Abstract
The activity of heparin cofactor, the major natural anticoagulant in human plasma, is deficient in disorders such as disseminated intravascular coagulation (DIC). Heparin cofactor activity was measured in plasmas from 20 burned patients and from Pseudomonas-infected and non-infected scald-burned rats by a modified thrombin time method using dilutions of test plasma in the presence of excess heparin and fibrinogen. Heparin cofactor activity appears to behave as an acute-phase reactant in the burned patients, increasing immediately after the burn is sustained. While with small burns it slowly returns to normal, with large burns there is a substantial reduction in activity, which is associated with infection with gram-negative organisms, coagulation changes suggestive of intravascular coagulation, and a 70% mortality rate. Heparin cofactor activity, higher in control rats than in control patients, increased immediately after the injury was sustained and remained elevated in the rat. When the animal was lethally infected with Pseudomonas aeruginosa after the thermal injury, there was a precipitous decline in activity subsequent to the initial increase. While alterations in the procoagulant system in burned patients have been studied, changes in the anticoagulant system have not. The present data indicate that heparin cofactor activity appears related to the size of the burn wound and the presence of infection, and may mirror the general hemostatic balance of the patient. The in-creased incidence of DIC and thromboembolic phenomena in thermally injured patients may reflect the role of heparin cofactor activity in the pathophysiology of thermal injury.
Published Version
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