› Incidence and global burden
› Incidence 1.6–10 per 10,000 deliveries in developed countries
› Up to 151 per 10,000 in developing countries
› Leading cause of maternal mortality globally
› Temporal distribution
› 50% antepartum
› 50% intrapartum or postpartum (most within 48 hours)
› Demographics and disparities
› Nulliparity is strongest single obstetric risk factor
› Risk decreases in subsequent pregnancies unless chronic risk factors persist
› Black patients have disproportionately higher prevalence and complication rates
› Structural and systemic factors contribute to racial health disparities
› Preeclampsia affects 5–8% of pregnancies; eclampsia develops in 2–3% of severe preeclampsia cases
› Mortality
› Remains a leading cause of maternal morbidity and mortality in both developed and developing settings
› Complications include placental abruption, DIC, pulmonary edema, aspiration pneumonia, cardiopulmonary arrest, acute renal failure, and maternal death
› Long-term sequelae: increased cardiovascular risk, recurrence risk, cognitive effects
› Central nervous system mechanism
› Cerebral vasospasm and loss of autoregulation leading to vasogenic edema
› Manifests as posterior reversible encephalopathy syndrome (PRES) in most cases
› Posterior cerebral regions most vulnerable due to reduced sympathetic innervation
› Seizure threshold lowered by cerebral edema, ischemia, and microhemorrhages
› Not fully explained by hypertension alone
› 20–38% have no prior documented hypertension or proteinuria
› Placental pathophysiology
› Abnormal placentation with inadequate spiral artery remodeling
› Placental ischemia leads to release of anti-angiogenic factors (sFlt-1) and reduced PlGF
› Endothelial dysfunction, vasoconstriction, and organ injury result
› Two-stage model
› Stage 1: abnormal placentation (subclinical)
› Stage 2: maternal systemic inflammatory response and endothelial activation
› End-organ effects
› Renal: glomerular endotheliosis, proteinuria, AKI
› Hepatic: periportal hemorrhage, necrosis (HELLP)
› Hematologic: microangiopathic hemolytic anemia, thrombocytopenia, DIC
› Cardiac: increased afterload, diastolic dysfunction, pulmonary edema
Therapeutic Considerations
› Why magnesium works
› Mechanism not fully elucidated; proposed mechanisms include:
› Cerebral vasodilation reducing ischemic threshold
› N-methyl-D-aspartate (NMDA) receptor antagonism reducing neuronal excitability
› Membrane stabilization
› Superiority established over phenytoin, diazepam, and lytic cocktail in Magpie Trial and Collaborative Eclampsia Trial
› Antihypertensive selection rationale
› Labetalol preferred: combined alpha and beta blockade; rapid, titratable effect
› Avoids reflex tachycardia seen with hydralazine
› Hydralazine: direct arteriolar vasodilator; well-established in obstetric use
› Less predictable response; risk of maternal hypotension
› Nifedipine IR: rapid oral onset; convenient when IV access unavailable
› Evidence does not support avoidance with magnesium, but close BP monitoring required
› Delivery timing evidence
› Delivery at >=37 weeks recommended for all preeclampsia
› At >=34 weeks for severe features (including eclampsia): deliver after stabilization
› Expectant management <34 weeks only in selected patients at tertiary center with maternal stabilization
› Magnesium prophylaxis post-delivery reduces recurrent eclampsia risk
› Long-term cardiovascular risk
› Eclampsia associated with significantly increased lifetime risk of:
› Hypertension, ischemic heart disease, stroke
› Risk persists decades after pregnancy
› Cognitive effects: memory and concentration difficulties reported
› Permanent white matter loss on MRI in up to 25% of patients
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