Acute Complications
of Preeclampsia
ERROL R. NORWITZ, MD, PhD,* CHAUR-DONG HSU, MD,
MPH,† and JOHN T. REPKE, MD†
Departments of Obstetrics & Gynecology, *Brigham & Women’s
Hospital, Harvard Medical School, Boston, Massachusetts, and
†University of Nebraska Medical Center, University of Nebraska
Medical School, Omaha, Nebraska
Preeclampsia is an idiopathic multisystem
disorder specific to human pregnancy and
the puerperium.
1
More precisely, it is a dis-
ease of the placenta, because it has also been
described in pregnancies where there is tro-
phoblast but no fetal tissue (complete molar
pregnancies). Although the pathophysiol-
ogy of preeclampsia is poorly understood, it
is clear that the blueprint for its development
is laid down early in pregnancy. It has been
suggested that the pathologic hallmark is a
complete or partial failure of the second
wave of trophoblast invasion from 16 to 20
weeks’ gestation, which is responsible in
normal pregnancies for destruction of the
muscularis layer of the spiral arterioles.
2
As
pregnancy progresses, the metabolic de-
mands of the fetoplacental unit increase.
However, because of the abnormally shal-
low invasion of the placenta, the spiral arte-
rioles are unable to dilate to accommodate
the required increase in blood flow, result-
ing in “placental dysfunction” that manifests
clinically as preeclampsia. Although attrac-
tive, this hypothesis remains to be validated.
Preeclampsia is a clinical diagnosis. The
classic definition of preeclampsia encom-
passes three elements: new-onset hyperten-
sion (defined as a sustained sitting blood
pressure 140/90 mm Hg in a previously
normotensive woman); new-onset protein-
uria (defined as >300 mg/24 hours or 2+
on a clean-catch urinalysis in the absence of
urinary tract infection); and new-onset sig-
nificant nondependent edema.
1
However,
more recent consensus reports have sug-
gested eliminating edema as a criterion for
the diagnosis.
3
A more extensive synopsis of preeclamp-
sia is beyond the scope of this discussion.
This monograph serves to review in detail
the diagnosis and management of several
acute maternal complications of preeclamp-
sia: eclampsia, HELLP (hemolysis, elevated
liver enzymes, low platelets) syndrome,
liver rupture, pulmonary edema, renal fail-
ure, disseminated intravascular coagulopa-
thy (DIC), hypertensive emergency, and hy-
pertensive encephalopathy and cortical
blindness.
Correspondence: Errol R. Norwitz, MD, PhD, Depart-
ment of Obstetrics & Gynecology, Brigham & Women’s
Hospital, Harvard Medical School, 75 Francis Street,
Boston, MA 02115. E-mail: enorwitz@partners.org
CLINICAL OBSTETRICS AND GYNECOLOGY
Volume 45, Number 2, 308–329
© 2002, Lippincott Williams & Wilkins, Inc.
CLINICAL OBSTETRICS AND GYNECOLOGY / VOLUME 45 / NUMBER 2 / JUNE 2002
308