Pocket Obstetrics and Gynecology

COMPLICATED PREGNANCY AND DELIVERY

GESTATIONAL HYPERTENSIVE DISORDERS

Definition and see Chap. 12 (Hypertension in Pregnancy, ACOG Task Force, 2013).

• Chronic HTN: SBP ≥140 or DBP ≥90 prior to Preg, prior to 20 w gest, or persisting longer than 12 w postpartum

• Gestational HTN: SBP ≥140 or DBP ≥90 after 20 w w/o proteinuria

• Preeclampsia: New onset HTN (as below) w or w/o proteinuria >20 w

Nonsevere: SBP ≥140 or DBP ≥90; proteinuria ≥300 mg/24 h (or 1+ urine dip or protein: creatinine ratio ≥0.3)

Sev: SBP ≥160 or DBP ≥110; proteinuria ≥5 g/24 h (or 3+ urine dip); oliguria <500 mL/24 h; sx such as HA, visual changes, difficulty breathing, or RUQ pain; elevated liver fxn tests, low Plts. Preeclampsia can → eclampsia. Newest guidelines do not use proteinuria to rule out preeclampsia. New onset HTN with sxs = diagnosis [thrombocytopenia (<100,000/uL) or serum Cr >1.1 mg/dL or elevated LFTs (2× upper limit normal) or pulmonary edema or cerebral/visual symptoms].

• Chronic HTN w/ superimposed preeclampsia: Worsening HTN w/ new onset proteinuria

• All BP should be taken on 2 occasions 4 h apart (after pt has been seated quietly for several minutes, cuff level w/ heart). Also see HELLP (Chap. 15) & Eclampsia (Chap. 18).

See detailed discussion and management of these disorders in Chap. 12.

Epidemiology and Etiology

• Preeclampsia found in ∼7% of pregnancies. True cause unk.

• Risk factors: Age <18 or >40; nulliparity; h/o preeclampsia, FHx of preeclampsia

• Poss causes: Endothelial damage, altered metabolism, inflammation, oxidative stress

Clinical Manifestations

• Preeclampsia: HA, visual changes (scotomata, photophobia), edema, abdominal pain (specifically epigastric or RUQ). Often asymptomatic.

Physical Exam

• Perform full neurologic exam: Evaluate for HA, visual changes, clonus

• Palpate abd to assess abdominal tenderness (specifically RUQ)

• Visualize/palpate extremities to evaluate for periph edema

Diagnostic Workup/Studies

• CBC, CMP (evaluate liver & renal fxn), assessment of proteinuria (by spot prot to Cr ratio, urinalysis, or 24 h urine collection)

• CT can show cerebral edema in the post hemispheres, a form of PRES (Post reversible encephalopathy syn)

Treatment and Medications

• Acute HTN (Chest 2007; 131:1949; Obstet Gynecol 2011;118:1465):

Labetalol: 20 mg IV, rpt at 10-min intervals, double dose w/ max dose of 80 mg at one given time; total max dose of 300 mg (eg, 20 mg → 40 mg → 80 mg → 80 mg → 80 mg)

Hydralazine: 5 mg IV over 1–2 min, rpt at 20 min intervals, max dose at one time of 20 mg; not 1st line as can see mat HoTN

Nifedipine: 10–20 mg PO q30min

Nitroprusside: 0.20-4 mcg/kg/min iv drip, titrate to effect. Only in critical illness resistant to max dose of other agents. Risk of cyanide toxicity with prolonged use.

Nicardipine: 2.5 mg/h IV titrating, do not exceed 15 mg/h

DO NOT USE: ACEI, or ARB

Goal: ↓ risk of mat stroke but maintain pres for placental perfusion

• Oral, outpt treatments

Labetalol: 100–800 mg PO BID–TID (max dose 2400 mg/24 h)

Methyldopa: 250 mg PO BID (max dose 3 g/24 h)

Nifedipine XR: 30–90 mg PO daily (max dose 120 mg/24 h)

• Preeclampsia with severe features, or chronic HTN w/ superimposed preeclampsia

Magnesium sulfate (MgSO4): Bolus 4–6 g IV w/ maintenance of 1–2 g/h for sz prevention, titrate and consider no bolus if pt has renal failure

Goal magnesium level = 4–6 mg/dL

Monit closely for pulm edema as MgSO4 is a smooth muscle relaxer

• Timing for deliv based on limited scientific evid & should always be dependent upon the individualized clinical picture (Obstet Gynecol 2011;118:327)

Chronic HTN: On no meds (38–39 w), controlled on meds (37–39 w), not well controlled on meds (36–37 w)

Gestational HTN: 37–38 w

Preeclampsia: Nonsevere (37 w), sev (at time of dx if ≥34 w, otherwise dependent upon clinical picture)

HYDROPS FETALIS

Definition and Epidemiology

• Accum of fluid in 2 of the following 5 extravascular compartments: Heart (pericardial effusion), lungs (pleural effusion), abd (ascites), subcutaneous tissue best seen around fetal skull (edema), amnion (polyhydramnios)

• Immune Hydrops: Rh isoimmunization

RhD– Mom w/ RhD+ fetus has 16% chance of undergoing isoimmunization

↓ to 2% w/ postpartum anti-D immune globulin administration

↓ to 0.1% w/ additional administration in the 3rd trimester (Transfus Med Rev 1988:2:129)

6/1000 live births undergo Rh isoimmunization

2nd Preg more affected than 1st (1st usually mildly affected, if affected at all, as 1st Ig produced is IgM – DOES NOT cross placenta)

• Nonimmune Hydrops: All other causes

Genetic (aneuploidy, Turner syn, trisomies), CV (structural, arrhythmias, vascular abnormalities), hematologic (α-thal), respiratory (pulm hypoplasia), infectious (CMV, syphilis, Parvovirus, Rubella)

1/1500–1/3800 births affected

Etiology

• Immune: Unclear, possibly from fetal anemia/hypoxia leading to heart failure

Mom RhD–, fetus RhD+ → Mom makes antibodies → cross placenta → antibodies bind to fetal bld → hemolysis of fetal bld → release of bilirubin & fetal anemia → fetal cardiac failure & damaged myocardium → fluid accum → hydrops fetalis

• Nonimmune: Dependent upon the underlying d/o

Clinical Manifestation

• US findings can include enlarged liver/spleen/placenta/heart, ascites

• Fetal HR tracings: Sinusoidal pattern indicative of fetal anemia

• Mirror syn: Mother gets edema that mimics the hydropic fetus

Physical Exam

• Mother may appear edematous if experiencing mirror syn

• Infant can range from hyperbilirubinemic to pale, limp, edematous

Diagnostic Workup/Studies

• Immune: All women have Rh(D) typing & Ab screening at 1st prenatal visit → if antibodies present indirect Coombs test detects Ab titer

Titer <1:32

Rpt titer every 4 w

After 24 w gest, rpt titer every 2 w

If remains <32 deliver at term vs. if ≥32 proceed w/ w/u below

Titer ≥1:32

Test father’s Ag & genotype

Homozygous: MCA Dopplers q1–2w starting at 18–24 w gest

Heterozygous: Perform amniocentesis for fetal DNA

RhD+: Proceed w/ MCA Dopplers

RhD–: Deliver fetus at term, no further testing

• Nonimmune:

Detailed personal (inquire about infectious contacts) & FHx

Perform detailed US & consider fetal ECHO

Obtain MCA Dopplers to assess fetal anemia

Offer amniocentesis (karyotype, TORCH panel)

Obtain mat bld (anemia w/u, type & screen, serologies for CMV, parvovirus B19, toxoplasmosis, syphilis)

Subsequent Workup

• MCA Dopplers

Peak MCA velocity >1.5 MoM → check fetal HCT via PUBS → transfuse fetus if HCT <30%

Peak MCA velocity ≤1.5 MoM → continue MCA Dopplers q1–2w

Nomogram to monit MCA Doppler results is valid until 35 w gest

Treatment and Medications

• Immune: PUBS, intrauterine fetal bld xfusion when needed, Phenobarb 30 mg PO TID to mother prior to deliv if received multi PUBs and need for delivery

• Nonimmune: Prog dependent upon etiology; worse prog when diagnosed earlier in gest & w/ pleural effusions or polyhydramnios

CV issues: ∼40% of nonimmune hydrops

Fetal arrhythmias (eg, SVT) can be treated w/ mat rate controlling meds

Mortality rate 50–98% (approaches 100% if <30 w gest w/ pleural effusions)

Often may require supportive care or offering termination of Preg

Continue to monit MCA Dopplers as above if dx is anemia

INTRAUTERINE GROWTH RESTRICTION

Definition and Epidemiology (Obstet Gynecol 2013;121:1122)

• Defined as sonographic EFW <10th percentile

• By definition is present in 10% of all gestations. Often, not signif until EFW <5%

Etiology

• Mat factors:

Behavioral: Smoking, substance use, decreased nutritional intake

Medical: Extremes of reproductive age, HTN, renal dz, lung dz, lupus, cyanotic heart dz, collagen vascular dz, viral or protozoal illness

• Fetal factors:

Congen d/o (eg, aneuploidy), constitutional

Clinical Manifestation

• Small for gestational age infant (<10%)

• Neonat morbidity: Dependent on cause; infants born constitutionally small generally have no sequelae & those w/ congen anomalies have poorer outcomes

• Perinatal morbidity & mortality is increased, particularly below 3%ile EFW

Physical Exam

• Lagging fundal height compared to gestational age. Nml fundal height measurements from 20–36 w are defined as 1 cm per week of gest ±2 cm.

Diagnostic Workup/Studies

• Goal: Identify true placental insufficiency causing IUGR vs. constitutional or other

• Clinical dx:

Screening is accomplished via fundal height measurements

Lagging fundal height (≥3 cm) → US eval for growth

• US:

Eval after identifying lagging fundal height includes EFW using fetal biometry

Fetal biometry: Head circumference, biparietal diameter, abdominal circumference, & femur length

EFW <10% = IUGR

AFI should be performed for prog

Oligohydramnios (AFI <5 cm) correlates w/ an increased risk of fetal death

• Umbilical artery Doppler:

Measurement of velocity of flow through umbilical artery during systole & diastole

Peak systolic velocity is elevated in IUGR → indicates ↑ placental resistance

W/ progression of IUGR, diastolic flow ↓ as placental resistance ↑ → AEDF or REDF

AEDF: Risks of continuing Preg begin to outweigh the risks of prematurity

REDF: Move toward deliv

Management (Am J Obstet Gynecol 2011;204:34.e1)

• Initial US is performed after lagging fundal height is found (65–85% sens and 96% spec). Growth US repeated in 3–4 w

• At least weekly antenatal testing is indicated & may include:

NST, BPP, modified BPP + umbilical artery Doppler

Negative predictive values are >99% for each of the above tests – ie, a negative test is highly reassuring that IUFD will not occur w/i 1 w

• Deliv: (Obstet Gynecol 2011;118:323)

38–39 w6d gest w/ nml testing and isolated IUGR; Deliv plan tailored to individual risks and ongoing eval

34–37 w6d gest w/ abnormal umbilical artery Dopplers or other risk factors (eg, oligo, maternal comorbities)

Earlier delivery (≤34 w) considered for the most severe cases (eg, REDF), after steroids for FLM and with MgSO4 for fetal neuroprotection (for ≤32 w GA)

MULTIPLE GESTATION

Definition and Epidemiology (Obstet Gynecol 2014;123:1118)

• Pregnancies in which more than one fetus implants in the uterus

• Multi gestations account for 3% of all births

• 65% rise in twins & 500% rise in triplets or higher since 2002, likely secondary to ART

Etiology

• Described in terms of zygosity – number of eggs initially fertilized

Monozygotic = one egg fertilized by one sperm; splitting of initial zygote

Dizygotic = usu two eggs fertilized by two sperm; two separate fertilization events

• Chorionicity vs. amnionicity

Determined by timing of embryonic splitting

0–4 d after fertilization → dichorionic diamnionic twins

4–8 d after fertilization → monochorionic diamnionic twins

8–12 d after fertilization → monochorionic monoamnionic twins

>12 d post fertilization → conjoined twins

Chorionicity: Number of placentas shared by embryos (di = 2, mono = 1)

Amnionicity: Number of amnionic sacs around embryos (mono = both embryos in 1 sac)

Physical Exam

• Measurement of size > dates

Diagnostic Workup/Studies

• Best test is US in early Preg → determines number of embryos

Cannot always tell chorionicity

1st trimester twin peak sign = dichorionic gest

Figure 11.1 A: Monochorionic diamnionic twins have fused amnionic membranes with no intervening placental tissue (<1 mm thick). B: Dichorionic diamnionic twins show twin peak sign with membrane separation and intervening chorion

Complications

• Almost all complications of Preg are more likely w/ multi gestations

• Discordance: One twin larger than the other; clinically signif when greater than 20%. Calculate discordance % as: [(larger EFW - smaller EFW) / larger EFW] × 100.

• Monochorionic monoamnionic twins: Cord entanglement & subseq cord accident; delivered early at 32–34 w

• Monochorionic diamnionic twins: Twin to twin transfusion syndrome (TTTS)

Due to bld vessel anastomoses w/i single placenta w/ pressure diff

Occurs in ∼15% of monochorionic diamniotic twin gestations

Donor twin: Bld shunted away

Recipient twin: Bld shunted toward

Stages of TTTS (J Perinatol 1999;19:550):

1. Polyhydramnios/oligohydramnios, donor bladder present

2. Poly/oli, donor bladder absent

3. Poly/oli, abn Dopplers

4. Poly/oli, hydrops of recipient

5. IUFD of one or both fetuses

Rx:

Laser photocoagulation of vessel anastomoses (Stage II or worse)

Serial amnioreduction

Selective reduction (termination) of one fetus

CERVICAL INSUFFICIENCY/SHORT CERVIX

Definition and Epidemiology (Obstet Gynecol 2012;120:964)

• Inability of cervix to maintain a Preg until term

• Weakened cervical tissue leading to loss of Preg, often 2nd trimester

Etiology

• Congen: Collagen dz, Müllerian fusion anomalies, h/o DES exposure in utero

• Acq: Cervical trauma, D&C, cervical manipulation (LEEP, cold knife cone)

• Abnormality in cervical remodeling (4 steps: Softening, ripening, dilation, repair)

Clinical Manifestation

• Asymptomatic/painless cervical dilation/effacement

• Often h/o painless dilation & deliv in the 2nd trimester w/ prior pregnancies

Physical Exam

• Speculum exam can show a dilated cervix

• Digital exam reveals soft, effaced, & possibly dilated cervix

Diagnostic Workup/Studies

• When performing fetal anatomy US at 18–22 w, can perform CL via transabdominal US. CL <25 mm on transabdominal → transvaginal US

Treatment and Medications

• For short cervix: Vaginal progesterone 200 mg micronized or 90 mg gel daily

• For short cervix or cervical insufficiency: Cervical Cerclage (Obstet Gynecol 2014;123:372)

Surgical stitch placed circumferentially around the cervix

McDonald: “Purse-string” placed at cervicovaginal junction

Shirodkar: Requires dissection of the vesicovaginal & rectovaginal fascia to the level of the internal os

• When to treat:

Singleton Preg w/:

No prior spont preterm births → offer vaginal progesterone suppl if CL ≤20 mm at ≤24 w

Prior spont preterm birth (start progesterone injections weekly from 16–36 w) → consider cerclage if CL ≤25 mm at ≤24 w

Dilated cervix <24 w → consider rescue cerclage on individual basis

Multiples show no improv w/ progesterone & worse outcomes w/ cerclage

Figure 11.2 Management of short cervix

PRETERM PREMATURE RUPTURE OF MEMBRANES

Definition and Epidemiology (Obstet Gynecol 2013;122:918)

• PROM: Rupture of membranes before the onset of active labor (“premature” to labor)

• PPROM: Premature rupture of membranes <37 w (preterm GA and prior to labor)

• Occurs prior to 1/3 of preterm births

Etiology

• No consensus on the cause of PPROM – thought to be on spectrum of preterm labor

• Risk factors include intra-amniotic infxn, uterine over distension, smoking, connective tissue disorders, 2nd & 3rd trimester bleeding, nutritional deficiency, prior preterm deliv, symptomatic contractions, amniocentesis (leakage after amniocentesis more likely to stop & not lead to deliv)

Clinical Manifestation

• Leakage of amniotic fluid prior to labor

• If accompanied by mat fever or tachy, uterine fundal tenderness, fetal tachy, purulent or malodorous fluid there should be concern for intra-amniotic infxn

Physical Exam

• Sterile speculum exam (Obstet Gynecol. 1992;80:630; Am J Obstet Gynecol. 2000;183:1003)

• Avoid digital exam, esp if preterm. Single digital exam decreases latency to deliv.

Diagnostic Workup/Studies

• Clinical dx:

Leakage of fluid per vagina that is consistent w/ amniotic fluid (see below)

Signs of infxn should prompt deliv, regardless of prematurity, to ↓ risk of mat & neonat sepsis

Sterile speculum exam: Pooling of fluid in the vaginal vault sugg ROM

US: Oligohydramnios is often present, though not diagnostic

NST: Fetal tachy is often present w/ intra-amniotic infxn

Oligohydramnios → variable decelerations

• Lab tests:

Ferning: Place fluid from vaginal vault on a dry slide; salts in the amniotic fluid produce a delicate ferning pattern under microscope.

pH: Amniotic fluid has a basic pH → turns pH paper blue (nitrazine test)

Also nitrazine positive: Bld, bact vaginosis, semen.

• Diagnostic procedures

Indigo carmine amniotic infusion “tampon test”

Indigo carmine injected into the amniotic sac via amniocentesis

Tampon inserted vaginally to detect blue color indicating leakage of amniotic fluid

If amniocentesis performed to assess chorioamnionitis, get cell count, gram stain, gluc, & cx (aerobic/anaerobic/myco- and ureaplasma)

Management

• Previable (<24 w): May be managed outpt, w/o Abx, until viability

Major complications: Limb contractures, pulm hypoplasia

Should be offered termination via D&E or induction

• Early preterm (24–34 w):

Antenatal corticosteroids (up to 32–34 w depending on institutional protocol)

Admit to inpt observation in nearly all cases

No indication for tocolytics

Collect GBS culture

Latency Antibiotics

↑ duration of Preg (“latency period”) on avg 1 w

↓ neonat morbidity (respiratory distress, NEC)

Does not ↓ incid of chorio

Induction at 34 w gest or w/ signs of preterm labor, chorio, abruption, fetal distress

• ≥34 w (PLoS Med 2012;9:e1001208):

Unless contraindications exist to vaginal deliv, induction may be attempted

After 34 w, no difference in neonat sepsis btw induction & conservative mgmt, but trend toward ↓ neonat morbidity w/ induction

More likely to see variable decelerations during labor → ↑ CD for fetal intolerance

GBS status should be assessed during latency & appropriate therapy in labor

PRETERM LABOR

Definition and Epidemiology

• Labor (ctx + cervical dilation) occurring before 37 w gest

• Preterm labor occurs in ∼40–50% of all pregnancies

• Preterm deliv occurs in roughly 12% of pregnancies → ∼35% of all health care spending for infants in US

Etiology

• Poorly understood, but risk factors include multi gest/uterine over distension, bact infxn, placental abruption, cervical insufficiency, prior preterm labor

Clinical Manifestation

• Physical exam findings of labor including persistent uterine contractions (>4/20 min or 8/h) leading to changes in cervical effacement & dilation.

• Occ includes rupture of membranes

Physical Exam

• Painful uterine contractions leading to cervical change, and eval for PPROM, abruption, etc

Diagnostic Workup/Studies (Obstet Gynecol 2012;120:964)

• Pelvic exam:

Sterile speculum and digital exam to evaluate cervical dilation

Collect fFN swab

GBS swab if deliv is not imminent & has not been collected previously

Sterile vaginal exam to directly assess cervix (must be after fFN collected!)

• Labs:

fFN: Basement membrane peptide present in amniotic membranes. Can be tested via cervical swab – not reliable w/ vaginal bleeding, recent (<24 h) intercourse or vaginal exam. If negative, 95% do notdeliver in 14 d (Br J Obstet Gyneacol 1996;103:648)

• US:

Transvaginal US measurement of cervical length <25 mm is a/w preterm deliv

Treatment and Medications (Obstet Gynecol 2012;119:1308)

• Prior to 34 w gest:

Administer corticosteroids for fetal lung maturation

Tocolytics only to allow for Cort administration or mat xfer – no pharmacotherapy proven to stop preterm labor

• Prior to 32 w gest:

Magnesium sulfate administration for fetal neuroprotection (N Engl J Med 2008;359:895)

• Prevention of recurrent preterm birth:

17-OH progesterone caproate (250 mg IM weekly) starting at 16 w until 36 w (30% reduction in recurrent preterm deliv) (N Engl J Med 2003;348:2379)

Serial cervical length measurements starting at 16–24 w/ poss cerclage placement if cervical length <25 mm. See short cervix, above. (Am J Obstet Gynecol 2009;201:375)

POSTPARTUM HEMORRHAGE (PPH)

Definition and Epidemiology (Obstet Gynecol 2006;108:1039)

• Bld loss >500 cc w/ a vaginal deliv or >1000 cc w/ a CD (total EBL)

• Common, w/ incid 2–3% of all births in the United States (Am J Obstet Gynecol 2010;202:353). Clinically, excessive bld loss causing symptomatic anemia (palps, SOB, lightheadedness) &/or signs of hypovolemia (tachy, HoTN, hypoxemia)

• Major cause of mat mortality (Cochrane Database Syst Rev 2007;1:CD003249). Risk of death 1:1000 births in developing countries & 1:100,000 births in developed countries.

• Primary (Early) PPH: W/i 24 h of deliv, caused by uterine atony, genital tract lacerations, bladder or urethral lacerations, retained products of conception, invasive placentation (eg, accreta), uterine rupture or inversion, coagulopathy

• Secondary (Late) PPH: From 24 h–12 w after deliv, caused by infxn, retained products of conception, placental site subinvolution, coagulopathy

Etiology

Uterine atony (most common cause) from: Distended uterus (multi gest, polyhydramnios); impaired uterine contractility (tocolytic meds or anesthetics, prolonged use of meds for labor induction) (Am J Obstet Gynecol2011;204:56); intraamniotic infxn (chorio); distended bladder (prevents lower uterine segment contraction)

• Trauma: Genital tract laceration (vaginal or cervical); surgical injury

• Retained placental tissue (normally or abnormally implanted)

• Coagulopathy: Consumptive coagulopathy from ongoing hemorrhage; HELLP syn; sev preeclampsia; amniotic fluid embolism (w/ DIC); sepsis; fetal demise

• Bleeding may not be apparent if intra- or retroperitoneal bleed, or if genital tract hematoma

Physical Exam

• Bimanual exam to assess for atony or retained placental tissue. Consider bedside US to evaluate for retained placental tissue.

• Thorough inspection of the genital tract for laceration or hematoma

• Tachy & HoTN seen when bld loss approaches 1500–2000 cc

Diagnostic Workup/Studies

• Identify origin of bleeding:

Visualize cervix & vagina to evaluate for lacerations

Bimanual uterine massage to assess for uterine atony

Bedside US to view poss retained products

Manual evacuation of uterine cavity for poss extraction of retained products

Place Foley catheter (distended bladder may contribute to poor uterine tone)

• Labs: Bld type & cross, CBC, PT/INR, PTT, fibrinogen. 5 mL of bld in red top tube at bedside → clot in 8–10 min if fibrinogen >150 mg/dL.

• Immediately begin treating for the suspected origin of hemorrhage (eg, for uterine atony administer uterotonics, perform bimanual uterine massage)

Medical Therapies for PPH

• Oxytocin (Pitocin) Routine use during the 3rd stage of labor significantly reduces the incid of PPH (Cochrane Database Syst Rev 2001;(4):CD001808). Can bolus for PPH, though some risk for HoTN. Onset of action: ∼1 min (IV), 3–5 min (IM).

• Misoprostol May cause fever, chills/shivering, GI distress. Onset of action: 100 min (PR) (vs. 8 min PO, 11 min SL, 20 min PV)

• Methylergonovine Onset of action: 2–5 min (IM).

• Carboprost tromethamine (Hemabate) May cause bronchospasm in asthmatics. May rpt q15–90 min as needed, w/ max cumulative dose 2 mg. Onset of action: 15–30 min (IM).

Procedural Therapies for PPH

• Uterine massage for atony (external, bimanual)

• Manual extraction of placenta

• D&C/ Suction curettage of the uterus for retained placenta

• Uterine tamponade: Balloon catheter placement (Foley or Bakri balloon, or lap packing) for tamponade, esp lower uterine segment atony

• Uterine compression sutures (eg, B-Lynch) or mattress sutures

• Uterine artery embolization (interv radiol)

Figure 11.3 Management of uterine atony with bimanual massage

Figure 11.4 Initial surgical management of uterine atony.

• Exploratory laparotomy

Compression sutures: B-Lynch, Hayman, Pereira (physically ↑ uterine tone)

Vessel ligation: Uterine arteries (O’Leary sutures), hypogastric arteries (↓ perfusion)

• Hysterectomy (definitive therapy)

PLACENTAL ABRUPTION

Definition and Epidemiology (Am J Epidemiol 2001;153:332)

• Decidual hemorrhage causing premature separation of the placenta

• Incid: 1/120 pregnancies. ↑ w/ PPROM (2–5%)

Pathophysiology

• Decidual hemorrhage → decidual cells release tissue factor → thrombin (uterotonic) is formed, up-regulates apoptosis, induces expression of inflamm cytokines → tissue necrosis (Am J Obstet Gynecol2004;191:1996)

Etiology

• Mechanical force (trauma) or abn uteroplacental vessels (constriction from vascular dz such as smoking or hypertensive dz)

• Acute: High pres arterial bleeding

• Chronic: Low pres venous hemorrhage, often due to inflamm necrosis

• Factors a/w abruption: Smoking, cocaine use, mat vascular dz, prolonged ruptured membranes, abruption in prior Preg, uterine leiomyoma, multiparity, advanced mat age, HTN

Clinical Manifestation and Physical Exam

• Acute: Vaginal bleeding, abdominal/back pain, contractions (high frequency, low amplitude), abdominal/uterine tenderness, bright red bld in vaginal vault

• Chronic: Intermittent vaginal bleeding, often in small amounts, dark/old bld in vagina

• Couvelaire uterus: Purple tinged uterus due to bld in myometrium seen at cesarean

• Placenta: Gross retroplacental clots & histologic decidual necrosis or placental infarction

Diagnostic Workup/Studies

• Clinical dx by Hx, exam, sono, & suspicion

• Continuous electronic fetal monitoring & uterine tocometry: Frequent uterine contractions (tetany) & nonreassuring fetal heart tracing

• US: 25–50% sens

Retroplacental clot: Elevated region of placenta less echogenic than placental tissue → if seen, likelihood of abruption HIGH

Subchorionic clot: Elevated highly echogenic region of membrane

Thickened placenta that moves w/ mat mvmt

• Labs: CBC, T&C, coags, Kleihauer–Betke (trauma, Rh-mother)

↑ early mat serum AFP: 10× risk of abruption if AFP not a/w a fetal anomaly (Prenat Diagn 2007;27:240)

↓ fibrinogen (<200 mg/dL) = most sensitive lab predictor for sev abruption

DIC commonly seen w/ abruption

Treatment and Medications

• Large bore IV placement & fluid/bld resusc as necessary

• Term or near term: Deliv. If nonreassuring fetal heart tones → emergent CS

• Preterm: Generally delay deliv if fetal well-being is reassuring

Many chronic abruptions will not require deliv

Antenatal steroids if deliv anticipated prior to 34 w gest

Tocolysis not used in women w/ acute abruption

Antenatal testing & serial growth ultrasounds w/ expectant mgmt

Be prepared w/ uterotonics in the postpartum period

PLACENTA PREVIA

Definition and Epidemiology

• Placenta overlying or proximate to internal cervical os (definitions have varied)

Complete: Placenta completely covers os (>20–30%)

Partial: Placental edge partially covers os

Marginal: Placental edge w/i 2 cm of the internal os but does NOT cover os

Low-lying placenta: Placental edge extends into lower uterine segment

• Incid: 0.4% of pregnancies over 20 w (J Matern Fetal Neonatal Med 2003;13:175)

• ↑ w/ increasing parity, cigarette smoking, h/o placenta previa, prior uterine Surg, & prior CD

1–4% in the Preg following a CD

Up to 10% if ≥4 CDs

Etiology

• Trophoblastic implantation: Scarred endometrium may ↑ this process

• Increased need for placental oxygen or nutrient deliv (smokers, multi gest, higher altitude residence)

• ↑ risk of previa at earlier gestational age as the unidirectional growth of trophoblastic tissue toward fundus (trophotropism) is limited. Lower uterine segment ↑ w/ gestational age → Over 90% of placenta previa identified in the 2nd trimester resolve at term

Clinical Manifestation and Physical Exam

• Painless vaginal bleeding in the 2nd & 3rd trimesters

• DO NOT perform digital cervical exam on a pt suspected to have a previa

• A sterile speculum exam is used to visually assess cervical dilation

Diagnostic Workup/Studies

• Identification of placenta during routine US, usually performed from 18–22 w

• If concern for previa → rpt US to assess extent of previa or verify resolution

• Prior CSs + previa = look carefully for evid of placenta accreta (below)

Treatment and Medications

• Pelvic rest (no intercourse or digital exams for duration of Preg)

• Outpt mgmt: Small bleeds resolved for >7 d, live close to the hospital, & are highly compliant

• Inpt mgmt: Actively bleeding placenta previa, ≥2 episodes of vaginal bleeding

If pt can be stabilized & deliv is not needed immediately for fetal distress:

Large-bore IV access

Baseline labs (H/H, platelet count, type & screen, coags)

Antenatal steroids should be administered <34 w gest

• CD at 36–37 w gest (Obstet Gynecol 2011;118:326)

VASA PREVIA

Definition and Epidemiology (Ultrasound Obstet Gynecol 2001:109)

• Umbilical vessels cross internal cervical os in front of fetal presenting part

• Prevalence: 1:2500 deliveries (OBG Survey 2004:245)

• Type 1: From a velamentous cord insertion (vessels not surrounded by Wharton’s jelly)

• Type 2: From vessels btw lobes of a bilobed or succenturiate lobed placenta

Clinical Manifestation

• Vaginal bleeding w/ rupture of membranes → fetal vessel laceration

• Sinusoidal fetal HR (indicating fetal anemia)

Diagnostic Workup/Studies

• Transvaginal US w/ color Dopplers to diagnose before labor

• Once identified, continue to monit w/ US throughout Preg

15% resolve (Obstet Gynecol 2000;95:572)

Begin NSTs twice weekly from 28–30 w to evaluate for cord compression

• Apt test: Qualitative test on vaginal bleeding + fetal bld = indicative of vasa previa

Negative = mat bld, no ruptured vasa previa. Rarely used test in clinical practice.

Treatment and Medications

• Highly consider administration of antenatal corticosteroids prior to 34 w gest

CD pior to rupture of membranes. Suggested gestational age: 34–36 w.

• Pelvic rest (no intercourse or digital exams for duration of Preg)

PLACENTA ACCRETA

Definition and Epidemiology

• Abn placental implantation: Placental villi attach to the myometrium or grow through it instead of being contained by decidual cells

• Risk of accreta ↑ w/ placenta previa & increasing number of CDs (Obstet Gynecol 2006;107:1226)

Pathology

• Accreta: Chorionic villi attached to myometrium

• Increta: Chorionic villi invade the myometrium just up to the serosa

• Percreta: Chorionic villi protrude through the uterine serosa

Risk Factors

• Advanced mat age, smoking, advanced parity, submucosal fibroids, Asherman’s syn

• Most strongly correlated w/ placenta previa + prior uterine incision (eg, CD, myomectomy)

Clinical Manifestation

• Given US advancements, often diagnosed prior to clinical presentation

• Placenta does not detach after deliv → PPH.

Diagnostic Workup/Studies

• Women w/ placenta previa or low lying anter placenta & prior uterine Surg → sono for accreta at 20–24 w

• Ultrasonographic findings suggestive of placenta accreta:

Loss of hypoechoic boundary btw placenta & bladder or thin myometrium <1 mm

Placental lacunae w/ turbulent flow

Irreg bladder wall w/ extensive vascularity

Loss of retroplacental clear space

• Consider color Doppler sono, 3D sono, & MRI. Cystoscopy if bladder invasion suspected

Subsequent Workup

• If accreta identified, pt should be seen by a team of physicians (Anesthesia, General Surg, Interventional Radiology, Uro) to prepare for cesarean hysterectomy

• Monit closely for vaginal bleeding & abdominal pain throughout Preg

Treatment and Medications

• CD at 34–36 w, be prepared for hysterectomy (Obstet Gynecol 2011;118:323)

• Steroids for fetal lung maturity if deliv prior to 34 w gest

• PPH w/ extreme bld loss likely. Maintain IV access & T&C for bld products. Consider internal iliac artery balloon catheters, postsurgical embolization. See Chap. 16 for massive xfusion protocol & bld products.

UTERINE INVERSION

Definition and Epidemiology

• Complete: Internal lining of fundus extrudes through cervical os

• Incomplete: Portion of fundus extrudes to the cervix but not through the os

• 1 in 2500 deliveries (J Reprod Med 1989;34:173)

Etiology

• Excessive umbilical cord traction during 3rd stage of labor on a fundally implanted placenta

• Impaired uterine contraction after deliv of placenta

• Uterine malformations. Abn placentation (eg, placenta accreta)

Physical Exam

• Visualization of endometrial lining through the cervical os (meaty, red tissue)

• Inability to palpate fundus of uterus

Treatment and Medications

• Reinvert the uterus w/ constant/gentle pres, in a cephalad direction, on the fundally inv portion of the uterus. Reinversion becomes more difficult w/ delay. Bleeding ↑↑↑

• General anesthesia & tocolytic agents may be needed to assist w/ replacing the uterus; monit closely for HoTN & increased bleeding, such as:

Magnesium sulfate 2 g IV

Terbutaline 0.25 mg IV or IM

Nitroglycerine 50 mcg IV

Halogenated anesthesia (isoflurane, sevoflurane)

• Obstetrical emergency if reinversion is not successful → laparotomy → elevate fundus by round ligaments & restore cephalad with a hand below in the vagina.

AMNIOTIC FLUID EMBOLISM

Definition and Epidemiology

• Presence of amniotic fluid in mat circulation, occurring usually at deliv

• Incid of 7.7/100000 births. Unpredictable & unpreventable

Pathology

• Poorly understood. Amniotic fluid enters mat circulation → precipitation of DIC & shock in mother (cardiogenic vs. distributive)

• Thought to be due to tumultuous labor or uterine manipulation, but unk

Clinical Manifestation and Physical Exam

• Sudden profound HoTN from cardiogenic shock, hypoxemia, DIC

• Acute in onset & sev, life threatening → ICU admission. Often rapidly fatal

• Acute destabilization of vital signs – usually becoming unresponsive rapidly

Diagnostic Workup/Studies

• Clinical dx: HoTN, hypoxemia, cardiorespiratory failure

• Ddx: Placental abruption, uterine rupture, peripartum cardiomyopathy, sepsis, PE, anaphylaxis, MI

Treatment and Medications

• If deliv has not yet occurred, emergent (often bedside) deliv of the fetus is warranted

• Supportive rx of hemodynamic instability is the mainstay of rx. Call for help.

MALPRESENTATION

Definition and Epidemiology

• Fetal presentation refers to the presenting part of the fetus (lowest or nearest cervix). Poss presentations include:

Cephalic presentation divided into vertex, sinciput, brow, & face

Breech presentation divided into frank, complete, & footling

Incid of breech presentation declines w/ increasing gestational age, starting at ∼33% at 21–24 w → 11% at 32 w → 3–4% at ≥37 w

Other presentation: back (up or down), shoulder, etc

Etiology and Diagnosis

• Uterine anomalies (bicornuate, septum), fibroids, placentation defects (previa), multiparity, poly/oligohydramnios, contracted mat pelvis, fetal or neuro defect, short umbilical cord

• Presenting part is felt w/ vaginal exam, identified on Leopold maneuvers. Verify w/ sono.

Treatment

• Breech & mentum post face presentations → usually CD. Planned vaginal breech deliv a/w ↑ perinatal mortality, neonat mortality, & serious neonat morbidity than planned CD (5% vs. 1.6%) (Lancet2000;356:1375)

• External cephalic version may be attempted (at >36 w, usu 36–38 weeks) to convert a breech presentation to a cephalic. Contraindicated in pregnancies where CD is indicated (eg, placenta previa), gestational age <36 w (high rate of reversion). (ACOG Practice Bulletin #17, Reaffirmed 2012)

FETAL MECONIUM

Definition and Epidemiology

• Fetal mec stool usu passed in the 1st days of life. If prior to deliv → meconium-stained amniotic fluid, which if breathed by fetus can → mec aspiration syn

• Meconium-stained amniotic fluid in ∼9% of live births w/ 0.1% mec aspiration syn

• Most common in pregnancies reaching 41–42 w gest (post term)

• More likely during labor c/b fetal hypoxia → possibly indicating fetal stress resp

Pathology

• Aspiration of mec by the fetus → dz in neonat lungs. Hypoxemia in neonate secondary to pulm injury

• Injury from mechanical obst of the airway, inflamm damage caused by irritation in the lungs, or by inactivation of surfactant w/i alveoli

Clinical Manifestations

• Dark brown to green amniotic fluid when membranes rupture or after (describe as thin, mod, thick)

• Note color & presence or absence of particulate matter

Diagnostic Workup/Studies

• Mec aspiration can occur during deliv – mec aspiration syn is diagnosed w/ neonat hypoxemia in the presence of aspiration

Treatment and Medications

• Amnioinfusion does not prevent mec aspiration syn

• Peds should be at deliv when mec is noted on rupture of membranes

• To prevent aspiration, nonvigorous neonates should not be initially stimulated at the perineum. Allow peds to evaluate & perform tracheal suction w/ laryngoscope.

CHORIOAMNIONITIS

Definition and Epidemiology

• Infxn of the amniotic membrane & chorion of the placenta

• Complicates 1–4% of all births in US

• Risk factors – ↑ duration of membrane rupture, GBS bacteriuria, prolonged labor, multi vaginal exams, internal monitoring

Etiology

• Infxn is present in the chorionic membranes, umbilical cord, or placenta

• May be transmitted via ascending infxn from lower genital tract, transplacentally from mat bld stream, or iatrogenically (eg, via amniocentesis)

• Typical organisms: Ureaplasma, Mycoplasma hominis (more common in ascending infections), GBS, Escherichia coli, Gardnerella vaginalis, Listeria monocytogenes (more common w/ transplacental spread from mat infxn)

Physical Exam

• Mat: Fever (>38°C or 100.4°F), fundal tenderness, purulent or foul smelling discharge, tachy >100 bpm. Fetal: tachy >160 bpm

• Mat fever + tachy is highly suggestive. Clinical dx.

• Rule out other causes fever/tachy (eg, epidural fever, administration of ephedrine)

Diagnostic Workup/Studies

• Clinical dx: Mat fever is the most important marker of the condition

• Lab eval: Rarely performed, though amniotic fluid culture is the gold std for dx; other suggestive amniotic fluid markers include gluc ≤15 mg/dL, IL-6 >7.9 ng/mL, positive MMP, WBC > 30/mm3, leukocyte esterase positive on dipstick. IL-6, MMP, & leukocyte esterase ↑ sens/spec.

Treatment and Medications

• Acetaminophen for fever control → ↓ incid of neonat encephalopathy

• IV Abx:

Vaginal deliv: Ampicillin 2 g IV q6h + Gentamicin 1.5 mg/kg IV q8h until deliv; one additional dose after deliv of each antibiotic → ↓ endomyometritis

CD: Same as vaginal deliv + Clindamycin 900 mg IV once OR Metronidazole 500 mg IV once; consider continuing Abx until pt is afebrile for 24–48h (generally w/ Gentamicin/Clindamycin or Ampicillin/Gentamicin/Clindamycin).

ENDOMYOMETRITIS

Definition and Epidemiology

• Infxn of the endometrial, parametrial, or myometrial tissue usually >24 h after deliv (low grade mat fever common during this period). Clinical suspicion guides dx.

• Incid varies w/ mode of deliv:

Vaginal deliv: 0.2–0.9%; higher if chorio was present

CD: 5–30%; decreased w/ perioperative prophylactic Abx

Etiology

• Similar to chorio (ascending infxn from lower genital tract). Also introduced infxn from surgical trauma. Usually polymicrobial.

• Infxn from genital tract can invade the surgical wound

Physical Exam

• Physical exam is similar to chorio w/ mat fever & fundal tenderness

• Malodorous lochia may be present

Diagnostic Workup/Studies

• ↑ WBC (although commonly elevated in labor & postoperatively anyway)

• Largely clinical dx & depends on context/suspicion. Imaging generally unnecessary unless suspecting pelvic abscess or larger/progressing infxn.

• Cx for chlamydia & gonorrhea could be considered if not already obtained

• Routine endometrial culturing is not helpful secondary to genital tract contamination

Treatment and Medications

• Treat w/ broad spectrum Abx. >90% respond to Gentamicin (5 mg/kg IV q24h) + Clindamycin (900 mg IV q8h). IV Abx until asymptomatic/afebrile for 24–48 h; no data exist to support continued oral antibiotic rx. Clinical response guides antibiotic coverage/spectrum (eg, broaden if no response in ~24 h or clinically worsening) and duration of treatment.

• Acetaminophen/Ibuprofen for mat fever. Breastfeeding okay.