Eduovisual
Pregnancy, Childbirth & Puerperium
Eclampsia: prevention and management
— Complicates ~1.5–10 per 10,000 deliveries in high-income countries; higher in low-resource settings.
— ~50% occur antepartum, ~20% intrapartum, ~30% postpartum (most within 48 h, but "late postpartum eclampsia" can occur up to 4–6 weeks).
— Abnormal placental spiral artery remodeling → endothelial dysfunction → systemic vasospasm, increased vascular permeability.
— Cerebral autoregulation failure → hyperperfusion, vasogenic edema (posterior > anterior — overlaps with PRES on MRI).
— Pregnant or recently postpartum patient with seizure, severe headache unresponsive to acetaminophen, visual scotomata/blurring, RUQ or epigastric pain, or sudden altered mental status.
— BP ≥140/90 (often ≥160/110), proteinuria, or known preeclampsia — but eclampsia can occur without prior diagnosis and even with normal-range BP in ~15%.
— Persistent frontal/occipital headache, photophobia, hyperreflexia/clonus, epigastric pain, oliguria, rapid weight gain/edema.
Board pearl: A postpartum woman returning to the ED on day 5 with headache and one witnessed seizure — even if BP is 138/88 — should be treated as eclampsia until proven otherwise. Do not anchor on "she already delivered." Late postpartum eclampsia is a classic Step 3 trap, often misdiagnosed initially as migraine, viral illness, or primary seizure disorder, delaying magnesium and antihypertensive therapy.
— Generalized tonic-clonic, typically 60–90 seconds, followed by postictal confusion lasting 10–20 minutes.
— Usually self-limited; status epilepticus is uncommon but possible.
— Recurrence within hours is common without magnesium prophylaxis.
— Headache (frontal, persistent, throbbing, not relieved by acetaminophen).
— Visual changes: scotomata, blurred vision, photopsia, cortical blindness.
— Epigastric/RUQ pain (hepatic capsule stretch from periportal hemorrhage/edema).
— Nausea, vomiting, altered mentation, dyspnea (pulmonary edema), brisk reflexes.
— Gestational age and last prenatal visit BP/urine results.
— History of chronic hypertension, prior preeclampsia, pregestational diabetes, lupus, antiphospholipid syndrome, CKD, obesity, twins, IVF.
— Family history of preeclampsia/eclampsia.
— Postpartum: delivery date, mode, blood loss, NSAID use (worsens hypertension), pain medication exposure.
— Eclampsia without proteinuria (~15%).
— Eclampsia at BP <140/90 ("normotensive eclampsia," ~15–20%) — diagnosis is clinical.
— Postpartum patient with seizure plus thunderclap headache — must also consider PRES, RCVS, cerebral venous thrombosis.
Key distinction: Preeclampsia with severe features (BP ≥160/110, platelets <100k, Cr >1.1, LFTs 2× normal, pulmonary edema, persistent headache/visual symptoms) is the immediate precursor — but eclampsia is defined by the seizure, not severity criteria. Step 3 management: Even before lab confirmation, in a pregnant patient with a first seizure, start IV magnesium sulfate empirically while obtaining CBC, CMP, LDH, uric acid, urine protein/creatinine ratio, and fetal monitoring. Treat first, document later.
— BP often ≥160/110, but may be only mildly elevated or normal.
— Tachycardia, tachypnea (suggests pulmonary edema or acidosis).
— SpO₂ — desaturation suggests pulmonary edema, aspiration, or amniotic fluid embolism.
— Postictal lethargy, confusion, focal deficit (transient).
— Hyperreflexia with clonus — sensitive prodromal finding; absence of reflexes after magnesium initiation suggests toxicity.
— Persistent focal deficit → urgent neuroimaging (rule out intracranial hemorrhage, ischemic stroke, cerebral venous thrombosis).
— Visual field defects, cortical blindness — concerning for occipital vasogenic edema (PRES).
— Crackles, S3, JVD — pulmonary edema (occurs in ~3% of severe preeclampsia, more common postpartum from fluid mobilization).
— Murmurs (rule out underlying valvular disease, peripartum cardiomyopathy).
— RUQ tenderness — hepatic capsule distension; severe → consider hepatic hematoma/rupture.
— Fundal height, uterine tenderness (placental abruption — eclampsia is a strong risk factor).
— Vaginal exam (after stabilization) — assess labor status, bleeding.
— Continuous EFM as soon as mother is stable.
— Transient fetal bradycardia is common during/after maternal seizure (maternal hypoxemia/hypercarbia) and typically resolves within 5–10 minutes with maternal stabilization.
— Persistent fetal bradycardia >10 minutes despite maternal recovery suggests placental abruption — proceed to urgent delivery.
CCS pearl: On a CCS case, after seizure stabilization, simultaneously order: "magnesium sulfate IV load," "labetalol IV," "continuous fetal monitoring," "OB consult STAT," "type and screen," "CBC, CMP, LDH, haptoglobin, uric acid, coags, urine protein/Cr." Do not wait for one result before ordering the next — parallel orders score higher than serial workup.
— CBC — thrombocytopenia (<100k = severe feature; HELLP if <100k with hemolysis + ↑AST).
— Peripheral smear — schistocytes suggest microangiopathic hemolysis.
— LDH (>600 supports hemolysis), haptoglobin (low), indirect bilirubin (elevated).
— AST/ALT — ≥2× upper limit of normal = severe feature; >1000 raises concern for hepatic infarction/hematoma.
— Creatinine — ≥1.1 mg/dL or doubling of baseline = severe feature.
— Uric acid — supportive but not diagnostic (elevated >5.5 mg/dL).
— Coagulation panel — PT/PTT/fibrinogen (DIC screen, especially with abruption).
— Urine protein/creatinine ratio ≥0.3, or dipstick ≥2+ (24-hr collection not needed acutely).
— Type and screen — anticipate delivery and possible transfusion.
— Glucose — rule out hypoglycemic seizure.
— Magnesium level — baseline before infusion, then 4–6 hourly if renal impairment or signs of toxicity.
— Fingerstick glucose, ECG (rule out arrhythmia, look for QTc, electrolyte effects), urine pregnancy test if gestational status unclear in reproductive-age woman.
— Head CT (noncontrast): focal deficit, prolonged coma, atypical seizure, recurrent seizure despite magnesium, thunderclap headache, or suspicion of ICH.
— MRI brain: persistent neuro deficits — may show posterior reversible encephalopathy syndrome (PRES) — bilateral parieto-occipital vasogenic edema.
— CXR: if dyspnea, hypoxia — pulmonary edema.
— RUQ ultrasound: if severe RUQ pain or AST >500 — assess for subcapsular hematoma.
Board pearl: Neuroimaging is not required to diagnose eclampsia — diagnosis is clinical. Image only when the seizure is focal, recurrent despite therapeutic magnesium, the patient fails to return to baseline, or you suspect an alternative diagnosis (stroke, CVST, ICH). Ordering routine CT delays magnesium and is a wrong-answer trap.
— MRI brain with MRV: gold standard for PRES, cerebral venous sinus thrombosis (postpartum hypercoagulability), and ischemic stroke. Look for symmetric parieto-occipital T2/FLAIR hyperintensities (PRES) vs. asymmetric infarct vs. empty delta sign (CVST).
— CTA/MRA head/neck: if RCVS (reversible cerebral vasoconstriction syndrome) suspected — beaded "string-of-beads" cerebral arteries; presents with thunderclap headache, common postpartum.
— Lumbar puncture: if meningitis/SAH suspected after negative CT.
— EEG: only if recurrent seizures despite therapeutic magnesium, suspicion of nonconvulsive status, or prior epilepsy on the differential.
— ADAMTS13 — distinguish TTP from HELLP (TTP: ADAMTS13 <10%; HELLP: normal/mildly low).
— Complement levels (C3/C4), soluble C5b-9 — atypical HUS overlap in postpartum thrombotic microangiopathy.
— Lupus serologies, antiphospholipid panel — if recurrent preeclampsia, fetal loss history, or atypical features.
— sFlt-1/PlGF ratio — emerging biomarker, available at some centers; ratio >38 supports preeclampsia diagnosis, helpful in atypical presentations (not yet standard of care in US).
— Ultrasound for growth (IUGR common), amniotic fluid index, umbilical artery Dopplers.
— Biophysical profile if non-reassuring tracing.
— Betamethasone if 24⁰–33⁶ weeks and delivery anticipated within 7 days.
Key distinction: Eclampsia vs. TTP vs. HELLP vs. aHUS vs. AFLP — all can present postpartum with thrombocytopenia and end-organ injury. AFLP: profound hypoglycemia, hyperammonemia, coagulopathy out of proportion to platelet count. TTP: ADAMTS13 <10%, neurologic symptoms predominant, does not improve with delivery. HELLP improves within 48–72 h postpartum — if it doesn't, reconsider TTP/aHUS and consider plasma exchange or eculizumab.
— ABCs: left lateral decubitus, suction, oxygen via nonrebreather, IV access ×2, padded rails.
— Stop the seizure / prevent recurrence: IV magnesium sulfate (see chunk 7).
— Control severe hypertension: BP ≥160/110 sustained ≥15 min → IV labetalol, hydralazine, or oral nifedipine immediate-release.
— Fetal monitoring once mother stabilized.
— Plan delivery — definitive treatment.
— ≥34 weeks: deliver after maternal stabilization. Vaginal delivery acceptable if no obstetric contraindication.
— <34 weeks: still deliver if eclampsia (uncontrollable BP, non-reassuring fetal status, abruption, pulmonary edema, DIC, renal failure, persistent neuro symptoms) — but administer betamethasone if time permits and there are no contraindications to brief delay.
— <24 weeks: counsel regarding maternal risk; delivery still typically indicated for eclampsia.
— Mode of delivery: eclampsia is not itself an indication for cesarean — vaginal delivery is preferred if cervix favorable and fetal status reassuring.
— Restrict crystalloid to ~80 mL/hr — these patients are at high risk for pulmonary edema (low oncotic pressure, capillary leak).
— Foley catheter for strict I/Os.
— HELLP, DIC, abruption, pulmonary edema, AKI, hepatic hematoma, persistent neuro deficit → ICU-level care.
Step 3 management: The four parallel orders in the first 15 minutes are: (1) magnesium sulfate 4–6 g IV load + 1–2 g/hr drip, (2) labetalol 20 mg IV (or hydralazine 5–10 mg IV) for BP ≥160/110, (3) continuous fetal monitoring + OB/MFM consult, (4) labs (CBC, CMP, LFTs, LDH, coags, T&S). Definitive therapy is delivery of the placenta — magnesium and antihypertensives are bridges.
— Loading dose: 4–6 g IV over 15–20 minutes (or 5 g IM in each buttock = 10 g IM if no IV access).
— Maintenance: 1–2 g/hr IV infusion; continue for 24 hours after delivery or after last seizure (whichever later).
— Therapeutic level 4.8–8.4 mg/dL (4–7 mEq/L).
— Superior to phenytoin and diazepam in preventing recurrent eclamptic seizures (Magpie, Collaborative Eclampsia Trial).
— Mechanism: NMDA antagonism, cerebral vasodilation, membrane stabilization — not a traditional anticonvulsant.
— Loss of patellar reflexes (~9–12 mg/dL) → first sign.
— Respiratory depression (~12–17 mg/dL).
— Cardiac arrest (>25 mg/dL).
— Antidote: calcium gluconate 1 g IV over 10 minutes.
— Reduce dose in renal impairment (Cr >1.0): give load, then 1 g/hr or less, follow levels q4–6h.
— Additional 2 g IV bolus magnesium.
— If still seizing: lorazepam 2–4 mg IV or midazolam; consider levetiracetam.
— Persistent/focal → image and reassess diagnosis.
— Labetalol 20 mg IV → 40 → 80 → 80 mg q10 min (max 300 mg). Avoid in asthma, bradycardia, decompensated heart failure.
— Hydralazine 5–10 mg IV q20 min (max 30 mg). Watch for reflex tachycardia, maternal hypotension → fetal distress.
— Nifedipine IR 10 mg PO, repeat q20 min (max 50 mg). Useful if no IV access.
Board pearl: Do not use ACE inhibitors, ARBs, nitroprusside (cyanide toxicity), or atenolol in pregnancy. Avoid furosemide unless pulmonary edema is present. The triad to memorize: magnesium for seizures, labetalol/hydralazine/nifedipine for BP, delivery for cure.
— Stabilize seizure, BP, and oxygenation first; emergent cesarean during active seizure increases maternal morbidity.
— Typical stabilization window: 1–4 hours.
— Vaginal delivery preferred when feasible — induce with oxytocin if cervix favorable.
— Cesarean indications: non-reassuring fetal status, abruption with hemodynamic instability, failed induction, malpresentation, unfavorable cervix at very preterm gestation, other obstetric indications.
— Eclampsia alone is NOT a cesarean indication.
— Neuraxial (epidural/spinal) is preferred if platelets ≥70k (institution-dependent; many use ≥80k for epidural, ≥50k for spinal), no DIC, no rapidly falling counts.
— Avoid general anesthesia when possible — laryngoscopy triggers BP surges, risk of airway edema, aspiration. If GA needed: pretreat with labetalol/remifentanil to blunt intubation response.
— Avoid ergot alkaloids (methylergonovine) for postpartum hemorrhage — causes hypertensive crisis. Use oxytocin first-line, then carboprost (avoid in asthma) or misoprostol.
— Continuous EFM, q15 min BP, strict I/O, magnesium continued throughout.
— Pulse ox, lung exam q1–2h for pulmonary edema.
— Continue magnesium 24 h postpartum or 24 h post-last seizure.
— BP monitoring q4h; continue antihypertensives — peak postpartum BP often occurs days 3–6.
— Avoid NSAIDs if uncontrolled hypertension (controversial; ACOG now states NSAIDs can be used cautiously, but many still avoid in severe-feature patients with persistent BP elevation).
CCS pearl: After delivery, the case is not over — continue magnesium for 24 h, monitor BP q4h, restrict IV fluids, and reassess labs at 12 and 24 h. Discharge planning starts at 24–48 h with BP recheck at 3–7 days and outpatient follow-up.
— Magnesium is renally cleared — accumulation risk if Cr >1.0 or oliguric (UOP <30 mL/hr × 4 h).
— Adjusted regimen: standard load (4–6 g), but maintenance reduced to 1 g/hr or lower.
— Check serum magnesium q4–6h; clinical exam (DTRs, RR, mental status) is more reliable than levels alone.
— Dialysis rarely needed acutely; AKI usually reverses postpartum within days to weeks.
— Differential of AKI: pre-renal (volume depletion, hemorrhage), intrinsic (cortical necrosis from severe hypoperfusion or abruption, TMA), post-renal (rare).
— Severe AST/ALT elevations (>1000) raise concern for hepatic infarction or subcapsular hematoma — order RUQ ultrasound or CT.
— Hepatic rupture is rare but catastrophic — sudden RUQ pain, hypotension, shoulder pain (Kehr sign), hemoperitoneum. Management: emergent laparotomy, hepatic packing, IR embolization.
— Coagulopathy: correct fibrinogen <150 with cryoprecipitate; platelets <50k with platelet transfusion (or <20k spontaneous); FFP for active bleeding with INR >1.5.
— Profound hypoglycemia, hyperammonemia, severe coagulopathy, often without thrombocytopenia early.
— Swansea criteria for diagnosis.
— Management: urgent delivery, supportive ICU care, consider liver transplant evaluation if no recovery.
Key distinction: HELLP improves within 48–72 h of delivery; AFLP may require days to weeks of ICU support, and recovery hinges on early delivery + correction of hypoglycemia, coagulopathy, and ammonia. If LFTs and INR worsen postpartum instead of improving, reconsider AFLP, TTP, aHUS, or drug injury — do not anchor on HELLP.
— Higher baseline risk of preeclampsia/eclampsia, especially primigravidas <17.
— Often present late due to inconsistent prenatal care.
— Counsel on contraception postpartum (LARCs preferred); future pregnancies higher risk.
— 2–3× preeclampsia risk; consider low-dose aspirin starting 12–28 weeks (ideally before 16 wk) in subsequent pregnancies.
— Superimposed preeclampsia risk ~25%; baseline antihypertensives continued (labetalol, nifedipine, methyldopa); switch off ACE/ARB at conception.
— Aspirin 81 mg daily from 12–28 weeks is standard prevention.
— All are USPSTF-listed high-risk indications for prophylactic low-dose aspirin.
— APS: add prophylactic LMWH + aspirin.
— 2–3× risk; aspirin prophylaxis recommended.
— ~15–20% recurrence risk; earlier and more severe recurrence possible.
— Aspirin 81 mg daily next pregnancy starting 12 weeks.
— Future CV risk: 2× lifetime risk of chronic HTN, stroke, CAD, CKD — counsel on lifestyle, annual BP screening.
— Estrogen-containing methods generally avoided in first 21–42 days postpartum (VTE risk) and longer if persistent HTN.
— Progestin-only pills, IUDs, implants are safe and preferred.
Step 3 management: For any patient with one high-risk factor (prior preeclampsia, chronic HTN, diabetes, CKD, autoimmune, multiple gestation) or ≥2 moderate risk factors (nulliparity, BMI ≥30, age ≥35, family history, low SES, Black race, IVF), prescribe low-dose aspirin 81 mg daily starting at 12–28 weeks (ideally by 16 weeks) and continue until delivery. This is a USPSTF Grade A recommendation and a recurring Step 3 prevention question.
— Pulmonary edema (~3%) — postpartum fluid mobilization, capillary leak; treat with O₂, furosemide, fluid restriction.
— Stroke — ischemic or hemorrhagic; eclampsia is a leading cause of pregnancy-related stroke; sustained SBP >160 is the major driver — hence aggressive BP control.
— HELLP syndrome with hepatic hematoma/rupture.
— DIC — especially with abruption, hepatic failure.
— Acute kidney injury — usually reversible.
— Placental abruption (~7–10%) — sudden pain, bleeding, fetal distress.
— Postpartum hemorrhage — coagulopathy, atony (magnesium causes uterine relaxation).
— Aspiration pneumonia, posterior tongue laceration from seizure.
— Cortical blindness — usually reverses within days to weeks with BP control.
— PRES — typically reversible with BP control.
— Maternal death — eclampsia accounts for a significant share of maternal mortality globally; in US, hypertensive disorders cause ~7% of pregnancy-related deaths.
— Prematurity, IUGR, fetal hypoxia during maternal seizure, neonatal magnesium effects (hypotonia, respiratory depression — usually transient), stillbirth.
— 2× lifetime cardiovascular disease risk.
— 4× risk of chronic hypertension.
— Increased risk of CKD, type 2 diabetes, VTE.
— Possible cognitive and mood sequelae; increased PPD risk.
Board pearl: The leading cause of death in eclampsia is intracranial hemorrhage from uncontrolled severe hypertension, not the seizure itself. This is why BP ≥160/110 sustained ≥15 minutes mandates IV antihypertensive within 30–60 minutes — a quality metric tracked by The Joint Commission and ACOG (severe maternal morbidity bundles).
— Recurrent seizures despite therapeutic magnesium.
— Refractory hypertension despite two IV agents.
— Pulmonary edema requiring noninvasive or invasive ventilation.
— AKI with oliguria, rising creatinine, or need for CRRT.
— DIC, massive transfusion, ongoing hemorrhage.
— Stroke, ICH, persistent neurologic deficit, status epilepticus.
— Hepatic hematoma or rupture.
— Hemodynamic instability.
— Neurology: persistent deficit, atypical seizure, status epilepticus, suspected stroke or CVST.
— Nephrology: rising creatinine, oliguria, electrolyte derangements.
— Hematology: TMA workup (TTP vs. aHUS vs. HELLP), DIC, refractory thrombocytopenia.
— Cardiology: pulmonary edema, suspected peripartum cardiomyopathy, arrhythmia.
— Anesthesia: early involvement for delivery planning, especially if platelets borderline.
— Neonatology: anticipate preterm delivery, magnesium effects.
— Interventional radiology: hepatic hematoma embolization.
— Community ED without OB capability: stabilize with magnesium and antihypertensives, then transfer to tertiary center with MFM and NICU.
— Do not delay magnesium awaiting transfer.
— If delivery is imminent or fetal distress severe — deliver locally, then transfer.
CCS pearl: On a CCS case, "consult OB/GYN" should be ordered within the first 5 simulated minutes — alongside, not after, initial pharmacology. Failing to consult appropriate specialists in a timely manner is one of the most common reasons CCS cases lose points despite correct clinical management.
— BP ≥160/110, thrombocytopenia, elevated LFTs, Cr ≥1.1, pulmonary edema, persistent headache/visual symptoms.
— Distinguished from eclampsia by absence of seizure or unexplained coma.
— Hemolysis (LDH >600, schistocytes, low haptoglobin), Elevated Liver enzymes (AST >2× ULN), Low Platelets (<100k).
— Class 1: platelets <50k; Class 2: 50–100k; Class 3: 100–150k.
— Can occur without significant hypertension or proteinuria.
— Treatment: magnesium + delivery; supportive care.
— BP ≥140/90 after 20 weeks without proteinuria or end-organ features; ~50% progress to preeclampsia.
— Pre-existing HTN + new proteinuria or new end-organ features after 20 weeks.
— Third trimester; nausea, vomiting, jaundice, hypoglycemia, hyperammonemia, coagulopathy out of proportion to platelet drop.
— Microvesicular steatosis; associated with fetal LCHAD deficiency.
— Late pregnancy through 5 months postpartum; dyspnea, edema, reduced EF; can mimic preeclamptic pulmonary edema. Echo differentiates.
— TTP: ADAMTS13 <10%; neuro symptoms predominant; needs plasma exchange.
— Atypical HUS: complement-mediated; consider eculizumab.
Key distinction: HELLP improves with delivery (within 48–72 h). If platelets continue to drop, hemolysis persists, or AKI worsens beyond 72 h postpartum, stop assuming HELLP and pursue TTP/aHUS workup — wrong answer to keep saying "HELLP" on day 5 postpartum with worsening labs.
— Known epilepsy, subtherapeutic AED levels, sleep deprivation, postpartum hormonal shifts.
— Treat acutely with benzodiazepines + AEDs; but in pregnant patient with prodromal headache/HTN, start magnesium concurrently until eclampsia excluded.
— Postpartum hypercoagulability; headache, seizure, focal deficit, papilledema.
— Diagnosis: MRV or CTV (empty delta sign).
— Treatment: anticoagulation (LMWH/heparin) even with hemorrhagic infarct.
— Focal deficit, asymmetric findings; CT/MRI.
— Eclampsia is a major risk factor — these can coexist.
— Thunderclap headache, meningismus; CT then LP if negative within 6 h limits.
— Aneurysmal SAH risk is elevated in pregnancy.
— Thunderclap headache(s), often postpartum or with vasoactive drug exposure; CTA shows segmental vasoconstriction. Treat with nimodipine, avoid vasoactives.
— Symmetric posterior vasogenic edema on MRI; reverses with BP control.
— Hypoglycemia (check fingerstick), hyponatremia (oxytocin-induced water intoxication, especially intrapartum), hypocalcemia.
— Meningitis, encephalitis, abscess — fever, neck stiffness, photophobia; LP after imaging.
— Cocaine, amphetamines, serotonin syndrome, local anesthetic systemic toxicity (LAST) from epidural — treat with intralipid.
— Sudden cardiovascular collapse, hypoxemia, DIC, often with seizure-like activity intrapartum.
Board pearl: Any pregnant or postpartum patient with seizure plus focal deficit, thunderclap headache, fever, or persistent altered mentation after seizure resolution needs neuroimaging — eclampsia is a clinical diagnosis but does not protect against coexisting CVST, ICH, or stroke.
— Continue oral antihypertensive if BP ≥150/100 on >2 readings or any single ≥160/110.
— Preferred agents: labetalol, nifedipine ER, methyldopa; if breastfeeding, all three are compatible.
— Avoid ACE inhibitors/ARBs while breastfeeding only certain ones — enalapril and captopril are considered safe in lactation and are reasonable if HTN persists beyond first weeks.
— Goal BP: <140/90 by 6 weeks postpartum; <130/80 long-term per ACC/AHA.
— Low-dose aspirin 81 mg daily starting 12–16 weeks in next pregnancy (ideally before 16 weeks, continue until delivery).
— Calcium supplementation 1.2–2.5 g/day if dietary calcium <600 mg/day (WHO/USPSTF).
— Optimize BMI, BP, glucose preconception.
— Counsel on 15–25% recurrence risk.
— Lifestyle: DASH diet, exercise, weight loss, smoking cessation.
— Annual BP, fasting lipids, glucose; consider HbA1c.
— Document history of preeclampsia/eclampsia in chart — it is now recognized as a CV risk-enhancing factor in ACC/AHA prevention guidelines.
Step 3 management: At discharge, every patient gets: (1) BP cuff for home monitoring with log, (2) oral antihypertensive if indicated, (3) clear return precautions (headache, visual changes, RUQ pain, swelling, SOB, seizure), (4) follow-up BP check within 3–7 days, (5) postpartum visit at 1–2 weeks (not 6 weeks alone), (6) lifetime CV risk counseling.
— Inpatient: BP q4h until 24 h post-magnesium discontinuation.
— Outpatient: BP check at 72 hours and within 7–10 days of discharge (ACOG quality metric).
— Peak postpartum BP often days 3–6 — patients can become severely hypertensive after discharge.
— Continue home BP monitoring 2–4 weeks; escalate if SBP ≥150 or DBP ≥100 on home readings.
— Repeat CBC, CMP, LFTs at 24–48 h post-delivery; expect HELLP improvement.
— If not improving by 72 h → reconsider TTP, aHUS, AFLP.
— Proteinuria typically resolves over weeks to months; persistent proteinuria >12 weeks → nephrology referral, suspect underlying CKD.
— Return precautions: severe headache, visual disturbance, chest pain, dyspnea, RUQ pain, seizure, leg swelling/asymmetry — call/return immediately.
— Mental health: increased PPD/PTSD risk after eclampsia or NICU course — screen at every visit using EPDS/PHQ-9.
— Breastfeeding: encouraged; almost all antihypertensives compatible.
— Contraception: progestin-only methods, IUDs, implants preferred; avoid estrogen-containing methods at least 21–42 days postpartum, longer if persistent HTN.
— BP, weight, fasting lipid panel, glucose/HbA1c yearly.
— Document preeclampsia history in problem list — affects ASCVD risk modification.
— Recurrent severe early-onset preeclampsia or HELLP → consider thrombophilia, APS, complement pathway evaluation.
CCS pearl: A common missed step on CCS is not scheduling the 3–7 day postpartum BP recheck. Always order "BP check in 3–7 days" and "postpartum visit in 1–2 weeks" — not just the routine 6-week visit. The 6-week-only model is outdated for hypertensive disorders of pregnancy.
— A postictal or altered eclamptic patient cannot consent to cesarean or transfusion. Use substituted judgment (spouse, parent, healthcare proxy) or, in true emergency with fetal/maternal jeopardy, implied consent doctrine permits life-saving intervention.
— Document the urgency, attempts to reach surrogate, and clinical necessity.
— If a competent patient refuses cesarean despite fetal compromise, the patient's autonomy generally prevails — courts have repeatedly ruled against forced cesarean. Engage ethics, social work, and offer continued counseling.
— Do not obtain a court order as a routine — only in extraordinary circumstances and with institutional ethics committee involvement.
— Maternal mortality and severe maternal morbidity events trigger state-level maternal mortality review committee (MMRC) reporting — not provider-initiated typically, but cooperate fully.
— Severe maternal morbidity (massive transfusion, ICU admission, eclampsia) should be flagged in QI systems.
— ED-to-OB triage handoff: ensure magnesium continuity and BP monitoring are explicit.
— Postpartum discharge: early hospital discharge (<48 h after vaginal, <72 h after cesarean) is a high-risk transition for hypertensive disorders. Document 72-h BP follow-up plan, give a home BP cuff, ensure patient has phone access and a clear contact number.
— AIM (Alliance for Innovation on Maternal Health) Severe Hypertension in Pregnancy bundle is a national standard: timely treatment within 30–60 minutes of sustained BP ≥160/110 is a tracked quality metric.
— If treatment delays occur (e.g., severe HTN not treated within 60 min), institutions follow disclosure protocols. Honest, empathic communication is the standard.
Board pearl: A "wrong answer" trap: obtaining court order for emergent cesarean in a refusing competent patient. The correct answer is continued counseling, ethics consult, and respecting autonomy — never force-treat a competent adult.
Key distinction: Magnesium is not an anticonvulsant in the traditional sense — it does not treat status epilepticus from epilepsy. Use benzodiazepines/AEDs for those. In eclampsia, magnesium uniquely outperforms standard anticonvulsants because the mechanism involves cerebral vasospasm and endothelial dysfunction, not epileptogenic foci.
Step 3 management: When in doubt on any pregnant/postpartum seizure stem — magnesium first, BP control second, delivery third, neuroimaging only if atypical. This algorithm answers the majority of eclampsia questions.
Eclampsia is preeclampsia complicated by seizure or unexplained coma in pregnancy through 6 weeks postpartum, and its management hinges on immediate IV magnesium sulfate for seizure control/prevention, rapid IV antihypertensive therapy for sustained BP ≥160/110, and timely delivery as the only definitive cure.
Board pearl: The three highest-yield wrong-answer traps are (1) delaying magnesium to obtain head CT, (2) using phenytoin or lorazepam first-line instead of magnesium, and (3) failing to schedule the 3–7 day postpartum BP follow-up — each of these costs points on Step 3 stems and CCS cases. Master the parallel-order mindset: magnesium, antihypertensive, fetal monitoring, OB consult, labs — all within the first 15 simulated minutes.