Abstract
Acute liver failure (ALF) is a rare but rapidly progressing syndrome, marked by severe liver dysfunction and altered mental status. While definitions of ALF vary across different guidelines, with timelines ranging from 4 to 26 weeks between jaundice onset and encephalopathy, the key defining features remain encephalopathy and coagulopathy. Elevated coagulation markers, particularly prothrombin time and international normalized ratio, have traditionally been associated with bleeding risks. However, emerging evidence suggests a rebalanced state of coagulation in ALF, similar to cirrhosis, where bleeding risks—both spontaneous and procedural—are surprisingly low. Viscoelastic hemostatic assays and thrombin generation assays further confirm this rebalanced hemostatic state. Current guidelines for correcting coagulopathy in ALF remain limited, typically reserved for active bleeding or prior to high-risk invasive procedures.
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