Search

High blood pressure in the postpartum period is most commonly seen in women with antenatal hypertensive disorders, but it can develop de novo in the postpartum time frame. Whether postpartum preeclampsia or eclampsia represents a separate entity from preeclampsia or eclampsia with antepartum onset is unclear. Although definitions vary, the diagnosis of postpartum preeclampsia should be considered in women with new-onset hypertension 48 hours to 6 weeks after delivery. New-onset postpartum preeclampsia is an understudied disease entity with few evidence-based guidelines to guide diagnosis and management. We propose that new-onset hypertension with the presence of any severe features (including severely elevated blood pressure in women with no history of hypertension) be referred to as postpartum preeclampsia after exclusion of other etiologies to facilitate recognition and timely management. Older maternal age, black race, maternal obesity, and cesarean delivery are all associated with a higher risk of postpartum preeclampsia. Most women with delayed-onset postpartum preeclampsia present within the first 7 to 10 days after delivery, most frequently with neurologic symptoms, typically headache. The cornerstones of treatment include the use of antihypertensive agents, magnesium, and diuresis. Postpartum preeclampsia may be associated with a higher risk of maternal morbidity than preeclampsia with antepartum onset, yet it remains an understudied disease process. Future research should focus on the pathophysiology and specific risk factors. A better understanding is imperative for patient care and counseling and anticipatory guidance before hospital discharge and is important for the reduction of maternal morbidity and mortality in the postpartum period., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Objective: This study was undertake to determine risk factors for adverse maternal outcomes among women with HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome., Study Design: Maternal medical records of pregnancies complicated by HELLP syndrome managed between July 1, 1992, and April 30, 1999, were reviewed. Risk factors evaluated included maternal age, parity, race, previous preeclampsia, chronic hypertension, gestational age at diagnosis, mean arterial blood pressure, nadir blood platelet count (<50,000 cells/microL vs > or =50,000 cells/microL), and peak serum levels of aspartate aminotransferase and lactate dehydrogenase. Maternal outcome variables analyzed included eclampsia, abruptio placentae, disseminated intravascular coagulopathy, pulmonary edema, pleural effusion, ascites, acute renal failure, liver hematoma, need for transfusion of blood products, cesarean delivery, and death. Statistical analysis was performed with the Student t test, the chi(2) test, and logistic regression analysis., Results: A total of 183 women with HELLP syndrome were studied. Eclampsia was present in 6%, abruptio placentae was present in 10%, and disseminated intravascular coagulopathy was present in 8%. Forty-one women (22%) required transfusion of blood products. Incidence of eclampsia significantly decreased with increasing gestational age, from 16% at < or =28 weeks' gestation to 3% at >32 weeks' gestation (P <.05) and was higher among African American patients than among white patients (12% vs 3%; P <.05). Logistic regression analysis showed an independent relationship between eclampsia and race (P <.05). Incidence of abruptio placentae was higher among women with previous preeclampsia than among women without this clinical history (26% vs 5%; P <.05). Disseminated intravascular coagulopathy was significantly associated with abruptio placentae (P <.0001) and acute renal failure (P <.0001). A nadir platelet count of <50, 000/microL, a peak serum aspartate aminotransferase level of >150 U/L, and a peak serum lactate dehydrogenase level of >1400 U/L were not independent risk factors for adverse outcome., Conclusions: Among women with HELLP syndrome, African American race is a risk factor for eclampsia. Both acute renal failure and abruptio placentae are associated with disseminated intravascular coagulopathy. Laboratory parameters of HELLP syndrome are not independent risk factors for adverse maternal outcome.

Objective: This study was undertaken to identify risk factors associated with adverse maternal outcome in pregnancies complicated by eclampsia., Study Design: This was a descriptive study of 399 consecutive women with eclampsia whose cases were managed at one perinatal center between August 1977 and July 1998. Data were collected. Risk factors studied included maternal age, race, parity, preexisting medical complications, and clinical and laboratory findings. Outcome variables were maternal morbidities. Data were analyzed by either chi(2) analysis or the unpaired Student t test as appropriate., Results: In the entire cohort of women with eclampsia major maternal complications included abruptio placentae (10%), HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome (11%), disseminated intravascular coagulopathy (6%), neurologic deficits and aspiration pneumonia (7%), pulmonary edema (5%), cardiopulmonary arrest (4%), acute renal failure (4%), and death (1%, n = 2 patients with antepartum onset). Women with antepartum eclampsia had significantly higher incidences of abruptio placentae (12% vs 6%; P <.05) and HELLP syndrome (14% vs 4%; P =. 005) than did those in whom eclampsia developed post partum. In contrast, women with postpartum eclampsia were more likely to have neurologic deficits develop (9% vs 2%; P =.0006) than were those with antepartum eclampsia. In addition, women in whom eclampsia developed at

A case of eclampsia in association with partial molar pregnancy is described. Cytogenetic analysis confirmed a 69,XXX karyotype, and pathologic examination of the fetus showed a meningomyelocele, exomphalos, incomplete intestinal rotation, and cerebral ventricular dilatation.

Experiments were performed on two groups of pregnant baboons. In the experimental group, the subrenal aortic blood flow was reduced by 58% of its original value at 100 days of gestational age. In the control group, the blood flow was measured but not restricted. In the experimental group fetal death occurred in three of 12 animals following the use of a single left-flank incision to approach both the renal artery and the abdominal aorta. In the control group, pregnancies in eight of nine animals went successfully to 165 days. In the experimental group the development of hypertension, a decrease in plasma renin activity, an increase in renal resistance, an increase in serum uric acid, and the development of glomerular changes consistent with those seen in human pregnancy-induced hypertension were noted. These studies demonstrate that pregnancy-induced hypertension can be produced experimentally in a pregnant baboon, and this model should prove useful in expediting studies on the pathophysiologic features and treatment of this condition.

The possibility that the etiology of toxemia might be immunologic has been held for over 70 years. In the past decade, numerous studies have been instituted in attempts to verify the possible role of the immune system in this disease. The present study was undertaken as a probe to determine if a gross difference in the numbers of T and B cell lymphocyte populations might exist between pre-eclamptic and normally pregnant women. Twenty-five normally pregnant women in the third trimester were compared to 25 pre-eclamptic women, and significant differences were noted. If, indeed, there is an immunologic basis for pre-eclampsia, it is more subtle than the methodology used in this study is capable of detecting.

The maternal coagulation mechanism has been investigated in an effort to identify its role, if any, in the pathogenesis of eclampsia. Thrombocytopenia was identified in 28 of 95 cases (29 per cent), a prolonged thrombin time in 19 of 38 (50 per cent), abnormally elevated serum fibrinogen-fibrin degradation products in two of 65 (3 per cent), and circulating fibrin monomer in one out of 20 (5 per cent). Overt hemolysis was rare (2 per cent). Thus the pattern as well as the degree of change in the maternal coagulation mechanism differed remarkably from that typical of severe abruptio placentae and of prolonged retention of a dead fetus, the classic obstetric models of fast and slow disseminated intravascular coagulation. It is concluded that the coagulation changes when present in eclampsia are effect rather than cause. Moreover, the changes may evolve primarily from platelet adherence at sites of vascular endothelial damage as the consequence of segmental vasospasm and vasodilatation rather than be triggered by the escape of thromboplastin from the placenta into the maternal circulation.

The purpose of this report was to investigate the potential usefulness of average mean arterial pressure, maximal mean arterial pressure, and maximal diastolic pressure during the second trimester in predicting the development of eclampsia in 207 nulliparas and 20 multiparas with eclampsia. In the nulliparas, both the mean arterial pressure and the maximal mean arterial pressure during the second trimester were greater than or equal to 90 mm Hg in 22% and 34% of the patients, respectively. For the multiparas, the percentages with greater than or equal to 90 mm Hg were 30% and 35%, respectively. Only 8.7% of nulliparas with eclampsia had a maximal diastolic pressure during the second trimester greater than or equal to 80 mm Hg and no patient had a diastolic pressure of greater than or equal to 90 mm Hg. A review of the literature suggests that the mean arterial pressure observed during the second trimester has poor predictive value for future development of preeclampsia-eclampsia. We conclude that there is no correlation between second-trimester blood pressure recordings and subsequent eclampsia.