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Obstetrics and Gynecology · Obstetrics

Eclampsia

Eclampsia

Eclampsia is a severe complication of pregnancy and childbirth, manifested by seizures and developing against the background of preeclampsia. The pathology is accompanied by generalized vasospasm, multiorgan failure, and severe microcirculatory disorders.

Key symptomSeizures during pregnancy, childbirth, or the postpartum period
Pathogenesis basisGeneralized vascular spasm, hypovolemia, and tissue ischemia
Postpartum timingEarly eclampsia — up to 48 hours, late eclampsia — up to 28 days postpartum
Critical stageDirectly precedes eclampsia, including severe markers
3 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Classification and forms of eclampsia

In modern practice, eclampsia is considered within a single pathological continuum with preeclampsia. According to the classification, the following varieties and associated conditions are distinguished:

  • Eclampsia during gestation and childbirth.
  • Early postpartum eclampsia (developing within the first 48 hours).
  • Late postpartum eclampsia (occurring up to 28 days postpartum).
  • Development of pathology against the background of chronic arterial hypertension, which carries an unfavorable prognosis.

Before the manifestation of seizure syndrome, there is typically a critical stage of preeclampsia accompanied by specific symptoms and laboratory shifts.

Pathogenesis and vascular disorders

The development of severe conditions is based on profound placentation disorders and systemic angiopathy:

  1. Suppressed trophoblast invasion: spiral uterine arteries do not undergo the necessary gestational remodeling, retaining their muscle layer and narrow lumen.
  2. Placental ischemia: the lack of vessel dilation leads to reduced intervillous blood flow and primary hypoxia.
  3. Endothelial dysfunction: imbalance of angiogenic factors (decreased PlGF and VEGF against the background of increased sFlt-1) causes damage to the vascular endothelium.
  4. Systemic effects: generalized spasm, hypovolemia, impaired blood rheology and microcirculatory disturbances lead to ischemia and dystrophy of vital organs.
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Clinical variants of preeclampsia

The pathology may present either classically or have masked or atypical forms. Typical preeclampsia with the classic triad of symptoms is distinguished, as well as atypical variants:

  • Blood pressure elevation without concomitant proteinuria.
  • Appearance of protein in the urine against the background of normal blood pressure.
  • Development of generalized edema without hypertension.
  • Appearance of symptoms before the 20th week of pregnancy or their progression after delivery.
  • Combination of a moderate clinical picture with laboratory markers of severe organ damage.

Briefly: answers to topical questions

What symptoms are included in the classic triad of preeclampsia (Zangemeister triad)?

  • Arterial hypertension.
  • Proteinuria.
  • Edema.

What prodromal clinical symptoms are characteristic of the critical stage of preeclampsia?

  • Headache — heaviness in the occipital region and/or headache.
  • Visual disturbances — blurred vision, veil/fog before the eyes, flashing "floaters" or sparks.
  • Nausea and vomiting.
  • Epigastric and right upper quadrant pain — caused by stretching of Glisson's capsule of the liver.
  • Central nervous system symptoms — insomnia, agitation or drowsiness, memory impairment, irritability, lethargy, apathy.
  • Other manifestations — difficulty breathing through the nose, coughing, hypersalivation.

What sequential phases does an eclamptic seizure consist of?

  • First period — introductory (up to 30 s) — fine fibrillar twitching of facial muscles and eyelids.
  • Second period — tonic seizures (10–20 s) — tetanus of all body muscles with cessation of breathing and increasing cyanosis.
  • Third period — clonic seizures (from 30 s to 1.5 min) — continuous clonic seizures spreading from top to bottom.
  • Fourth period — seizure resolution — deep noisy inspiration with snoring, foaming at the mouth, and return of pulse.

Which drug is the first-line agent for halting and preventing seizures in eclampsia?

  • Magnesium sulfate — an agent for terminating and preventing seizures in eclampsia, administered parenterally.

What life-threatening maternal complications develop against the background of multiorgan failure in eclampsia?

  • Brain damage — ischemia, edema, hemorrhage.
  • Renal and hepatic pathology — acute hepato-renal failure.
  • Hemorrhage — massive postpartum hemorrhage.
  • Infectious complications — sepsis.
How to memorize

Eclampsia is an EMERGENCY: Endothelium suffers, Circulation drops, Spasm of vessels everywhere, Seizures on the background of preeclampsia.

Class and exam questions

What are the main periods distinguished in postpartum eclampsia?

Postpartum eclampsia is subdivided into early, which occurs within the first 48 hours after delivery, and late, developing within the subsequent 28 days.

What is the primary link in the pathogenesis of vascular disorders?

The primary link is a defect in cytotrophoblast invasion into the spiral uterine arteries, due to which the vessels do not dilate, retain their muscular layer, and cause placental ischemia.

What factors determine the development of endothelial dysfunction?

Dysfunction develops due to a decrease in the level of pro-angiogenic factors (PlGF, VEGF) and a simultaneous increase in the synthesis of the anti-angiogenic factor sFlt-1 against the background of oxidative stress.

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What else to study on this topic

  • Immunological mechanisms and disruption of maternal tolerance to fetal antigens
  • The role of oxidative stress and free radicals in endothelial damage
  • Comparison of the structure of spiral arteries in normal state, during pregnancy, and in preeclampsia
  • Diagnostic criteria for severe preeclampsia and laboratory markers
  • Features of the course of preeclampsia against the background of chronic arterial hypertension

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