Shock in pregnancy: pathophysiology and morphologic findings.
Sepsis and non-septic shock in pregnancy show characteristic modifications which are caused a) by physiologic changes in hemostasis primarily in the third trimester of pregnancy, b) by etiologic distinctions of shock regarded as pregnancy-specific, c) by hemodynamic changes in the circulation during pregnancy, d) by the ability of the healthy, young organism to compensate adequately. In the dead fetus syndrome and in non-septic shock, i.e., in amnionic fluid embolism and in abruptio placentae, the clinical picture is often governed by marked secundary fibrinolysis. Retroplacental hematoma, the characteristic feature of premature placental separation, remains controversial as either the cause or sequela of the hemostatic disorder. Etiologic, pathogenetic, and morphologic similarities exist between septic abortion, chorioamnionitis, and puerperal sepsis, but the varying response of the maternal organism during the course of pregnancy leads to different clinical and morphologic pictures. Due to a decrease in fibrinolytic activity as a consequence of pregnancy, the hypercoagulability state in a septic endotoxic shock predisposes the kidneys to bilateral renal cortical necrosis, principally in the amnion infection syndrome.
D000031:Abortion, Septic / Q000150:complications; D004619:Embolism, Amniotic Fluid / Q000473:pathology; D005260:Female; D005313:Fetal Death / Q000473:pathology; D006801:Humans; D007673:Kidney Cortex Necrosis / Q000150:complications; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000473:pathology / Q000503:physiopathology*; D011263:Pregnancy Trimester, Third; D012769:Shock / Q000473:pathology / Q000503:physiopathology*; D012772:Shock, Septic / Q000150:complications / Q000473:pathology; D013577:Syndrome