The incidence of hypertensive disorders of pregnancy is 2% to 8%. These disorders can be thought of as a continuum from gestational hypertension to eclampsia. Pre-eclampsia is defined as systolic blood pressure (SBP) ≥140 and diastolic blood pressure (DBP) ≥90, diagnosed after 20 weeks’ gestation and accompanied by proteinuria >300 mg/24 hours. Severe pre-eclampsia is defined as SBP ≥160, DBP ≥110, proteinuria >5 g/24 hours. In addition, signs of end-organ dysfunction (oliguria, elevated serum creatinine, pulmonary edema, visual disturbances, headaches, epigastric pain), fetal growth restriction, oligohydramnios, or HELLP syndrome (Hemolysis, Elevated Liver Enzymes, and Low Platelets) make the diagnosis of severe pre-eclampsia. Eclampsia is diagnosed by the presence of seizures.

The etiology of pre-eclampsia is poorly understood. Currently, it is believed that initially there is abnormal trophoblastic invasion during placental implantation. Trophoblastic invasion of the decidual and myometrial portions of the spiral arteries results in an increase in diameter of these arteries. In pre-eclampsia, only the decidual portions change; the myometrial segments remain small and exceptionally responsive to vasomotor stimuli. This abnormality explains the drop in placental perfusion and the predisposition to uterine growth retardation. In turn, this leads to the changes that characterize the systemic maternal disease. There is endothelial dysfunction that can cause platelet aggregation, downregulation of circulating anticoagulants, and capillary leaks. In addition, an imbalance between decreased prostacyclin I₂ and increased thromboxane A₂exists. Prostacyclin I₂ is a potent vasodilator and activator of platelets. Thromboxane A₂ is a potent vasoconstrictor and promoter of platelet aggregation. Endothelial dysfunction may impair nitric oxide and increase endothelin-1. Endothelin-1 is also a potent vasoconstrictor and platelet aggregator. These changes result in generalized vasospasm, reduced intravascular volume, decreased glomerular filtration rate, generalized edema, and a hypercoagulable state.

Obesity, among others, is an independent risk factor for developing pre-eclampsia. When the two entities are combined, anesthetic management can be quite challenging. Current obstetric management involves treating elevated blood pressure with labetalol first, then using oral nifedipine. These
patients will likely be receiving magnesium sulfate for seizure prophylaxis. It is crucial to have open and complete communication with the obstetricians regarding these patients. The only definitive treatment is delivery of the fetus.

The anesthetic management of labor should involve the early placement of a continuous lumber epidural catheter. Given the obese body habitus and generalized edema, intravenous line placement may be difficult at best. Next, it is important to check a platelet count and prothrombin time/international normalized ratio prior to proceeding. Early involvement of anesthesia can allow placement before platelet counts fall to an unacceptable level. Most obstetric anesthesiologists are comfortable placing an epidural with platelet counts >80,000. Obesity increases the technical difficulty of placing an epidural catheter. Help should be recruited to ensure optimal positioning. Early placement of an epidural has benefits besides patient comfort. Controlling the pre-eclamptic patient’s pain can blunt the hypertensive response to pain, decrease circulating catechols, and improve uteroplacental blood flow. In addition, early epidural catheter placement may avoid a general anesthetic in case of a C section. Fluid bolus must be done with some caution because too much fluid may result in pulmonary edema. If there is presence or suspicion of pulmonary issues, boluses of 250 mL at a time may be wise. Vasoactive medications such as ephedrine or phenylephrine may have a much greater effect than anticipated on the already exceptionally responsive vascular system.