A central role in the emergence of acute traumatic coagulopathy
is thought to be played by hypoperfusion resulting due to
shock and hypotension.5 There is a direct correlation between
the degree of hypotension and the laboratory derangements
in the coagulation profile.
Hypoperfusion in trauma patients is associated with a
moderate, dose-dependent reduction in the activity of coagulation
factors II, VII, IX, X, and XI, and a more pronounced
reduction in factor V activity, which is relatively independent
of the severity of shock. The mechanisms underlying
decreased factor V activity may be due to activated protein C
mediated cleavage