We have reviewed 47 patients (pts.) with severe acute DIG (mean fibrirogen 100.5 mg/dl,
platelets 45,700/μl, prothrombin time 19.4 sec, partial thrcmboplastin tiire 86.5
sec). Most pts. were critically ill. Predisposing conditions included infection (32),
shock (32), and surgery or trauma (21). Routine treatment included aggressive therapy
for underlying diseases and metabolic disturbances, vitamin K, folate, and blood components.
Twelve pts. were treated with heparin and 10 (83%) died. Ifeparin apparently benefited
only 1 pt, and in 7 bleeding increased. Thirty (86%) of 35 pts. who did not receive
heparin died. Analysis suggested that heparin would not have affected the outcome
in any of them. In all pts. who died multiple potential causes were present. Thrombosis,
ischemia, or hemorrhage were the apparent immediate cause of death in only 2 pts.
but were contributory causes in others. In most pts. with significant complications
potentially attributable to Die other causative pathology was present. Twenty-five
pts. had autopsies. Microvascular thrombi were not found but large vessel thrombi
were relatively common. We conclude that 1) Severe DIG is usually a preterminal event
in criticallv ill pts. 2) Other pathology may be more important than DIC when death
or significant thrombosis or bleeding occur. 3) Heparin is rarely beneficial and often
increases bleeding. 4) Microvascular thrombi may not be the only mechanism responsible
for DIC.
