The clinical presentation of liver failure can arise from many factors: hepatitis, alcoholic liver disease, etc. The end-result is cirrhosis and a fatty liver, which leads to intrahepatic obstruction and decreased liver function. Unfortunately, there is no other treatment of liver failure than transplantation. Instead, most patients receive treatment for complications that arise as a result of liver disease.
The following complications of liver failure can occur:
- Increased pressure in the portal vein (portal hypertension) resulting from intrahepatic obstruction.
- Oesophageal varices: portal hypertension causes increased pressure and dilation of the cardiac and oesophageal veins.
- Ascites: increased intra-abdominal pressure results in increased fluid transudation.
- Encephalopathy: high circulating levels of ammonia result from an increased ammonia uptake in the GI tract and decreased conversion of ammonia in the liver. High ammonia levels in the brain are associated with encephalopathic symptomatology.
Liver failure causes significant changes in the pharmacokinetic profile of drugs. In general, liver failure does all the following EXCEPT:
Extra info: Plasma clearance would be expected to DECREASE as a result of liver failure, thereby increasing a drugs terminal half-life. The volume of distribution can increase or decrease depending on the hydrophilicity of the drug. Finally, since there are fewer circulating proteins, it is likely that protein binding will decrease.
A patient can present with the clinical symptoms of liver failure within:
Extra info: Symptoms can occur after a few days if the liver failure is acute (such as that resulting from eating Amanita mushrooms or a paracetamol overdose), over months (e.g. as the result of hepatitis B infection), or over many years (as the result of alcohol use).