Obstetrics

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 OBSTETRICS

HEMATOLOGIC CHANGES IN PREGNANCY .....................................................................................................1

CHRONIC HYPERTENSION .........................................................................................................................2
WHITE COAT HYPERTENSION ....................................................................................................................2
BREAST ENGORGEMENT...........................................................................................................................3
BREASTFEEDING CONTRAINDICATIONS.........................................................................................................5
MOLAR PREGNANCY ...............................................................................................................................6
BIOPHYSICAL PROFILE .............................................................................................................................6
HYDATIFORM MOLE ...............................................................................................................................7
PREECLAMPSIA DUE TO HYDATIFORM MOLE .................................................................................................7
MANAGEMENT OF HYDATIFORM MOLE .......................................................................................................8
THECA LUTEIN CYSTS...............................................................................................................................9
UTERINE ATONY ....................................................................................................................................9
POSTPARTUM HEMORRHAGE .................................................................................................................. 11
ASSESSING AMOUNT OF BLEEDING ........................................................................................................... 13
AMNIOTIC FLUID EMBOLISM ................................................................................................................... 13
BASELINE FETAL HEARTBEAT ................................................................................................................... 14
FETAL HEARTBEAT VARIABILITY ............................................................................................................... 14
FHR TRACINGS .................................................................................................................................... 15
EARLY DECELERATIONS .......................................................................................................................... 15
LATE DECELERATIONS ............................................................................................................................ 15
VARIABLE DECELERATIONS ..................................................................................................................... 16
SINUSOIDAL FETAL HEART RATE TRACING .................................................................................................. 16
PRETERM FHR TRACINGS ....................................................................................................................... 17
MANAGEMENT OF FHR CATEGORY III ....................................................................................................... 17
FETAL TACHYCARDIA ............................................................................................................................. 17
FETAL STATIONS .................................................................................................................................. 18
UTERINE CONTRACTION ABNORMALITIES ................................................................................................... 19
CALCULATING MONTEVIDEO UNITS .......................................................................................................... 20
DECELERATIONS ................................................................................................................................... 21
TWIN PREGNANCY................................................................................................................................ 22
MONOCHORIONIC MONOAMNIOTIC TWINS RISKS ....................................................................................... 23
T SIGN AND LAMBDA SIGN ...................................................................................................................... 25
TWIN-TWIN TRANSFUSION SYNDROME...................................................................................................... 27
HYPEREMESIS GRAVIDARUM ................................................................................................................... 28
WERNICKE ENCEPHALOPATHY DUE TO HYPEREMESIS GRAVIDARUM ................................................................. 30
THYROID HORMONE PRODUCTION DURING PREGNANCY ............................................................................... 31
NEONATAL THYROTOXICOSIS .................................................................................................................. 32
SHEEHAN SYNDROME............................................................................................................................ 32
MIGRAINES ........................................................................................................................................ 33
TYPES OF ABORTIONS............................................................................................................................ 35
SPONTANEOUS ABORTION ..................................................................................................................... 36

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MISSED ABORTION ............................................................................................................................... 37

COMPLETE ABORTION ........................................................................................................................... 38
THREATENED ABORTION ........................................................................................................................ 38
SEPTIC ABORTION ................................................................................................................................ 39
SUBCHORIONIC HEMATOMA ................................................................................................................... 40
UTERINE RUPTURE ............................................................................................................................... 41
INTRAUTERINE FETAL DEMISE.................................................................................................................. 43
ANTIPHOSPHOLIPID ANTIBODY SYNDROME ................................................................................................ 45
SLE .................................................................................................................................................. 46
SLE NEPHRITIS IN PREGNANCY ................................................................................................................ 47
PRETERM LABOR .................................................................................................................................. 48
EXTERNAL CEPHALIC INVERSION............................................................................................................... 49
ABRUPTIO PLACENTAE........................................................................................................................... 50
VASA PREVIA ...................................................................................................................................... 52
PREECLAMPSIA .................................................................................................................................... 53
PREECLAMPSIA PREVENTION ................................................................................................................... 56
STROKE DUE TO PREECLAMPSIA ............................................................................................................... 56
SEIZURE PREVENTION IN PREECLAMPSIA PATIENT WITH MYASTHENIA GRAVIS .................................................... 57
ECLAMPSIA ......................................................................................................................................... 58
PATHOPHYSIOLOGY OF PULMONARY EDEMA IN PREECLAMPSIA/ECLAMPSIA ...................................................... 59
POSTPARTUM PREECLAMPSIA ................................................................................................................. 59
ANTIHYPERTENSIVES IN PREGNANCY ......................................................................................................... 60
ANTEPARTUM FETAL SURVEILLANCE ......................................................................................................... 61
DECREASED FETAL MOVEMENT MANAGEMENT ........................................................................................... 62
INFERTILITY ......................................................................................................................................... 62
FIBROIDS............................................................................................................................................ 63
TYPES OF FIBROIDS ............................................................................................................................... 64
DEGENERATING UTERINE FIBROIDS ........................................................................................................... 64
UTERINE SARCOMA .............................................................................................................................. 65
INTRAUTERINE SYNECHIAE ...................................................................................................................... 66
INTRAHEPATIC CHOLESTASIS OF PREGNANCY............................................................................................... 67
CHOLELITHIASIS IN PREGNANCY ............................................................................................................... 68
POLYMORPHIC ERUPTION OF PREGNANCY .................................................................................................. 69
FETAL GROWTH RESTRICTION ................................................................................................................. 70
HYPERTENSION AND ASYMMETRIC GROWTH RESTRICTION ............................................................................. 71
SEPTIC PELVIC THROMBOPHLEBITIS .......................................................................................................... 72
ANEMIA IN PREGNANCY......................................................................................................................... 72
DIFFERENTIALS OF THROMBOCYTOPENIA IN PREGNANCY ............................................................................... 73
GESTATIONAL THROMBOCYTOPENIA ......................................................................................................... 74
HEPARIN-INDUCED THROMBOCYTOPENIA .................................................................................................. 74
NORMAL PHYSIOLOGIC CHANGES IN PREGNANCY......................................................................................... 75

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RENAL CHANGES IN PREGNANCY .............................................................................................................. 76

CARDIOPULMONARY ADAPTATIONS IN PREGNANCY...................................................................................... 76
COAGULATION CASCADE ........................................................................................................................ 77
PLACENTA PREVIA ................................................................................................................................ 78
CERVICAL INSUFFICIENCY ........................................................................................................................ 79
CERVICAL CONIZATION .......................................................................................................................... 80
CERCLAGE PLACEMENT .......................................................................................................................... 81
COLPOSCOPY ...................................................................................................................................... 82
HELLP SYNDROME ............................................................................................................................... 83
MAGNESIUM SULPHATE TOXICITY ............................................................................................................ 84
ECTOPIC PREGNANCY ............................................................................................................................ 85
RISKS OF OBESITY IN PREGNANCY ............................................................................................................ 86
OPERATIVE VAGINAL DELIVERY................................................................................................................ 86
UTERINE INVERSION ............................................................................................................................. 87
WATER INTOXICATION DUE TO OXYTOCIN TOXICITY...................................................................................... 88
OXYTOCIN CONTRAINDICATIONS .............................................................................................................. 88
LATE-TERM PREGNANCY ........................................................................................................................ 89
FETAL DYSMATURITY SYNDROME: ............................................................................................................ 90
LUMBAR PUNCTURE ............................................................................................................................. 90
POSTPARTUM URINARY RETENTION ......................................................................................................... 91
PERINEAL LACERATIONS ......................................................................................................................... 92
VAGINAL ATROPHY ............................................................................................................................... 93
ERB-DUCHENNE PALSY .......................................................................................................................... 94
FETAL MALPOSITION ............................................................................................................................. 95
APPROPRIATE WEIGHT GAIN IN PREGNANCY .............................................................................................. 96
RISK FACTORS FOR FETAL ANEMIA ........................................................................................................... 96
ROUTINE SCREENINGS AND INTERVENTIONS DURING PREGNANCY.................................................................... 97
NEURAL TUBE DEFECT ........................................................................................................................... 98
FOLATE SUPPLEMENT ............................................................................................................................ 98
STI SCREENING .................................................................................................................................... 99
SYPHILIS ............................................................................................................................................ 99
HIV MANAGEMENT DURING PREGNANCY ................................................................................................ 100
HEPATITIS C IN PREGNANCY .................................................................................................................. 101
FETAL FIBRONECTIN ............................................................................................................................ 101
SHORT CERVIX ................................................................................................................................... 102
GBS INFECTION ................................................................................................................................. 103
BRAXTON-HICKS CONTRACTIONS ........................................................................................................... 103
PRENATAL TESTING............................................................................................................................. 104
QUADRUPLE TEST .............................................................................................................................. 105
CELL-FREE FETAL DNA TESTING............................................................................................................. 105
ACUTE CERVICITIS .............................................................................................................................. 106

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DEPOT MEDROXYPROGESTERONE ACETATE (DMPA) .................................................................................. 107

AMNIOTIC FLUID INDEX ....................................................................................................................... 108
POLYHYDRAMNIOS ............................................................................................................................. 108
OLIGOHYDRAMNIOS ........................................................................................................................... 108
PRETERM PRELABOR RUPTURE OF MEMBRANES (PPROM) ......................................................................... 109
ASYMPTOMATIC BACTERIURIA .............................................................................................................. 111
PYELONEPHRITIS IN PREGNANCY ............................................................................................................ 112
INTRA-AMNIOTIC INFECTION (CHORIOAMNIONITIS) .................................................................................... 113
CAUSES OF FETAL TACHYCARDIA ............................................................................................................ 114
INDICATIONS FOR ANTI-D IMMUNE GLOBULIN .......................................................................................... 114
KLEIHAUER-BETKE TEST ....................................................................................................................... 115
ABO HEMOLYTIC DISEASE.................................................................................................................... 115
VAGINAL HEMATOMA ......................................................................................................................... 116
LOW BACK PAIN ................................................................................................................................ 117
NORMAL LABOR ................................................................................................................................ 118
ACTIVE PHASE ARREST ........................................................................................................................ 119
PROTRACTED ACTIVE PHASE ................................................................................................................. 119
2ND STAGE ARREST OF LABOR ................................................................................................................ 120
PHYSIOLOGIC HYDRONEPHROSIS OF PREGNANCY ....................................................................................... 121
HYDRONEPHROSIS FROM URETERAL SUTURE ............................................................................................ 121
RENAL INTERVENTIONS ........................................................................................................................ 122
CONGENITAL ZIKA SYNDROME............................................................................................................... 122
RUBELLA INFECTION DURING PREGNANCY ................................................................................................ 123
CONGENITAL TOXOPLASMOSIS .............................................................................................................. 123
CONGENITAL HERPES .......................................................................................................................... 124
CONGENITAL CMV ............................................................................................................................. 125
CONGENITAL LISTERIA ......................................................................................................................... 126
SEQUELAE OF CONGENITAL INFECTIONS ................................................................................................... 126
VACCINES DURING PREGNANCY ............................................................................................................. 127
SYPHILIS IN PREGNANCY ...................................................................................................................... 128
GRANULOMATOSIS INFANTISEPTICA........................................................................................................ 129
PUBIC SYMPHYSIS DIASTASIS ................................................................................................................ 130
MCROBERTS MANEUVER ..................................................................................................................... 131
BREECH PRESENTATION ....................................................................................................................... 132
INTERNAL PODALIC VERSION................................................................................................................. 133
GESTATIONAL DIABETES....................................................................................................................... 134
METABOLIC EFFECTS OF HPL ................................................................................................................. 136
SHOULDER DYSTOCIA .......................................................................................................................... 137
MANAGEMENT OF SHOULDER DYSTOCIA ................................................................................................. 139
ERB-DUCHENNE AND KLUMPKE PALSY .................................................................................................... 139
STRESS URINARY INCONTINENCE ............................................................................................................ 140

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CAUSES OF HYPERANDROGENISM IN PREGNANCY ...................................................................................... 141

MALIGNANT HYPERTHERMIA ................................................................................................................ 141
CESARIAN SECTION INCISION TYPES ........................................................................................................ 142
TRIAL OF VAGINAL BIRTH AFTER UTERINE SURGERY .................................................................................... 142
SHORT INTERPREGNANCY INTERVAL ........................................................................................................ 143
ILLICIT DRUG USE IN PREGNANCY ........................................................................................................... 143
DELIVERY PLAN FOR NONVIABLE FETUS ................................................................................................... 144
ACUTE FATTY LIVER OF PREGNANCY ....................................................................................................... 145
NONALCOHOLIC FATTY LIVER DISEASE ..................................................................................................... 146
HYDROPS FETALIS .............................................................................................................................. 147
Α THALASSEMIA ................................................................................................................................. 148
EARLY POSTPARTUM SIGNS .................................................................................................................. 149
POSTPARTUM FEVER ........................................................................................................................... 150
POSTPARTUM ENDOMETRITIS ............................................................................................................... 150
TREATMENT OF CHOICE ....................................................................................................................... 150
POSTPARTUM DIFFICULTY IN VOIDING..................................................................................................... 151
LOCHIA ............................................................................................................................................ 151
POSTPARTUM THYROIDITIS................................................................................................................... 152
TYPES OF THYROIDITIS ......................................................................................................................... 153
POSTPARTUM CONTRACEPTION ............................................................................................................. 153
POSTPARTUM DEPRESSION................................................................................................................... 154
HYPOTENSION AS A SIDE EFFECT OF EPIDURAL........................................................................................... 155
PREGNANCY & EXERCISE ...................................................................................................................... 156
MELASMA ........................................................................................................................................ 157
OSTEOGENESIS IMPERFECTA ................................................................................................................. 158
PLACENTA ACCRETA............................................................................................................................ 158
RECTUS ABDOMINIS DIASTASIS ............................................................................................................. 159
DIGITAL CERVICAL EXAMINATION ........................................................................................................... 160
ANEMBRYONIC GESTATION .................................................................................................................. 161
POSTDURAL PUNCTURE HEADACHE ........................................................................................................ 161
PSEUDOCYESIS................................................................................................................................... 162
UTERINE INCARCERATION ..................................................................................................................... 162
ULCERATIVE COLITIS DURING PREGNANCY ................................................................................................ 162
APPENDICITIS DURING PREGNANCY ........................................................................................................ 163
VAGINAL CUFF DEHISCENCE .................................................................................................................. 164
OOPHORECTOMY DURING PREGNANCY.................................................................................................... 164
DIABETES INSIPIDUS DURING PREGNANCY ................................................................................................ 164
POLYURIA ........................................................................................................................................ 165
BIPOLAR MANAGEMENT DURING PREGNANCY .......................................................................................... 165
SICKLE CELL DISEASE IN PREGNANCY ....................................................................................................... 166
ROUND LIGAMENT PAIN ...................................................................................................................... 166

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BUPIVACAINE TOXICITY ....................................................................................................................... 167

ACUTE PANCREATITIS DURING PREGNANCY .............................................................................................. 167
TRIGLYCERIDE-INDUCED PANCREATITIS .................................................................................................... 168
PERIPARTUM CARDIOMYOPATHY ........................................................................................................... 168
CARPAL TUNNEL SYNDROME................................................................................................................. 169

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HEMATOLOGIC CHANGES IN PREGNANCY

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CHRONIC HYPERTENSION
1. To make a diagnosis of chronic hypertension during pregnancy, 2 measurements should be
elevated ≥4 hours apart
2. Risks
a. Maternal
i. Superimposed preeclampsia
ii. Postpartum hemorrhage
iii. Gestational diabetes
iv. Abruption placentae
v. Cesarean delivery
b. Fetal
i. Fetal growth restriction
ii. Perinatal mortality
iii. Preterm delivery
1. ↑ in systemic vascular resistance and arterial stiffness → placental
dysfunction
iv. Oligohydramnios
1. Note: poorly controlled diabetes leads to polyhydramnios

WHITE COAT HYPERTENSION

1. Seen in patients with anxiety over medical care
2. Causes ↑ BP in patients who don’t have high blood pressure otherwise

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BREAST ENGORGEMENT
1. Occurs 3-5 days after delivery when colostrum is replaced by milk, resulting in high milk
production volumes
2. Engorgement is also exacerbated by physiologic ↑ in interstitial edema because of ↓ in
progesterone levels after delivery
3. Symptoms
a. Bilateral breast fullness
b. Diffuse tenderness and erythema
4. Treatment
a. Breastfeeding
b. Regular pumping
c. Cool compresses
d. Acetaminophen
e. NSAIDs
5. Differentials
a. Lactational Mastitis
i. Unilateral breast
ii. Focal tenderness and erythema
iii. Fever
b. Breast Abscess
i. Area of fluctuancy
ii. Axillary lymphadenopathy
c. Mammary candidosis
i. Unilateral
ii. Stabbing breast pain which is out of proportion to examination
iii. Scaling of skin of nipple
d. Galactocele and plugged ducts
i. Palpable mass

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BREASTFEEDING CONTRAINDICATIONS

1. It is recommended that patients with hepatitis B and C breastfeed. However, they should
abstain from breastfeeding if their nipples are cracked or bleeding
2. Cocaine is expressed into breast milk and can lead to fetal intoxication and withdrawal
symptoms. In addition, cocaine may cause long-term neurobehavioral problems (eg,
hyperactivity, cognitive delay)

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MOLAR PREGNANCY

BIOPHYSICAL PROFILE

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HYDATIFORM MOLE

1. Another risk factor is Vitamin A deficiency

2. Differentials
a. Embryonal carcinoma
i. Elevated b-hCG and abdominal mass but patient has ascites rather than
hypertension or neurologic symptoms

PREECLAMPSIA DUE TO HYDATIFORM MOLE

1. Preeclampsia at <20 weeks gestation can be a complication of hydatiform mole
2. The abnormal trophoblastic tissue proliferation can result in preeclampsia and leads to an
enlarged uterus (eg, pelvic mass)
a. Preeclampsia is due to abnormal placental spiral artery development, which leads to:
i. Placental hypoperfusion
ii. Placental ischemia
iii. Maternal hypertension
3. USG: anechoic cystic spaces (eg, snowstorm appearance)

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MANAGEMENT OF HYDATIFORM MOLE

1. Suction curettage, followed by serial beta-hCG levels until levels are Poly and
undetectable for at least 6 months (to diagnose gestational trophoblastic Oligohydroamnios
1. Poly: AFI ≥24 cm or a
neoplasia, if any)
single deepest pocket ≥8
2. OCPs are prescribed during this time period as pregnancy can make it
cm
difficult to determine the significance of rising beta-hCG
2. Oligo: AFI ≤5 cm or a
single deepest pocket <2
cm

Chance of uterine
rupture
It rarely occurs in patients
who have not had any
uterine surgery

Category I Tracing
Management
Expectant.

• Progesterone
supplementation is used
to prevent recurrence of
preterm labor in the
form of IM
hydroxyprogesterone
• Most common cause of
puerperal fever is
endometritis
• Most common cause of
nonreactive NST is quiet
fetal sleep cycle (which
lasts ≤40min)
o Extend
nonreactive NST
to 40-120
minutes because
of this reason
• Infertility is also one of
the risk factors for
hydatiform mole

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THECA LUTEIN CYSTS

UTERINE ATONY
1. Most common cause of primary postpartum hemorrhage (PPH)
a. Primary PPH occurs <24 hours after delivery
b. Hemostasis after delivery is achieved by:
i. Clotting
ii. Compression of placental site blood vessels by myometrial contraction
iii. Disruption of either of these can lead to PPH
2. Atony occurs when uterus becomes:
a. Fatigued
i. Prolonged labor
b. Over-distended
i. Fetal weight >4000g
ii. Multiple gestations
c. Unresponsive to oxytocin from saturation
3. Other risk factors for atony are:
a. Forceps-assisted delivery
b. Hypertensive disorders
4. Uterus is soft (“boggy”) and enlarged (eg, above umbilicus)

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POSTPARTUM HEMORRHAGE
1. First line is bimanual message and oxytocin
2. If that fails, use tranexamic acid
3. If that fails, use other uterotonics
a. Methylergonovine
i. Contraindicated in hypertensive patients (causes vasoconstriction)
b. Carboprost
i. Contraindicated in asthma patients (causes bronchoconstriction)
4. A pelvic ultrasound may be indicated to evaluate for retained products of conception

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ASSESSING AMOUNT OF BLEEDING

AMNIOTIC FLUID EMBOLISM

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BASELINE FETAL HEARTBEAT

FETAL HEARTBEAT VARIABILITY

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FHR TRACINGS

EARLY DECELERATIONS
1. These are caused by fetal head compression, when the fetal head descends closer to the cervix
2. Fetal head compression → narrowing of fetal anterior fontanelle → transient alteration in
cerebral blood flow → stimulation of vagal response → ↓ heart rate
3. These are benign, physiologic findings and don’t require any intervention

LATE DECELERATIONS
1. Occurs because of placental dysfunction, which leads to intermittent hypoxemia in the fetus
a. Placental dysfunction can occur in cases of late-term pregnancies (≥41 weeks gestation)
due to age-related placental changes (↑ placental vascular resistance)
2. Progressive placental dysfunction can lead to chronic fetal hypoxemia → uteroplacental
insufficiency
a. Blood is distributed more to brain than the peripheral tissues, which leads to:
i. ↓ fetal activity
ii. ↓ fetal renal perfusion → oligohydroamnios (single deepest pocket of amniotic
fluid <2 cm)

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VARIABLE DECELERATIONS
1. Well-tolerated if umbilical cord compression occurs with <50% of contractions
2. In contrast, umbilical cord compressions with ≥50% of contractions (recurrent variable
decelerations) increases the risk of fetal hypoxemia and acidosis
3. Management of recurrent variable decelerations
a. Maternal repositioning reduces cord compression:
i. Left lateral
ii. All-fours
b. If initial management doesn’t work, we can do amnioinfusion
i. It increases amniotic fluid volume → ↓ cord compression
ii. It is contraindicated in a patient with history of uterine surgery
c. If the FHR tracings become a category III tracing (absent variability + recurrent variable
decelerations) → caesarian delivery

SINUSOIDAL FETAL HEART RATE TRACING

1. Smooth, wave-like oscillation, with fixed amplitude (5-15/min) and frequency (3-5 cycles/min)
2. This tracing is considered a category III tracing and associated with severe fetal anemia likely
from fetal blood loss from ruptured vasa previa (presents as bright-red amniotic fluid)
3. Patients with this CTG require urgent C-section

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PRETERM FHR TRACINGS

1. ↑ FHR baseline
2. ↓ variability
3. Lower-amplitude accelerations
a. This is because FHR accelerations require mature sympathetic nervous system which
develops at 26-28 weeks gestation. Therefore, extremely premature fetuses (<28 weeks
gestation) often do not demonstrate reactivity

MANAGEMENT OF FHR CATEGORY III

1. Initial management of category III tracings is with:
a. Maternal repositioning
b. Intrauterine resuscitative interventions
i. Oxygen administration
ii. IV fluids
iii. Discontinuing uterotonics
2. Patients remote from delivery (ie, not completely 10 cm dilated) who do not improve from
initial resuscitative measures require an immediate C-section
a. Patients with complete cervical dilation can undergo operative vaginal delivery (eg,
vacuum-assisted vaginal delivery)

FETAL TACHYCARDIA

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FETAL STATIONS

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UTERINE CONTRACTION ABNORMALITIES

1. Tachysystole
a. >5 contractions in 10 minutes
b. Uterine contractions temporarily interrupt intervillous blood flow; excessive and
frequent contractions lead to fetal compromise → late decelerations
c. Management
i. Supportive measure
1. Lateral maternal repositioning
2. Tocolysis
ii. Discontinuation of uterotonic agents

2. Tetanic contractions
a. Contractions lasting >2 minutes
3. Management
a. Tocolytics (eg, terbutaline)

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CALCULATING MONTEVIDEO UNITS

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DECELERATIONS

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TWIN PREGNANCY

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MONOCHORIONIC MONOAMNIOTIC TWINS RISKS

1. Preterm birth
a. Common to all types of twin gestations
b. Due to uterine crowding and uterine overdistension → ↑ prostaglandin production, ↑
oxytocin receptors and ↑ contractility within the uterus
c. It can also be induced because of increase in maternal (eg, preeclampsia) and fetal (eg,
fetal growth restriction, discordant growth) complications
2. Single placental risks
a. Twin-twin transfusion syndrome
3. Single amniotic sac risks
a. Umbilical cord entanglement
b. Intrauterine fetal demise
4. Management
a. Inpatient management starting at 28 weeks gestation
i. Frequent fetal monitoring
ii. Antenatal corticosteroids administration
iii. Delivery at 32-34 weeks (preterm) via C-section

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T SIGN AND LAMBDA SIGN

1. T sign signifies 1 placenta (monochorionic) but 2 amniotic sacs
2. Lambda sign signifies 2 fused placenta (dichorionic) with 2 amniotic sacs

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TWIN-TWIN TRANSFUSION SYNDROME

1. Complications in donor
a. Anemia
b. Renal failure
c. Oligohydramnios
d. Low-output heart failure
e. Fetal growth restriction
2. Complications in recipient
a. Polycythemia
b. Polyhydramnios
c. Cardiomegaly
d. High-output cardiac failure
e. Hydrops fetalis
3. Treatment
a. Mild TTTS
i. Serial ultrasounds to look for worsening clinical features
b. Moderate to severe TTTS
i. Laser coagulation of placental anastomoses

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HYPEREMESIS GRAVIDARUM
1. Pathophysiology: ↑ ß-hCG and progesterone in pregnancy
a. ↑ ß-hCG symptom: nausea
b. ↑ progesterone symptom: vomiting
i. Because of relaxation of LES (ie, gastroesophageal reflux) and stomach (ie,
delayed gastric emptying)
2. Risk factors
a. Prior history of hyperemesis gravidarum
b. Multiple gestations
c. Hydatiform mole
d. History of esophageal reflux
e. History of migraines or motion sickness
3. Self-note: it seems that hyperemesis gravidarum is linked with ↑ b-hCG levels and its risk factors
are the same which are accompanied by ↑ b-hCG.
4. Resolves by 16-20 weeks gestation but can persist until delivery
5. Characterized by:
a. Dehydration
i. Dry mucous membranes
ii. Delayed capillary refill
iii. Tachycardia
b. Hypoglycemia
i. Ketonuria
c. Orthostatic hypotension
d. Electrolyte abnormalities
e. >5% loss of prepregnancy weight
6. Serum chemistry
a. Hypochloremic metabolic alkalosis
b. Hypokalemia
c. Ketonuria (basis for differentiating it from normal vomiting)
d. ↑ serum aminotransferases
7. It can also be associated with transient hyperthyroidism (eg, thyrotoxicosis of hyperemesis) due
to stimulation of thyroid by elevated b-hCG
8. Tobacco use protects against hyperemesis gravidarum because it ↑ metabolism of estrogen →
↓ serum estrogen

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WERNICKE ENCEPHALOPATHY DUE TO HYPEREMESIS GRAVIDARUM

1. A neurological disease due to thiamine deficiency
2. Presentation
a. Altered mental status
b. Oculomotor dysfunction (eg, nystagmus)
c. Gait ataxia
d. Bilaterally absent ankle reflex
3. Lab findings
a. Hypochloremic metabolic alkalosis
b. Hypokalemia
c. Hypoglycemia
d. ↑ serum aminotransferases
4. Treatment
a. Antiemetics
b. Fluids
c. Thiamine supplementation
d. Glucose infusion
i. Glucose infusion prior to thiamine supplementation can exacerbate the disease
and should be delayed until the patient has received thiamine
5. This disease increases the risk for spontaneous abortion
6. Differentials
a. Acute fatty liver of pregnancy
i. Occurs in third trimester
ii. Jaundice is present

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THYROID HORMONE PRODUCTION DURING PREGNANCY

1. Thyroid hormone production increases during pregnancy by following 2 mechanisms:
a. Estrogen stimulates synthesis of thyroxine-binding globulin (TBG) and decreases TBG
clearance. This leads to increase in bound thyroid hormone which in turn leads to
increased thyroid hormone production to maintain free hormone levels
b. hCG has a common alpha unit with TSH and a similar beta unit. Thus, it stimulates TSH
receptors directly to increase thyroid hormone production
2. Net effect is subclinical hyperthyroidism with ↑ total T3 and T4, normal (or mildly elevated) free
T4, and suppressed TSH.
3. Patient remains clinically euthyroid
4. However, patients with preexisting hypothyroidism (eg, chronic lymphocytic [Hashimoto]
thyroiditis) cannot increase thyroid hormone production, resulting in a relative hypothyroid
state
a. Hence, such patients with baseline hypothyroidism who become pregnant should have
their replacement thyroxine dose increased

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NEONATAL THYROTOXICOSIS

SHEEHAN SYNDROME

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MIGRAINES
1. Migraine headaches are common during childbearing age due to cyclic changes in estrogen and
progesterone
a. Headaches improve during pregnancy due to loss of these cyclic changes, but some
women have worsening symptoms, likely due to an increase in other migraine risk
factors (eg, sleep disturbance, physical exertion, emotional stress) that occur during
pregnancy
2. Treatment is written below in the table
3. For pregnant patients, the drugs are chosen based on fetal safety profile:
a. Preventive medications:
i. Beta blockers (first-line)
ii. CCBs
b. Abortive medications:
i. Acetaminophen
ii. Add codeine, antiemetics (eg, promethazine), or caffeine/butalbital to
acetaminophen if monotherapy with acetaminophen does not work
iii. Oxycodone (if combination therapy does not work)
4. Ergotamines and triptans are contraindicated during pregnancy
a. Ergotamine and triptans cause hypertonic uterine contractions and vasoconstriction →
preterm labor, fetal growth restriction
5. Prolonged beta blocker use can cause growth restriction due to decreased placental perfusion
from low blood pressure. Therefore, patients should be initiated on the lowest effective dose
and require frequent monitoring
6. NSAIDs can only be used in 2nd trimester. Use in other trimesters have following complications:
a. 1st trimester use: Risk of miscarriage
rd
b. 3 trimester use: Risk of fetal complications (eg, premature ductus arteriosus
closure, oligohydramnios, renal dysfunction)

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OBSTETRICS

34
 OBSTETRICS

TYPES OF ABORTIONS

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SPONTANEOUS ABORTION
1. Inevitable abortion presentation
a. Heavy vaginal bleeding
b. Cramping
c. Dilated cervix
d. Nonviable intrauterine gestation in the lower segment of uterus
2. Treatment
a. Hemodynamically stable
i. Expectant management
ii. Misoprostol
b. Hemodynamically unstable
i. Suction curettage
c. Oxytocin is not effective as there are few oxytocin receptors in early pregnancy

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MISSED ABORTION
1. Intrauterine pregnancy demise at <20 weeks gestation
2. Risk factors
a. Advanced maternal age (due to ↑ risk of fetal chromosomal abnormalities)
3. Presentation
a. Asymptomatic
b. Decreased pregnancy symptoms (eg, nausea, breast tenderness)
4. Physical examination
a. Closed cervix
b. No bleeding
5. Ultrasound findings
a. Embryo without cardiac activity
b. Empty gestational sac without fetal pole
i. Some early pregnancies can present without a fetal pole. Hence viability is
determined by serial ultrasounds and serial b-hCG levels
1. Repeat b-hCG levels normally increase until the end of first trimester
but in case of missed abortion, decreasing levels are seen

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 OBSTETRICS

COMPLETE ABORTION
1. Risk factors
a. Cocaine
b. Alcohol
c. Tobacco
2. Presentation
a. Lower abdominal pain
b. Heavy vaginal bleeding with passage of clots at <20 weeks gestation
3. Examination
a. Closed cervix
4. Diagnosis
a. Ultrasonography
i. Empty uterus
ii. Normal adnexa
b. ß-hCG is positive because it can take up to 6 weeks for ß-hCG to become undetectable

THREATENED ABORTION
1. Features
a. Closed cervix
b. Viable intrauterine gestation
c. Vaginal bleeding
d. Subchorionic hematoma

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SEPTIC ABORTION
1. Management
a. IV fluids
b. Broad-spectrum antibiotics
c. Suction curettage
2. Note: hysterectomy is not indicated. It is indicated in following case:
a. Pelvic abscess
b. If the patient does not improve after suction curettage and 48 hours of broad-spectrum
antibiotics
3. Note #2: misoprostol causes uterine contractions and expels products of conception for
spontaneous abortion. However it is not used for septic abortion because of slow onset of action

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 OBSTETRICS

SUBCHORIONIC HEMATOMA

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 OBSTETRICS

UTERINE RUPTURE
1. Occurs in patients with prior history of uterine surgery
2. Pain presentation:
a. Focal and intense, which is relieved by rupture
b. Diffuse pain after the rupture
3. Signs of imminent rupture
a. Hyperventilation
b. Agitation
c. Tachycardia
d. Bleeding (can be vaginal or intra-abdominal)
4. Loss of fetal station is pathognomonic for rupture
5. There is no presenting fetal part
6. Diagnosis
a. Fetal limbs palpable on abdominal exam
b. Fetal heart tracings are abnormal (eg, fetal tachycardia, recurrent decelerations)
c. Disordered contractions occur because ruptured myometrial fibers cannot contract in
unison, leading to progressively decreasing contraction amplitude (ie, staircase sign on
tocodynamometry)

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OBSTETRICS

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 OBSTETRICS

INTRAUTERINE FETAL DEMISE

1. Fetal death at ≥20 weeks
2. Pathophysiology can be:
a. Maternal
i. Antiphospholipid antibody syndrome
ii. Fetomaternal hemorrhage
b. Fetal
i. Fetus should undergo autopsy and karyotype/genetic studies
c. Placenta
i. Check for thrombosis, abruption, infection, or other disease
3. Risk factors
a. Fetal growth restriction
b. Abnormal fetal karyotype
c. Tobacco use
d. Nulliparity
e. Obesity
f. Hypertension
g. Diabetes mellitus
h. Up to half of the cases have no identifiable etiology
4. Presentation
a. Decreased or absent fetal movement
5. Diagnosis
a. Confirmed by absence of cardiac activity on ultrasound
b. Inability to find fetal heart rate by Doppler sonography is not diagnostic as it can also be
due to fetal malpresentation or maternal obesity
6. Labor induction can be delayed until the patient is ready, however delay for several weeks can
lead to coagulopathy

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OBSTETRICS

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 OBSTETRICS

ANTIPHOSPHOLIPID ANTIBODY SYNDROME

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 OBSTETRICS

SLE

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 OBSTETRICS

SLE NEPHRITIS IN PREGNANCY

1. Similar to preeclampsia, except:
a. Joint pain
b. Malar rash
c. RBC casts on urinalysis
d. ↓ complement levels
e. ↑ ANA titers
2. Risk factors
a. Discontinuation of hydroxychloroquine
b. Active disease prior to conception

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 OBSTETRICS

PRETERM LABOR

1. Cervical dilation in the setting of regular, painful contractions at <37 weeks gestation
2. Risk factors
a. History of preterm delivery (strongest risk factor)
b. Short cervical length on transvaginal ultrasound in 2nd trimester
i. Short cervix is defined as ≤2 cm without history of preterm labor or ≤2.5 cm
with history of preterm labor
c. History of cervical surgery
d. Multiple gestation
e. Advanced maternal age
f. Iron deficiency anemia
3. Transvaginal ultrasound measurement of cervical length in 2nd trimester is gold standard for
further evaluation of preterm labor risk
4. Management
a. Given below in the table
b. Note: indomethacin is used for tocolysis. It can lead to fetal vasoconstriction (ie,
premature closure of ductus arteriosus) → decreased renal perfusion → fetal oliguria →
oligohydramnios
i. Patients are given indomethacin for ≤48 hours
ii. Oligohydramnios associated with indomethacin use is reversible and can be
corrected if the medication is discontinued

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 OBSTETRICS

EXTERNAL CEPHALIC INVERSION

1. Relative contraindication
a. Ruptured membranes
b. ↓ amniotic fluid
c. Fetal prematurity
2. It is not recommended during active labor due to its low success at that time

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 OBSTETRICS

ABRUPTIO PLACENTAE
1. Risk factors
a. Trauma
b. Smoking
c. Cocaine use
d. Hypertension
2. Clinical features
a. Constant abdominal pain (unlike pain associated with preterm labor, which is
intermittent as uterus relaxes and softens between contractions)
b. Back pain may also be present
c. Bleeding
d. Fetal decelerations and loss of variability
3. Physical examination
a. Tender uterus
b. Distended uterus → fundal height larger than expected
c. Unusually low-amplitude but frequent contractions of a firm uterus
i. This is due to uterotonic effect of blood concealed behind placenta
4. Due to physiologic hypervolemia, the patient may appear hemodynamically stable until up to
20% of the blood volume has been lost
5. FHR tracings
a. Minimal variability
b. Decelerations
c. Uterine tachysystole (eg, >5 contractions in a 10-minute period)
6. Complications
a. Maternal
i. DIC (due to tissue factor released by decidual bleeding)
ii. Hypovolemic shock
b. Fetal
i. Hypoxia
ii. Preterm delivery
7. Management
a. IV fluids (first step)
b. Place the patient in left lateral decubitus position to displace the uterus off the
aortocaval vessels and increase cardiac output

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8. Differentials
a. Uterine rupture
i. +ve history of uterine surgery or myomectomy
ii. Loss of fetal station
iii. Diminishing contractions
iv. Palpable fetal parts
b. Vasa previa
i. Painless vaginal bleeding and FHR abnormalities after amniotomy

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VASA PREVIA

1. Management:
a. Vasa previa is diagnosed on fetal anatomy ultrasound at 18-20 weeks
b. It is managed with C-section at 34-35 weeks gestation (ie, prior to spontaneous labor)

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PREECLAMPSIA
1. It is defined as new-onset hypertension at
a. ≥20 weeks gestation
b. Proteinuria
i. >300 mg/24 hr
ii. Protein/creatinine ratio ≥0.3
iii. Dipstick ≥1+
2. Risk factors
a. Nulliparity
b. Multiple gestation
c. Maternal age <18
d. Advanced maternal age
e. Diabetes mellitus:
i. It is a risk factor because its sequelae are individual risk factors for preeclampsia
(eg, diabetic nephropathy, vascular disease)
f. Chronic kidney disease
g. Prior preeclampsia
3. Patients at high risk for preeclampsia should get a 24-hour urine collection for total protein at
the initial prenatal visit for following reasons:
a. To establish baseline renal function
b. To look for nephrotic range proteinuria so that those patients can be put on
anticoagulation during pregnancy and postpartum
4. Pathophysiology
a. Abnormal placental development and function → chronic uteroplacental insufficiency →
fetal growth restriction/low birth weight
5. Preeclampsia can be divided as
a. Preeclampsia without severe features
b. Preeclampsia with severe features
i. Severe hypertension (defined as systolic blood pressure ≥160 mm Hg or
diastolic pressure ≥110 mm Hg for ≥15 minutes)
ii. Platelet count <100,000/mm3
iii. Transaminitis
iv. Creatinine ≥1.1 mg/dL
v. Headache
vi. Visual changes
6. Generalized hyperreflexia is also commonly seen in preeclampsia patients. A sustained ankle
clonus may also be present
7. Maternal complications
a. Abruption placentae
b. DIC
c. Eclampsia

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d. Hepatic rupture
e. Pulmonary edema
i. Generalized arterial vasospasm → ↑ systemic vascular resistance and ↑ cardiac
output → pulmonary edema
ii. ↓ renal function and ↓ serum albumin and ↑ capillary permeability can also
lead to PE
iii. Management includes supplemental oxygen, fluid restriction and diuresis in
severe cases.
8. Antihypertensive drugs to administer:
a. IV Hydralazine (vasodilator)
b. IV labetalol
i. Contraindicated in bradycardia
c. Oral nifedipine
i. Cannot give in case of ongoing emesis
d. Methyldopa is indicated in chronic hypertension due to slow-onset, not in acute cases
9. Differentials
a. Gestational hypertension
i. No proteinuria or severe features
b. Eclampsia
i. Seizures are present
c. Intrahepatic cholestasis
i. Pruritis is present
ii. Elevated bilirubin

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OBSTETRICS

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 OBSTETRICS

PREECLAMPSIA PREVENTION

STROKE DUE TO PREECLAMPSIA

1. Mechanisms:
a. Activation of coagulation system, platelet aggregation, and vascular microthrombi
formation → cerebral vessel occlusion (ischemic stroke)
b. Dysregulated cerebral blood flow → inappropriate cerebral vasospasm → ↑ perfusion
pressure → rupture of intracerebral vessels (hemorrhagic stroke)
2. Most patients with preeclampsia do not require CT scan but those with focal neurologic deficits
require a CT scan of the head to evaluate for possible stroke and help guide management

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SEIZURE PREVENTION IN PREECLAMPSIA PATIENT WITH MYASTHENIA GRAVIS

1. MgSO4 is contraindicated in patients with myasthenia gravis because it may trigger myasthenic
crisis
2. Valproic acid is given for seizure prophylaxis

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 OBSTETRICS

ECLAMPSIA

1. Seizures are preceded by:

a. Severe headaches
b. Visual disturbances (eg, blurry vision, photophobia, loss of vision)
c. Epigastric/RUQ pain
2. There are no focal neurologic defects
3. Postictal state +
4. Differentials
a. Epilepsy
i. Occur in the absence of provocation
ii. They are followed rather than preceded by headaches

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 OBSTETRICS

PATHOPHYSIOLOGY OF PULMONARY EDEMA IN PREECLAMPSIA/ECLAMPSIA

POSTPARTUM PREECLAMPSIA
1. Preeclampsia can present in postpartum patients up to 6 weeks after delivery
2. Presentation:
a. Severe headache in bilateral occipital or frontal regions (most common presentation)
i. This headache does not improve with acetaminophen or NSAIDs

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 OBSTETRICS

ANTIHYPERTENSIVES IN PREGNANCY

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 OBSTETRICS

ANTEPARTUM FETAL SURVEILLANCE

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DECREASED FETAL MOVEMENT MANAGEMENT

1. Do a nonstress test
a. To account for fetal sleep cycle, NST should continue for ≥40 minutes (20 minutes for
fetal sleep cycle, 20 minutes for NST)
2. If it is nonreactive, do a BPP or CST
3. BPP has a total score of 10
a. 0/10, 2/10 or 4/10 is an abnormal BPP → urgent delivery
b. 6/10 is equivocal → repeat in 24 hours
c. 8/10 or 10/10 is normal
d. Abnormal BPP indicates fetal hypoxia due to placental dysfunction
i. Risks for placental dysfunction include hypertension, smoking, diabetes or
advanced maternal age
e. If a BPP has been performed, a CST is not needed
4. Contraindications to CST are the same as contraindications to labor, eg:
a. Placenta previa
b. Prior myomectomy

INFERTILITY
1. It is the inability to conceive after 6 months of unprotected intercourse in women age ≥35 years
(or after 12 months in women age <35 years)

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FIBROIDS
1. Physical examination
a. Irregular uterine contour
b. Enlarged uterus
2. Pressure effects
a. Urinary frequency or Incomplete voiding
b. Constipation
c. These effects are caused by subserosal or pedunculated fibroids
3. Recurrent pregnancy lost
a. Due to submucosal, intramural and intracavitary fibroids
4. Can lead to size-date discrepancy
5. Obstetrical complications
a. Miscarriage
b. Malpresentation
c. Abruption placentae
d. Preterm birth
6. For surgical management of fibroids, do hysterectomy if patient has completed her family. If the
patient still desires to conceive, do hysteroscopic myomectomy instead

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TYPES OF FIBROIDS

DEGENERATING UTERINE FIBROIDS

1. Fibroids can grow rapidly during pregnancy due to ↑ estrogen and progesterone levels.
However, because myometrial blood flow shifts towards the developing fetus and placenta
during pregnancy, fibroids can outgrow their blood supply, leading to fibroid infarction and
necrosis
2. Presentation:
a. Uterine contractions (due to prostaglandin release)
b. Fundal tenderness
c. Tender mass
d. Leukocytosis (due to inflammatory cytokine release)
3. Diagnosis:
a. Ultrasound
4. Management:
a. Conservative management with acute pain control (eg, indomethacin for patients <32
weeks gestation)

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UTERINE SARCOMA

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INTRAUTERINE SYNECHIAE
1. Seen in patients who undergo intrauterine surgery
2. Damage to endometrial basalis layer → inflamed and denuded endometrium → uterus adheres
to itself → obliteration of cavity
3. Lack of endometrium results in:
a. Light menses
b. Secondary amenorrhea
c. Infertility
d. Negative progesterone withdrawal test
4. Patients presents with complaint of inability to conceive and monthly pelvic pain with little or no
bleeding
5. Diagnosis
a. Hysteroscopy
6. Treatment
a. Lysis of adhesions
7. Differentials
a. Endometriosis
i. Fixed, tender uterus
ii. Not associated with amenorrhea
b. Recurrent fibroids
i. Enlarged uterus
ii. Heavy menses

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INTRAHEPATIC CHOLESTASIS OF PREGNANCY

1. ↑ estrogen and progesterone → hepatobiliary stasis and ↓ bile excretion → ↑ total bile acids
(>10 µmol/L)
2. Risk factors:
a. Prior intrahepatic cholestasis of pregnancy
b. Maternal age ≥35
c. Multiple gestations
3. Presentation
a. Pruritis that is worst on palms and soles
b. No associated rash
c. RUQ pain
4. Labs
a. ↑ aminotransferases
b. Alkaline phosphatase may be elevated but is not diagnostic because it is also produced
by placenta
5. Complications:
a. Intrauterine fetal demise:
i. Risk is particularly high when serum bile acids ≥100 µmol/L
b. Preterm delivery
c. Meconium-stained amniotic fluid
d. Neonatal respiratory distress
6. Treatment
a. First line: ursodeoxycholic acid

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CHOLELITHIASIS IN PREGNANCY

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POLYMORPHIC ERUPTION OF PREGNANCY

1. Also called pruritic urticarial papules and plaques of pregnancy

2. Causes pruritis within the abdominal striae that spreads centrifugally but spares the palms and
the soles
3. Treatment is topical corticosteroids

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FETAL GROWTH RESTRICTION

1. It is an ultrasound-estimated fetal weight <10th percentile for gestational age
2. It may be
a. Symmetric
b. Asymmetric
3. Features
a. Thin, loose skin
b. Thin umbilical cord
c. Wide anterior fontanel
d. Decreased subcutaneous fat
e. Meconium-stained amniotic fluid
4. Placenta should undergo histopathologic examination to evaluate for further infarction and/or
infection

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HYPERTENSION AND ASYMMETRIC GROWTH RESTRICTION

1. Due to placental insufficiency in 2nd and 3rd trimester
a. Abdomen size increases in 2nd and 3rd trimester but in case of placental insufficiency,
blood goes to vital organs (ie, brain) and leads to asymmetric or “head-sparing” growth
pattern

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SEPTIC PELVIC THROMBOPHLEBITIS

1. Several factors predispose postpartum patients to thrombosis:

a. Hypercoagulable state of pregnancy
b. Pelvic venous stasis and dilation
c. Endothelial damage from infection and/or trauma during delivery

ANEMIA IN PREGNANCY
1. It is defined as:
a. Hb <11 g/dl in the first and third trimesters
b. Hb <10.5 g/dl in the second trimester

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DIFFERENTIALS OF THROMBOCYTOPENIA IN PREGNANCY

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GESTATIONAL THROMBOCYTOPENIA
1. It is a benign condition with isolated, mild thrombocytopenia (ie, platelets 100,000-
150,000/mm3)
2. It is commonly diagnosed in third trimester
3. Management:
a. Reassurance and observation

HEPARIN-INDUCED THROMBOCYTOPENIA

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NORMAL PHYSIOLOGIC CHANGES IN PREGNANCY

1. ↑ cardiac output
a. ↑ stroke volume in early pregnancy
b. ↑ heart rate in later pregnancy
2. ↓ serum creatinine (0.4 to 0.8 mg/dL)
a. Because of ↑ renal perfusion
3. Leukocytosis
a. Because of inflammation
4. ↑ urinary protein (up to 300 mg/day)
a. Due to ↑ renal basement membrane permeability
5. Platelets are normal or decreased
a. Some patients acquire Gestational Thrombocytopenia (<100,000/mm3 but
>70,000/mm3) which does not require any further evaluation

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RENAL CHANGES IN PREGNANCY

CARDIOPULMONARY ADAPTATIONS IN PREGNANCY

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COAGULATION CASCADE

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PLACENTA PREVIA
1. Usually diagnosed routinely at 18-20 weeks
2. Can present with severe painless hemorrhage through vagina and nonpainful contractions
3. Irregular contractions are seen on tocodynamometry
4. Risk Factors include:
a. Prior C-section
b. Prior placenta previa
c. Multiple gestation (due to ↑ placental surface area)
d. Advanced maternal age (>35 years)
e. Multiparity
f. Smoking
5. Majority cases resolve spontaneously by 3rd trimester due to:
a. Lower segment lengthening
b. Placental growth toward the fundus
6. Management
a. Initial management is routine obstetric care as it resolves spontaneously mostly
b. Pelvic rest is advised
c. Repeat ultrasound is performed at 3rd trimester (ie, ≥28 weeks gestation)
d. Asymptomatic patients undergo scheduled cesarean at 36-37 weeks gestation
7. Many patients have reassuring fetal monitoring initially (eg, accelerations, no decelerations) as
the bleeding is primarily maternal

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CERVICAL INSUFFICIENCY
1. It can be due to following reasons:
a. Intrinsic cervical instability
b. Reduced cervical length (eg, prior cervical conization)
c. Congenital abnormalities (eg, in utero diethylstilbestrol exposure)
2. It causes 2nd trimester pregnancy loss
3. It is diagnosed by any 1 of the following criteria:
a. Painless cervical dilation in the current pregnancy (ie, examination-based)
b. A second-trimester cervical length of ≤2.5 cm plus a prior preterm delivery (ie,
ultrasound-based)
c. ≥2 prior consecutive, painless, second-trimester losses (ie, history-based)
4. USG:
a. Shortened cervix
b. Dilated cervix
5. No vaginal bleeding is present
6. Symptoms
a. Pelvic pressure
b. Painless cervical dilation
7. Differentials
a. Abortion
i. Pain is present
ii. Bleeding is present
b. Abruption placentae
i. Decelerations
present
ii. Pain present
c. Hydatiform mole
i. Absent fetus on
USG
ii. 1st trimester
bleeding
d. Placenta previa
i. Bleeding is present
ii. Cervix is closed

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CERVICAL CONIZATION

1. It is indicated in case of CIN grade 2 & 3

a. Colposcopy is the gold standard method for diagnosing CIN
2. Methods
a. Cold knife conization
i. Via scalpel
b. Loop electrosurgical excision procedure (LEEP)
i. Via electrocautery

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CERCLAGE PLACEMENT
1. It treats cervical insufficiency by reinforcing cervix with suture or synthetic tape
2. Candidates include:
a. Patients with history of 2nd trimester deliveries
b. Patients with short cervix
i. Short cervix can also be treated by vaginal progesterone

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COLPOSCOPY
1. It evaluates cervix and vagina under magnification after application of acetic acid to contrast and
identify abnormal (eg, aceto-white changes) from normal cells
a. Abnormal vessels (a sign of high-grade lesions) also become more visible
2. It is indicated in case of high-grade lesions, regardless of HPV status. In case of low-grade
lesions, do HPV co-testing to differentiate between atypical squamous cell of undetermined
significance (ASCUS) and low-grade intraepithelial lesion
3. CIN during pregnancy
a. Colposcopy can be performed during pregnancy
b. In case of “inadequate” colposcopy, we normally do endocervical curettage but it is
deferred during pregnancy due to risk of miscarriage and preterm delivery
c. Cervical biopsy is performed in pregnancy if a lesion has high-grade features (eg,
abnormal vessels)

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HELLP SYNDROME
1. Serious liver problems include:
a. Centrilobular necrosis
b. Hematoma formation
c. Thrombi in the post capillary system
2. These processes can cause liver swelling with distension of the hepatic (Glisson’s) capsule →
RUQ or epigastric pain

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MAGNESIUM SULPHATE TOXICITY

1. Its toxicity can cause neuromuscular depression
2. Characteristics
a. Apnea
b. Muscle paralysis
c. Somnolence
d. Visual disturbances
e. ↓ or absent deep-tendon reflexes
f. Respiratory depression
g. Cardiac arrest
3. Renal insufficiency is a common risk factor for magnesium toxicity
4. Range:
a. Therapeutic range 5-8 mg/dL
b. Toxic concentrations ≥8 mg/dL
5. Antidote: Calcium gluconate

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 OBSTETRICS

ECTOPIC PREGNANCY
1. Presentation
a. Hypotension
b. Positive b-hCG
c. Vaginal bleeding
2. Blood in abdomen can present with following:
a. Acute abdomen
b. Cervical motion tenderness
c. Shoulder pain (referred pain from
diaphragm)
d. Urge to defecate (blood in posterior
cul-de-sac)
3. Risk factors for cornual/interstitial ectopic
pregnancy include:
a. Uterine anomalies
i. Bicornuate “heart-shaped”
uterus
b. In vitro fertilization

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RISKS OF OBESITY IN PREGNANCY

1. Obesity in pregnancy is prepregnancy BMI ≥30 kg/m2
2. It increases risks of:
a. Fetal demise
b. Fetal macrosomia (>90th percentile)

OPERATIVE VAGINAL DELIVERY

1. Other indications are:

a. Maternal exhaustion
b. Maternal contraindications to Valsalva maneuver (eg, Hypertrophic cardiomyopathy)

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UTERINE INVERSION
1. Risk factors
a. Nulliparity
b. Fetal macrosomia
c. Rapid labor and delivery
d. Placenta accreta
2. Uterine inversion can result from excessive fundal pressure and traction on the umbilical cord
before placental separation
3. Presentation
a. Severe lower abdominal pain
b. Hemorrhagic shock
c. Smooth, round mass protruding through cervix or vagina
d. Uterine fundus is no longer palpable transabdominally
4. The inverted uterus should immediately be replaced
a. Placental removal and administration of uterotonic drugs should be initiated only after
the uterus is replaced
b. Uterine relaxants can be used to aid in uterine replacement if the initial attempt is
unsuccessful. However, reduction of an inverted uterus is preferable without uterine
relaxants

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WATER INTOXICATION DUE TO OXYTOCIN TOXICITY

1. Oxytocin works like ADH and its toxicity can lead to water retention
a. Water retention → hyponatremia → tonic-clonic seizures
2. Management
a. Hypertonic saline (eg, 3% saline)

OXYTOCIN CONTRAINDICATIONS
1. Prior classical C-section
2. Fetal heart decelerations

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LATE-TERM PREGNANCY
1. Pregnancy at ≥41 weeks gestation is late-term (post term is ≥42 weeks)
2. Age-related changes in placenta (eg, infarctions, calcifications) → ↑ placental vascular
resistance → uteroplacental insufficiency → chronic fetal hypoxemia → CNS depression →
demise
3. To prevent CNS depression, blood is distributed preferentially to brain → ↓ blood to kidneys →
oligohydramnios
4. Signs of utero-placental insufficiency
a. Late decelerations on NST
b. Oligohydramnios on ultrasound
5. If utero-placental insufficiency is positive → immediate delivery due to the risk of IUFD

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FETAL DYSMATURITY SYNDROME:

1. It occurs in post-term (≥42 weeks gestation) pregnancies due to age-related placental changes
2. Neonatal presentation
a. Small for gestational age
b. Thin body with loose skin
c. Meconium-stained amniotic fluid

LUMBAR PUNCTURE

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POSTPARTUM URINARY RETENTION

1. Inability to void ≥6 hours after vaginal delivery or ≥6 hours after urinary catheter removal
following cesarean delivery
2. Presentation
a. Overflow incontinence → urinary dribbling
b. Overdistended bladder → lower abdominal pressure
3. Causes
a. Pudendal nerve injury
i. Due to perineal trauma from:
1. Prolonged 2nd stage of labor
2. Perineal laceration
b. Epidural anesthesia
i. Suppresses micturition reflex and ↓ detrusor tone → bladder atony
4. Diagnosis:
a. Postvoid residual volume ≥150 mL
5. Management
a. Intermittent urethral catheterization
i. Resolution in <1 week

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PERINEAL LACERATIONS

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VAGINAL ATROPHY
1. It can present with urinary symptoms:
a. Urethral discomfort
b. Stress urinary incontinence
2. Unlikely to occur immediately postpartum (due to high estrogen levels during pregnancy)
a. Low estrogen level can lead to vaginal atrophy, eg:
i. Old age
ii. Lactational amenorrhea

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ERB-DUCHENNE PALSY
1. Due to shoulder dystocia due to fetal
macrosomia (birth weight >4.5 kg)
2. Involves C5-C7
a. C5: deltoid and infraspinatus
b. C6: biceps
c. C7: wrist/finger extensors
3. Damage to C5-C7 → waiter’s tip posture
4. Management
a. Observation and physical therapy
because resolution occurs within 3
months
b. Surgical intervention can be
considered if there is no
improvement by age 3-9 months
i. Nerve graft
ii. Reconstruction
iii. Decompression

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FETAL MALPOSITION
1. Fetal position is the relationship of the fetal presenting part to the maternal pelvis
2. Optimal position is occiput anterior
3. Occiput transverse can cause cephalopelvic disproportion and 2nd stage arrest
a. Molding and caput suggest cephalopelvic disproportion
b. Molding is the change in fetal skull shape as maternal expulsive efforts sculpt the fetal
head into the shape of the pelvis to facilitate delivery
c. Caput is scalp edema due to prolonged pressure

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APPROPRIATE WEIGHT GAIN IN PREGNANCY • Fetal growth restriction

1. Average women should increase their intake by 350-450 kcal/day can lead to
during 2nd and 3rd trimesters polycythemia

Gastroschisis risk:
It is increased with 1st
trimester NSAIDs use

Continuation of Menses
in Non-lactating mothers:
Within 10 weeks of birth

Prophylactic Platelet
Transfusion
• Normal delivery: if
platelet count is
<20,000/mm3
• C-section: if platelet
count is <40,000/mm3

ß-hCG levels after

Pregnancy:
They become undetectable
2-4 weeks after delivery.
Increased levels are a
concern for gestational
trophoblastic disease
RISK FACTORS FOR FETAL ANEMIA
1. Fetomaternal hemorrhage
2. Maternal alloimmunization
3. In utero infection (eg, parvovirus)

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ROUTINE SCREENINGS AND INTERVENTIONS DURING PREGNANCY

1. All pregnant women should receive screening for:
a. HIV
b. Hepatitis B
c. Chlamydia
d. Syphilis
e. Illicit drug use
2. Anti-D immune globulin administration
a. 28-32 weeks gestation
i. First trimester administration is justified only in case of uterine bleeding
b. <72 hours after delivery of Rh(D)-positive infant
3. GBS screening
a. 35-37 weeks (because results are valid for approx. 5 weeks)
4. HIV Screening
a. In first prenatal visit as early antiretroviral therapy initiation ↓ risk of HIV transmission
to fetus
b. Rescreening in high-risk individuals (eg, IV drugs users, multiple sexual partners)
5. Maternal serum AFP
a. Measured at 15-20 weeks gestation (optimally at 16-18 weeks)
b. If increased, follow up with ultrasound to look for fetal anatomical defects, gestational
age, or multiple gestations
c. Benign causes of ↑ MSAFP:
i. Multiple gestations
ii. Incorrect gestational age dating (most common cause)
6. Urine culture
a. In first trimester to rule out asymptomatic bacteriuria because it has 40% chance of
progressing to pyelonephritis because smooth muscle relaxation and ureteral dilation
allow urine to ascend from bladder to kidneys
b. Rescreening if positive culture in first trimester or positive risk factors (eg, urinary tract
abnormalities, sickle cell disease)

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NEURAL TUBE DEFECT

FOLATE SUPPLEMENT
1. Women should take folate supplement 1 month prior to conception
2. Dosage:
a. Average-risk patients: 0.4 mg daily
b. High-risk patients: 4 mg daily

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STI SCREENING
1. All patients undergo HIV, HBV, and syphilis screening at initial prenatal visit because these STIs
can cause congenital infection
2. High-risk patients also require gonorrhea and chlamydia screening because these infections can
cause preterm prelabor rupture of membranes and neonatal infections (eg, conjunctivitis)
a. These high-risk patients also require repeat screening for all STIs in the third trimester

SYPHILIS

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HIV MANAGEMENT DURING PREGNANCY

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HEPATITIS C IN PREGNANCY

FETAL FIBRONECTIN
1. Fibronectin is a glycoprotein found at the decidual-chorionic interface
2. Normal levels
a. High until 22 weeks gestation
b. Low during mid-second and third trimesters
c. Again high during third trimester
i. Because of decidual-chorionic interface disruption due to contractions
3. Measurement:
a. In patients with preterm contractions between 22 and 35 weeks gestation, fFN can help
distinguish between preterm and false labor
b. fFN is not tested before 22 weeks because of high rate of false-positive results

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SHORT CERVIX
1. Short cervix is defined as ≤2 cm without history of preterm labor or ≤2.5 cm with history of
preterm labor
2. Prevention of preterm labor
a. History of preterm birth = IM progesterone starting in 2nd trimester & serial TVUS for
cervical length measurement
i. If TVUS shows short cervix → cerclage
b. No history of preterm birth with short cervix = vaginal progesterone

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GBS INFECTION
1. GBS screening is done at 35-37 weeks gestation
2. Intrapartum penicillin is administered to prevent the early-onset neonatal GBS infection
3. In case of low risk for anaphylaxis, use cefazolin
4. In case of high risk for anaphylaxis:
a. If patient is sensitive to both clindamycin and erythromycin → use clindamycin
b. If patient is resistant to either clinda or erythro, or sensitivities are not available → use
vancomycin along with neonatal observation and evaluation (because vanco does not
reach bactericidal concentrations in amniotic fluid, like the others)
5. Patients who should receive GBS prophylaxis:
a. ALL patients who are GBS positive or unknown and who will deliver vaginally
b. Patients at <37 weeks who will deliver by C-section if they are GBS positive or unknown
and have ruptured membranes
6. A few patients do not undergo GBS screening because they are considered to have persistent,
heavy GBS colonization. They are patients having:
a. GBS asymptomatic bacteriuria
b. GBS UTI
c. Prior delivery of an infant with early-onset neonatal infection

BRAXTON-HICKS CONTRACTIONS
1. Features
a. Mild, irregular contractions
b. No cervical change
c. Reactive NST
2. Discharge the patient with labor precautions

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PRENATAL TESTING

1. In case of abnormal 1st trimester combined test, go for a diagnostic test:

a. Chorionic villus sampling at 10-13 week
b. Amniocentesis at 15-20 week
2. If patient declines invasive testing, do following:
a. Anatomy ultrasound
b. Cell-free fetal DNA test

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QUADRUPLE TEST
1. Performed in 2nd trimester (15-20 weeks)
2. Patients with abnormal quadruple test should be offered cell-free fetal DNA testing
3. Ultrasound should be performed to evaluate for fetal anomalies

CELL-FREE FETAL DNA TESTING

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ACUTE CERVICITIS

1. Presentation
a. Postcoital bleeding
b. Thick malodorous mucopurulent discharge
2. Signs
a. Friable cervix (bleeds easily on contact)
3. Diagnosis
a. NAAT
4. Treatment should be started empirically before infection ascends:
a. Azithromycin + ceftriaxone
5. Differentials
a. Bacterial vaginosis
i. Thin, grey discharge instead of thick, purulent
ii. Fishy odor

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DEPOT MEDROXYPROGESTERONE ACETATE (DMPA)

1. Form of contraception administered every 3 months
a. Inhibits release of GnRH from hypothalamus
2. Side effects
a. Menstrual irregularities during the first 6 months
b. Amenorrhea after 1 year of use
c. Weight gain
d. Fatigue
e. Nausea
f. Breast tenderness

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AMNIOTIC FLUID INDEX

POLYHYDRAMNIOS
1. It is defined as amniotic fluid index ≥24 cm or a deepest vertical pocket of ≥8 cm
2. Management is based on severity, maternal symptoms, and gestational age:
a. Severe or symptomatic polyhydramnios at preterm gestation:
i. Do amnioreduction
b. Mild, asymptomatic polyhydramnios at term gestation:
i. Expectant management is carried out

OLIGOHYDRAMNIOS
1. It is defined as amniotic fluid index of ≤5 cm or a deepest vertical pocket of <2 cm
2. Causes:
a. Early Gestation Oligohydramnios: Fetal etiologies (eg, aneuploidy, renal
agenesis, posterior urethral valves)
b. Second- and Third-Trimester Oligohydramnios: Uteroplacental insufficiency (with fetal
growth restriction) or maternal causes,
such as dehydration or rupture of
membranes (with normal fetal growth)

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PRETERM PRELABOR RUPTURE OF MEMBRANES (PPROM)

1. It can be easily understood by breaking it down:

a. Preterm = <37 weeks gestation
b. Prelabor = closed cervix (ie, prior to labor)
c. Rupture of membranes = vaginal pooling of nitrazine-positive fluid in posterior fornix
i. Ferning is noticed
ii. ↑ on Valsalva
2. Risk factors are those that distend or weaken the membranes:
a. Multiple gestation
b. Prior preterm delivery
c. Prior history of PPROM
d. Genital tract infection (eg, bacterial vaginosis)
e. Antepartum bleeding
f. Polyhydramnios
3. Management: primarily inpatient management
a. If <34 weeks
i. Give corticosteroids for fetal lung maturity
ii. Give latency antibiotics
b. If ≥34 weeks gestation, intraamniotic infection or deteriorating fetal/maternal status:
i. Delivery
ii. GBS prophylaxis

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ASYMPTOMATIC BACTERIURIA

1. It can lead to PPROM or preterm labor

a. Mechanism
i. Intrauterine bacterial enzymatic activity
1. Stimulates prostaglandin release → contractions → preterm labor
ii. ↑ membrane fragility
1. By degrading collagen or activating inflammatory cytokines → PPROM
2. Diagnosis:
a. All women should undergo a screening urine culture at the initial prenatal visit
3. Management:
a. Antibiotics
4. Follow-up:
a. Repeat urine culture:
i. This is done because a third of patients do no completely eradicate the
bacteriuria with initial treatment
ii. If repeat urine culture comes out negative, patient can proceed with routine
prenatal care

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PYELONEPHRITIS IN PREGNANCY

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INTRA-AMNIOTIC INFECTION (CHORIOAMNIONITIS)

1. Common in patients with PROM (PROM occurs before the onset of regular contractions) and in
those with prolonged membrane rupture (>18 hours)
2. These infections are usually polymicrobial
3. Symptoms
a. Nausea
b. Vomiting
c. Uterine fundal tenderness
4. Diagnosis
a. Maternal fever + ≥1 of the following:
i. Fetal tachycardia >160/min for at least 10 minutes
ii. Maternal leukocytosis
iii. Purulent amniotic fluid
5. Management
a. Broad-spectrum IV antibiotics
i. Ampicillin
ii. Gentamicin
iii. Clindamycin
b. Augmentation of labor

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CAUSES OF FETAL TACHYCARDIA

1. Maternal infection
2. Medication use (eg, terbutaline)
3. Poorly controlled maternal hyperthyroidism
4. Abruption placentae
5. ↑ cardiac output demand (eg, hydrops fetalis)

INDICATIONS FOR ANTI-D IMMUNE GLOBULIN

• Notes: if the mother is already sensitized (↑ antibody titers), administration of anti-D immune
globulin is not helpful
o Close fetal monitoring for hemolytic disease is done in such a case

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KLEIHAUER-BETKE TEST

ABO HEMOLYTIC DISEASE

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VAGINAL HEMATOMA
1. Typically presents with hypotension and anemia due to concealed bleeding into the
retroperitoneum
2. Patients also have
a. Vaginal pain
b. Vaginal mass

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LOW BACK PAIN

1. Presentation
a. Pain that radiates down the thighs
b. Pain worsens with activity and improves with rest
2. Pregnancy related causes of acute low back pain should be evaluated and ruled out, for
example:
a. Preterm labor
b. Pyelonephritis

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NORMAL LABOR

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ACTIVE PHASE ARREST

1. Active phase of labor is 6 cm→10 cm cervical dilation at rate of ≥1 cm every 2 hours
2. Active phase arrest is defined as:
a. No cervical change in ≥6 hours with inadequate contraction
b. No cervical change in ≥4 hours with adequate contraction
3. Risk factors:
a. Late-term gestation
b. Fetal macrosomia
c. Cephalopelvic disproportion
4. Management
a. C-section
5. Notes:
a. Oxytocin is used to augment labor if contractions are inadequate (<200 Montevideo
units)
i. It is also used in protracted labor (ie, cervical dilation rate <1 cm/2 hours but not
arrested labor)
b. Prostaglandin is used for cervical ripening in early labor induction, not in active labor

PROTRACTED ACTIVE PHASE

1. It is <1 cm/2 hours increase in cervical dilation after it has reached 6 cm dilation
2. Causes
a. Cephalopelvic disproportion (more common in late-term pregnancies)
b. Fetal malposition (eg, occiput posterior)
c. Maternal obesity
d. Maternal excessive weight gain
e. Nulliparity
f. Advanced maternal age
g. Inadequate contractions
3. Note: epidural lengthens SECOND STAGE of labor, not the active phase of 1st stage

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2ND STAGE ARREST OF LABOR

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PHYSIOLOGIC HYDRONEPHROSIS OF PREGNANCY

1. Normal change in pregnancy
a. Bilateral kidney involvement
b. Bilateral dilation of renal pelvises and proximal ureters
2. Causes of hydronephrosis
a. 1st trimester
i. ↑ progesterone → ureteral dilation and ↓ peristalsis
nd
b. 2 trimester
i. Uterine enlargement → compression of ureters at pelvic brim
1. Right hydronephrosis is often more pronounced due to dextrorotation
of uterus
3. Management
a. No management

HYDRONEPHROSIS FROM URETERAL SUTURE

1. It usually occurs during hysterectomy when ureter is accidentally sutured during ligation of
uterine artery or vaginal cuff closure
2. Risk of ureteral injury:
a. Obesity
b. Distorted pelvic architecture from malignancy
c. Prior pelvic surgery
3. Presentation:
a. Initially:
i. Painless because of postoperative pain medications
b. Later:
i. Non-radiating back pain
ii. Costovertebral angle tenderness
4. Labs:
a. Creatinine and urinalysis may be normal if 1 ureter is affected
5. Diagnosis:
a. Renal ultrasound
6. Treatment:
a. Surgery (eg, suture removal)
7. Differentials:
a. Ureteral injury:
i. Ascites is seen
b. Renal vein thrombosis/Renal infarction:
i. Hematuria is seen

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RENAL INTERVENTIONS
1. Ureteral stents and nephrostomy tubes
a. When etiology of hydronephrosis is ureteral blockage
2. Foley catheter
a. In disorders of bladder outlet obstruction
3. Urodynamic studies
a. Performed to evaluate mixed urinary incontinence (eg, urgency and stress) outside of
pregnancy

CONGENITAL ZIKA SYNDROME

1. Transmission:
a. Aedes mosquito bite
b. Sexually transmitted
2. Virus destroys neural progenitor cells
a. Neuronal destruction → thin cerebral cortices
b. Neuronal necrosis → intracranial calcification
3. Newborn has closed anterior fontanelle and severe microcephaly
4. Diagnosis
a. Reverse-transcriptase PCR
b. Neuroimaging

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RUBELLA INFECTION DURING PREGNANCY

1. It can lead to:
a. Spontaneous abortion
b. IUFD
c. Congenital Rubella Syndrome
2. Congenital rubella syndrome
a. Deafness
b. Cardiac defects
c. Hepatosplenomegaly
d. Microcephaly
e. Cataracts
3. MMR vaccine is contraindicated during pregnancy but patients should be vaccinated during the
immediate postpartum period if they haven’t been vaccinated before

CONGENITAL TOXOPLASMOSIS
1. Particularly common in Europeans due to their consumption of undercooked or cured meat
2. It destroys fetal neural tissue:
a. Bilateral ventriculomegaly
b. Intracranial calcifications particularly within basal ganglia

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CONGENITAL HERPES
1. Mothers have a history of painful genital ulcers
2. Fetal features:
a. Placental and umbilical cord calcifications
b. Temporal lobe involvement
c. Meningoencephalitis
d. Sepsis
e. Long-term sequelae
i. Blindness
ii. Neurocognitive disability
iii. Persistent seizures
3. Prevention
a. Prophylactic antiviral (acyclovir or valacyclovir) beginning at 36 weeks regardless of
symptoms
i. It reduces asymptomatic viral shedding and outbreak recurrence
4. Delivery
a. Vaginal delivery if asymptomatic at the time of delivery
b. C-section if active lesions are present at time of delivery

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CONGENITAL CMV
1. Maternal infection can lead to vertical transmission and can spread to following organs:
a. Placenta
i. Fetal growth restriction
ii. Hydrops fetalis
b. Liver
i. Hepatosplenomegaly
ii. Intrahepatic calcifications
c. CNS
i. Microcephaly
ii. Ventriculomegaly
iii. Bilateral periventricular intracranial calcifications
2. Diagnosis
a. Maternal infection: serology
b. Fetal infection: amniocentesis
3. Management
a. Maternal antiviral therapy has not been proven effective
b. Hence, management is generally expectant
c. Abortion in cases where fetuses have severe congenital CMV infection

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CONGENITAL LISTERIA
1. Listeria infection occurs after consumption of unpasteurized dairy product
2. Fetal infection leads to following
a. Spontaneous abortion
b. Preterm delivery
i. Multiple abscesses
ii. Granulomatous infantiseptica
c. Ultrasound findings:
i. Dilated loops of bowl
ii. Ascites

SEQUELAE OF CONGENITAL INFECTIONS

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VACCINES DURING PREGNANCY

1. All pregnant women without any contraindication (ie, prior allergic response to vaccine) should
receive inactivated influenza vaccination as soon as it becomes available
a. This is because pregnancy is associated with high risk for influenza-associated morbidity
and mortality
2. Inactivated vaccine is safe during every trimester and while breastfeeding
a. Activated vaccine is safe only during breastfeeding

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SYPHILIS IN PREGNANCY
1. Patients are tested with 2 categories: nontreponemal and treponemal serology
a. Either may be used for screening, but positive results require confirmation with a test
from the alternate category as false positives are common
2. Treatment
a. Benzathine penicillin G (IM)
i. 1 dose weekly for 3 weeks
b. Patients who are allergic to penicillin need to be desensitized because alternate
medications are either ineffective, contraindicated, or have limited data in pregnancy

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GRANULOMATOSIS INFANTISEPTICA
1. Causative organism: Listeria monocytogenes
2. Pregnant women (due to relative immunosuppression) are at increased risk of invasive disease
(ie, bacteremia) and fetal infection via transplacental transmission
3. Granulomatosis infantiseptica is caused by acquiring infection in early pregnancy (eg, 1st and 2nd
trimesters)
a. This can lead to intrauterine fetal demise
4. Infection in the third trimester does not lead to fetal demise but can lead to fetal distress,
preterm delivery, or early-onset neonatal sepsis
5. Prevention:
a. Avoiding foods contaminated with Listeria, for example:
i. Raw meats and vegetables
ii. Unpasteurized dairy products
iii. Processed (eg, deli) meats
b. Proper handwashing after handling soil or decaying vegetation

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PUBIC SYMPHYSIS DIASTASIS

1. It is the symptomatic widening of pubic symphysis
a. During pregnancy, ↑ progesterone and relaxin → physiologic widening of pubic
symphysis
b. Symptomatic diastasis can occur after traumatic delivery
2. The pain is exacerbated by walking, weight-bearing, or position changes
3. Management is conservative with supportive care
a. Most patients recover within first 4 weeks postpartum
4. Differentials
a. Femoral nerve damage
i. Can occur as a result of McRoberts Maneuver
ii. Numbness over anterior and medial thigh
iii. Inability to extend the leg or flex the hip
iv. Diminished patellar reflexes

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MCROBERTS MANEUVER

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BREECH PRESENTATION

1. Risk factors
a. Multiparity
b. Multiple gestation
c. Uterine anomalies (eg, septate uterus)
d. Fetal anomalies (eg, hydrocephaly)
e. Leiomyomas
i. Limit fetal mobility
ii. Prevent fetal cephalic engagement
f. Placenta previa
2. Physical examination
a. Subcostal pain
b. Palpation of a hard mass near the uterine fundus (due to fetal head)
c. Lack of fetal presenting part on digital cervical examination
3. Management
a. Other contraindications to vaginal delivery present → C-section
b. No contraindications to vaginal delivery → external cephalic version
i. Done at ≥37 weeks gestation

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INTERNAL PODALIC VERSION

1. Indicated in delivery of second twin
2. Procedure: grasp the feet by inserting hand in uterus and perform breech extraction

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GESTATIONAL DIABETES

1. New-onset diabetes after 20 weeks gestation

2. ↑ hPL and placental somatomammotropin in 3rd trimester → pancreatic ß cell hyperplasia and
↑ insulin resistance → gestational diabetes
3. Patients are universally screened for GDM at 24-28 weeks gestation
4. Diagnosis
a. 1 hr GTT
i. If positive → 3 hr GTT
5. Management
a. Dietary modifications
i. 3 meals and 2-4 snacks with evenly distributed carbohydrates, proteins and fats
b. Insulin as 2nd line
6. Follow-up:
a. Postpartum screening is carried out because patients are at risk for developing type 2
diabetes mellitus
i. If screening is negative, repeat screening should occur at 3-year intervals

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METABOLIC EFFECTS OF HPL

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SHOULDER DYSTOCIA

1. Infant risks
a. Brachial plexus injuries
b. Clavicular or humeral fractures
c. Hypoxic encephalopathy
2. Maternal risks
a. Fourth-degree (eg, rectal mucosa) perineal lacerations
b. Postpartum hemorrhage
3. Shoulder dystocia is caused by impaction of anterior shoulder behind pubic symphysis

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MANAGEMENT OF SHOULDER DYSTOCIA

ERB-DUCHENNE AND KLUMPKE PALSY

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STRESS URINARY INCONTINENCE

1. Most common cause of involuntary urine leakage in pregnant women
2. It occurs with ↑ intrabdominal pressure
a. Standing from sitting position
b. Coughing
c. Laughing
3. It should be differentiated from rupture of membranes because urine can enter posterior vagina
through retrograde vaginal voiding due to effects of growing uterus and positional changes
while voiding. The differentiating points are:
a. No ferning on microscopy
b. No ↑ in fluid in vagina on Valsalva
c. Nitrazine testing is negative
4. Stress urinary incontinence is common following labor and delivery due to following
mechanisms:
a. Weakening of pelvic floor muscles
b. Stretch injury to pudendal nerve, which helps maintaining continence by innervating
contraction of external urethral sphincter
i. Pudendal nerve is also a main sensory nerve of pelvis and damage to it can
result in a decreased voiding sensation
5. Management of Postpartum Stress Urinary Incontinence:
a. Observation and reassurance till <6 weeks postpartum
b. Patients with chronic stress urinary incontinence:
i. Continence pessary
ii. Midurethral sling procedure

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CAUSES OF HYPERANDROGENISM IN PREGNANCY

MALIGNANT HYPERTHERMIA

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CESARIAN SECTION INCISION TYPES

TRIAL OF VAGINAL BIRTH AFTER UTERINE SURGERY

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SHORT INTERPREGNANCY INTERVAL

ILLICIT DRUG USE IN PREGNANCY

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DELIVERY PLAN FOR NONVIABLE FETUS

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ACUTE FATTY LIVER OF PREGNANCY

1. Develops in third trimester, particularly in patients with multiple gestation
2. It is an intrinsic hepatic disease with microvesicular fatty infiltration of hepatocytes secondary to
abnormal maternal-fetal fatty acid metabolism
3. Clinical features
a. Hepatic inflammation
i. Epigastric/RUQ pain
ii. Leukocytosis
iii. ↑ aminotransferases
b. Fulminant liver failure
i. Scleral icterus
ii. Hyperbilirubinemia
iii. Profound hypoglycemia
c. DIC
d. Acute kidney injury (from hepatorenal syndrome)
4. Management
a. Maternal stabilization
b. Immediate delivery

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NONALCOHOLIC FATTY LIVER DISEASE

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HYDROPS FETALIS
1. Causes
a. Rh alloimmunization
b. Parvovirus B19
c. α thalassemia
2. Features
a. Ascites (echolucent abdominal fluid)
b. Skin edema → skin peeling
c. Polyhydramnios
d. Placental thickening (reflecting
intravillous edema)
e. Pleural effusion
f. Pericardial effusion
3. Management
a. Serial ultrasounds
b. Intrauterine transfusion

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Α THALASSEMIA

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EARLY POSTPARTUM SIGNS

1. Shivering
2. Uterus contracts and becomes firm and globular with fundus typically 1-2 cm above or below
the umbilicus
3. Vaginal discharge (normal uterine decidua shedding and blood). It can normally last up to 8
weeks
a. Lochia rubra:
i. Few days after delivery
ii. Red or reddish-brown
b. Lochia serosa:
i. After 3-4 days
ii. Thin
iii. Pink or brown colored
c. Lochia alba:
i. After 2-3 weeks
ii. White or yellow colored

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POSTPARTUM FEVER
1. Temperature ≥100.4 F after the first 24 hours post delivery
2. Look for signs of endometritis:
a. Uterine tenderness
b. Foul-smelling lochia

POSTPARTUM ENDOMETRITIS
1. Most common cause of puerperal fever
2. Presentation
a. Fever >24 hours postpartum
b. Purulent lochia
c. Uterine tenderness
3. Diagnosis
a. Neither blood or endometrial cultures are required for diagnosis
b. Further evaluation is indicated if there is no improvement after 48 hours of antibiotic
therapy
4. Treatment
a. Clindamycin + gentamycin
b. Continue treatment until patient is afebrile for >24 hours

TREATMENT OF CHOICE
1. Clindamycin + Gentamycin = Endometritis
2. Ceftriaxone = Pyelonephritis in pregnancy
3. Dicloxacillin = Lactational Mastitis
4. Penicillin = GBS prophylaxis and syphilis
5. Vancomycin = Breast abscesses

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POSTPARTUM DIFFICULTY IN VOIDING

1. It is a common occurrence
2. Patient voids spontaneously but has difficulty in voiding
3. Causes
a. Suppression of micturition reflex and/or ↓ in bladder tone after regional anesthesia
b. Pudendal nerve palsy from injury
c. Periurethral swelling
4. If the patient is unable to void, they may require urethral catheterization

LOCHIA
1. It is vaginal discharge postpartum
2. It is due to slow process of endometrial shedding and regeneration
3. It can be bloody with small clots.
4. Patients should be evaluated for delayed postpartum hemorrhage in following cases:
a. Passage of large blood clots
b. Increased pad counts (eg, saturation of ≥1 pad/hr for ≥2 consecutive hours)
c. Signs and symptoms of anemia due to acute blood loss
5. Lochia bleeding can last up to 6-8 weeks

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POSTPARTUM THYROIDITIS
1. It is a form of painless autoimmune thyroiditis
2. It can occur within 12 months of delivery
3. Presentation can be variable:
a. Hyperthyroid
b. Hypothyroid
c. Hyperthyroid then hypothyroid
4. Diagnosis:
a. Decreased radioactive iodine uptake
b. Thyroid peroxidase antibody assay is positive
5. Management:
a. Most patients return to euthyroid state and do not require treatment
6. Differentials:
a. Subacute Granulomatous Thyroiditis (ie, de Quervain thyroiditis):
i. Patient presents with fever and have a severely painful and tender goiter

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TYPES OF THYROIDITIS

POSTPARTUM CONTRACEPTION
1. In patients who are <1 month postpartum, OCPs are contraindicated because they increase risk
of thromboembolism and can negatively affect breastfeeding
2. Copper IUDs are good choices for contraception if there are no other IUD-related
contraindications present
3. Progestin-only pill can also be used because they don’t affect breastfeeding. However, they are
less effective
4. Progestin subdermal implants are very good and reliable contraceptive options. They do not
affect breastfeeding and don’t have any negative effect on menstrual bleeding. Also, they don’t
increase the risk of thromboembolism

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POSTPARTUM DEPRESSION

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HYPOTENSION AS A SIDE EFFECT OF EPIDURAL

1. It is caused by blockage of sympathetic nerve fibers → loss of vascular tone → vasodilation and
venous pooling
2. Prevention: aggressive IV fluids prior to epidural placement
3. Treatment
a. Left uterine displacement by positioning patient on left side
b. Additional IV fluid bolus
c. Vasopressor administration
4. Complication
a. High spinal or total spinal
i. When local anesthesia ascends towards the head
ii. It may happen with intrathecal injection or overdose of anesthetics
iii. Signs
1. Hypotension
2. Bradycardia
3. Respiratory difficulty
4. Diaphragmatic paralysis
5. Cardiopulmonary arrest
b. Wet tap
i. Leakage of spinal fluid if dura is punctured
ii. Leads to postural headaches
1. Worse with sitting up
2. Improves with lying down
iii. No hypotension

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PREGNANCY & EXERCISE

1. 20-30 minutes of moderate intensity exercise on most or all days of the week is recommended
a. Moderate intensity: should be able to engage in normal conversation during the activity
2. Patients should stop exercising if following symptoms develop:
a. Vaginal bleeding
b. Leakage of fluid
c. Contractions
d. Chest pain
3. Avoid exercises with high risk of blunt trauma or falling

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MELASMA

1. Acquired hyperpigmentation disorder that occurs on sun-exposed areas of the face

2. Due to UV radiation triggering melanocyte proliferation and pigment deposition in sun-exposed
areas
3. Risk factors
a. Pregnancy
i. Estrogen & progesterone also stimulate melanocyte proliferation
b. Darker skin color
c. Thyroid dysfunction
d. Medication (eg, antiepileptics)
e. Cosmetic use
4. Presentation
a. Irregularly shaped
b. Hyperpigmented macules
c. Varying color
i. Light to dark brown
ii. Ash/blue
d. Symmetric centrofacial, mandibular or malar distribution
5. Diagnosis is clinical and no further evaluation is required
6. Management
a. Sun avoidance
b. Broad-spectrum sunscreen use
7. Melasma resolves after pregnancy. Areas that do not resolve can be treated with:
a. Skin-lightening agents
b. Topical retinoids

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OSTEOGENESIS IMPERFECTA
1. Types
a. Mild (type I)
b. Moderate (types III-IX)
c. Severe (type II)

PLACENTA ACCRETA
1. When placental villi attach directly to myometrium instead of the decidua
2. Risk factors
a. Prior C-section
b. History of D&C
c. Maternal age >35
3. Diagnosis
a. Antenatal ultrasound: irregularity or absence of placental-myometrial interface and
intraplacental villous lakes
4. Presentation
a. Placenta that does not detach
b. Manual extraction leads to severe hemorrhage
5. Management
a. Antenatally diagnosed: cesarean hysterectomy
b. Postnatally diagnosed: hysterectomy

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RECTUS ABDOMINIS DIASTASIS

1. Weakening of linea alba, the fascia that lies between the rectus abdominis muscles and keeps
them in close proximity
2. Risk factors
a. Chronic abdominal stretching
i. Pregnancy
ii. Multiparity
b. Surgical weakness
i. Prior C-section
c. ↑ intraabdominal pressure
i. Constipation
3. Presentation
a. Nontender midline mass
b. No associated fascial defect
c. No pain, acute GIT symptoms (rebound or guarding) or risk of bowel strangulation
4. Management
a. Observation and reassurance (resolves by itself in postpartum)
b. Abdominal binders are not recommended in pregnancy because they cause external
compression on the abdomen and may cause fetal growth restriction
5. Differential
a. Hernia
i. Associated fascial defect

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DIGITAL CERVICAL EXAMINATION

1. Helps in determining:
a. Cervical dilation
b. Fetal presentation
2. It is usually adequate for determining fetal presentation; however, it may be insufficient in
patients with a bulging bag
a. Do a transabdominal ultrasound instead
i. This ultrasound is also indicated before performing amniotomy to avoid
umbilical cord prolapse in patients with funic (ie, cord first) presentation

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ANEMBRYONIC GESTATION
Anembryonic Gestation

POSTDURAL PUNCTURE HEADACHE

1. Occurs due to unintentional dural puncture during epidural anesthesia
2. Headache develops within 72 hours of the procedure

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PSEUDOCYESIS
1. It is a condition in which the woman believes she is carrying a baby but in reality, she is not
pregnant
2. Mechanism:
a. It occurs due to somatization of stress which affects the hypothalamic-pituitary-ovarian
axis and causes early pregnancy symptoms (eg, amenorrhea, breast fullness, morning
sickness, and abdominal distension)
3. This leads to a nonpsychotic patient who believes she is pregnant
a. The belief is so strong that the patient may misinterpret negative home pregnancy tests
as being positive
4. Management:
a. Psychiatric evaluation and treatment

UTERINE INCARCERATION
1. It is a rare disorder that occurs during pregnancy
a. It does not occur postpartum because the uterus becomes progressively smaller, and
therefore unlikely to become entrapped
2. Mechanism:
a. As the retroverted uterus enlarges, it becomes entrapped under the sacral promontory
3. Presentation:
a. Pelvic pain
b. Urinary retention due to bladder obstruction

ULCERATIVE COLITIS DURING PREGNANCY

1. Ulcerative colitis worsens in pregnancy due to placental cytokines that worsen colonic
inflammation
2. Complications:
a. Maternal:
i. Worsening UC disease activity
ii. Severe hematochezia
iii. Anemia
iv. Toxic megacolon
b. Fetal:
i. Preterm delivery
ii. Small for gestational age
3. Fertility rates are lower in those with active ulcerative colitis
4. Management:
a. The usual ulcerative colitis medications (eg, mesalamine, TNF-α) are considered safe for
use during pregnancy and during breastfeeding. Sulfasalazine is contraindicated during
pregnancy due to insufficient safety data

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APPENDICITIS DURING PREGNANCY

1. The appendix undergoes cephalad displacement by the gravid uterus during pregnancy. This
leads to an atypical presentation of pain in the right mid-to-upper quadrant or right flank
2. Features:
a. Signs of intraabdominal inflammation and peritonitis
b. Uterine irritability
c. Uterine contractions
d. Fetal tachycardia (due to maternal fever)
3. Due to atypical presentation, pregnant patients often have a delayed diagnosis and increased
risk of complications (eg, appendiceal rupture, fetal demise)
4. Management:
a. Surgery

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VAGINAL CUFF DEHISCENCE

1. It may present after hysterectomy with increased watery vaginal discharge (from peritoneal
fluid leaking through defect)

OOPHORECTOMY DURING PREGNANCY

1. Progesterone is released from corpus luteum until 10 weeks gestation and after that it is
released from placenta
2. Hence, patients who have corpus luteum removed through oophorectomy before 10 weeks
should be given supplemental progesterone

DIABETES INSIPIDUS DURING PREGNANCY

1. DI can remain undiagnosed because the body often compensates for water losses with a
demand for increased fluid intake (eg, increased thirst)
2. However, during pregnancy, placentally produced enzymes (eg, vasopressinase) increase ADH
breakdown and can worsen symptoms, thereby unmasking undiagnosed DI
a. Some women develop transient DI of pregnancy due to exaggerate response to
vasopressinase. This phenomenon resolves with delivery but recurs with subsequent
pregnancies
3. Features of DI:
a. Low urine specific gravity (<1.006)
b. Polyuria (24-hr urinary output >3 L)

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POLYURIA

BIPOLAR MANAGEMENT DURING PREGNANCY

1. Valproate has a bad pregnancy safety profile. Hence, bipolar patients wishing to get pregnant
should be switched to lamotrigine
a. Lithium is potentially teratogenic (Ebstein anomaly), but the absolute risk is very low
due to the rarity of the condition. Hence, patients with severe bipolar who are stable on
lithium can be continued on this medication with close monitoring. However, if a new
medication has to be introduced, it is better to start with lamotrigine which has a lower
teratogenic risk
2. Pregnancy should be delayed for 3-6 months to assess the efficacy of the medication

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SICKLE CELL DISEASE IN PREGNANCY

1. Acute pain episodes (eg, vasoocclusive pain crisis) due to sickle cell disease occur more
commonly during pregnancy due to following reasons:
a. ↑ metabolic demands
b. Hypercoagulable state
2. Acute pain episodes increase during first trimester especially if there are other precipitating
factors (eg, stress, nausea/vomiting, dehydration)

ROUND LIGAMENT PAIN

1. This pain may occur due to the ligament being stretched by gravid uterus during pregnancy
2. It presents as sharp pain that radiates to vagina

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BUPIVACAINE TOXICITY
1. Normally epidural analgesia is given with bupivacaine by injecting it in epidural space
a. However, sometimes the epidural catheter may be inadvertently inserted into the
epidural vasculature, leading to systemic bupivacaine toxicity
2. Bupivacaine blocks inhibitor neural pathways to cause symptoms of CNS overactivity
3. Presentation:
a. CNS overactivity:
i. Perioral numbness
ii. Metallic taste
iii. Tinnitus
iv. Generalized tonic-clonic seizure
b. Cardiovascular sympathetic activation:
i. Tachycardia
ii. Hypertension
4. Management:
a. Drug cessation
b. Benzodiazepines for seizure control
c. Supportive care

ACUTE PANCREATITIS DURING PREGNANCY

1. Patient needs 2 of 3 classic features to be diagnosed:
a. Classic symptoms (eg, severe epigastric pain radiating to the back)
b. ↑ amylase/lipase
c. Characteristic image finding
2. If classic symptoms and amylase/lipase levels are positive, there is no need to get a CT scan

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TRIGLYCERIDE-INDUCED PANCREATITIS
1. Triglyceride level typically rises in third trimester (↑ triglyceride-rich lipoprotein production and
↓ LPL activity)
2. Diagnosis:
a. Lipid panel:
i. Triglyceride level >100 mg/dL is required for diagnosis
3. Management:
a. Insulin is helpful in limiting fatty-acids release from adipocytes (given if glucose ≥500
mg/dL)
b. Apheresis is helpful if glucose ≤500 mg/dL or severe pancreatitis

PERIPARTUM CARDIOMYOPATHY
1. Features:
a. Rapid-onset systolic heart failure at >36 weeks gestation or early Puerperium

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CARPAL TUNNEL SYNDROME

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