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