PRACTICE
BULLETIN
CLINICAL MANAGEMENT GUIDELINES FOR
OBSTETRICIANGYNECOLOGISTS
NUMBER 33, JANUARY 2002
Diagnosis and
Management of
Preeclampsia and
Eclampsia
Hypertensive disease occurs in approximately 1222% of pregnancies, and it is
directly responsible for 17.6% of maternal deaths in the United States (1, 2).
However, there is confusion about the terminology and classification of these
disorders. This bulletin will provide guidelines for the diagnosis and management of hypertensive disorders unique to pregnancy (ie, preeclampsia and
eclampsia), as well as the various associated complications. Chronic hypertension has been discussed elsewhere (3).
Background
Definition
The National High Blood Pressure Education Program Working Group (hereafter
referred to as the Working Group) has recommended that the term gestational hypertension replace the term pregnancy-induced hypertension to describe
cases in which elevated blood pressure without proteinuria develops in a woman
after 20 weeks of gestation and blood pressure levels return to normal postpartum (4). According to the criteria established by the Working Group, in pregnant women, hypertension is defined as a systolic blood pressure level of 140
mm Hg or higher or a diastolic blood pressure level of 90 mm Hg or higher that
occurs after 20 weeks of gestation in a woman with previously normal blood
pressure (4). As many as one quarter of women with gestational hypertension
will develop proteinuria, ie, preeclampsia (5).
Preeclampsia is a syndrome defined by hypertension and proteinuria that
also may be associated with myriad other signs and symptoms, such as edema,
Pathophysiology
The etiology of preeclampsia is unknown, although much
of the literature has focused on the degree of trophoblastic invasion by the placenta (4). In cases of preeclampsia,
invasion by the trophoblast appears to be incomplete
(1618). Moreover, the severity of hypertension may be
related to the degree of trophoblastic invasion (19).
Preeclampsia also may be associated with significant
alterations in the immune response (4).
Vascular Changes
HELLP Syndrome
Women with severe preeclampsia and hepatic involvement may develop HELLP syndrome. In one study,
HELLP syndrome occurred in approximately 20% of
women with severe preeclampsia (26). As with severe
preeclampsia, HELLP syndrome is associated with an
increased risk of adverse outcomes, including placental
abruption, renal failure, subcapsular hepatic hematoma,
recurrent preeclampsia, preterm delivery, and even fetal
or maternal death (2630).
Hematologic Changes
Various hematologic changes also may occur in women
with preeclampsia, especially when the preeclampsia is
severe. Both thrombocytopenia and hemolysis may occur
as part of the HELLP syndrome, although the etiology is
unknown. Interpretation of hematocrit levels in the face
of severe preeclampsia should take into consideration
that hemolysis or hemoconcentration or both may occur.
Thus, the hematocrit level may be very low because of
hemolysis or very high secondary to hemoconcentration
in the absence of hemolysis. Lactate dehydrogenase is
present in erythrocytes in high concentration. A disproportionate elevation of levels of lactate dehydrogenase in
serum may be a sign of hemolysis.
Hepatic Changes
Renal Changes
As a result of vasospasm, the normal expected increase in
glomerular filtration rate and renal blood flow and the
expected decrease in serum creatinine may not occur in
women with preeclampsia, especially if the disease is
severe. Oliguria, commonly (albeit arbitrarily) defined as
less than 500 mL in 24 hours, also may occur secondary
to the hemoconcentration and decreased renal blood
flow. Rarely, persistent oliguria may reflect acute tubular
necrosis, which may lead to acute renal failure (8).
Fetal Changes
As a result of impaired uteroplacental blood flow or placental infarction, manifestations of preeclampsia also
may be seen in the fetal placental unit. These include
intrauterine growth restriction, oligohydramnios, placental abruption, and nonreassuring fetal status demonstrated on antepartum surveillance.
For mild preeclampsia, vaginal delivery at term is preferred. No randomized clinical trials have evaluated the
optimal method of delivery for women with severe
preeclampsia or eclampsia. Two retrospective studies
comparing induction of labor with cesarean delivery in
women with severe preeclampsia remote from term concluded that induction of labor was reasonable and was
not harmful to low-birth-weight infants (49, 50). The
decision to perform cesarean delivery should be individualized.
The following recommendations are based on limited or inconsistent scientific evidence (Level B):
The management of a woman with severe preeclampsia remote from term is best accomplished in
a tertiary care setting or in consultation with an
obstetriciangynecologist with training, experience,
and demonstrated competence in the management of
high-risk pregnancies, such as a maternalfetal medicine subspecialist.
Practitioners should be aware that although various
laboratory tests may be useful in the management of
women with preeclampsia, to date there is no reliable predictive test for preeclampsia.
The following recommendations are based primarily on consensus and expert opinion (Level C):
Summary of
Recommendations
Invasive hemodynamic monitoring should be considered in preeclamptic women with severe cardiac
disease, renal disease, refractory hypertension, pulmonary edema, or unexplained oliguria.
References
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(Level III)
2. Koonin LM, MacKay AP, Berg CJ, Atrash HK, Smith JC.
Pregnancy-related mortality surveillanceUnited States,
19871990. Mor Mortal Wkly Rep CDC Surveill Summ
1997;46(4):1736 (Level III)
3. Chronic hypertension in pregnancy. ACOG Practice Bulletin
No. 29. American College of Obstetricians and Gynecologists. Obstet Gynecol 2001;98:177185 (Level III)
4. Report of the National High Blood Pressure Education
Program Working Group on High Blood Pressure in
Pregnancy. Am J Obstet Gynecol 2000;183:S1S22
(Level III)
5. Saudan P, Brown MA, Buddle ML, Jones M. Does gestational hypertension become pre-eclampsia? Br J Obstet
Gynaecol 1998;105:11771184 (Level II-2)
6. North RA, Taylor RS, Schellenberg JC. Evaluation of a
definition of pre-eclampsia. Br J Obstet Gynaecol 1999;
106:767773 (Level II-2)
7. Levine RJ, Ewell MG, Hauth JC, Curet LB, Catalano PM,
Morris CD, et al. Should the definition of preeclampsia
include a rise in diastolic blood pressure >/= 15 mm Hg to
a level < 90 mm Hg in association with proteinuria? Am J
Obstet Gynecol 2000;183:787792 (Level II-2)
35. Friedman SA, Lindheimer MD. Prediction and differential diagnosis. In: Lindheimer MD, Roberts JM,
Cunningham FG, eds. Chesleys hypertensive disorders in
pregnancy. 2nd ed. Stamford, Connecticut: Appleton &
Lange, 1999:201227 (Level III)
36. Stamilio DM, Sehdev HM, Morgan MA, Propert K,
Macones GA. Can antenatal clinical and biochemical
markers predict the development of severe preeclampsia?
Am J Obstet Gynecol 2000;182:589594 (Level II-2)
37. Helewa ME, Burrows RF, Smith J, Williams K, Brain P,
Rabkin SW. Report of the Canadian Hypertension Society
Consensus Conference: 1. Definitions, evaluation and
classification of hypertensive disorders in pregnancy.
CMAJ 1997;157:715725 (Level III)
38. Lim KH, Friedman SA, Ecker JL, Kao L, Kilpatrick SJ.
The clinical utility of serum uric acid measurements in
hypertensive disease of pregnancy. Am J Obstet Gynecol
1998;178:10671071 (Level II-2)
53. Gilbert WM, Towner DR, Field NT, Anthony J. The safety and utility of pulmonary artery catheterization in severe
preeclampsia and eclampsia. Am J Obstet Gynecol 2000;
182:13971403 (Level II-3)
54. Clark SL, Cotton DB, Hankins GD, Phelan JP. Critical
care obstetrics. 3rd ed. Malden, Massachusetts: Blackwell
Science, 1997 (Level III)
41. The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood
pressure. Arch Intern Med 1997;157:24132446 [erratum
Arch Intern Med 1998;158:573] (Level III)
58. Sibai BM. Prevention of preeclampsia: a big disappointment. Am J Obstet Gynecol 1998;179:12751278
(Level III)
45. 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;105:300303
(Level I)
61. Levine RJ, Hauth JC, Curet LB, Sibai BM, Catalano PM,
Morris CD, et al. Trial of calcium to prevent preeclampsia. N Engl J Med 1997;337:6976 (Level I)
63. Chappell LC, Seed PT, Briley AL, Kelly FJ, Lee R, Hunt
BJ, et al. Effect of antioxidants on the occurrence of preeclampsia in women at increased risk: a randomised trial.
Lancet 1999;354:810816 (Level I)
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Diagnosis and management of preeclampsia and eclampsia. ACOG
Practice Bulletin No. 33. American College of Obstetricians and
Gynecologists. Obstet Gynecol 2002;99:159167
Evidence obtained from at least one properly designed randomized controlled trial.
II-1 Evidence obtained from well-designed controlled
trials without randomization.
II-2 Evidence obtained from well-designed cohort or
casecontrol analytic studies, preferably from more
than one center or research group.
II-3 Evidence obtained from multiple time series with or
without the intervention. Dramatic results in uncontrolled experiments could also be regarded as this
type of evidence.
III Opinions of respected authorities, based on clinical
experience, descriptive studies, or reports of expert
committees.
Based on the highest level of evidence found in the data,
recommendations are provided and graded according to the
following categories:
Level ARecommendations are based on good and consistent scientific evidence.
Level BRecommendations are based on limited or inconsistent scientific evidence.
Level CRecommendations are based primarily on consensus and expert opinion.