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| Decidual Vasculopathy |
| Etiology • Unknown |
| Pathogenesis • Unknown • Blood vessels either fail to undergo normal physiologic conversion or develop pathologic changes following conversion, |
| Epidemiology • Associated with pregnancy induced hypertension • Associated with anticardiolipin antibodies and lupus anticoagulant |
| General Gross Description • Not grossly visible lesions in the blood vessels • Sequelae to decidual vasculopathy may be grossly evident as a small placenta (acceleration of villus maturation) or one displaying infarcts or abruption |
| General Microscopic Description • Unconverted vessels exhibit round cross section with a preserved muscularis and intima • Thrombosed vessels may exhibit mural or occlusive thrombosis with or without recanalization; thrombi may organize with smooth muscle proliferation • Lymphocytes or plasma cells may involve the wall of the vessel • Fibrinoid necrosis can be recognized as acellular, brilliantly eosinophilic and glassy transformation of the vessel wall • Atherosis, often accompanying fibrinoid necrosis, consists of an intramural accumulation of foamy macrophages resembling cells seen in atherosclerosis • These changes may occur in converted or unconverted vessels |
| Clinical Correlation • Severity of clinical disease does not correlate well with severity of pathology • Thrombosed vessels may result in villous infarct • Necrotic vessels may rupture with abruption • Unconverted vessels may respond to vasospasm and also lead to abruption |
| References • Benirschke K, Kaufmann P. Pathology of the Human Placenta, third edition, New York: Springer Verlag, 1995, pp. 484-500. |
| Decidual Vasculopathy |
| Synopsis by: Melinda Sanders M.D. (T4F190M35100)[422] |
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