ABSTRACT
The liver is the primary site of synthesis of most coagulation and fibrinolytic proteins,
and also plays a role in the clearance of hemostasis factors and their degradation
products. In acute liver failure, these functions are severely disturbed, and the
risk of hemorrhage is increased. Following a brief summary of the physiology of hemostasis,
this review describes the nature and frequency of hemostatic abnormalities in acute
liver failure. These abnormalities include quantitative and qualitative platelet defects,
impaired synthesis and clearance of the coagulation factors and related inhibitory
proteins, and enhanced fibrinolysis. Disseminated intravascular coagulation may also
play a role, although this syndrome is difficult to distinguish from changes due to
the failure of hepatic synthesis and clearance alone. At present, management options
are limited to support with blood products, although pharmacological manipulation
of the coagulation and fibrinolytic systems represent a potential area for future
study.
KEY WORDS
acute liver failure - platelets - coagulation factors - fibrinoly sis - disseminated
intravascular coagulation
