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Acute Inflammation

Cardiovascular Risk Factors

Chronic Inflammation

Coagulation Related Pathology

Introduction to IVF

Perinatal Pathology

Recurrent Obstetric Compromise

Uteroplacental Vascular Pathology

Uteroplacental Vascular Pathology Case Reports

Recurrent Obstetric Compromise

The single best predictor of obstetric compromise is a prior history of poor pregnancy outcome. However, the risk for subsequent pregnancies is not outcome specific; patients with early recurrent pregnancy loss are at risk for problems later in gestation including preeclampsia, spontaneous prematurity, fetal growth restriction and late fetal death if they maintain pregnancy past the first trimester. It would follow, therefore, that although the clinical manifestations may vary, there may be some pathophysiological links among these conditions that are potentially influenced by environmental and temporal factors, resulting in outcome variability. There is comparatively little documentation detailing the pathology of successive pregnancies with different sub-optimal pregnancy outcomes. It would seem logical that identification of the underlying pathophysiology would facilitate cost-effective clinical intervention to improve subsequent pregnancy outcome. The frustration and, in some cases, desperation, of patients with recurrent pregnancy loss has fostered the proliferation of interventions that are at the very least hotly contested both as far as scientific basis and efficacy. In order to create a sound strategy for patient management in cases of recurrent obstetric compromise, it is our thesis that diagnostic schemes should be established utilizing not only clinical, genetic but also histopathologic assessment.

The mechanisms by which pregnancy loss and/or compromise are effected are imprecisely understood and probably only indirectly assessed by current laboratory modalities. However, the goal of this perinatal pathology group has been to identify broad pathophysiologic processes that are biologically reasonable, including lesions that have been well documented in the placental histology literature. We acknowledge that there is neither complete consensus nor lack of inter-observer variance regarding the diagnosis of these lesions. Nevertheless, we present a framework for the classification of placental histopathologic diagnosis. This framework we use, and propose that such a framework, which permits identification of general pathophysiologic mechanisms underlying placental histopathology, is clinically relevant to the determination of causes of recurrent obstetric compromise.

 


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