Liver failure coagulopathy

Coagulopathy is a common complication of liver disease. Synthesis of vitamin K and clotting factors is impaired in patients with cirrhosis and acute liver failure. Cirrhosis can also cause a reduced platelet synthesis of thromboxane-2, and a platelet adhesion defect is sometimes seen [8]. Cholestatic patients may have deranged clotting due to vitamin K malabsorption. 

Acute liver failure (ALF) is defined as an acute clinical picture with jaundice due to a most severe disorder in the liver function and/or massive liver cell necrosis which, without any pre-existing liver disease, culminates in hepatic coma (= endogenous coma) within 8 weeks. Potentially, the condition is fully reversible (C. Trey et al., 1970). In addition, coagulopathy must also be present (D.F. Schafer et al., 1989). 

The clinical and laboratory findings of this sudden deterioration largely correspond to those of acute liver failure (see above). This also applies to potential complications such as coagulopathy, HE, ascites and/or HRS. 

Niacin is a safe drug to use and its toxicity is dose related. Niacin toxicity has been shown to manifest itself as altered mental status, nausea and vomiting (Mittal et al. 2007). Evidence shows that excess niacin can cause hepatic dysfunction with associated coagulopathy, jaundice and fulminant liver failure (Etchason et al. 1991 Fischer et al. 1991). In addition niacin overdose can cause impaired glucose control (Mittal et al. 2007). 

Acute liver failure (ALF) Acute severe injury to the liver in patients without prior liver disease resulting in synthetic dysfunction (such as coagulopathy) and encephalopathy. 

Complications The possible outcome of oesophageal haemorrhage can take the following forms (7.) haemorrhagic shock, (2.) acute liver or kidney failure, (S.) hepatic encephalopathy (culminating in hepatic coma), (4.) consumptive coagulopathy, and (5.) aspiration pneumonia. 

Summary 21-year-old female at 35-week gestation with malaise, nausea and vomiting, jaundice, elevated blood pressures, elevated Uver function tests, coagulopathy, hypoglycemia, and subsequently hepatic coma and renal failure. She has been diagnosed with acute fatty liver of pregnancy. 

B. Hepatic failure. Liver injury may be apparent within 24-36 hours, with rapidly rising transaminase levels. Fulminant hepatic failure may follow, with jaundice, encephalopathy, and death. Encephalopathy, metabolic acidosis, severe coagulopathy, and hypoglycemia are grave prognostic signs and usually predict a fatal outcome. 

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