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Pregnancy, Eclampsia
Updated: Sep 28, 2006
Introduction
Background
Preeclampsia is a hypertensive disorder of pregnancy associated with proteinuria with or without edema. If hypertension and proteinuria are complicated by seizures or coma, the condition is known as eclampsia.
Pathophysiology
Eclampsia develops after the 20th week of gestation and is considered a complication of severe preeclampsia. The progression from severe preeclampsia to seizures and coma is thought to be due to hypertensive encephalopathy, vasogenic edema associated cortical ischemia, edema, or hemorrhage.
The cause of preeclampsia and later eclampsia remains unclear. Genetic, immunologic, endocrine, nutritional, and perhaps infectious agents also likely have a role in this complex process. Current research implicates uterine and placental ischemia and the subsequent release of humoral agents resulting in widespread vasoconstriction. The direct cause of the defining seizure activity of eclampsia remains unknown. Cerebral ischemia, infract, hemorrhage, and edema have all been known to occur in patients with edema, evidenced by MRI and by autopsy. Research evidence of endothelial damage in the uterus and placenta with resulting edema suggests a similar secondary central nervous system (CNS) event, but a unifying theory remains elusive.
Eclampsia is a clinical diagnosis with patients having seizures without evidence for CNS, metabolic, or other etiology of the seizure activity. Most patients have systolic BPs higher than 160 mm Hg or diastolic BPs higher than 110 mm Hg and proteinuria; however, eclampsia can occur with minimally elevated BP or elevated related to baseline and without proteinuria. Evidence of end-organ damage prior to development of seizures is common; symptoms include altered mental status; headache; visual disturbances; and abdominal pain; and signs include hemoconcentration; hemolysis, impaired liver function with elevated liver enzyme levels, and thrombocytopenia (HELLP); proteinuria; oliguria; pulmonary edema; generalized peripheral edema; microangiopathic hemolytic anemia; and fetal growth retardation.
Specific laboratory studies, invasive monitoring, and biopsy may show evidence of altered cardiovascular and pulmonary dynamics, hematologic alterations and coagulopathy, and multisystem cellular damage.
Eclampsia is most common during the antepartum period, yet 20-25% of cases occur during the postpartum period. Although postpartum eclampsia may occur as long as 3 weeks postpartum, most cases (98%) occur on the first postpartum day. Eclampsia is not the cause of seizures that occur during the first trimester or well into the postpartum period. These seizures are suggestive of CNS pathology.
The following are considered risk factors for development of preeclampsia preceding eclampsia: extremes of maternal age, primigravida, multiple gestations, molar pregnancy, preexisting hypertension, diabetes mellitus or renal disease, preexisting connective tissue or vascular disease, fetal growth restriction, genetic factors, prior history of preeclampsia or eclampsia, and family history of preeclampsia or eclampsia.
Frequency
United States
Eclampsia complicates approximately 0.05-0.2% of all pregnancies.
Mortality/Morbidity
- The most significant maternal complications of eclampsia are related to permanent CNS damage secondary to recurrent seizures or intracranial bleeding. The maternal mortality rate is 8-36%
- The definitive treatment for eclampsia is delivery of the fetus. Premature delivery and its complications often contribute to the fetal mortality rate of 13-30%. Placental infarcts, abruptio placentae, and intrauterine growth retardation also contribute to fetal demise.
- Mortality rates vary according to the level of care provided by the medical center. Patients must be treated in a facility that offers high-risk obstetric care.
Age
Eclampsia usually occurs in patients at both extremes of reproductive age; however, the risk of eclampsia is greatest in women younger than 20 years.
Clinical
History
- Most eclampsia patients present with hypertension and seizures, with some combination of proteinuria and edema.
- The natural progression of the disease is from symptomatic severe preeclampsia (differentiated from preeclampsia by specific vital signs, symptoms, and laboratory abnormalities) to seizures.
- Features include the following:
- Seizure or postictal state (100%)
- Headache (80%)
- Generalized edema (50%)
- Vision disturbance (40%)
- Abdominal pain with nausea (20%)
- Amnesia and other mental status changes
Physical
Findings at physical examination may include the following:
- Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg
- Tachycardia
- Tachypnea
- Rales
- Mental status changes
- Hyperreflexia
- Clonus
- Papilledema
- Oliguria or anuria
- Localizing neurologic deficits
- Right upper quadrant (RUQ) or epigastric abdominal tenderness
- Generalized edema
- Small fundal height for the estimated gestational age
- Apprehension
Causes
- The etiology of eclampsia is not fully understood.
- Animal modes have suggested dysfunction of the uteroplacental bed related to altered endothelial and angiogenic factors and vascular implantation. This results in decreased uteroplacental perfusion pressure and ischemia and subsequent release of cytokines and reactive oxygen species. The effect is sympathetic and neurohormonal dysregulation of blood pressure, generalized vasoconstriction, and cellular and organ system dysfunction.
- Other causes may include the following:
- Altered cardiovascular reactivity
- Increased capillary permeability
- Widespread vasospasm
- Microthrombi
- Hypertension
- Improper implantation of the placenta
- Risk factors include the following:
- Prior preeclampsia and eclampsia, familial incidence (Paternal and maternal inheritance, HLA, angiotensinogen gene, and altered endothelial function have all been implicated.)
- Obesity, chronic hypertension, renal disease, thrombophilias, vascular and connective tissue disorders, gestational diabetes, and systemic lupus erythematosus
- Multiple fetuses, hydatid mole, fetal hydrops
- Primigravida, teenaged patient or patient older than 35 years, lower socioeconomic status
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References
ACOG. ACOG Practice Bulletin: Diagnosis and Management of Preeclampsia and Eclampsia: The American College of Obstetricians and Gynecologists Number 33. Jan 2002.
Abbott J. Complications related to pregnancy. In: Emergency Medicine: Concepts and Clinical Practice. 3rd ed. 1992:1984-7.
Brady WJ, DeBehnke DJ, Carter CT. Postpartum toxemia: hypertension, edema, proteinuria and unresponsiveness in an unknown female. J Emerg Med. Sep-Oct 1995;13(5):643-8. [Medline].
Coomarasamy A, Honest H, Papaioannou S. Aspirin for prevention of preeclampsia in women with historical risk factors: a systematic review. Obstet Gynecol. Jun 2003;101(6):1319-32. [Medline].
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Hals G, Crump T. The pregnant patient: guidelines for management of common life-threatening medical disorders in the emergency department. Emerg Med Rep. Mar 13 2000;21(6):57-9.
Hansen WF. Problems in pregnancy. In: Emergency Medicine: A Comprehensive Study Guide. 4th ed. 1996: 573.
Moussouttas M, Abubakr A, Grewal RP. Eclamptic subarachnoid haemorrhage without hypertension. J Clin Neurosci. May 2006;13(4):474-6. [Medline].
Rivers EP. Preeclampsia, eclampsia, and other hypertensive disorders of pregnancy. In: The Clinical Practice of Emergency Medicine. 2nd ed. 1996: 315-21.
Robinson CJ, Johnson DD, Chang EY. Evaluation of placenta growth factor and soluble Fms-like tyrosine kinase 1 receptor levels in mild and severe preeclampsia. Am J Obstet Gynecol. Jul 2006;195(1):255-9. [Medline].
Stennett AK, Khalil RA. Neurovascular mechanisms of hypertension in pregnancy. Curr Neurovasc Res. May 2006;3(2):131-48. [Medline].
Which anticonvulsant for women with eclampsia?. Evidence from the Collaborative Eclampsia Trial. Lancet. Jun 10 1995;345(8963):1455-63. [Medline].
Further Reading
Keywords
eclampsia, hypertension of pregnancy, seizures in pregnancy, toxemia of pregnancy, coma in pregnancy, preeclampsia, hypertensive disorder, proteinuria
