American Journal of Obstetrics and Gynecology 

Abstract: This article presents a standard system of terminology recently approved by the International Continence Society, the American Urogynecologic Society, and the Society of Gynecologic Surgeons for the description of female pelvic organ prolapse and pelvic floor dysfunction. An objective site-specific system for describing, quantitating, and staging pelvic support in women is included. It has been developed to enhance both clinical and academic communication regarding individual patients and populations of patients. Clinicians and researchers caring for women with pelvic organ prolapse and pelvic floor dysfunction are encouraged to learn and use the system.

Abstract: In utero estimates of fetal weight were evaluated prospectively in 109 fetuses with the use of sonographic models developed in a previous study. This report confirms that the best in utero weight estimates result from the use of models based on measurements of head size, abdominal size, and femur length. Since the accuracy of these models (1 SD = 7.5%) is significantly better than those based on measurements of head and body (e.g., biparietal diameter, abdominal circumference), we recommend routine use of such models in obstetric sonography.

Abstract: Despite intense study preeclampsia remains enigmatic and a major cause of maternal and fetal morbidity and mortality. Most investigative efforts have focused on the hypertensive component of this disorder with reduced attention given to other equally important characteristics. Increased sensitivity to pressor agents and activation of the coagulation cascade occur early in the course of preeclampsia, often antedating clinically recognizable disease. Inasmuch as endothelial cell injury reduces the synthesis of vasorelaxing agents, increases the production of vasoconstrictors, impairs synthesis of endogenous anticoagulants, and increases procoagulant production, these cells are likely to be implicated in the pathophysiology of preeclampsia. Indeed, evidence of endothelial cell injury is provided by the most characteristic morphologic lesion of preeclampsia, glomerular endotheliosis. Additional support for this hypothesis is derived from reports that indicate increased levels of circulating fibronectin (which can be released from injured endothelial cells) and increased factor VIII antigen present in the blood of preeclamptic women. More recently, direct evidence of activities that injure endothelial cells in vitro and increase the contractile sensitivity of isolated vessels has been presented. We propose that poorly perfused placental tissue releases a factor(s) into the systemic circulation that injures endothelial cells. The changes initiated by endothelial cell injury set in motion a dysfunctional cascade of coagulation, vasoconstriction, and intravascular fluid redistribution that results in the clinical syndrome of preeclampsia.