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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

Uteroplacental Vascular Pathology Case Reports

CASE 1: This 32 year old woman presented at 32 weeks for evaluation of decreased fundal height. Ultrasonography showed oligohydramnios, fetal biometry at the 5th percentile, and absent end-diastolic flow on umbilical artery Doppler velocimetry. After one course of antenatal steroids, delivery was induced for non-reassuring fetal testing. The 180 gram placenta showed uteroplacental vessels with absent physiologic conversion, fibrinoid necrosis/atherosis and chronic vasculitis. Small distal villi were fibrotic and poorly vascularized. This is a "typical" case of preterm preeclampsia with chronically abnormal uteroplacental vascular conversion, with a small placenta, defective arborization, reduced placental nutrient transport capacity and fetal compromise.

CASE 2: This 28 year old woman with two previous preeclamptic pregnancies presented at 29 weeks’ gestation with complaints of headache and excessive weight gain. Physical examination and admission laboratory tests confirmed a diagnosis of severe preeclampsia, with thrombocytopenia and elevated liver enzymes. Fetal biometry showed all measurements to be at or greater than the 60th percentile for gestational age. The patient was induced for maternal indications and delivered a viable infant. The 340 gram placenta (normal to large for gestational age) demonstrated diffuse chronic marginating choriodeciduitis with dense decidual plasma cell infiltrates. Multifocal uteroplacental thrombi were accompanied by subacute placental abruption. When preeclampsia is recurrent, the possibility of maternal subclinical auto/allo-immune pathology, as well as underlying renal or metabolic disease, should be considered. In comparison to Case 1, this placenta showed normal development until the apparently acute onset of uteroplacental thrombosis. At 2 months post partum, she was found to have phospholipid antibodies. We have found thrombosis of otherwise structurally normal uteroplacental vessels plus plasma cells to be common in the phospholipid antibody syndrome. When vascular pathology is accompanied by chronic inflammatory lesions, simple anticoagulation may not be effective, if the principal drive to tissue injury is immune in nature. This type of evaluation of the underlying processes of tissue injury in a compromised pregnancy are obviously useful when a treatment appears to have "failed"; histology may show that treatment was rather misdirected to trying to remedy a symptom of a very different principal disease.

 


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