•  This is a view of the basal plate.

•  The large spaces are fully converted decidual or uteroplacental vessels.

•  The black arrows point to vessels which are much smaller and which retain a muscular wall.

• Unknown

• Unknown

• Blood vessels either fail to undergo normal physiologic conversion or develop pathologic changes following conversion

• Associated with pregnancy induced hypertension

• Associated with anticardiolipin antibodies and lupus anticoagulant

• 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

• 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

• 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

• Benirschke K, Kaufmann P. Pathology of the Human Placenta, third edition, New York: Springer Verlag, 1995, pp. 484-500.

• Current literature from PubMed at National Library of Medicine