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.

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.

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.

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.

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.

Hypertension and proteinuria, the two most important signs of preeclampsia, are often not obvious. By the time the patient has developed symp­toms, such as epigastric pain and severe headache, the disorder may be far advanced. For this reason, prenatal care for early detection of this disorder is imperative (Fig.

One of the earliest signs of preeclampsia may be a sudden increase in weight. Whenever weight gain exceeds 0.91 kg in any given week, or 2.73kg in a month, early preeclampsia should be considered. Sudden and excessive weight gain may be attributed to abnormal retention of fluid and is demonstrable before significant edema of the face or upper extremities.

The most dependable warning sign of preeclampsia is hypertension. The dia­stolic blood pressure is a more reliable prognostic sign than the systolic, and a per­sisting diastolic pressure of ≥90mm Hg is abnormal. Proteinuria varies greatly from case to case and, in the same patient, from hour to hour. This variability is likely due to intermittent renal vasospasm. Frequent urinary dipstick readings or a 24-hour urinary collection is often necessary to diagnose proteinuria.

Other signs and symptoms of preeclampsia, such as severe headache, epi­gastric pain, blurry vision, shortness of breath, and decreased urinary output, usually appear late and in severe cases (see Table 7.1). However, hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome) may be an early portent of severe preeclampsia (10-12).

Prepartum management

The goal of therapy is to prevent eclampsia, as well as other severe complications of preeclampsia. The only definitive therapy for preeclampsia/eclampsia is deliv­ery. Once this has been achieved in a form that assures maximum safety for both the mother and the newborn, the patient is usually on her way to full recovery. This decision is fairly simple in patients with mild preeclampsia at term or with severe preeclampsia at any time during gestation. However, the management of patients with mild preeclampsia far from term is very controversial (13). Some of the areas of controversy include the need for hospitalization, the use of antihy­pertensive agents, and the use of sedatives and anticonvulsants. Most obstetricians in this country usually advise bed rest in the hospital for the

FIGURE 7.2 Signs and symptoms of preeclampsia.

duration of the pregnancy. Ambulatory treatment may be appropriate for a minority of compliant private patients with very mild preeclampsia.

Preterm patients with mild preeclampsia are admitted to the hospital and placed on bed rest. Although this seems a reasonable form of therapy, its efficacy is not clearly established. Strict sodium restriction or diuretic therapy has no role in the prevention or treatment of preeclampsia. Patients are usually placed on a regular diet, although some authorities recommend a high-protein diet. Close monitoring of both the mother and the fetus is initiated. Daily monitoring should include hematocrit and platelet count, frequent blood pressure checks, maternal weight estimation, and search for clinical evidence of severe disease. Important clinical signs and symptoms of severe disease include headache, epi­gastric pain, blurred vision, and shortness of breath.

If deterioration is progressive, as determined by laboratory findings, symp­toms, and clinical signs, the decision to continue the pregnancy must be reevalu­ated daily. Important clinical signs that need to be monitored include blood pressure, urinary output, and fluid retention as evidenced by daily weight increase. Laboratory studies (24-hour urinary collection for total protein and creatinine clearance, complete blood count, serum uric acid, blood urea nitro­gen, and creatinine) should be performed at intervals of no more than 48 hours. Once it has been determined that the patient has developed severe preeclampsia, steps should be taken for prompt delivery.

Fetal size, determined by ultrasonic biometry, is an accurate guide to the functional status of the fetus. Lack of growth suggests insufficient blood flow, which places the fetus in danger because of lack of placental reserve. Another indirect measure of altered maternal circulation is uterine artery Doppler veloci­metry, which may serve as an early marker for preeclampsia.

Every effort should be made to deliver the baby as close to term as possible.

The most important test of maturity is the lecithin/sphingomyelin ratio, which can be used to determine the risk of severe respiratory distress syndrome. The risk is high when the ratio is and good nutrition are still the most effective means of decreasing the incidence and severity of this disease.

References

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