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.5
Markers of hypoperfusion, such as base deficit, might be
better and more readily available predictors of who all require
coagulation support than international normalized ratio or
activated partial thromboplastin time.
A central role in the emergence of acute traumatic coagulopathyis thought to be played by hypoperfusion resulting due toshock and hypotension.5 There is a direct correlation betweenthe degree of hypotension and the laboratory derangementsin the coagulation profile.Hypoperfusion in trauma patients is associated with amoderate, dose-dependent reduction in the activity of coagulationfactors II, VII, IX, X, and XI, and a more pronouncedreduction in factor V activity, which is relatively independentof the severity of shock. The mechanisms underlyingdecreased factor V activity may be due to activated protein Cmediated cleavage.5Markers of hypoperfusion, such as base deficit, might bebetter and more readily available predictors of who all requirecoagulation support than international normalized ratio oractivated partial thromboplastin time.
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