Quick facts on eclampsia
Incidence
- The maternal death rate for eclampsia varies geographically, according to the quality of the area’s health-care system. In developed countries, the rate ranges from 1.8% to 7.2%, while in countries with less available medical care, it can exceed 25%.1-3
- Although the maternal mortality rate for preeclampsia is lower (approximately 0.34% in the United States) than for eclampsia, preeclampsia still accounts for more than half of the maternal deaths linked to pregnancy “toxemia.”3,4
- Eclampsia-associated perinatal mortality remains high—about 10%—even in developed countries.
Risk of eclampsia
- Eclampsia usually involves reversible cerebral edema and endangers the mother principally through seizure-related aspiration (2%) or underlying disturbances such as acute renal failure (5%), pulmonary edema (4%), cardiorespiratory arrest (3%), and abruptio placentae.5,6
- Eclamptic seizures also carry the risk of permanent brain injury or death when they are associated with hemorrhagic or ischemic stroke or with tentorial herniation.
- Recurrent seizures—in which prolonged activation of N-methyl-D-aspartate receptors can produce toxic brain levels of calcium—also may lead to permanent injury and death.
- About 7% of eclamptic women develop significant neurologic sequelae, including aphasia, psychosis, cortical blindness, weakness, coma, or cerebrovascular accident.7
- More than half of eclamptic women who die within 48 hours after the onset of convulsions have cerebral petechiae, hemorrhage, or ischemic softening (nonhemorrhagic) of the brain,8 which may result from thrombosis of cerebral vessels9 or other complications of cerebral vasospasm.8,10
- Necrosis of the walls and endothelium of precapillary arterioles also can occur.
- Cerebral edema in gross specimens has not been a consistent finding at autopsy.8,11 Although this seems to run counter to expectations, a detailed microscopic analysis of the brain would be necessary to identify focal edema affecting a small brain sector.
REFERENCES
1. Douglas KA, Redman CWG. Eclampsia in the United Kingdom. BMJ. 1994;309:1395-1400.
2. Majoko F, Mujaji C. Maternal outcome in eclampsia at Harare Maternity Hospital. Cent Afr J Med. 2001;47:123-128.
3. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol. 2001;97:533-538.
4. The Magpie Trial Collaborative Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359:1877-1890.
5. Lawson J. Complications of eclampsia: Abruptio placentae, cardiac failure, renal failure, hyperpyrexia, uncontrollable fits, prolonged coma. Clinics Obstet Gynaecol. 1982;9:711-721.
6. Usta IM, Sibai BM. Emergent management of puerperal eclampsia. Obstet Gynecol Clin N Am. 1995;22:315-333
7. Usta IM, Sibai BM. Emergent management of puerperal eclampsia. Obstet Gynecol Clin N Am. 1995;22:315-333.
8. Sheehan JL, Lynch JB. Pathology of Toxaemia of Pregnancy. London: Churchill Livingston; 1973;524-582.
9. McKay DG. Clinical significance of the pathology of toxemia of pregnancy. Circulation. 1964;30(suppl 2):66-75.
10. Will AD, Lewis KL, Hinshaw DB, Jr, et al. Cerebral vasoconstriction in toxemia. Neurology. 1987;37:1555-1557.
11. Hibbard LT. Maternal mortality due to acute toxemia. Obstet Gynecol. 1973;42:263-270.
Give magnesium to all preeclamptic patients to be delivered
Clinical symptoms and signs are unreliable predictors of which pregnant women will develop seizures. For example, eclampsia can occur in gravidas without hypertension or proteinuria. When these conditions are present, the risk of eclampsia is not proportional to their severity.1,17-20 Thus, given the relative safety of magnesium therapy with appropriate monitoring, a reasonable approach is to initiate therapy at the time of diagnosis in all preeclamptic patients who are to be delivered.
If all clinicians followed this management approach, about 5% of gravidas would receive therapy to prevent a rare but potentially injurious event, although for most (more than 97%) the treatment would be unnecessary.
Pregnancy-induced hypertension. The administration of magnesium sulfate to women with new-onset hypertension (arterial blood pressure of 140/90 mm Hg or more) without proteinuria is controversial. Some physicians do not give magnesium to these patients because the risk of eclampsia is lower than in those with preeclampsia (as characterized by hypertension and proteinuria).
About 25% of women with pregnancy-induced hypertension will develop preeclampsia, but those who will go on to develop proteinuria or seizures cannot be identified prospectively. For this reason, other physicians favor prophylactic magnesium for this group.5 They point out that, once a seizure has occurred, recurrence may be more difficult to prevent. We do not routinely administer magnesium to women with pregnancy-induced hypertension unless they have or develop prodromal symptoms (e.g., headache, epigastric pain), high arterial pressures (more than 160/105 mm Hg), proteinuria, or hemolysis, elevated liver enzymes, and low platelets syndrome.
Clinical symptoms and signs are unreliable predictors of which pregnant women will develop seizures.
Mild preeclampsia. Similar arguments also have been given for and against magnesium prophylaxis in women with mild preeclampsia. In the Magpie trial, magnesium sulfate administration was associated with a reduction in the incidence of eclampsia of approximately 56% (placebo: 1.6%; magnesium: 0.7%) in 7,468 gravidas who did not have severe preeclampsia by the definition used in the study. In light of this evidence, we have maintained our practice of giving magnesium to those with mild preeclampsia.