How is Shock Liver Diagnosed?

Hepatic shock is also called as shock liver, ischemic hepatopathy or hypoxic hepatitis. This condition is very complex to identify, hence, a differential diagnostic procedure is followed. Clinical diagnosis is based on some characteristic feature that includes

• Cardio-pulmonary or circulatory failure with or without associated hypotension.
• Massive and rapidly reversible increases in serum aminotransferase levels.
• Exclusion of other causes of severe acute liver injury, for example, acetaminophen overdose, viral hepatitis, and toxin-mediated liver damage.
• Hypoxic hepatitis, toxin- or drug-induced liver injury, autoimmune hepatitis, and liver trauma are some of the leading causes of rapidly elevated liver enzymes.

The diagnosis of hypoxic hepatitis can be presumed without liver biopsy if the patients fulfill the above 3 criteria (characteristic feature). In some cases, liver biopsy may be helpful in the diagnosis of hypoxic hepatitis. The identification of centrilobular necrosis in the liver biopsy indicates the reduced supply of arterial oxygen. Centrilobular necrosis is essential if the hypoxic hepatitis diagnosis is uncertain. It is difficult to predict particularly when aminotransferase levels are less than 20 times the upper limit of normal. Biopsy is commonly not advisable in hypoxic hepatitis patients because of multiple co-morbidities cause excess of bleeding.

Non-invasive imaging options like abdominal ultrasonography can be supportive in the diagnosis of hypoxic hepatitis. Other imaging techniques, like computed tomography or magnetic resonance imaging, are not required for diagnosis but may help to exclude other causes of liver injury. Dilation of the inferior vena cava and suprahepatic veins due to passive congestion is suggestive of hypoxic hepatitis. However, the diagnostic utility of ultrasonography in hypoxic hepatitis has not yet been validated.

For example, viral hepatitis typically has lower peaks in serum lactate dehydrogenase than does hypoxic hepatitis. In addition, the pattern of liver injury in hypoxic hepatitis is hepatocellular rather than cholestatic, so large increases in alkaline phosphatase are atypical.

It is generally acknowledged that the diagnosis of ischemic hepatitis mainly depends on the relevant lab tests, such as ALT, AST, LDH, ALP, TB, γ-GT, coagulation factor and albumin levels. A decrease in albumin and coagulation factors is the pivotal laboratory finding. Although these parameters have low sensitivity and specificity, they emerge as a result of hepatocellular or bill ducts injury and widely used to detect hepatic injury. The incidence of liver dysfunction may be underestimated if traditional static measures such as aminotransferase or bilirubin only are considered. Dynamic tests such as indocyanine green clearance are useful for monitoring perfusion and global liver function.

There are multiple causes of low blood pressure, also called hypotension, which can lead to hepatic ischemia including a) Abnormal heart rhythms, b) Dehydration, c) Heart Failure, d) Infection, e) Severe bleeding, f) Blood clot in the main artery to the liver (hepatic artery), g) Swelling of blood vessels leading to reduced blood flow (vasculitis)

Hepatic shock is also known as shock liver, ischemic hepatopathy or hypoxic hepatitis, which all has the same pathophysiology causing hepatic ischemia or hypoxia. Shock liver is characterized by elevation of hepatic enzymes either transient or persistent because of hepatic cellular injury. This rise in hepatic enzymes is subtle most of the times, but researches have shown some cases with high enzyme levels. It is detected frequently in critically ill patients, especially ICU patients.

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