Hypertensive Disorders of Pregnancy: Preeclampsia/Eclampsia
Luis Sanchez-Ramos
Hypertensive disorders of pregnancy, including preeclampsia and eclampsia, are the second leading cause of maternal mortality in the United States. Preeclampsia is a disorder that affects women exclusively during pregnancy. It is a disease of unknown etiology that presents in pregnant women at both extremes of reproductive age. Reported incidences range from 2% to 30%, depending on the diagnostic criteria used and the population studied (1). Conditions associated with an increased incidence include previous preeclampsia, multifetal pregnancy, molar pregnancy, and triploidy. It is a clinical condition that comprises a wide spectrum of signs and symptoms that have been observed to develop alone or in combination. Complications resulting from preeclampsia are also a leading cause of perinatal morbidity and mortality.
The diagnosis of the disease is based on the presence of hypertension in association with significant proteinuria. Preeclampsia is usually classified clinically as mild or severe (2). However, even in a seemingly stable patient with minimal signs and symptoms, this disease can rapidly progress to life-threatening eclampsia, with seizures and complications that may include pulmonary edema, intracerebral hemorrhage, acute renal failure, disseminated intravascular coagulation, and abruptio placentae. The criteria for severe preeclampsia are summarized in Table 7.1.
There appears to be an increased incidence of preeclampsia in patients with minimal or no prenatal care and in those of low socioeconomic status (3). All these types of patients are frequently seen for the first time by physicians in the emergency department. Consequently, it is not unusual for such physicians to be the first to make the diagnosis and initiate appropriate management.
PATHOPHYSIOLOGY
The basic disorder underlying preeclampsia is vasospasm. Constriction of the arterioles causes resistance to blood flow and subsequent arterial hypertension. Vasospasm and damage to the vascular endothelium in combination with local hypoxia presumably lead to hemorrhage, necrosis, and other end-organ disturbances of severe preeclampsia.
Vascular reactivity to infused angiotensin II and other vasopressors is decreased in normotensive pregnancy (4,5). The refractoriness to angiotensin II may be mediated by vascular endothelium synthesis of vasodilatory prostaglandins such as prostacyclin. There are data to suggest that preeclampsia may be associated with inappropriately increased production of prostaglandins with vasoconstrictor properties such as thromboxane. Several authors have shown increased vascular reactivity to pressor hormones in patients with early preeclampsia. The increased reactivity to vasopressors may be due to altered ratios of thromboxane and prostacyclin (6).
Pregnancy normally increases blood volume by as much as 40%, but the expansion may not occur in a woman destined to develop preeclampsia. Vasospasm contracts the intravascular space and leaves her highly sensitive
to fluid therapy or blood loss at delivery. The vascular contraction impairs uteroplacental blood flow, contributes to intrauterine growth restriction, and may lead to intrauterine fetal demise. Circulatory impairment reduces renal perfusion and glomerular filtration, and swelling of intracapillary glomerular cells and glomerular endotheliosis may result. Edema probably occurs because of maldistribution of extracellular fluid, since plasma fluid is not increased.
to fluid therapy or blood loss at delivery. The vascular contraction impairs uteroplacental blood flow, contributes to intrauterine growth restriction, and may lead to intrauterine fetal demise. Circulatory impairment reduces renal perfusion and glomerular filtration, and swelling of intracapillary glomerular cells and glomerular endotheliosis may result. Edema probably occurs because of maldistribution of extracellular fluid, since plasma fluid is not increased.
TABLE 7.1 Criteria for Severe Preeclampsia | |||||||||
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DIAGNOSIS
The diagnosis of preeclampsia is usually straightforward: the blood pressure is at least 140/90 mm Hg on at least two occasions 6 or more hours apart. In the past, it was recommended that an increase of 30 mm Hg in systolic or 15 mm Hg in diastolic blood pressure be used as a diagnostic criterion, even when absolute values remained lower than 140/90 mm Hg. During the last decade, the former definition has been accepted by the Working Group on High Blood Pressure in Pregnancy, because the only available evidence shows that women with blood pressures meeting the old criterion are not likely to have adverse outcomes (7,8).
In addition to hypertension, the patient often presents with significant proteinuria, defined as the presence of at least 300 mg of protein in a 24-hour urine collection or a reading of 1+ or higher on random dipstick samples. The degree of proteinuria often fluctuates widely over a 24-hour period. Therefore, a single random sample may fail to detect significant proteinuria.
Although in the past, edema was an accepted criterion for the diagnosis of preeclampsia, it is such a common finding in pregnant women that its presence should not validate the existence of preeclampsia any more than its absence should rule out the diagnosis. However, significant edema of the hands and face associated with a sudden increase in weight may be a valuable warning sign (Fig. 7.1).
In addition to the classic findings of hypertension and proteinuria, other laboratory clues may be helpful in the diagnosis of preeclampsia. Thrombocytopenia may at times be an early warning in patients who subsequently will develop hypertensive disorders of pregnancy. Increased serum levels of uric acid may be of both prognostic and diagnostic values. Patients with preeclampsia have markedly decreased urinary excretion of calcium; in fact, hypocalciuria can be detected prior to the appearance of clinical signs and symptoms (9).
 FIGURE 7.1 Preeclampsia: edema of face, hand, and foot. |
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