Perspective

Preeclampsia is a disease of pregnancy characterized by a sustained elevation in blood pressure (sitting blood pressure of ≥140 mm Hg systolic or ≥90 mm Hg diastolic) and proteinuria (≥1+ in a random urine sample or 300 mg in a 24-hour urine sample) occurring after the 20th week of gestation. Edema is common in patients with preeclampsia but is not necessary for the diagnosis. Eclampsia is defined by seizures, usually in the setting of preeclampsia. Seizures are rare without underlying preeclampsia. Although preeclampsia develops most commonly after the 20th week of pregnancy, it may occur in the postpartum period, usually within the first 24 to 48 hours, but delayed manifestations of 2 weeks or longer have been reported.

Epidemiology

Preeclampsia complicates 5% to 11% of pregnancies in the United States. The rate is higher in developing nations. This disease accounts for a significant percentage of both maternal and fetal mortality. Fetal complications such as prematurity and low birth weight are common, with death occurring in 129 of every 1000 cases. Maternal complications are common in both eclampsia and severe preeclampsia, including HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) (11%), placental abruption (10%), disseminated intravascular coagulation (DIC) (6%), neurologic deficits (6%), aspiration pneumonia (6%), pulmonary edema (5%), renal failure (4%), and death (1%).

First pregnancies are at greatest risk. Other risk factors include extremes of reproductive age, more than 10 years between pregnancies, multiple gestations, molar pregnancies, previous or family history of preeclampsia, underlying diseases (hypertension, diabetes, autoimmune or renal diseases, obesity), and thrombophilia (e.g., antiphospholipid syndrome, factor V Leiden deficiency, activated protein C resistance).¹

Pathophysiology

Preeclampsia is a multisystem disorder of gestation. Its exact cause is unclear and several mechanisms have been implicated. The disease is thought to originate within the placenta, which for reasons that remain obscure, has inappropriately decreased perfusion. Hypoperfusion and multiorgan effects ensue in some patients as a result of decreased intravascular volume and endothelial vascular leakage causing increased interstitial volume, interstitial protein leakage, and vasoconstriction.² Preeclampsia affects nearly every organ system.

Severe preeclampsia is characterized by hypertension secondary to increased peripheral resistance. However, the profound elevation in blood pressure is the result rather than the cause of the underlying pathophysiology. Effects on the liver include edema, hepatocellular necrosis, and periportal and subcapsular hematomas. Decreased renal flow with high perfusion pressure can cause glomerular and tubular injury resulting in proteinuria or, worse, renal failure. Cerebral vasospasm leads to edema, microinfarction, and hemorrhage. Patients experience a variant of chronic DIC with thrombocytopenia and hemolysis that can worsen the already present organ system dysfunction.

HELLP syndrome is a particularly severe form of preeclampsia associated with severe maternal morbidity.

Preeclampsia has long-term implications for the health of these patients. After delivery, women with preeclampsia are at increased risk for the development of chronic hypertension, cardiovascular diseases, and psychosomatic disorders.³

Presenting Signs and Symptoms

Classic clinical findings in patients with preeclampsia include proteinuria and an associated elevation in blood pressure; when these signs develop late in the pregnancy of a previously healthy woman, the diagnosis of preeclampsia is clear. However, preeclampsia does not always occur in such a straightforward manner. For instance, a patient with chronic hypertension complicated by chronic renal disease can be difficult to differentiate from one who has preeclampsia. Likewise, seizures in pregnant patients do not always herald eclampsia, and other structural, toxic, and metabolic causes have to be considered.

Patients may have the classic symptoms of severe preeclampsia, such as seizures superimposed on hypertension and proteinuria, or may have incidentally noted hypertension and proteinuria with or without edema.

Persistent elevation in blood pressure is the hallmark of preeclampsia. Hypertension is defined as a sitting blood pressure of 140 mm Hg systolic or 90 mm Hg diastolic or greater. Blood pressure readings should ideally be taken more than 6 hours apart; however, for most patients in the emergency department (ED), if concern is high, therapy should not be delayed. Early in pregnancy, diastolic blood pressure decreases but returns to normal toward the 28th week of gestation. Therefore, a sustained diastolic blood pressure of greater than 90 mm Hg at the midpoint of pregnancy should be considered elevated unless the patient has a clearly documented history of hypertension.

If the patient’s blood pressure before pregnancy is known, an increase in systolic blood pressure of 30 mm Hg or greater and an increase in diastolic blood pressure of 15 mm Hg or greater are diagnostic of preeclampsia. In addition to hypertension, the patient will have proteinuria of 1+ or greater on urinalysis.

Patients with severe preeclampsia may have additional symptoms of organ involvement (Box 121.1),⁴ including significant edema, especially facial edema, and documented weight gain of more than 5 pounds per week. Findings ominous for severe preeclampsia include a blood pressure of 160 mm Hg systolic and 110 mm Hg diastolic or greater, visual disturbances (blurred vision or scotomata), severe headache, altered mental status, seizures (which defines eclampsia), hyperreflexia with clonus, severe epigastric or right upper quadrant pain on examination, retinal hemorrhage with exudates and papilledema (which is rare and more commonly indicates underlying chronic hypertension), bibasilar rales and evidence of frank pulmonary edema, oliguria, and petechiae and bleeding from puncture sites.

Fetal growth retardation and oligohydramnios may be seen in cases of severe preeclampsia, but this information is not usually available. Sudden onset of abdominal pain with a firm painful uterus suggests placental abruption, which complicates up to 10% of preeclamptic pregnancies.

Differential Diagnosis and Medical Decision Making

The current classification of hypertension in pregnancy is divided into four categories: preeclampsia, gestational or transient hypertension, chronic hypertension, and preeclampsia superimposed on chronic hypertension (Box 121.2).⁵ In addition, occult renal disease can be manifested as proteinuria and associated hypertension.

The differential diagnosis of severe preeclampsia is broad and distinction may be difficult, particularly with concomitant HELLP syndrome.⁶ Thrombotic thrombocytopenic purpura (TTP) and preeclampsia can have identical findings of thrombocytopenia, hemolytic anemia, renal disease, and neurologic abnormalities. In patients with preeclampsia, the hypertension, proteinuria, and edema tend to precede the hematologic findings. In patients with TTP, they generally follow and are a result of the hematologic abnormalities. However, by the time that the patient arrives in the ED, these subtle distinctions may be almost impossible to delineate.

Laboratory tests may help clarify the diagnosis and determine the severity of the preeclampsia. If proteinuria is 1+ or greater on urinalysis, a hypertensive pregnant woman should be considered to have preeclampsia unless proved otherwise. A 24-hour urine collection is more sensitive for this purpose, but its use is not realistic in the ED.

A complete blood count should be performed with a manual differential and haptoglobin assay to evaluate for hemolysis. Decreased platelet counts (<100,000/mm³) are associated with severe disease. Fibrinogen levels, fibrin split products, and a prothrombin time (PT) and partial thromboplastin time (PTT) should be ordered to evaluate for DIC, which may complicate severe preeclampsia.

A comprehensive metabolic profile should be obtained because elevated serum creatinine, especially when associated with oliguria, and elevated liver transaminases suggest severe preeclampsia. Uric acid levels should be assayed; the degree of elevation of uric acid has been shown to correlate with the severity of the preeclampsia. Elevated lactate dehydrogenase (LDH) levels indicate hemolysis but can also be a result of liver involvement. Typing plus crossmatching of blood is necessary in cases of severe preeclampsia or anticipated delivery.

HELLP syndrome is characterized by peripheral smears showing schistocytes and burr cells, elevated LDH levels (>600 U/L), elevated liver enzymes (bilirubin >1.2 and aspartate transaminase >70 U/L), and low platelet count (<100,000).⁷ In addition, the abnormal laboratory test results in patients with HELLP syndrome can be seen in the other diseases noted in Box 121.3.

Table 121.1 shows the frequency of certain signs and laboratory values that may help distinguish between several of the key conditions that mimic severe preeclampsia with HELLP syndrome.⁶

Table 121.1 Differentiating HELLP Syndrome From Other Critical Conditions

 Documentation

Preeclampsia and Eclampsia

Pregnant women being evaluated should have their blood pressure documented; any elevation needs to be addressed. A complete history should include symptomatic clues (e.g., headache, vision changes, abdominal pain) identifying causes of the elevation.

Review of records may indicate that the elevation is chronic and that the patient is being monitored for this finding.

If the blood pressure is not dangerously high and no other evidence of preeclampsia is present, it may be addressed by making arrangements for close outpatient follow-up.

Documentation should include completion of appropriate laboratory testing.

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