Disseminated intravascular coagulation in a horse with postpartum ulcerative colitis and laminitis.
Hemostatic studies were conducted on a five year old Belgian mare presented two days postpartum with colic and laminitis that was unresponsive to treatment.The mare was moderately thrombocytopenic with plasma fibrinogen levels more than twice that of a normal control horse. Platelet function as evaluated by aggregometry indicated that the circulating platelets were markedly hyporesponsive. Activated partial thromboplastin times and prothrombin times were prolonged. Para-coagulation tests (protamine sulfate and ethanol gelation) were strongly positive and fibrin degradation products were significantly elevated in the serum.The laboratory data suggested that the clinical bleeding was the result of the development of disseminated intravascular coagulation. The data were compatible with intravascular activation of the clotting mechanism, consumption of hemostatic factors, inhibition of platelet function and enhanced stimulation of the fibrinolytic mechanism.This report illustrates the complexity of the hemostatic abnormalities associated with pathological overactivation of the hemostatic mechanism. Factors such as tissue thromboplastins and/or endotoxins can stimulate disseminated intravascular coagulation, particularly during pregnancy or in the early postpartum period when a physiological "hypercoagulable" state already exists.
Johnstone
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Blackwell
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