) with red cell transfusion despite antihistamine treatment
• Preventing neonatal group B Streptococcus infection Antenatal screening- Rectovaginal culture at 36-38 weeks gestation Indications for intrapartum prophylaxis- GBS bacteriuria or GBS urinary tract infection in current pregnancy (regardless of treatment)- GBS-positive rectovaginal culture in current pregnancy- Unknown GBS status PLUS any of the following:→ <37 weeks gestation→ Intrapartum fever→ Rupture of membranes for ≥18 hours- Prior infant with early-onset neonatal GBS infection  Intrapartum prophylaxis- Intravenous penicillin
• Subchorionic hematoma Etiology: Separation of chorion from the uterus Clinical presentation:- Ultrasound: Blood collection by gestational sac± Vaginal bleeding Risk factors:- Infertility treatment- Anticoagulation- Uterine anomalies- Recurrent pregnancy loss Complications:- Spontaneous abortion- Abruptio placentae- Preterm premature rupture of membranes- Preterm delivery Management:- Expectant± Serial ultrasounds
• Adolescent pregnancy Definition: Pregnancy at age <19 Maternal complications:- Hydatidiform mole- Preeclampsia- Anemia- Operative vaginal delivery- Postpartum depression Fetal complications:- Gastroschisis  - Omphalocele- Preterm birth- Low birth weight- Perinatal death
• Anticoagulation during pregnancy Low-molecular-weight heparin:- SubQ- Throughout pregnancy- Avoid in severe renal insufficiency Unfractionated heparin:- SubQ or IV- Before delivery- Used in renal insufficiency- Best for high bleeding risk (term pregnancy, surgery) Warfarin: - Oral- Preconception & postpartum- Sometimes used in 2nd & 3rd trimester for patients with mechanical heart valve - Teratogenic (bone & cartilage)- ↑ bleeding
• Exercise during pregnancy Exercise should be avoided by: Patients at risk for preterm delivery- Cervical insufficiency- Preterm labor during current pregnancy- Preterm premature rupture of membranes Patients at risk for antepartum bleeding- Placenta previa- Persistent second- or third-trimester bleeding Patients with an underlying condition that could be exacerbated by exercise- Severe anemia- Hypertensive disorders of pregnancy (eg, preeclampsia)- Restrictive lung disease- Severe heart disease

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