Mentor: Anita K. Blanchard, MD
Editor: Roger Smith, MD
Eclampsia is a neurological manifestation of preeclampsia defined as new onset generalized tonic-clonic seizures that can result in significant maternal morbidity and death. In recent decades there has been a marked decrease in the incidence of eclampsia, attributable to improved prenatal care, early detection of preeclampsia, and use of peripartum magnesium sulfate prophylaxis. There has been an increase in frequency of postpartum eclampsia, which now accounts for 10 to 44% of all cases of eclampsia. The majority of patients with postpartum eclampsia present with symptoms within a week of delivery.
Delayed diagnosis remains a major obstacle towards treating postpartum preeclampsia, making eclampsia more likely. Early hospital discharge is the norm, so postpartum hypertensive disorders can go unrecognized. In retrospective reviews, the majority of women with postpartum eclampsia cite one or more prodromal symptoms. Headache is the most common symptom, preceding seizure by hours to days before presentation. Additionally, discharge instructions may lack information about the signs, symptoms, and possibility of postpartum preeclampsia and eclampsia. As a result, only one third of these patients seek medical care and when sought it is often from primary or emergency department health care providers who may be less familiar with hypertensive disorders of pregnancy. Moreover, many women who present with postpartum eclampsia have not had signs nor symptoms of preeclampsia pre or intrapartum. The differential diagnoses of postpartum seizures includes hypertensive encephalopathy, cerebrovascular accident, cerebral venous thrombosis, infection, metabolic abnormalities, and drug intoxication or withdrawal.
Eclampsia is diagnosed clinically based on generalized tonic-clonic seizures, which are sometimes accompanied by visual disturbances, headaches, epigastric or right upper quadrant pain and altered mental status. Hyper-reflexia and non-dependent edema may be present. Laboratory abnormalities may include elevated liver transaminases, thrombocytopenia, proteinuria, hypoalbuminemia, and hyperuricemia. Alternatively, laboratory values may be minimally abnormal. Overt proteinuria and severe range blood pressures are less prevalent in late onset postpartum eclampsia, which also may confound the diagnosis. Electroencephalogram has limited value in distinguishing seizures due to eclampsia from other causes. MRI can support the diagnosis and rule out other causes of new onset convulsions. The classic finding is symmetric, extensive vasogenic edema in the parieto-occipital region described as reversible posterior leukoencephalopathy. The posterior cerebral edema is best treated by normalizing blood pressures, diuresis and administering magnesium sulfate. Magnesium sulfate should be continued at least 24 to 48 hours after the last convulsion.
Although it is debatable whether postpartum eclampsia is preventable, improved awareness and heightened surveillance are important measures to identify women with increased risk. Improved patient education with verbal counseling and written discharge information including danger signs and symptoms may impact the incidence of this condition. Extended postpartum medical care for 72 hours and early follow up care within the first 7-10 days in women with hypertensive disorders is advised. Collaborative efforts to improve symptom recognition among primary care providers may promote early intervention.
Al-Safi Z, et al. Delayed postpartum preeclampsia and eclampsia: demographics, clinical course, and complications. Obstet Gynecol. 2011 Nov; 118(5): 1102-7.
Hirshfeld-Cytron J, Lam C, Karumanchi SA, Lindheimer M. Late postpartum eclampsia: examples and review. Obstet Gynecol Surv. 2006 Jul; 61(7):471-80.
ACOG Task Force on Hypertension in Pregnancy. Hypertension in Pregnancy. American College of Obstetricians and Gynecologists, Washington, DC, 2013.
Initial Approval November 2015; Reaffirmed January 2017
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