An eclamptic convulsion is frightening to behold. First, the woman’s face becomes distorted, and her eyes protrude. Then her face acquires a congested expression, and foam may exude from her mouth. Breathing stops.
Because eclampsia is so frightening, the natural tendency is to try to stop a convulsion, but this is not the wisest strategy.
Rather, the foremost priorities are to avoid maternal injury and support cardiovascular functions. How to do this, and how to prevent further convulsions, monitor and deliver the fetus, and avert complications are the focus of this article.
Since eclampsia may be fatal for both mother and fetus, all labor and delivery units and all obstetricians should be prepared to diagnose and manage this grave threat. However, few obstetric units encounter more than 1 or 2 cases a year; most obstetricians have little or no experience managing acute eclampsia. In the Western world, it affects only 1 in 2,000 to 1 in 3,448 pregnancies.1-4
How a convulsion happens
Most convulsions occur in 2 phases and last for 60 to 75 seconds. The first phase, lasting 15 to 20 seconds, begins with facial twitching, soon followed by a rigid body with generalized muscular contractions.
In the second phase, which lasts about a minute, the muscles of the body alternately contract and relax in rapid succession. This phase begins with the muscles of the jaw and rapidly encompasses eyelids, other facial muscles, and body. If the tongue is unprotected, the woman often bites it.
Coma sometimes follows the convulsion, and deep, rapid breathing usually begins as soon as the convulsion stops. In fact, maintaining oxygenation typically is not a problem after a single convulsion, and the risk of aspiration is low in a well managed patient.
Upon reviving, the woman typically remembers nothing about the seizure.
If convulsions recur, some degree of consciousness returns after each one, although the woman may become combative, agitated, and difficult to control.
Harbingers of complications
In the developed world, eclampsia increases the risk of maternal death (range: 0 to 1.8%).1-5 A recent review of all reported pregnancy-related deaths in the United States from 1979 to 1992 found 4,024 cases.6 Of these, 790 (19.6%) were due to preeclampsia-eclampsia, 49% of which were caused by eclampsia. The risk of death from preeclampsia or eclampsia was higher for the following groups:
- women over 30,
- no prenatal care,
- African Americans, and
- onset of preeclampsia or eclampsia before 28 weeks.6
Pregnancies complicated by eclampsia also have higher rates of maternal morbidity such as pulmonary edema and HELLP syndrome (TABLE 1). Complications are substantially higher among women who develop antepartum eclampsia, especially when it is remote from term.1-3
Antepartum eclampsia, especially when it is remote from term, is much more likely to lead to complications
|Death||0.5-–2||Risk of death is higher: |
|Intracerebral hemorrhage||<1||Usually related to several risk factors|
|Aspiration pneumonia||2–3||Heightened risk of maternal hypoxemia and acidosis|
|Disseminated coagulopathy||3–5||Regional anesthesia is contraindicated in these patients, and there is a heightened risk of hemorrhagic shock|
|Pulmonary edema||3–5||Heightened risk of maternal hypoxemia and acidosis|
|Acute renal failure||5–9||Usually seen in association with abruptio placentae, maternal hemorrhage, and prolonged maternal hypotension|
|Abruptio placentae||7–10||Can occur after a convulsion; suspect it if fetal bradycardia or late decelerations persist|
Adverse perinatal outcomes
Perinatal mortality and morbidity are high in eclampsia, with a perinatal death rate in recent series of 5.6% to 11.8%.1,7 This high rate is related to prematurity, abruptio placentae, and severe growth restriction.1
Preterm deliveries occur in approximately 50% of cases, and about 25% occur before 32 weeks’ gestation.1
Diagnosis can be tricky
When the patient has generalized edema, hypertension, proteinuria, and convulsions, diagnosis of eclampsia is straightforward. Unfortunately, women with eclampsia exhibit a broad spectrum of signs, ranging from severe hypertension, severe proteinuria, and generalized edema, to absent or minimal hypertension, nonexistent proteinuria, and no edema (TABLE 2).1