Liver Decompensation

The anatomy and physiology of the liver make it susceptible to injury from infection, autoimmune disorders, toxins and ischemia. The liver can compensate for a significant amount of damage through regeneration but if disease inhibits replacement of lost hepatocytes a decompensation threshold is reached after which liver functions will decline markedly. During the compensated stage, patients usually exhibit few signs or symptoms of hepatic insufficiency except perhaps jaundice. Their routine lab values can be within normal range or mildly impaired. However, tests like galactose tolerance or indocyanine green can demonstrate significant loss of hepatocytes.

When the liver fails to meet the needs of the body, the patient may exhibit minor signs of liver disease including: nausea, diarrhea, anorexia and fatigue.

More serious signs of liver failure include:


ALF Classification
Causes of ALF in the U.S.*
  • Hyperacute - jaundice to encephalopathy 0-7 days
  • Acute - jaundice to encephalopathy 8-28 days
  • Subacute - jaundice to encephalopathy 29-84 days
  • Acetaminophen overdose 46%
  • Unknown 14%
  • Drug/toxin reactions 12% (antibiotics, NSAIDs, anticonvulsants)
  • Hepatitis B virus 7.7%
  • Autoimmune Hepatitis 5.9%
  • Ischemia 4.6%
  • Hepatitis A virus 2.6%
  • Wilson disease 1.4%
  • Budd-Chiari syndrome 0.9%
  • Pregnancy 0.8%
  • Other 4.8%

Acetaminophen Toxicity

Acetaminophen is oxidized to the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI).* At normal therapeutic dosage any NAPQI produced is rapidly neutralized by the chief hepato-cellular anti-oxidant, glutathione. Neutralizing NAPQI depletes available stores of glutathione. If the amount of NAPQI exceeds available glutathione the hepatocyte is exposed to oxidative damage which can cause inflammation or cell death. Glutathione is also consumed in the process of neutralizing the metabolic by-products of ethanol. Therefore, consuming ethanol with acetaminophen increases the toxicity of acetaminophen or any other source of oxidative stress.*

Acute Liver Failure(ALF) is a rare life threatening syndrome characterized by: a. abrupt loss of liver function affecting a previously asymptomatic patient, b. coagulopathy (INR >1.5), c. altered mental status. Acute liver failure has been classified as "hyperacute", "acute" and "subacute" based upon the time from jaundice to hepatic encephalopathy.*

The etiology of ALF varies geographically. In the U.S., hyperacute liver failure is usually caused by acetaminophen overdose. Acetaminophen overdose with a jaundice to encephalopathy interval of 0-7 days has a fair likelihood of spontaneous recovery. A jaundice-to-encephalopathy interval of >28 days is usually caused by idiosyncratic drug reactions. It has a very poor prognosis without liver transplantation. Improvements in intensive care and liver transplantation have significantly affected survival rates. Today a U.S. patient receiving care in a liver transplant center has about a 40% chance of spontaneous recovery and about 65% survival rate following liver transplantation.*

Management of ALF requires a thorough history/physical and labs to determine etiology and rule out the presence of chronic liver disease or sepsis. If acetaminophen overdose is suspected IV administration of N-acetylcysteine is the first line of treatment. N-acetylcysteine assists remaining hepatocytes to replace glutathione needed to reduce further oxidative stress. The third step is to determine if the patient should be transferred to a liver transplant center. Management of multi-organ system failure (MOSF) often complicates ALF and is best managed in an experienced facility capable of providing transplant if indicated. Patients with an INR >2 or a Grade 2 hepatic encephalopathy or whose prognosis is poor due to age and etiology should be considered for transfer to a liver transplant center where experienced professionals can evaluate for transplant listing.*

Chronic Liver Disease (CLD) and cirrhosis combined were the 12th most frequent cause of death in the U.S. in 2004.* CLD by definition is a liver illness which has not resolved within 6 months. CLD is characterized by progressive replacement of hepatocytes by fibrosis and eventual cirrhosis. The scar tissue associated with fibrosis and cirrhosis disrupts liver architecture obstructing blood flow and bile excretion. Cirrhotic scarring eventually isolates and encapsulates islands of hepatocytes. Cirrhosis is the common end stage for most chronic liver diseases.

Symptoms of cirrhosis reflect a loss of hepatocyte function resulting in symptoms which include:

Diagnosis of cirrhosis is made based upon:

Cirrhosis is classified by morphology:

Treatment of cirrhosis is focused on slowing progression and the risk of complications associated with the underlying cause:

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