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Context: Subinvolution of the placental site is an anatomic cause of delayed postpartum uterine bleeding that may be underrecognized by general surgical pathologists., Objective: To review the physiology of uteroplacental arterial development and normal postpartum involution, and to present the characteristic clinical and histopathologic features of subinvolution., Data Sources: Literature review (MEDLINE via PubMed and Ovid) regarding the pathology and pathophysiology of placental site subinvolution. Review of the clinical and pathologic characteristics of our own institution's previously diagnosed cases of subinvolution from hysterectomy and endomyometrial curettage specimens., Conclusions: Surgical pathologists must be aware of the cardinal histopathologic findings of subinvolution, and this diagnosis must be considered in every postpartum curettage or hysterectomy specimen presented to the surgical pathologist. Subinvolution of the placental site is an important diagnosis, as this process implies an idiopathic cause, rather than an iatrogenic cause, of postpartum uterine bleeding. The etiology of placental site subinvolution remains poorly characterized.

Subarachnoid hemorrhage represents a rare event in pregnancy with a high mortality rate. We present the case of a 39-year-old pregnant woman who developed right vertebral artery dissection with subsequent massive subarachnoid hemorrhage with fatal outcome. The macroscopic and microscopic autopsy findings are described. A review of the literature with a discussion of the varied predisposing factors for vertebral artery dissection and subarachnoid hemorrhage and the rarity of these events in pregnancy is provided.

This case report describes a 31-year-old woman at 8 weeks' gestation with large arteriovenous malformation of the uterus involving bilateral uterine and ovarian arteries. She had a history of multiple pregnancy losses, as well as spontaneous copious vaginal hemorrhage. The patient underwent an embolization procedure followed by total abdominal hysterectomy and bilateral salpingo-oophorectomy. The uterus was very small (30 g) despite its gravid status, and the overall microscopic findings indicated Müllerian system hypoplasia in addition to vascular malformation.

A clinicohistologic study of acute atherosis in late complicated pregnancy was undertaken. Maternal vessels in the placental basal plate, underlying the amniochorial membranes and in placental bed biopsy specimens, were examined histologically. The earliest histologically convincing lesion acceptable as acute atherosis was fibrinoid necrosis with a perivascular mononuclear cell infiltrate, while lipophages were a late phenomenon. Any maternal uterine vessel that had not undergone physiologic vascular changes could be affected by acute atherosis. Acute atherosis was not seen in normal pregnancies or in pregnancies of diabetic women but was seen in pregnancies complicated by preeclampsia, small-for-gestational-age infants, or both. In pregnancies complicated by small-for-gestational-age infants, acute atherosis was not seen in the vessels in the decidua parietalis.

We describe herein circulating IgM antitrophoblast antibodies in a patient with recurrent pregnancy-associated vasculitis and intrauterine fetal demise. The patient also exhibited a lupus anticoagulant. Direct and indirect immunofluorescence studies were carried out with the patient's placenta, normal placentas, the patient's serum, and normal serum controls. The antitrophoblast antibodies may have contributed further to the risk of intrauterine death, already known to be associated with lupus anticoagulants. More information about the frequency of such antibodies is desirable and could be obtained in similar cases by the methods discussed.

We report a case of fetal death at 30 weeks' gestation followed by the unexpected death of the mother 28 1/2 hours later. At postmortem examination, extensive small-vessel thrombi were found in the maternal organs, including the uterus, kidney, and heart. In retrospect the mother had evidence of chronic pericarditis and myocarditis. Laboratory tests of antemortem serum demonstrated elevated titers of anti-double-stranded DNA and of anticardiolipin antibodies.

The purpose of this article is to provide a critical review of our current knowledge of the pathogenic mechanisms of human cardiomyopathy in the context of accepted morphologic findings (gross, microscopic, ultrastructural) and the clinical presentation of this disease. It is our intent to emphasize the numerous difficulties encountered in categorizing patients with cardiomyopathy to pursue investigations in the pathogenesis and origins of this puzzling cardiac condition. It is our belief that such difficulties stem primarily from the existing classification of cardiomyopathies, which is mostly empirical and somewhat vague. This is particularly true in regard to the dilated cardiomyopathies that probably encompass multiple entities grouped under the umbrella of cardiomegaly and dilation. The article's objective is to summarize clinical symptoms and signs, modalities of diagnostic investigations, and prognosis for each category of cardiomyopathy. However, the main purpose of this article is to present recent findings on the origins, possible autoimmune basis of the disease, and results of immunologic studies in patients with cardiomyopathy.