Pre-Eclampsia and Eclampsia (Toxemia of Pregnancy)

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Chapter 219 Pre-Eclampsia and Eclampsia (Toxemia of Pregnancy)

INTRODUCTION

Description: Pre-eclampsia is a pregnancy-specific syndrome (occurring after 20 weeks of gestation) of reduced organ perfusion, vasospasm, and endothelial activation characterized by hypertension, proteinuria, and other symptoms. Pregnancy can induce hypertension or aggravate existing hypertension. Edema and proteinuria (one or both) are characteristic pregnancy-induced changes. If pre-eclampsia is untreated, convulsions (eclampsia) may occur. Chronic hypertension may be worsened by or superimposed on pregnancy-induced changes. Severe cases may include hemolysis, elevated liver enzymes, and low platelet counts (HELLP syndrome; occurs in up to 20% of severe pre-eclampsia cases).
Prevalence: Five to eight percent of all births, 250,000 cases per year, result in 150 maternal deaths (18%) and 3000 fetal deaths per year. (Overall, hypertensive disease of some type occurs in approximately 12% to 22% of pregnancies, and it is directly responsible for 17.6% of maternal deaths in the United States.)
Predominant Age: Rare before 20 weeks of gestation.
Genetics: Multifactorial, runs in families.

ETIOLOGY AND PATHOGENESIS

Causes: Unknown, genetic, endocrine/metabolic (including altered prostaglandin production), uteroplacental ischemia, immunologic all proposed.
Risk Factors: Prior history, body mass index >32.3, African American race, nulliparity, age older than 35 (2-fold to 3-fold increase) or younger than 18 years, multifetal pregnancy, fetal hydrops, hydatidiform mole, thrombophilia.

CLINICAL CHARACTERISTICS

Signs and Symptoms

• Hypertension without proteinuria or edema (gestational hypertension)
• Hypertension with proteinuria or edema (pre-eclampsia) (severe pre-eclampsia: headache, abdominal pain, weight gain, visual disturbances, thrombocytopenia, oliguria, hemoconcentration, pulmonary edema, proteinuria >3+)
• Hypertension, proteinuria, or edema and seizures (grand mal type) (eclampsia)

DIAGNOSTIC APPROACH

Differential Diagnosis

• Chronic (essential) hypertension
• Transient hypertension
• Chronic renal disease
• Acute or chronic glomerulonephritis
• Coarctation of the aorta
• Cushing’s disease
• Systemic lupus erythematosus
• Periarteritis nodosa
• Obesity
• Epilepsy
• Encephalitis
• Cerebral aneurysm or tumor
• Lupus cerebritis
• Hysteria

Associated Conditions: Hypertension, heart disease, stroke, placental infarcts, and placental abruption.

Workup and Evaluation

Laboratory: Liver and renal function studies (enzymes, renal clearance, 24-hour urinary protein measurement).
Imaging: Ultrasonography to monitor fetal growth (frequently restricted).
Special Tests: Assessment of fetal lung maturation may be performed, but if maternal disease is severe, management is based on maternal factors and not fetal maturation. Invasive hemodynamic monitoring may be required for patients with the most severe cases.
Diagnostic Procedures: History, physical examination (with blood pressure), urinalysis (or “dipstick”), laboratory assessment.

Pathologic Findings

Results of 24-hour urinary protein measurement >300 mg/24 hours, blood pressure >140/90, characteristic renal glomerular lesions (capillary endotheliosis), premature aging of the placenta, increased vascular reactivity, elevated liver enzymes, thrombocytopenia. (In the past, hypertension indicative of pre-eclampsia has been defined as an elevation of more than 30 mm Hg systolic or more than 15 mm Hg diastolic above the patient’s baseline pressure; however, this has not proved to be a good predictor of outcome and is no longer part of the criteria for pre-eclampsia. These patients do require close monitoring.)

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: Aggressive evaluation, frequent prenatal visits, increased fetal surveillance (fetal growth). Hospitalization is required for all but the most benign conditions (mild gestational hypertension, stable chronic hypertension with normal fetal growth). Weekly antenatal testing should be strongly considered. (See table.)
Specific Measures: The only true treatment for pre-eclampsia or eclampsia is delivery. Management of symptoms may be used to get both mother and baby into optimal condition for delivery.
Diet: No specific dietary changes indicated except as dictated by labor or other management. (A low-salt diet has been advocated but is unproved. Supplementation with high-dose vitamins C, A, or E has been associated with adverse effects and is not recommended.)
Activity: Bed rest with severe conditions or for women in the process of delivery.

CRITERIA FOR PRE-ECLAMPSIA

Pre-eclampsia (Mild) Severe Pre-eclampsia (One or More)
• Blood pressure ≥140 mm Hg systolic or ≥90 mm Hg diastolic after 20 weeks of gestation with previously normal blood pressure
• Proteinuria (≥0.3 g/24 hours)

• Blood pressure ≥160 mm Hg systolic or ≥110 mm Hg diastolic on two occasions at least 6 hours apart, while the patient is on bed rest
• Proteinuria (≥5 g/24 hours or 3+ or greater on two random urine samples at least 4 hours apart)
• Oliguria (<500 mL in 24 hours)
• Cerebral or visual disturbances
• Pulmonary edema or cyanosis
• Epigastric or right upper quadrant pain
• Impaired hepatic function
• Thrombocytopenia
• Fetal growth restriction

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Patient Education: American College of Obstetricians and Gynecologists Patient Education Pamphlet AP034 (High Blood Pressure During Pregnancy).

Drug(s) of Choice

Drug treatment of mild pre-eclampsia has generally been disappointing. Glucocorticoids are often given to encourage fetal lung maturation. Drugs such as labetalol or nifedipine have been given as part of conservative management protocols. These have generally resulted in prolongation of the gestation and improved fetal outcome but no reduction in catastrophic events such as placental abruption. Magnesium sulfate is often given intravenously during labor to stabilize blood pressure and reduce the risk of seizures but is not associated with a reduction in fetal morbidity or mortality. Intravenous hydralazine may be used to lower blood pressure acutely during labor. Recent data suggest that antiplatelet/nonsteroidal anti-inflammatory agents may reduce the risk of recurrence or complications, but definitive data are lacking.
Contraindications: Angiotensin-converting enzyme (ACE) inhibitors are contraindicated in pregnancy.
Precautions: Excessive levels (>10 mEg/L) of magnesium sulfate may result in respiratory paralysis and cardiac arrest.
Interactions: See individual agents.

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Alternative Drugs

Verapamil, nimodipine, diazoxide, and nitroglycerin have all been studied or advocated at some time. (Prophylactic treatment with aspirin has not been proved to be effective in preventing pre-eclampsia except in selected patients.)

FOLLOW-UP

Patient Monitoring: Increased maternal and fetal surveillance (more frequent prenatal visits, laboratory tests, and ultrasonography evaluations).
Prevention/Avoidance: Early detection and treatment. Aggressive management of pre-eclampsia may reduce the risk of eclampsia. (The use of prophylactic aspirin remains controversial and unproven.) The risk of recurrence of pre-eclampsia in subsequent pregnancies is inversely proportional to the gestational age at which it occurred in the index pregnancy.
Possible Complications: Maternal—cardiac decompensation, stroke, pulmonary edema and respiratory failure, renal failure, seizures and seizure-related injuries, intracranial hemorrhage, coma, death (0.5% to 5% mortality). Fetal risk (growth restriction and death) is directly proportional to both the degree of proteinuria and the level of diastolic blood pressure. The risk to both mother and fetus increases dramatically in eclampsia.
Expected Outcome: Generally, gestational hypertension, pre-eclampsia, and eclampsia improve after delivery. Eclamptic seizures may occur up to 10 days after delivery but are uncommon beyond 48 hours.

MISCELLANEOUS

ICD-9-CM Codes: 642.4 (Mild pre-eclampsia), 642.5 (Severe pre-eclampsia), 642.6 (Eclampsia), 642.7 (With superimposed pre-existing hypertension).

REFERENCES

Level I

Barrilleaux PS, Martin JNJr, Klauser CK, et al. Postpartum intravenous dexamethasone for severely preeclamptic patients without hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome: a randomized trial. Obstet Gynecol. 2005;105:843.

Livingston JC, Livingston LW, Ramsey R, et al. Magnesium sulfate in women with mild preeclampsia: a randomized controlled trial. Obstet Gynecol. 2003;101:217.

Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995;333:201.

Magpie Trial Follow-Up Study Collaborative Group. The Magpie Trial: A randomised trial comparing magnesium sulphate with placebo for pre-eclampsia. Outcome for children at 18 months. BJOG. 2007;114:289. Epub 2006 Dec 12

Magpie Trial Follow-Up Study Collaborative Group. The Magpie Trial: A randomised trial comparing magnesium sulphate with placebo for pre-eclampsia. Outcome for women at 2 years. BJOG. 2007;114:300. Epub 2006 Dec 12

Level II

Askie LM, Duley L, Henderson-Smart DJ, Stewart LA, PARIS Collaborative Group. Antiplatelet agents for prevention of pre-eclampsia: a meta-analysis of individual patient data. Lancet. 2007;369:1791.

Conde-Agudelo A, Villar J, Lindheimer M. World Health Organization systematic review of screening tests for preeclampsia. Obstet Gynecol. 2004;104:1367.

Coomarasamy A, Honest H, Papaioannou S, et al. Aspirin for prevention of preeclampsia in women with historical risk factors: a systematic review. Obstet Gynecol. 2003;101:1319.

Nassar AH, Adra AM, Chakhtoura N, et al. Severe preeclampsia remote from term: labor induction or elective cesarean delivery? Am J Obstet Gynecol. 1998;179:1210.

Level III

American College of Obstetricians and Gynecologists. Chronic hypertension in pregnancy. ACOG Practice Bulletin 29. Obstet Gynecol. 2001;98:177.

American College of Obstetricians and Gynecologists. Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin 33. Obstet Gynecol. 2002;99:159.

Brown MA, Mackenzie C, Dunsmuir W, et al. Can we predict recurrence of pre-eclampsia or gestational hypertension? BJOG. 2007;114:984. Epub 2007 Jun 14

Duley L, Meher S, Abalos E. Management of pre-eclampsia. BMJ. 2006;332:463.

Martin JNJr, Rose CH, Briery CM. Understanding and managing HELLP syndrome: the integral role of aggressive glucocorticoids for mother and child. Am J Obstet Gynecol. 2006;195:914. Epub 2006 May 2

Sibai BM. Treatment of hypertension in pregnant women. N Engl J Med. 1996;335:257.

Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol. 2003;102:181.

Sibai BM. Magnesium sulfate prophylaxis in preeclampsia: lessons learned from recent trials. Am J Obstet Gynecol. 2004;190:1520.

Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005;105:402.

Sibai BM. Imitators of severe preeclampsia. Obstet Gynecol. 2007;109:956.

Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet. 2005;365:785.

Witlin AG, Sibai BM. Magnesium sulfate therapy in preeclampsia and eclampsia. Obstet Gynecol. 1998;92:883.

Zhang J, Villar J, Sun W, et al. Blood pressure dynamics during pregnancy and spontaneous preterm birth. Am J Obstet Gynecol. 2007;197:162.e1.

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