2d:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/0fma7nlq6immz.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/1chr5wkk3j58k.js","/_next/static/immutable/chunks/37kmmh_zm4dov.js","/_next/static/immutable/chunks/311zvdjfxff-f.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js"],"default"] 2e:T6447,

Summary Table

Feature	Detail
Risk Factors	Nulliparity, extremes of maternal age (<20 or >35), prior preeclampsia, chronic hypertension, diabetes mellitus, renal disease, antiphospholipid syndrome, multiple gestation, obesity, family history of preeclampsia
Etiology	New-onset tonic-clonic seizures in a patient with preeclampsia, caused by cerebral vasospasm and endothelial dysfunction of placental origin
Patient Presentation	Pregnant or recently postpartum woman with seizures, typically preceded by headache, visual disturbances (blurred vision, scotomata), right upper quadrant or epigastric pain, and hyperreflexia
Classic Physical Exam	Hypertension (often severe, blood pressure greater than or equal to 160/110 mmHg), generalized edema, hyperreflexia with clonus, altered mental status during or after seizure
Key Diagnostic Results	Proteinuria (protein/creatinine ratio greater than or equal to 0.3), elevated liver transaminases, thrombocytopenia, elevated uric acid, elevated LDH; cerebral imaging reserved for atypical cases
Management	Magnesium sulfate for seizure control and prevention, antihypertensives (IV labetalol or IV hydralazine) for severe hypertension, and delivery as the definitive treatment
Keywords	"Pregnant woman with seizures," "headache and visual changes in third trimester," "hyperreflexia with clonus," "magnesium sulfate," "seizure in postpartum period"

1. Pathophysiology

Eclampsia arises from the same underlying disease process as preeclampsia: abnormal placentation. During normal pregnancy, cytotrophoblasts invade the spiral arteries of the uterus and remodel them into low-resistance, high-capacity vessels. In preeclampsia, this remodeling fails. The spiral arteries remain narrow and high-resistance, leading to chronic placental ischemia.

The ischemic placenta releases a cascade of antiangiogenic factors, most notably soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin. These factors antagonize vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), creating a state of systemic endothelial dysfunction. This is why the disease does not confine itself to the uterus but instead damages the vasculature of the kidneys (proteinuria), liver (elevated transaminases, capsular distension causing RUQ pain), and brain.

The progression from preeclampsia to eclampsia reflects cerebral involvement. Severe hypertension overwhelms cerebral autoregulation, causing vasogenic edema in the posterior cerebral circulation. This is the same mechanism seen in posterior reversible encephalopathy syndrome (PRES), and indeed, MRI in eclamptic patients frequently shows PRES-pattern white matter changes in the parieto-occipital regions. The vasospasm and blood-brain barrier breakdown lower the seizure threshold, producing the tonic-clonic seizures that define eclampsia.

This pathophysiology directly explains the prodromal symptoms: headache reflects rising intracranial pressure and vasospasm, visual disturbances (scotomata, blurred vision, cortical blindness) reflect occipital lobe edema, and hyperreflexia with clonus reflects upper motor neuron irritability from cerebral edema. The presence of these symptoms in a preeclamptic patient signals impending eclampsia and should prompt immediate treatment with magnesium sulfate.

An important conceptual point: eclampsia can occur antepartum (most common, roughly 50%), intrapartum (roughly 25%), or postpartum (roughly 25%). Postpartum eclampsia most commonly develops within 48 hours of delivery but can occur up to 4 to 6 weeks postpartum. This means a vignette describing a woman who seizes days after delivery with no prior seizure history should immediately raise suspicion for late postpartum eclampsia.

2. Classification and Clinical Manifestation

Eclampsia itself is not traditionally subdivided into formal subtypes, but it is best understood as one point on the spectrum of hypertensive disorders of pregnancy. The table below contextualizes eclampsia within that spectrum and highlights how presentation differs at each stage.

Condition	Blood Pressure	Proteinuria	Distinguishing Features
Gestational Hypertension	Greater than or equal to 140/90 mmHg after 20 weeks	Absent	Hypertension alone without end-organ damage; may progress to preeclampsia
Preeclampsia without Severe Features	Greater than or equal to 140/90 mmHg after 20 weeks	Present (protein/creatinine ratio greater than or equal to 0.3)	Hypertension plus proteinuria or other end-organ criteria, but without severe-range values
Preeclampsia with Severe Features	Greater than or equal to 160/110 mmHg on two occasions 4 hours apart	May or may not be present	Any one of: severe-range BP, platelets < 100,000, liver transaminases more than twice the upper limit of normal, creatinine > 1.1, pulmonary edema, cerebral or visual symptoms
Eclampsia	Usually severely elevated, but can occur at any BP	Usually present	New-onset tonic-clonic seizures in the setting of preeclampsia with no other identifiable cause
HELLP Syndrome	Variable	Variable	Hemolysis (elevated LDH, schistocytes, low haptoglobin), Elevated Liver enzymes, Low Platelets; can coexist with eclampsia

A high-yield exam point: eclampsia is diagnosed clinically based on the occurrence of seizures in a preeclamptic patient (or a patient with features consistent with preeclampsia) after excluding other causes such as epilepsy, cerebral venous thrombosis, intracranial hemorrhage, or metabolic derangements. Notably, some patients present with eclampsia as their first manifestation, meaning they had no previously documented hypertension or proteinuria. Up to 20% of eclamptic patients may have blood pressure below 140/90 at the time of seizure. This is a classic exam trap.

3. Diagnostic Workup

Test	Role	Key Findings
Blood pressure measurement	Best initial assessment	Greater than or equal to 140/90 confirms hypertension; greater than or equal to 160/110 defines severe range
Urinalysis / Urine protein-creatinine ratio	Screening for proteinuria	Ratio greater than or equal to 0.3, or dipstick 1+ or greater
24-hour urine protein	Confirmatory for proteinuria (if time permits)	Greater than or equal to 300 mg/24 hours
CBC with peripheral smear	Evaluate for HELLP or DIC	Thrombocytopenia (< 100,000), schistocytes, low haptoglobin
Liver function tests (AST, ALT)	End-organ damage assessment	Elevated to more than twice the upper limit of normal
Serum creatinine	Renal function	> 1.1 mg/dL or doubling of baseline
LDH	Hemolysis marker	Elevated in HELLP syndrome
Uric acid	Supportive marker	Often elevated in preeclampsia, though not diagnostic alone
Coagulation panel (PT, aPTT, fibrinogen)	Evaluate for DIC	Prolonged PT/aPTT, low fibrinogen if DIC develops
MRI brain	Reserved for atypical presentations	PRES pattern (posterior white matter vasogenic edema); not routinely required
CT head	Exclude hemorrhage or other structural lesion	Used when seizure presentation is atypical or focal neurological deficits are present

Eclampsia is fundamentally a clinical diagnosis. When a pregnant or recently postpartum woman presents with new-onset generalized tonic-clonic seizures and features of preeclampsia, the diagnosis is eclampsia until proven otherwise. There is no single confirmatory laboratory test that "rules in" eclampsia. Instead, the workup serves two purposes: (1) confirming the underlying preeclamptic state and assessing its severity, and (2) excluding alternative diagnoses.

The best initial step when a pregnant woman seizes is to stabilize the patient (protect airway, lateral decubitus position to prevent aspiration, ensure IV access) and administer magnesium sulfate. Laboratory evaluation follows and should include a CBC, metabolic panel, liver enzymes, LDH, coagulation studies, and urine protein assessment. These results help determine whether HELLP syndrome is present and guide further management.

Neuroimaging is not routinely required in a straightforward eclamptic presentation. However, if the seizure is focal, if there are persistent neurological deficits after the postictal period, if seizures recur despite adequate magnesium levels, or if the presentation occurs at an unusual time (e.g., very early in pregnancy or very late postpartum), then CT or MRI of the brain becomes necessary to exclude cerebral venous sinus thrombosis, intracranial hemorrhage, or a space-occupying lesion.

The serum magnesium level becomes important after treatment has started: the therapeutic range is 4 to 7 mEq/L. Loss of deep tendon reflexes occurs at roughly 7 to 10 mEq/L, respiratory depression at 10 to 13 mEq/L, and cardiac arrest at levels exceeding 15 mEq/L. Monitoring DTRs, respiratory rate, and urine output is the clinical bedside method for detecting magnesium toxicity.

4. Management and Treatment

Phase	Intervention	Details
Immediate seizure control	Magnesium sulfate	Loading dose: 4 to 6 g IV over 15 to 20 minutes. Maintenance: 1 to 2 g/hour continuous IV infusion
Recurrent seizure	Additional magnesium bolus	2 g IV over 3 to 5 minutes; if refractory, consider lorazepam or phenytoin
Severe hypertension control	IV labetalol or IV hydralazine	Labetalol: 20 mg IV bolus, then escalate (40 mg, then 80 mg) every 10 to 15 minutes (maximum 300 mg). Hydralazine: 5 to 10 mg IV every 15 to 20 minutes. Alternative: oral nifedipine 10 mg
BP target	Reduce to < 160/110	Goal is to prevent hypertensive encephalopathy and hemorrhagic stroke without causing uteroplacental hypoperfusion
Definitive treatment	Delivery	The only cure for the underlying disease process; timing depends on gestational age and maternal-fetal status
Postpartum continuation	Magnesium sulfate for 24 to 48 hours after delivery or after the last seizure (whichever is later)	Continue monitoring DTRs, respiratory rate (must remain greater than or equal to 12/min), and urine output (must remain greater than or equal to 30 mL/hour)
Magnesium toxicity antidote	Calcium gluconate	10 mL of 10% calcium gluconate IV over 3 minutes; keep at bedside whenever magnesium is infusing

When a pregnant or postpartum patient presents actively seizing, the first action is to ensure maternal safety: protect the airway, position the patient in the left lateral decubitus position (prevents aspiration and optimizes uteroplacental perfusion), and secure IV access.

The next best step is administration of magnesium sulfate. This is the single most tested point about eclampsia management. Magnesium sulfate is superior to diazepam and phenytoin for both treatment and prevention of eclamptic seizures (established by the landmark Magpie and Eclampsia trials). The loading dose is 4 to 6 g IV over 15 to 20 minutes, followed by a continuous infusion of 1 to 2 g/hour. If the patient has a recurrent seizure despite the loading dose, an additional 2 g IV bolus can be given over 3 to 5 minutes.

Simultaneously, if the blood pressure is in the severe range (greater than or equal to 160/110), acute antihypertensive therapy must be initiated. The goal is not normalization but reduction to below 160/110 to prevent hemorrhagic stroke. IV labetalol is commonly used first-line: start with 20 mg IV, then escalate to 40 mg, then 80 mg at 10 to 15 minute intervals if needed, up to a cumulative maximum of 300 mg. IV hydralazine (5 to 10 mg every 15 to 20 minutes) is an alternative. Oral nifedipine (10 mg) is a third option if IV access is delayed.

Delivery is the definitive treatment. After maternal stabilization (seizure control, blood pressure management), the decision to deliver depends on gestational age. In eclampsia specifically, delivery is indicated regardless of gestational age once the mother is stabilized, because the disease poses ongoing risk of recurrent seizures, stroke, placental abruption, and maternal death. If the fetus is viable and the gestational age is at or beyond 34 weeks, delivery should proceed promptly. Even before 34 weeks, delivery is indicated after stabilization because the maternal risk of continuing the pregnancy outweighs the benefit of fetal maturity in the setting of eclampsia.

Vaginal delivery is preferred if the cervix is favorable and there are no obstetric contraindications. Cesarean section is reserved for standard obstetric indications (e.g., non-reassuring fetal status, failed induction, malpresentation).

Magnesium sulfate infusion should continue for 24 to 48 hours postpartum (or 24 hours after the last seizure, whichever is later). During this period, clinical monitoring is essential: check deep tendon reflexes hourly (loss of DTR is the earliest sign of magnesium toxicity), ensure respiratory rate remains at or above 12 breaths per minute, and confirm urine output is at least 30 mL/hour (magnesium is renally excreted, so oliguria raises toxicity risk). If toxicity is suspected, stop the infusion immediately and administer calcium gluconate 10 mL of 10% solution IV over 3 minutes.

A contraindication note: magnesium must be used with extreme caution in patients with renal impairment, as the drug depends on renal clearance. In such patients, the maintenance dose should be reduced (typically to 1 g/hour) and serum magnesium levels should be monitored directly.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Epilepsy	Tonic-clonic seizures in a pregnant woman	Pre-existing seizure history, normal blood pressure, absence of proteinuria, therapeutic anticonvulsant levels; eclampsia is a diagnosis of exclusion only when epilepsy has been ruled out
Cerebral venous sinus thrombosis (CVST)	Seizures and headache in pregnancy/postpartum; pregnancy is a hypercoagulable state	Focal neurological deficits, papilledema, CT venography or MR venography showing thrombus in the dural sinuses; blood pressure may not be severely elevated
Intracranial hemorrhage	Severe headache, seizure, altered consciousness	Sudden onset of worst headache, focal neurological signs (hemiparesis, cranial nerve palsies), CT head showing acute hemorrhage; can coexist with eclampsia as a complication
HELLP Syndrome	Overlaps with severe preeclampsia; presents with RUQ pain, nausea, thrombocytopenia	HELLP is defined by the triad of hemolysis (elevated LDH, schistocytes), elevated liver enzymes, and low platelets; it can occur with or without seizures; eclampsia requires seizures by definition
Thrombotic thrombocytopenic purpura (TTP)	Thrombocytopenia, neurological symptoms, renal dysfunction in pregnancy	Pentad: microangiopathic hemolytic anemia, thrombocytopenia, neurological changes, renal dysfunction, fever; severely deficient ADAMTS13 activity (< 10%); blood pressure often not as severely elevated
Posterior reversible encephalopathy syndrome (PRES) from other causes	Seizures, headache, visual disturbances, posterior white matter edema on MRI	PRES can be caused by hypertensive emergency of any etiology, immunosuppressant use (cyclosporine, tacrolimus), or renal failure; the clinical context (pregnancy, proteinuria) distinguishes eclampsia
Meningitis/Encephalitis	Seizures, headache, altered mental status	Fever, nuchal rigidity, photophobia, CSF analysis showing pleocytosis; no hypertension or proteinuria

6. Traps and High-Yield Pearls

The most common way students get eclampsia questions wrong falls into a few predictable patterns.

Trap 1: Choosing the wrong anticonvulsant. When a pregnant woman seizes, the reflexive temptation is to reach for a benzodiazepine (lorazepam, diazepam) or phenytoin, because these are the standard drugs for status epilepticus in the general population. In eclampsia, the correct answer is always magnesium sulfate first. This holds true for both seizure treatment and seizure prophylaxis in severe preeclampsia. The only time benzodiazepines or phenytoin enter the picture is when seizures are refractory to magnesium.

Trap 2: Assuming eclampsia requires severe hypertension. A vignette may describe a woman at 36 weeks with a blood pressure of 145/92, mild proteinuria, headache, and then a seizure. Students may hesitate to call this eclampsia because the blood pressure is not in the severe range. Remember: up to 20% of eclamptic patients have blood pressures below 140/90 at the time of seizure. The seizure itself, in the context of any features of preeclampsia, is what makes the diagnosis.

Trap 3: Forgetting postpartum eclampsia. A woman presents 3 days after an uncomplicated delivery with new-onset seizures, headache, and elevated blood pressure. Students often fail to consider eclampsia because the pregnancy is "over." Postpartum eclampsia is real and is managed identically: magnesium sulfate, blood pressure control, and monitoring.

Trap 4: Not recognizing magnesium toxicity. A follow-up question may describe a patient on magnesium infusion who develops loss of deep tendon reflexes and a respiratory rate of 10. The next best step is to stop the magnesium infusion and administer IV calcium gluconate. Students who do not monitor the clinical signs of toxicity (DTR, respiratory rate, urine output) will miss this.

Trap 5: Delaying delivery. In preeclampsia without severe features before 37 weeks, expectant management may be appropriate. In eclampsia, however, delivery is indicated after maternal stabilization regardless of gestational age. A question that tempts you to "continue pregnancy and monitor" in a patient who has already seized is testing whether you understand that eclampsia mandates delivery.

The core competency being tested is the ability to recognize eclampsia across variable presentations (including atypical blood pressure, postpartum timing, and overlap with HELLP), to prioritize magnesium sulfate as the cornerstone of management, and to understand that delivery is the definitive treatment once the mother is stabilized.

1e:["$","$L2d",null,{"article":{"id":"93a4b1d6-5da1-4e35-8dae-77cec6f8f288","title":"Eklamsia","content":"$2e","category":"Reproduksi","created_at":"2026-05-16T09:38:19.18721+00:00","status":"published","subcategory":null},"questionCount":2,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]