Preeclampsia is part of a spectrum of hypertensive disorders specific to pregnancy. Although the precise etiology of preeclampsia remains unknown, it is a disease that occurs only in the presence of placental tissue. A combination of chronic uteroplacental ischemia, immune maladaptation, lipoprotein toxicity, genetic predisposition, and an exaggerated maternal inflammatory response likely play a role in disease progression, which is characterized by abnormal vasospasm and ischemia. Hypertensive disorders of pregnancy account for 25% to 60% of ICU admissions in developed nations and are a major contributor to maternal morbidity.

Preeclampsia complicates 2% to 8% of pregnancies globally and around 5% of all pregnancies in the United States, and the incidence has been rising over the past three decades. Hypertensive disorders of pregnancy contribute to 16% of maternal deaths. Risk factors for preeclampsia include nulliparity, multifetal gestation, history of preeclampsia in prior pregnancies, gestational diabetes, maternal age older than 35, and maternal pre-pregnancy body mass index (BMI) greater than 30. A patient meets the criteria for a diagnosis of preeclampsia if she has persistently elevated blood pressure after 20 weeks’ gestation in the setting of previously normal blood pressure, and proteinuria of greater than 300 mg in 24 hours or signs of end-organ dysfunction. The diagnosis of preeclampsia is divided into preeclampsia and preeclampsia with severe features based on the presence or absence of specific signs, symptoms, and abnormal laboratory values (Table 35.3).

1. Two additional diagnoses, eclampsia and HELLP syndrome, are a part of this spectrum of disease.
1. Eclampsia is defined as the occurrence of seizures or coma in a woman with preeclampsia that cannot be attributed to other causes. Eclamptic seizures may occur antepartum, intrapartum, or postpartum. Eclampsia is a cause of significant maternal and fetal morbidity, and mortality ranges from 0% to 14%. However, in high-resource countries where patients are managed in tertiary care centers with experienced providers, the mortality is closer to 1% to 2%. Eclamptic seizures are usually preceded by headache and visual disturbances. The pathophysiology remains unknown but may be related to failure of cerebral autoregulation, endothelial dysfunction, and/or cerebral vessel vasoconstriction. Seizures are generally abrupt and self-limited, but may be complicated by cardiopulmonary arrest or pulmonary aspiration of gastric contents.
2. HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome is characterized by a constellation of laboratory abnormalities and was previously regarded as a subset of severe preeclampsia; however, it is now recognized as a potentially distinct clinical entity because 15% to 20% of cases do not have hypertension or proteinuria. The diagnosis of HELLP syndrome is also associated with an increased risk of adverse outcomes including placental abruption, renal failure, hepatic subcapsular hematoma, hepatic rupture, and fetal and maternal death. Management entails administering magnesium, supportive care with normalizing blood pressure in the face of severe hypertension, and delivery of the fetus with recognition of the increased risk of hemorrhage in this population. Platelet counts can fall precipitously, and platelet transfusions are indicated in any parturient with significant bleeding or with a platelet count of less than 20 000/mm³. Subcapsular hematoma, if it occurs, is an emergency and can result in shock and fulminant hepatic failure. Death is typically due to exsanguination and coagulopathy. Prompt surgical intervention and resuscitative measures have led to improvement in maternal survival.
2. Management
1. Delivery: The only definitive treatment for preeclampsia, eclampsia, or HELLP syndrome is delivery of the fetus and placenta. The decision of when to deliver is made on the basis of the gestational age and the severity of the disease. Each patient and clinical situation should be individualized with a management strategy that seeks to balance and minimize both maternal and fetal morbidity. If needed, maternal stabilization should precede delivery to reduce morbidity.
2. Pharmacologic therapy
1. Seizure prophylaxis: Although the mechanism of action is unknown, magnesium sulfate is the medication of choice for prophylactic prevention and treatment of eclamptic seizures. Dosage of magnesium is 4 to 6 g IV bolus over 30 minutes followed by 2 g/h IV, but because it is renally cleared, this may need to be adjusted if severe renal dysfunction is present. The drug is administered during active labor, delivery, and for 24 to 48 hours postdelivery. Because of its relaxant effect on vascular and visceral smooth muscle, magnesium may decrease maternal blood pressure and predispose to postpartum atony and hemorrhage. It also inhibits acetylcholine release at the motor endplate, leading to potentiation of neuromuscular blocking agents. Finally, magnesium therapy increases the risk of pulmonary edema.
2. Antihypertensive medications such as labetalol (IV), hydralazine (IV), and calcium channel blockers (po) are frequently administered for control of blood pressure. The goal is not to normalize blood pressure but to keep patients from progressing to a hypertensive crisis, encephalopathy, or stroke with a goal systolic blood pressure (SBP) less than 160 mm Hg. When administering antihypertensive medications, it is important to remember that the placenta has no ability to autoregulate flow. Thus, a sudden drop in maternal blood pressure may decrease placental perfusion and result in significant compromise to the fetus. In cases of refractory hypertension, continuous infusions of nicardipine, esmolol, sodium nitroprusside, or nitroglycerin may be indicated.