Why the study?
Does vitamin K deficiency or liver dysfunction contribute to prolonged prothrombin time and partial thromboplastin time in patients with DIC?
Does vitamin K deficiency or liver dysfunction contribute to prolonged prothrombin time and partial thromboplastin time in patients with DIC?
Prolonged prothrombin and partial thromboplastin times in DIC may be due to vitamin K deficiency or liver dysfunction, suggesting bleeding in these patients may be more appropriately treated with vitamin K than with heparin.
May indicate vitamin K deficiency contributing to coagulopathy in DIC; hypothesis-generating and should not yet change practice.
Summary. In an investigation of 34 patients with laboratory evidence of disseminated intravascular coagulation (DIC), 17 were found to have a prolonged prothrombin time, 11 a prolonged partial thromboplastin time, and only 10 a prolonged thrombin time. Coagulation factor assays in these patients revealed deficiency patterns compatible with vitamin K deficiency and/or liver disease. In addition, a prolonged prothrombin time rapidly returned to normal in five of seven patients given vitamin K1. It is suggested that vitamin K deficiency and liver dysfunction occurred as a complication of the primary condition that led to DIC. The practical implications of these findings are that a prolonged prothrombin time and partial thromboplastin time may occur in patients with laboratory evidence of DIC in the presence of a normal thrombin time. Under these circumstances bleeding in patients with laboratory evidence of DIC is likely to be caused by vitamin K deficiency or liver dysfunction and therefore may be more appropriately treated with vitamin K than with heparin.
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Mant et al. (1973) studied this question.
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