Acute Complications of Preeclampsia
Total Page：16
File Type：pdf, Size：1020Kb
PROD. # GRF20214 CLINICAL OBSTETRICS AND GYNECOLOGY Volume 45, Number 2, 308–329 © 2002, Lippincott Williams & Wilkins, Inc. 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 clinically as preeclampsia. Although attrac- disorder specific to human pregnancy and tive, this hypothesis remains to be validated. the puerperium.1 More precisely, it is a dis- Preeclampsia is a clinical diagnosis. The ease of the placenta, because it has also been classic definition of preeclampsia encom- described in pregnancies where there is tro- passes three elements: new-onset hyperten- phoblast but no fetal tissue (complete molar sion (defined as a sustained sitting blood pregnancies). Although the pathophysiol- pressure Ն140/90 mm Hg in a previously ogy of preeclampsia is poorly understood, it normotensive woman); new-onset protein- is clear that the blueprint for its development uria (defined as >300 mg/24 hours or Ն2+ is laid down early in pregnancy. It has been on a clean-catch urinalysis in the absence of suggested that the pathologic hallmark is a urinary tract infection); and new-onset sig- complete or partial failure of the second 1 nificant nondependent edema. However, wave of trophoblast invasion from 16 to 20 more recent consensus reports have sug- weeks’ gestation, which is responsible in gested eliminating edema as a criterion for normal pregnancies for destruction of the 3 muscularis layer of the spiral arterioles.2 As the diagnosis. pregnancy progresses, the metabolic de- A more extensive synopsis of preeclamp- mands of the fetoplacental unit increase. sia is beyond the scope of this discussion. However, because of the abnormally shal- This monograph serves to review in detail low invasion of the placenta, the spiral arte- the diagnosis and management of several rioles are unable to dilate to accommodate acute maternal complications of preeclamp- the required increase in blood flow, result- sia: eclampsia, HELLP (hemolysis, elevated ing in “placental dysfunction” that manifests liver enzymes, low platelets) syndrome, liver rupture, pulmonary edema, renal fail- ure, disseminated intravascular coagulopa- Correspondence: Errol R. Norwitz, MD, PhD, Depart- thy (DIC), hypertensive emergency, and hy- ment of Obstetrics & Gynecology, Brigham & Women’s Hospital, Harvard Medical School, 75 Francis Street, pertensive encephalopathy and cortical Boston, MA 02115. E-mail: [email protected] blindness. CLINICAL OBSTETRICS AND GYNECOLOGY / VOLUME 45 / NUMBER 2 / JUNE 2002 308 Acute Complications of Preeclampsia 309 Eclampsia ditions. Eclamptic seizures are almost al- Eclampsia refers to the occurrence of one or ways self-limiting and seldom last longer more generalized convulsions and/or coma than 3 to 4 minutes. Eclamptic seizures are in the setting of preeclampsia and in the ab- clinically and electroencephalographically sence of other neurologic conditions.1 In indistinguishable from other generalized the past, eclampsia was thought to be the tonic-clonic seizures. In general, women end result of preeclampsia, hence the no- with typical eclamptic seizures who do not menclature. However, it is now clear that have focal neurologic deficits or prolonged coma do not require either electroencepha- seizures are only one of several clinical 9 manifestation of “severe” preeclampsia. lographic or cerebral imaging studies. The precise cause of seizures in women Clinical conditions other than eclampsia that with eclampsia is not known. Proposed eti- should be considered when evaluating a ologies include cerebral vasospasm with pregnant woman who has had a seizure are local ischemia, hypertensive encephalopa- listed in Table 1. thy with hyperperfusion, vasogenic edema, Approximately half of all cases of 4 eclampsia occur before term, with more than and endothelial damage. Despite recent 7 advances in detection and management, 20% occurring before 31 weeks’ gestation. preeclampsia/eclampsia remains the second Three quarters of the remaining cases occur most common cause of maternal death in the at term, developing intrapartum or within 48 United States (after thromboembolic dis- hours of delivery. Seizures due to eclampsia ease), accounting for 15% of all maternal always resolve postpartum, often within a deaths.5 It is estimated that eclampsia ac- few hours to days. Diuresis (>4 L/day) is be- counts for 50,000 maternal deaths per year lieved to be the most accurate clinical indi- worldwide.6 cator of resolution of preeclampsia/eclampsia, but it is not a guarantee against the develop- ment of seizures.10 Indeed, late postpartum EPIDEMIOLOGY AND INCIDENCE eclampsia (eclamptic seizures developing Eclampsia is most common in nonwhite, >48 hours postpartum but <4 weeks postpar- nulliparous women from lower socioeco- nomic backgrounds. Peak incidence is in the TABLE 1. Differential Diagnosis of teenage years and early 20s, but there is also Eclampsia an increased prevalence in women older than 35. Eclampsia before 20 weeks’ gesta- Cerebrovascular accident tion is rare; this should raise the possibility Intracerebral hemorrhage of an underlying molar pregnancy or anti- Cerebral arterial or venous thrombosis Hypertensive diseases phospholipid antibody syndrome. Hypertensive encephalopathy The overall incidence of eclampsia is Pheochromocytoma relatively stable, at 4 to 5 cases per 10,000 Space-occupying lesions of the central nervous live births in developed countries.7 In devel- system oping countries, however, the incidence var- Brain tumor Abscess ies widely from 6 to 100 per 10,000 live Metabolic disorders 8 births. Hypoglycemia Uremia Inappropriate antidiuretic hormone secretion CLINICAL MANIFESTATIONS AND resulting in water intoxication DIAGNOSIS Infectious etiology Eclampsia is a clinical diagnosis based on Meningitis evidence of one or more generalized convul- Encephalitis sions and/or coma in a preeclamptic woman Thrombotic thrombocytopenic purpura Idiopathic epilepsy and in the absence of other neurologic con- 310 NORWITZ ET AL tum) accounts for 25% of postpartum cases system, where it achieves anticonvulsant and up to 16% of all cases of eclampsia.10,11 levels within 1 minute, and it will control seizures in greater than 80% of patients MANAGEMENT within 5 minutes.13 However, most investi- A number of management strategies have gators recommend avoiding benzodiaz- been developed to prevent maternal and fe- epines because of the potentially profound tal complications resulting from eclampsia depressant effects on the fetus. This effect during the peripartum period. The immedi- becomes clinically significant when the total ate issues in caring for an eclamptic woman maternal dose of diazepam exceeds 30 mg. include maintenance of maternal vital func- tions, control of convulsions and blood pres- Treatment of Hypertension sure, prevention of recurrent seizures, and Cerebrovascular accident accounts for 15– evaluation for delivery. If the seizure is wit- 20% of deaths from eclampsia. The risk of nessed, maintenance of airway patency and hemorrhagic stroke correlates directly with prevention of aspiration should be the first the degree of elevation in systolic blood responsibilities of management. The partu- pressure and is less related to, but not inde- rient should be rolled onto her left side and a pendent of, the diastolic pressure.14 It is not padded tongue blade placed in her mouth, if clear whether there is a threshold pressure possible. above which emergent therapy should be in- stituted.14 Most investigators recommend Control of Convulsions aggressive antihypertensive therapy for sus- Although eclamptic seizures usually resolve tained diastolic pressures of more than 105 without treatment within 3 to 4 minutes, an to 110 mm Hg and systolic blood pressures anticonvulsant can be administered to of 160 mmHg or greater,3 although these achieve resolution of an ongoing convul- thresholds have not been tested prospec- sion. The treatment of choice is magnesium tively. The cerebral vasculature of women sulfate. In women already receiving magne- with underlying chronic hypertension can sium seizure prophylaxis, a serum magne- probably tolerate higher systolic pressures sium level should be obtained immediately without injury, whereas adolescents with and a rapid intravenous infusion of 1 to 2 g normally low blood pressures may benefit administered while awaiting the results. In from starting treatment at lower levels. Per- women not receiving seizure prophylaxis, sistent, severe elevation in blood pressure magnesium should be given as a rapid intra- (Ն160/110 mm Hg) should be treated to pre- venous infusion of 2 g repeated every 15 vent cerebrovascular accident. Initial treat- minutes to a maximum of 6 g. This loading ment options include hydralazine (5 mg in- dose may be given safely even in the pres- travenous push followed by 5- to 10-mg bo- ence of renal insufficiency. Exactly how luses as needed q 20 minutes) or labetalol magnesium acts as an anticonvulsant in (10–20 mg intravenous push, repeat q 10–20 eclampsia is not known. Several mecha- minutes with doubling doses not to exceed nisms have been proposed, including selec- 80 mg in any single dose, for a maximum tive vasodilatation of the cerebral vascula- total cumulative dose