Pulmonary edema may follow shortly after eclamptic convulsions or to several hours later. This up usually is caused by aspiration pneumonitis from gastric-content inhalation during vomiting that frequently accompanies convulsions. In some women, pulmonary edema may be caused by ventricular failure from increased aterload that results from severe hypertension. Both pulmonary edema and hypertension can be further aggravated by vigorous intravenous fluid administration (Dennis, 2012b). Such pulmonary edema from ventricular failure is more common in morbidly obese women and in those with previously unappreciated chronic hypertension.
Occasionally, sudden death occurs synchronously with an eclamptic convulsion, or it follows shortly thereafter. Most often in these cases, a massive cerebral hemorrhage is the cause (see Fig. 40-10). Hemiplegia may result from sublethal hemorrhage. Cerebral hemorrhages are more likely in older women with underlying chronic hypertension.
In approximately 10 percent of eclamptic women, some degree of blindness follows a seizure. The causes of blindness or impaired vision were discussed earlier (p. 724). Blindness with severe preeclampsia without convulsions usually stems from retinal detachment (Vigil-De Gracia, 2011). Conversely, blindness with eclampsia is typically due to occipital lobe edema (Cunningham, 1995). In both instances, however, the prognosis for return to normal function is good and is usually complete within 1 to 2 weeks postpartum.
Up to 5 percent of women with eclampsia have substantively altered consciousness, including persistent coma, following a seizure. This is due to extensive cerebral edema, and associated trans tentorial herniation may cause death (p. 723).
Rarely, eclampsia is followed by psychosis, and the woman becomes violent. This may last for several days to 2 weeks. The prognosis for return to normal function is good, provided there was no preexisting mental illness. It is presumed to be similar to postpartum psychosis discussed in Chapter 61 (p. 1179). Antipsychotic medications have proven efective in the few cases of posteclampsia psychosis treated at Parkland Hospital.
Generally, eclampsia is more likely to be diagnosed too frequently rather than overlooked. Epilepsy, encephalitis, meningitis, brain rumor, neurocysticercosis, amnionic fluid embolism, postdural puncture cephalalgia, and ruptured cerebral aneurysm during late pregnancy or in the puerperium may simulate eclampsia. Until other such causes are excluded, however, all pregnant women with convulsions should be considered to have eclampsia.
FIGURE 40-18 Fetal heart rate tracing shows fetal bradycardia following an intrapartum eclamptic convulsion. Bradycardia resolved and beat-to-beat variability returned approximately 5 minutes following the seizure.
• Management of Eclampsia
Magnesium sulfate is highly efective to prevent convulsions in women with preeclampsia and to stop them in those with eclampsia. In his review, Chesley (1978) cited observational data by Pritchard and colleagues (1955, 1975) from Parkland Hospital and from his own institution. At that time, most eclampsia regimens in the United States adhered to a similar philosophy, and it is still in use today: 1.
Control of convulsions using an intravenously administered loading dose of magnesium sulfate that is followed by a maintenance dose, usually intravenous, of magnesium sulfate 2.
Intermittent administration of an antihypertensive medication to lower blood pressure whenever it is considered dangerously high 3.
Avoidance of diuretics unless pulmonary edema is obvious, limitation of intravenous luid administration unless fluid loss is excessive, and avoidance of hyperosmotic agents 4.