Clinical presentation of women readmitted with postpartum severe preeclampsia or eclampsia.

OBJECTIVE: To identify symptoms that prompted a group of women readmitted for postpartum severe preeclampsia or eclampsia to seek medical care. DESIGN: Retrospective, case-control. SETTING: Tertiary-care teaching hospital. SUBJECTS: The study group consisted of 53 women readmitted in the postpartum period with severe preeclampsia or eclampsia. The control group was matched two-to-one with an index study participant and consisted of 106 women who had intrapartum severe preeclampsia or eclampsia. MAIN OUTCOME MEASURES: Patient symptoms, physical findings, laboratory assays. RESULTS: Neurologic complaints, malaise, and nausea and vomiting were reported more often in women who were readmitted than in mothers with intrapartum preeclampsia (all p values less than .001). Headaches were positively correlated with systolic, diastolic, and mean arterial blood pressure in women who were readmitted (all p values less than .05), although there was no relationship between blood pressure and headaches in the control group. In addition, multivariate analysis revealed that study participants were more likely to deliver at full term, have headaches and malaise, have normal platelet values, and develop seizures than mothers in the control group, chi 2 = 155.7, p < .001. CONCLUSIONS: Women readmitted for postpartum severe preeclampsia or eclampsia have a clinical presentation that differs from that of intrapartum preeclampsia or eclampsia.

The antiphospholipid antibody syndrome: an overview.

The antiphospholipid antibody syndrome is characterized by the presence of maternal anticardiolipin antibodies and/or the lupus anticoagulant in association with recurrent pregnancy loss, thrombotic events, and/or thrombocytopenia. This disorder occurs rarely, but pregnant patients with antiphospholipid antibodies are at risk for adverse maternal and perinatal outcomes. This article reviews the antiphospholipid antibody syndrome, including its pathophysiology, clinical sequelae, diagnostic criteria, medical treatment, and nursing care.

Role of laminin in maintenance of type II pneumocyte morphology and function.

Loss of differentiated function by type II pneumocytes plated on plastic surfaces was demonstrated by decreased lamellar body content, increased cellular protein, and rapid cellular flattening, changes that were retarded modestly by plating cells on laminin-coated surfaces. Laminin surfaces also inhibited [3H]thymidine (THM) incorporation into cellular DNA by 40% compared with plastic at 40 h, but did not alter an additional mitogenic effect of rat serum over fetal calf serum. In contrast, cells plated on the laminin-rich basement membrane-like gel formed from an extract of EHS mouse sarcoma, matrix gel (MG), maintained a high content of intracellular lipids in lamellar inclusions and retained a rounded morphology for at least 3 days. MG markedly inhibited THM incorporation and morphological changes when cells were cultured on this surface or when MG was formed over cells initially plated on plastic for various intervals. The importance of the laminin component of MG was demonstrated when these surfaces were pretreated with a highly specific antilaminin serum. Type II cells commenced flattening on the treated MG surface, and THM incorporation increased with the same time course as did control cells on plastic. The data suggest that short-term culture and study of differentiated type II pneumocytes may require a laminin-rich substratum. THM incorporation into type II cell DNA provides an important early and sensitive index of cell-basement membrane interaction and subsequent maintenance of function.