Eclampsia
The onset of convulsions in a woman with preeclampsia that cannot be attributed to other causes is termed eclampsia. The seizures are generalized and may appear before, during, or after labor. In older studies, in about 10 percent of eclamptic women, especially nulliparas, seizures did not develop until after 48 hours postpartum (Brown and colleagues, 1987; Lubarsky and associates, 1994). As prenatal care improved, many antepartum and intrapartum cases are now prevented, and a more recent study reported that a fourth of eclamptic seizures developed beyond 48 hours postpartum (Chames and co-workers, 2002).
Preeclampsia Superimposed on Chronic Hypertension
All chronic hypertensive disorders, regardless of their cause, predispose to development of superimposed preeclampsia and eclampsia. These disorders can create difficult problems with diagnosis and management in women who are not seen until after midpregnancy. The diagnosis of chronic underlying hypertension is made when:
Hypertension (140/90 mm Hg or greater) is documented antecedent to pregnancy.
Hypertension (140/90 mm Hg or greater) is detected before 20 weeks, unless there is gestational trophoblastic disease.
Hypertension persists long after delivery.
Additional historical factors that help support the diagnosis are multiparity and hypertension complicating a previous pregnancy other than the first. There frequently is also a family history of essential hypertension.
The diagnosis of chronic hypertension may be difficult to make if the woman is not seen until the latter half of pregnancy, because blood pressure decreases during the second and early third trimesters in both normotensive and chronically hypertensive women (see Chap. 45, Diagnosis). Thus, a woman with chronic vascular disease, who is seen for the first time at 20 weeks, frequently has blood pressure within the normal accepted range. During the third trimester, however, if blood pressure returns to its former hypertensive level, it presents a diagnostic problem as to whether the hypertension is chronic or induced by pregnancy. In these situations, a search for evidence of end-organ damage from chronic hypertension may help elucidate the underlying cause of hypertension. Examples include left ventricular hypertrophy or retinal changes such as arteriolar narrowing, exudates, or cotton-wool spots.
Some of the many causes of underlying hypertension that are encountered during pregnancy are listed in Table 34–3. Essential or familial hypertension is the cause of underlying vascular disease in more than 90 percent of pregnant women. Obesity and diabetes are other common causes. In some women, hypertension develops as a consequence of underlying renal parenchymal disease. Although earlier studies of renal biopsies identified abnormalities, especially in multiparas, Fisher and co-workers (1969) did not confirm a high prevalence of chronic glomerulonephritis.
Depending on its duration, chronic hypertension can lead to ventricular hypertrophy and cardiac decompensation, cerebrovascular accidents, or renal damage. These complications are more likely during pregnancy if there is superimposed preeclampsia, which develops in up to 25 percent of these women (Sibai and colleagues, 1998). The risk of placental abruption is also increased substantively if there is superimposed preeclampsia (see Chap. 35, Etiology). Moreover, the fetuses of women with chronic hypertension are at appreciable risks for growth restriction, preterm delivery, and death.
In some women with chronic hypertension, blood pressure increases to abnormal levels, typically after 24 weeks. If accompanied by proteinuria, then superimposed preeclampsia is diagnosed. Often, superimposed preeclampsia develops earlier in pregnancy than "pure" preeclampsia, and it tends to be more severe and often accompanied by fetal growth restriction. Indicators of severity shown in Table 34–2 are also used to further characterize superimposed preeclampsia.
Incidence and Risk Factors
Gestational hypertension more often affects nulliparous women. Because of the increasing incidence of chronic hypertension with advancing age, older women are at greater risk for superimposed preeclampsia. Thus, women at either end of reproductive age are considered to be more susceptible (see Chap. 7, Maternal Age).
The incidence of preeclampsia is commonly cited to be about 5 percent, although rather wide variations are reported. The incidence is markedly influenced by parity; it is related to race and ethnicity—and thus to genetic predisposition, and environmental factors likely also play a role. For example, Palmer and associates (1999) reported that living at high altitude in Colorado increased the incidence of preeclampsia. Some investigators have concluded that socioeconomically advantaged women have a lesser incidence of preeclampsia, however, Lawlor and colleagues (2005) did not observe this in an Aberdeen cohort of 3485 women.
The incidence of hypertensive disorders in healthy nulliparous women was carefully studied in a trial of dietary calcium supplementation (Hauth and colleagues, 2000). Of 4302 nulliparous women delivered at or beyond 20 weeks, a fourth developed a pregnancy-related hypertensive disorder. When all nulliparas were considered, preeclampsia was diagnosed in 7.6 percent and severe disease developed in 3.3 percent. By contrast, Vatten and Skjærven (2004) reported an incidence of preeclampsia of 2.6 percent in more than 1.6 million Norwegian nulliparas.
Other risk factors associated with preeclampsia include chronic hypertension as discussed, multifetal gestation, maternal age over 35 years, obesity, and African-American ethnicity (Conde-Agudelo and Belizan, 2000; Sibai and colleagues, 1997; Walker, 2000). The relationship between maternal weight and the risk of preeclampsia is progressive. It increases from 4.3 percent for women with a body mass index less than 19.8 kg/m2 to 13.3 percent in those with a body mass index greater than 35 kg/m2. In women with twin gestations compared with those with singletons, the incidence of gestational hypertension (13 versus 6 percent) and the incidence of preeclampsia (13 versus 5 percent) are both significantly increased (Sibai and co-workers, 2000). The incidence is unrelated to zygosity (Maxwell and associates, 2001). Although smoking during pregnancy causes a variety of adverse pregnancy outcomes, ironically, smoking has consistently been associated with a reduced risk of hypertension during pregnancy (Bainbridge and associates, 2005; Zhang and colleagues, 1999). Placenta previa has also been reported to reduce the risk of hypertensive disorders in pregnancy (Ananth and colleagues, 1997).
Eclampsia
This condition is somewhat preventable, and its incidence has decreased in the United States because most women now receive adequate prenatal care. For example, in the 15th edition of Williams Obstetrics (1976), for the prior 25-year period, the incidence of eclampsia at Parkland Hospital was 1 in 700 deliveries. For the 4-year period from 1983 to 1986, it decreased to 1 in 1150 deliveries, and for the 3-year period ending in 1999, it was approximately 1 in 1750 deliveries (Alexander and associates, 2004). In the National Vital Statistics Report, Ventura and colleagues (2000) estimated that the incidence of eclampsia in the United States in 1998 was about 1 in 3250. In the United Kingdom in 1992, Douglas and Redman (1994) reported that the incidence of eclampsia was 1 in 2000.