Changes in the Coagulation Mechanism Following Wounding and Resuscitation with Stored Blood : A Study of Battle Casualties in Korea

1. The coagulation system was studied in eleven battle casualties immediately after they had been wounded and resuscitated and during the first days of their convalescence.

2. In general the clotting time was shorter than normal and the platelet count and fibrinogen concentration were greater than normal. Prothrombin activity as measured by the one-stage test averaged 50 per cent of normal immediately after resuscitation with large transfusions of stored blood. This defect corrected itself within one to three days, but about the fourth day prothrombin activity again was reduced to about 50 per cent of normal and thereafter recovered gradually.

3. The primary fall of prothrombin activity was not proved to be caused by a lack of prothrombin but appeared in some cases to be related to a lack of labile factor which may have been a consequence of large transfusions of stored blood deficient in the labile factor. The prothrombin time was not always corrected by addition of labile factor. The defect of the coagulation mechanism was never great enough to cause serious hemorrhage. A tendency to ooze was noted in patients who had received over 20 pints of blood in a short time. It is suggested that this may have been due to the presence of a great number of immature platelets in the circulation. No fibrinolytic reactions were observed.

4. The secondary fall of prothrombin activity was not due to the lack of prothrombin. The defect of the coagulation mechanism could be corrected by the addition of heated serum that was free of prothrombin, thrombin, labile factor, stable factor, and thromboplastic activity. The factor responsible for the correction of the coagulation defect was heat stable (56 C. for 30 minutes in the presence of oxalate) and was not absorbed by tricalcium phosphate gel. Of the known factors involved in the coagulation system, these two characteristics eliminate all except the platelet factor 3. This fall in prothrombin activity was not associated with any clinical hemorrhagic tendency.