The pregnant patient can be an intimidating encounter for many emergency physicians. Rarely do we find ourselves alone in managing the pregnant critically ill patient. Emergency physicians, however, are expected to handle these emergencies competently.

Preeclampsia is defined as hypertension and proteinuria that occur after 20 weeks gestation. The spectrum of illness ranges from gestational hypertension to severe preeclampsia to eclampsia. Preeclampsia and eclampsia can occur up to 6 weeks postpartum.

Occurring in approximately 5% of pregnancies in the United States, preeclampsia occurs in as many as 14% of pregnancies worldwide. Maternal mortality is estimated at 790 per 100,000 live births, and fetal complications arising from premature birth are common.

Management should focus on blood pressure control, seizure prophylaxis and treatment, fluid management, and delivery when necessary. Although obstetric consultation is warranted in every case of preeclampsia, emergency physicians should be comfortable with the initial management.

Pathophysiology

Theoretical causes of preeclampsia include an imbalance of thromboxane and prostacyclin, immunologic abnormalities, increased vascular reactivity to vasoactive agents, hyperdynamic increase in cardiac output, abnormal development of the placenta, and genetic variations of the angiotensinogen gene.

One theory is that abnormal placental vasculature causes underperfusion, which in turn leads to activation of these factors.

Risk factors include first pregnancy, preeclampsia in previous pregnancy, age, race, family history of preeclampsia, diabetes, obesity, chronic hypertension, renal disease, and periodontal disease. Pregnancy-associated risk factors include chromosomal abnormalities, hydatidiform mole, multifetal pregnancy, oocyte donation or donor insemination, and urinary tract infection.

Women with preexisting hypertension have a 10%-25% increased risk of superimposed preeclampsia and should be closely monitored for proteinuria and edema. Preeclamptic patients are at risk for seizures, placental abruption, thrombocytopenia, cerebral hemorrhage, pulmonary edema, liver hemorrhage, and renal failure. These risks are present until delivery. Hypertension caused by preeclampsia resolves spontaneously by 12 weeks postpartum.

Diagnosis

Diagnostic criteria for preeclampsia include a systolic blood pressure greater than 140 mm Hg or a diastolic blood pressure greater than 90 mm Hg in a woman who was normotensive prior to 20 weeks gestation.

If hypertension precedes pregnancy, is present before 20 weeks of gestation, or persists longer than 12 weeks postpartum, it is defined as preexisting hypertension. The elevation must be present in two successive measurements 4-6 hours apart.1

A rise in systolic blood pressure of 30 mm Hg or diastolic blood pressure increase of 15 mm Hg is diagnostic in a woman with preexisting hypertension.

Urine dipstick values greater than 2+ suggest significant proteinuria but are not reliable and should be followed with a 24-hour urine collection. Proteinuria is also present with greater than 300 mg of protein in a 24-hour urine.

Edema is also a symptom commonly associated with preeclampsia, although difficult to assess given that normal pregnancy also commonly has dependent edema.

Severe preeclampsia is diagnosed by a systolic blood pressure greater than 160 mm Hg or diastolic blood pressure greater than 110 mm Hg, excess proteinuria, severe oliguria, cerebral or visual disturbances, pulmonary edema, impaired liver function, epigastric or right upper quadrant pain, thrombocytopenia, or fetal growth retardation.

Additional studies include serum creatinine, platelet count, serum alanine and aspartate aminotransferase concentrations (ALT and AST), serum lactate dehydrogenase (LDH), and serum uric acid.¹

The HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) is a sign of severe preeclampsia.

Every patient should have fetal heart sounds checked to confirm viability as part of the patient’s vital signs. Sonographic evaluation of the fetus is necessary to confirm gestational age if prenatal care is not well documented.

Gestational age is important in determining optimal management if the severity of symptoms progresses. A nonstress test or biophysical profile is used to evaluate fetal well being.

Visual disturbances, severe headaches, lateralizing neurologic signs, and liver tenderness in patients with severe preeclampsia should be treated aggressively to prevent progression to seizures and maternal organ damage.

CT scanning of the head is necessary in the case of lateralizing neurologic signs to rule out the possibility of intracranial hemorrhage.

Treatment

Delivery is the definitive treatment for preeclampsia and should be considered after 34 weeks gestation in the case of severe preeclampsia and 37 weeks gestation in mild preeclampsia.

A conservative approach, rather than preterm delivery, may be the better option depending on gestational age, maternal and fetal condition, and severity of disease.

Limitation of physical activity, including bed rest, has been proven to decrease blood pressure and is a common initial treatment of mild preeclampsia.

Mild preeclampsia may be monitored on an outpatient basis, but patients with moderate to severe preeclampsia should be admitted and closely followed.

All cases of preeclampsia must be closely followed until delivery, which should occur by 40 weeks gestation.

Eclampsia, seizure in the setting of preeclampsia, is an indication for emergent delivery. Magnesium sulfate should be used as first-line seizure prophylaxis and treatment. Any patient with severe preeclampsia should be started on magnesium, because it has been proven to prevent progression to eclampsia.²

Dosing for seizure prophylaxis is 4-6 g by intravenous bolus given over 20 minutes, followed by 1-2 g per hour maintenance dosing. Magnesium toxicity is a risk; therefore, magnesium levels, respiratory rate, reflexes, and urinary output must be monitored. Hypotension is a known side effect of magnesium.

In the case of hypermagnesemia (levels 6-8 mEq/L), calcium gluconate 10% solution 10-20 mL can be given to correct effects. Phenytoin also has been studied in eclamptic seizures and shown to be successful, but lack of familiarity and difficulty with dosing regimens in pregnancy, along with required cardiac monitoring in IV dosing, have limited its appeal.

Lorazepam may be used as well, but it has been shown to be less reliable in controlling seizures when compared to magnesium and is associated with fetal CNS depression, which may create problems in case of emergency delivery.³

Antihypertensives should be started in patients with severe hypertension in order to prevent maternal end-organ damage and stroke.

Blood pressure control does not, however, alter the progression of preeclampsia. One retrospective study found systolic blood pressure was 159 to 198 immediately prestroke in 24 of 24 patients.⁴ The suggestion is to initiate antihypertensive therapy in preeclamptic women when the systolic blood pressure is 150 mm Hg and the diastolic blood pressure is 100 mm Hg, or if symptoms may be attributable to elevated blood pressure. Treating mild hypertension may lead to fetal growth impairment; therefore, mild hypertension is better monitored than treated.

Hydralazine is often used for blood pressure control in the admitted patient, although unpredictable hypotension is a known side effect. Dosing begins with 5 mg intravenously, followed by a second dose if the desired effect is not achieved within 20 minutes.

Labetalol (alpha- and beta-adrenergic blocking agent) has fewer side effects (such as reflex tachycardia) and should be considered as first-line therapy.⁵ Dosing of intravenous labetalol should start at 20 mg, followed by increasing doses at 10-minute intervals up to a maximum total dose of 300 mg.

Labetalol is not teratogenic and may preserve uteroplacental blood flow better than other antihypertensive drugs.

Nifedipine, methyldopa, and hydrochlorothiazide have been used safely in pregnancy, but have been studied less than hydralazine and labetalol and should be considered second- or third-line treatments.⁶

Diazoxide (potassium channel blocker) was shown to be beneficial and safe in treating hypertension when used in small doses (15 mg) with hydralazine.⁷ Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated in pregnancy because of adverse fetal outcomes.⁵ Nitroprusside is known to cause fetal cyanide poisoning if used for more than 4 hours and should be avoided during pregnancy.

Betamethasone for fetal lung maturity should be administered to women of less than 34 weeks gestation in case of emergent preterm delivery. The decision to use steroids should be made in consultation with the high-risk obstetrician.

Once stabilized, patients should be continued on oral antihypertensive therapy until delivery. There is no well-established target blood pressure for the pregnant patient.

Although severe preeclamptic patients are in total body fluid overload, they are often intravascularly depleted and very sensitive to changes in volume status. Uterine contractions are also increased because of dehydration; therefore, improving volume status is essential in management.

Intravenous hydration, however, must be carefully administered, because studies have shown that excessive fluid use leads to an increase in extravascular fluid stores and greatly increases the risk of pulmonary edema.

Summary

Pregnancy-induced hypertension, preeclampsia, and eclampsia are on a continuum of a disease process that emergency physicians must be able to handle adeptly in the emergency department. Preventing progression of preeclampsia to seizures or other end-organ damage is accomplished through a variety of methods, both nonpharmacologic (bed rest, hydration) and pharmacologic (magnesium, labetalol, hydralazine, etc.).

Although controversy persists, magnesium remains the mainstay of therapy because of its familiarity, wide safety margin, and physiologic advantages to the fetus.

References

1. Pearlman M, Tintinalli JE, Dye P, et al: Preeclampsia and Hypertensive Disorders in Pregnancy, in Obstetric and Gynecologic Emergencies: Diagnosis and Management. McGraw-Hill Professional, 2003. pp. 96-103.
2. Coetzee EJ, Dommisse J, Anthony J. A randomized controlled trial of intravenous magnesium sulphate versus placebo in the management of women with severe preeclampsia. Br J Obstet Gynaecol 1998;105:300.
3. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with Phenytoin for the prevention of eclampsia. N England J Med 1995;333:201.
4. Martin JN Jr, Thigpen BD, Moore RC, et al. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure. Obstet Gynecol 2005;105:246.
5. Podymow T, August P. Hypertension in pregnancy. Adv Chronic Kidney Disease. 2007 Apr; 14(2):178-90.
6. McCoy S, Baldwin K. Pharmacotherapeutic options for the treatment of preeclampsia. Am J Health Syst Pharm. 2009 Feb 15; 66(4):337-44.
7. Hennessy A, Thornton CE, Makris A, et al. A randomized comparison of hydralazine and mini-bolus diazoxide for hypertensive emergencies in pregnancy: The PIVOT trial. Aust N Z J Obstet Gynaecol 2007;47:279.