Anesthesia for Hypertensive Disorders

HYPERTENSIVE DISORDERS

Hypertension during pregnancy can be classified as pregnancy-induced hypertension (PIH, often also referred to as preeclampsia), chronic hypertension that preceded pregnancy, or chronic hypertension with superimposed preeclampsia. Preeclampsia is usually defined as a systolic blood pressure greater than 140 mm Hg or diastolic pressure greater than 90 mm Hg after the 20th week of ges-tation, accompanied by proteinuria (>300 mg/d) and resolving within 48 h after delivery. When sei-zures occur, the syndrome is termed eclampsia. The HELLP syndrome describes preeclampsia associated with hemolysis, elevated liver enzymes, and a lowplatelet count. In the United States, preeclampsiacomplicates approximately 7–10% of pregnancies; eclampsia is much less common, occurring in one of 10,000–15,000 pregnancies. Severe preeclamp-sia causes or contributes to 20–40% of maternal deaths and 20% of perinatal deaths. Maternal deaths are usually due to stroke, pulmonary edema, and hepatic necrosis or rupture.

Pathophysiology & Manifestations

The pathophysiology of preeclampsia is probably related to a vascular dysfunction of the placenta that results in abnormal prostaglandin metabolism. Patients with preeclampsia have elevated production of thromboxane A₂ (TXA₂) and decreased produc-tion of prostacyclin (PGI₂). TXA₂ is a potent vaso-constrictor and promoter of platelet aggregation, whereas PGI₂ is a potent vasodilator and inhibitor of platelet aggregation. Endothelial dysfunction may reduce production of nitric oxide and increase pro-duction of endothelin-1. The latter is also a potent vasoconstrictor and activator of platelets. Marked vascular reactivity and endothelial injury reduce placental perfusion and can lead to widespread sys-temic manifestations.

Severe preeclampsia substantially increases both maternal and fetal morbidity and mortal-ity, and is defined by a blood pressure greater than 160/110 mm Hg, proteinuria in excess of 5 g/d, oli-guria (<500 mL/d), elevated serum creatinine, intra-uterine growth restriction, pulmonary edema, central nervous system manifestations (headache, visual dis-turbances, seizures, or stroke), hepatic tenderness, or the HELLP syndrome (Table 41-6). Hepatic rupture may also occur in patients with the HELLP syndrome.

Patients with severe preeclampsia or eclampsia have widely differing hemodynamic profiles. Most patients have low-normal cardiac filling pressures with high systemic vascular resistance, but cardiac output may be low, normal, or high.

Treatment

Treatment of preeclampsia consists of bed rest, seda-tion, repeated doses of antihypertensive drugs (usually labetalol, 5–10 mg, or hydralazine, 5 mg intrave-nously), and magnesium sulfate (4 g intravenous loading, followed by 1–3 g/h) to treat hyperreflexia and prevent convulsions. Therapeutic magnesium levels are 4–6 mEq/L.

Invasive arterial and central venous monitor-ing are indicated in patients with severe hyperten-sion, pulmonary edema, or refractory oliguria; an intravenous vasodilator infusion may be necessary. Definitive treatment of preeclampsia is delivery of the fetus and placenta.

Anesthetic Management

Patients with mild preeclampsia generally require only extra caution during anesthesia; standard anes-thetic practices may be used. Spinal and epidural anesthesia are associated with similar decreases in arterial blood pressure in these patients. Patients with severe disease, however, are critically ill and require stabilization prior to administration of any anesthetic. Hypertension should be controlled and hypovolemia corrected before administration of anesthesia. In the absence of coagulopathy, continuous epidural anes-thesia is the first choice for most patients with pre-eclampsia during labor, vaginal delivery, and cesarean section. Moreover, continuous epidural anesthesia avoids the increased risk of a failed intubation due to severe edema of the upper airway.

A platelet count and coagulation profile should be checked prior to the institution of regional anes-thesia in patients with severe preeclampsia. It has been recommended that regional anesthesia be avoided if the platelet count is less than 100,000/μL, but a platelet count as low as 70,000/μL may be acceptable in selected cases, particularly when the count has been stable. Although some patients have a qualitative platelet defect, the usefulness of a bleeding time determination is questionable. Continuous epidural anesthesia has been shown to decrease catecholamine secretion and improve uteroplacental perfusion up to 75% in these patients, provided hypotension is avoided. Judicious fluid boluses with epidural activation may be required to correct the disease-related hypovolemia. Goal-directed hemodynamic and fluid therapy utiliz-ing arterial pulse wave contour analysis (Virgileo/ Flotrac, LiDCOrapid) or echocardiography may be employed to guide fluid replacement. Use of an epi-nephrine-containing test dose for epidural anesthe-sia is controversial because of questionable reliability (see earlier section Prevention of Unintentional Intravascular and Intrathecal Injection) and the risk of exacerbating hypertension. Hypotension should be treated with small doses of vasopressors because patients tend to be very sensitive to these agents. Recent evidence suggests that spinal anesthesia does not, as previously thought, result in a more severe reduction of maternal blood pressure. Therefore, this technique is a reasonable anesthetic choice for cesarean section in a preeclamptic patient.

Intraarterial blood pressure monitoring is indi-cated in patients with severe hypertension during both general and regional anesthesia. Intravenous vasodilator infusions may be necessary to control blood pressure during general anesthesia. Intravenous labetalol (5–10 mg increments) can also be effective in controlling the hypertensive response to intuba-tion and does not appear to alter placental blood flow. Because magnesium potentiates muscle relaxants, doses of nondepolarizing muscle relaxants should be reduced in patients receiving magnesium therapy and should be guided by a peripheral nerve stimu-lator. The patient with suspected magnesium toxic-ity, manifested by hyporef lexia, excessive sedation, blurred vision, respiratory compromise and cardiac depression, can be treated with intravenous admin-istration of calcium gluconate (1 g over 10 minutes).