eMedicine Specialties > Obstetrics and Gynecology > Obstetrical Complications

Eclampsia

Author: Michael G Ross, MD, MPH, Professor of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles; Professor, Department of Community Health Sciences, University of California at Los Angeles School of Public Health; Chair, Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center
Contributor Information and Disclosures

Updated: Apr 1, 2009

Introduction

Background

Eclampsia is commonly defined as new onset of grand mal seizure activity and/or unexplained coma during pregnancy or postpartum in a woman with signs or symptoms of preeclampsia. Nonetheless, eclampsia in the absence of hypertension with proteinuria has been demonstrated to occur in 38% of cases reported in the United Kingdom.1 Similarly, hypertension was absent in 16% of cases reviewed in the United States.2

Most cases of eclampsia present in the third trimester of pregnancy, with about 80% of eclamptic seizures occurring intrapartum or within the first 48 hours following delivery. Rare cases have been reported prior to 20 weeks' gestation or as late as 23 days’ postpartum. Other than early detection of preeclampsia, no reliable test or symptom complex predicts the development of eclampsia. In developed countries, most of recent reported cases have been classified as unpreventable.

Pathophysiology

Many investigators have proposed factors relating to genetics, immunology, endocrinology, nutrition, and infection as possible etiologies leading to the development of preeclampsia/eclampsia. Despite extensive research, no definitive cause for preeclampsia has been identified (see eMedicine article Preeclampsia). The pathogenesis of eclamptic seizures may include mechanisms of cerebral vasoconstriction, hypertensive encephalopathy, cerebral edema, hemorrhage, and infarction. Whether these findings are causes or results of seizure activity is unclear.

Preeclampsia/eclampsia produces multiple systemic derangements that can involve a diversity of organ systems including hematologic, hepatic, renal, and cardiovascular systems as well as the central nervous system. The severity of these derangements often correlates with maternal medical (eg, pre-existing renal or vascular pathology) or obstetric factors (eg, multifetal gestations or molar pregnancy).

Systemic derangements associated with eclampsia can include the following:

  • Cardiovascular 
    • Generalized vasospasm
    • Increased peripheral vascular resistance
    • Increased left ventricular stroke work index
    • Decreased central venous pressure
    • Decreased pulmonary wedge pressure
  • Hematologic
    • Decreased plasma volume
    • Increased blood viscosity
    • Hemoconcentration
    • Coagulopathy
  • Renal
    • Decreased glomerular filtration rate
    • Decreased renal plasma flow
    • Decreased uric acid clearance
  • Hepatic
    • Periportal necrosis
    • Hepatocellular damage
    • Sub capsular hematoma
  • Central nervous system
    • Cerebral over perfusion due to loss of autoregulation
    • Cerebral edema
    • Cerebral hemorrhage

Frequency

United States

Primigravid and multifetal pregnancies as well as pregnancies in women without access to prenatal care have been identified as having an increased frequency of eclampsia. In the United States, some studies have identified an increased frequency in African Americans and in women with pre-existing cardiovascular or renal complications.3

International

The incidence of eclampsia varies between and within countries. Overall, the rate of eclampsia is higher in developing countries. The highest rate was reported in Columbia (8.1/1000) and the lowest rate was reported in the United Kingdom (0.49/1000 deliveries).4 In the developed world, the reported incidence of eclampsia ranges from 1 in 1,000 to 1 in 3,448 pregnancies.1,3

Mortality/Morbidity

Eclampsia accounts for approximately 50,000 maternal deaths worldwide annually. In developed countries, the maternal death rate has been reported as 0-1.8%. A CDC study found an overall preeclampsia-eclampsia case-fatality rate of 6.4 per 10,000 cases at delivery with a rate twice as high for black women compared with white women. This same study found an increased risk of death among women older than 30 years and those with no prenatal care. The highest risk for maternal death was found in pregnancies at 28 weeks’ gestation or less. The maternal mortality rate is as high as 14% in developing countries.5 The perinatal mortality rate from eclampsia in recent reviews in the United States and Great Briton ranges from 5.6-11.8%.1,6

Maternal complications of eclampsia may include permanent CNS damage from recurrent seizures or intracranial bleeds, disseminated intravascular coagulopathy, renal insufficiency, pulmonary edema, and cardiopulmonary arrest.

Causes of neonatal death include prematurity, placental infarcts, intrauterine growth retardation, abruptio placentae, and fetal hypoxia.

Race

Ethnic or racial predilections are unclear. A higher incidence of this condition may exist in African Americans.

Sex

Only females are affected.

Age

Recent reviews confirm both an increase in frequency of preeclampsia/eclampsia and severity of complications (including an increased mortality) risk in older gravidas, especially women aged 40 years or older. Previously reported increased risk in younger women has not been found in recent reviews.

Clinical

History

  • Eclampsia is defined by tonic-clonic seizure activity (focal or generalized) or unexplained coma.
  • Frequency of signs or symptoms prior to seizure include the following:
    • Headache (83%)
    • Hyperactive reflexes (80%)
    • Marked proteinuria (52%)
    • Generalized edema (49%)
    • Visual disturbances (44%)
    • Right upper quadrant pain or epigastric pain (19%)
  • Absence of signs or symptoms prior to seizure include the following:
    • Lack of edema (39%)
    • Absence of proteinuria (21%)
    • Normal reflexes (20%)
  • Relation to delivery
    • More than 70% occur prior to delivery.
    • 25% occur before labor (antepartum).
    • 50% occur during labor (intrapartum).
    • 25% occur after delivery (postpartum).
  • Patients with severe preeclampsia are at greater risk to develop seizures.
  • 25% of patients have symptoms consistent with mild preeclampsia prior to the seizures.

Physical

  • Eclamptic seizure
    • One or more seizures may occur.
    • Seizures generally last 60-75 seconds.
    • The face initially may become distorted with protrusion of the eyes.
    • Foaming at the mouth may occur.
    • Respiration ceases for the duration of the seizure.
  • The seizure may be divided into 2 phases:
    • Phase 1 lasts 15-20 seconds and begins with facial twitching. The body becomes rigid, leading to generalized muscular contractions.
    • Phase 2 lasts about 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence.
  • A coma or a period of unconsciousness follows phase 2.
    • Unconsciousness lasts for a variable period.
    • Following the coma phase, the patient may regain some consciousness.
    • The patient may become combative and very agitated.
    • The patient has no recollection of the seizure.
  • A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apneic phase.
  • Seizure-induced complications may include tongue biting, head trauma, broken bones, or aspiration.

Causes

The cause of the seizures is not clear, although several processes have been implicated in their development.

  • Areas of cerebral vasospasm may be severe enough to cause focal ischemia, which may in turn lead to seizures.
  • Pathologic alterations in cerebral blood flow and tissue edema induced by vasospasm may result in headaches, visual disturbances, and hypertensive encephalopathy, resulting in a seizure.

More on Eclampsia

Overview: Eclampsia
Differential Diagnoses & Workup: Eclampsia
Treatment & Medication: Eclampsia
Follow-up: Eclampsia
References

References

  1. Douglas KA, Redman CW. Eclampsia in the United Kingdom. BMJ. Nov 26 1994;309(6966):1395-400. [Medline].

  2. Mattar, F, Sibai BM. Eclampsia. VIII. Risk Factors for maternal morbidity. Am J Obstet Gynecol. 1990;163:1049-55.

  3. Zhang J, Meikle S, Trumble A. Severe maternal morbidity associated with hypertensive disorders in pregnancy in the United States. Hypertens Pregnancy. 2003;22(2):203-12. [Medline].

  4. Sahin, G. Incidence, morbidity and mortality of pre-eclampsia and eclampsia. Available at www.gfmer.ch/Endo/Course2003/eclampsia.htm. Accessed February 18, 2009.

  5. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. Feb 2005;105(2):402-10. [Medline].

  6. Sibai BM, Sarinoglu C, Mercer BM. Eclampsia. VII. Pregnancy outcome after eclampsia and long-term prognosis. Am J Obstet Gynecol. Jun 1992;166(6 Pt 1):1757-61; discussion 1761-3. [Medline].

  7. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol. Apr 2001;97(4):533-8. [Medline].

  8. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. Jul 27 1995;333(4):201-5. [Medline].

Further Reading

Keywords

eclampsia, seizures in pregnancy, toxemia of pregnancy, coma in pregnancy, preeclampsia, cerebral vasospasm, focal ischemia, hypertensive encephalopathy

Contributor Information and Disclosures

Author

Michael G Ross, MD, MPH, Professor of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles; Professor, Department of Community Health Sciences, University of California at Los Angeles School of Public Health; Chair, Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center
Michael G Ross, MD, MPH is a member of the following medical societies: American Association for the Advancement of Science, American College of Obstetricians and Gynecologists, American Federation for Clinical Research, American Gynecological and Obstetrical Society, American Physiological Society, American Public Health Association, Association of Professors of Gynecology and Obstetrics, Perinatal Research Society, Phi Beta Kappa, Society for Gynecologic Investigation, Society for Maternal-Fetal Medicine, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Bruce A Meyer, MD, MBA, Vice President for Medical Affairs, Associate Dean for Health System Affairs and Director of the Faculty Practice Plan, Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School
Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Antonio V Sison, MD, Medical Director, Ob/Gyn Group, Robert Wood Johnson University Hospital at Hamilton
Antonio V Sison, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and Association of Professors of Gynecology and Obstetrics
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

David Chelmow, MD, Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Program Director, Tufts University Affiliated Hospitals OB/GYN Residency Program; Chair, Tufts University Health Sciences Campus Institutional Review Board; Vice Chair for Research and Education, Dept of OB/GYN, Tufts Medical Center
David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical Decision Making
Disclosure: Nothing to disclose.

 
 
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