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OB Emergencies — Preeclampsia, HELLP, Eclampsia, AFE, Peripartum CMP

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OB · 8 min read

The five obstetric emergencies that kill mothers. Preeclampsia is now diagnosed without proteinuria; AFE is now treated as a cardiac arrest with DIC; peripartum cardiomyopathy is increasingly survivable with mechanical support.

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Preeclampsia — modern diagnostic criteria + severe features

ACOG 2020 criteria: new-onset HTN (SBP ≥140 OR DBP ≥90 on two readings ≥4 hr apart) after 20 weeks gestation in previously normotensive woman, PLUS proteinuria (≥300 mg/24 hr or ≥0.3 protein:creatinine ratio) OR (in absence of proteinuria) any severe feature.

SEVERE FEATURES

SBP ≥160 or DBP ≥110
platelet <100k
transaminases ≥2× upper limit
serum creatinine >1.1 or doubled from baseline
pulmonary edema
new cerebral/visual symptoms (headache, scotomata, blurred vision)

Pathophysiology: abnormal placental cytotrophoblast invasionreduced spiral artery remodelingplacental ischemiarelease of antiangiogenic factors (sFlt-1, soluble endoglin)systemic endothelial dysfunctionvasoconstriction + capillary leak + organ injury.

Definitive treatment: delivery of placenta.

Magnesium for seizure prophylaxis; antihypertensives for severe BP.

BP management in severe preeclampsia: treat persistent SBP >=160 or DBP >=110 within 15-60 min; first-line agents labetalol IV, hydralazine IV, or nifedipine PO; definitive treatment is delivery.

Pleural effusion evaluation and management: transudate (CHF, cirrhosis, nephrotic - Light's criteria) vs exudate (infection, malignancy, PE). Diagnosed by CXR, ultrasound, CT; thoracentesis for symptoms or diagnostic workup. Anesthetic implications for volume removal and re-expansion pulmonary edema. — BP management in severe preeclampsia: treat persistent SBP >=160 or DBP >=110 within 15-60 min; first-line agents labetalol IV, hydralazine IV, or nifedipine PO; definitive treatment is delivery.

Magnesium sulfate — dosing, monitoring, toxicity

KeyMgSO4 4-6 g IV load over 15-20 min, then 1-2 g/hr infusion, OR 10 g IM (5 g each buttock) load + 5 g IM q4h if no IV access (Pritchard regimen).

Therapeutic level 4-7 mEq/L (4.8-8.4 mg/dL).

Reduces eclamptic seizure risk by ~50% vs placebo (Magpie trial, Lancet 2002) and beats phenytoin/diazepam (Collaborative Eclampsia Trial 1995).

Toxicity by level

5-9 mg/dL therapeutic

9-12 mg/dL loss of deep tendon reflexes

12-18 mg/dL respiratory depression

18-24 mg/dL respiratory paralysis

>24 mg/dL cardiac arrest

Monitor: hourly DTRs, respiratory rate, urine output (Mg renally cleared — accumulates in renal failure; reduce infusion to 0.5-1 g/hr if Cr >1.0).

ANTIDOTEcalcium gluconate 1 g (10 mL of 10%) IV over 3-5 min for severe toxicity.

Mg potentiates nondepolarizing NMBs (reduce dose ~50%) + prolongs sux mildly.

Magnesium sulfate toxicity ladder by serum level: therapeutic 4-7 mg/dL, loss of DTRs 8-12, respiratory depression 12-15, cardiac arrest >15-25; treat with calcium gluconate 1 g IV; used for preeclampsia seizure prophylaxis and tocolysis.

Lithium: narrow therapeutic window (0.6-1.2 mEq/L maintenance, toxic >1.5); toxicity causes tremor, confusion, ataxia, seizure; risk factors include NSAIDs, ACEi, diuretics, dehydration; prolongs neuromuscular blockade. — Magnesium sulfate toxicity ladder by serum level: therapeutic 4-7 mg/dL, loss of DTRs 8-12, respiratory depression 12-15, cardiac arrest >15-25; treat with calcium gluconate 1 g IV; used for preeclampsia seizure prophylaxis and tocolysis.

Hypertensive emergency in pregnancy

KeyTarget: when SBP ≥160 or DBP ≥110 sustained ≥15 min, reduce to SBP 140-150/DBP 90-100 within 30-60 min — avoid abrupt drop (placental hypoperfusion + fetal distress).

First-line agents: labetalol 20 mg IV, then 40 mg, then 80 mg q10min (max 220-300 mg total); hydralazine 5-10 mg IV q15-20 min (slower onset, more reflex tachycardia); nifedipine 10 mg PO (NOT sublingual) q20 min × 3. Avoid: ACE inhibitors + ARBs (fetal renal injury — contraindicated all trimesters), nitroprusside (cyanide toxicity to fetus with prolonged use), esmolol (excessive fetal bradycardia).

Once stable, transition to oral labetalol 200-400 mg PO bid or nifedipine XL 30-60 mg daily.

HELLP syndrome + neuraxial considerations

HELLPHemolysis + Elevated Liver enzymes + Low Platelets — often considered a severe variant of preeclampsia though 15-20% lack hypertension.

Criteria (Tennessee): platelets <100k, AST ≥70, LDH ≥600.

Classic presentation

RUQ pain
malaise
nausea late 2nd-3rd trimester

Complications

hepatic hematoma/rupture
abruption
AKI
DIC
eclampsia
stroke
ARDS
fetal demise

Maternal mortality 1%, perinatal 7-20%.

Definitive treatment: delivery.

Neuraxial decision (most contested OB topic): platelets ≥80k commonly accepted for epidural/spinal at most institutions when trend is stable + no other coagulopathy + recent count (within 6 hr ideal)

70k acceptable in some institutions with stable trend

≥100k essentially universally accepted

<70k usually contraindicated GA (with magnesium-attenuated sux response + careful intubation given airway edema)

Always check trajectory, not just the spot value.

HELLP syndrome features: Hemolysis (LDH >600, schistocytes), Elevated Liver enzymes (AST/ALT >70), Low Platelets (<100K); severe preeclampsia variant; delivery is definitive treatment.

Eclampsia + management of seizure

KeyEclampsia: generalized tonic-clonic seizure in a woman with preeclampsia or in postpartum period — incidence 1-2% of preeclampsia.

Usually preceded by warning signs (headache, vision changes, hyperreflexia, RUQ pain) — but can occur without warning.

Most occur intrapartum or within 48 hr postpartum; ~10% present >48 hr postpartum.

Acute management

protect airway + left lateral tilt + supplemental O2

MgSO4 IV bolus 4-6 g over 5 min (if not already running) or additional 2 g if already on infusion

benzodiazepine (lorazepam 2 mg IV or midazolam 2-5 mg IV) only for status refractory to magnesium

AVOID prolonged paralysis if possible (need to monitor neuro status)

maternal stabilization THEN delivery (do not deliver mid-seizure unless fetal distress + maternal hemodynamics permit)

MRI brain only if persistent neuro deficit (PRES is the classic finding — posterior reversible encephalopathy syndrome).

MgSO4 for seizure prophylaxis in severe preeclampsia: loading 4-6 g IV over 20-30 min, maintenance 1-2 g/h; monitor reflexes, RR, urine output, magnesium level; antidote is IV calcium gluconate.

Amniotic fluid embolism — catastrophic biphasic syndrome

KeyAFE incidence ~1:15,000-50,000 deliveries; mortality historically 60-80%, modern series 20-40% with aggressive resuscitation.

Pathophysiology: amniotic fluid + fetal cellular debris enters maternal circulation during labor, C/S, or postpartum biphasic response: Phase 1 (minutes) — pulmonary vasospasm, acute RV failure, hypoxia; Phase 2 (within hours) — LV failure, cardiogenic shock, and DIC (massive consumptive coagulopathy with hyperfibrinolysis).

Presentation: sudden hypoxia + hypotension + cardiovascular collapse + DIC + altered mental status (during/just after delivery).

Treatment: ACLS with high-quality CPR (left lateral tilt roll supine for compressions; perimortem C/S within 4-5 min if pregnant + arrest), 100% O2 + intubate, aggressive transfusion with balanced 1:1:1 ratio + fibrinogen replacement with cryoprecipitate (target fibrinogen >150-200), TXA 1 g IV, consider VA-ECMO + extracorporeal life support early at experienced centers.

The 'A-OK' regimen (atropine 1 mg + ondansetron 8 mg + ketorolac 30 mg) has anecdotal support but is unproven.

Amniotic fluid embolism (AFE) presents with sudden hypoxia, hypotension and DIC near labor/delivery; risk factors include advanced maternal age and multiparity. Management: call for help, ACLS, support coagulopathy, consider ECMO; mortality remains high.

Damage control resuscitation (DCR): permissive hypotension (SBP 80-90), hemostatic resuscitation (1:1:1), and damage control surgery; minimize crystalloid, treat coagulopathy with blood products and TXA. — Amniotic fluid embolism (AFE) presents with sudden hypoxia, hypotension and DIC near labor/delivery; risk factors include advanced maternal age and multiparity. Management: call for help, ACLS, support coagulopathy, consider ECMO; mortality remains high.

Peripartum cardiomyopathy — diagnosis + anesthetic plan

Definition (modern, AHA/ESC): new-onset systolic dysfunction (EF <45%) within the last month of pregnancy or within 5 months postpartum, in the absence of another identifiable cause.

Incidence ~1:1,000-4,000 in US; higher in African-American + multiparous + advanced maternal age + multiple gestation.

Presentation

dyspnea
orthopnea
edema
palpitations — often dismissed as 'normal pregnancy' until severe

Pathophysiology: thought to involve oxidative-stress fragments of prolactin (16-kDa fragment is antiangiogenic + cardiotoxic).

Treatment: standard HF therapy adjusted for pregnancy (avoid ACEi/ARB antepartum — use hydralazine + nitrates; beta-blockers acceptable; loop diuretics; anticoagulation if EF <35%).

Bromocriptine 2.5 mg/day × 7 days (then 2.5 mg bid × 6 weeks) is investigational in Europe (BRO-HF, IPAC trials) — controversial in US.

Anesthetic for delivery

SLOW incremental epidural is preferred when EF >30% + stable

GA with arterial line + cardiac monitoring + careful induction (etomidate or fentanyl-based) when EF <30% or unstable

VA-ECMO standby in severe cases

Future pregnancy strongly discouraged if EF doesn't normalize.

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