Ischemic hepatitis refers to reversible severe hypotension and hypoxia leading to central lobular necrosis of the liver, often caused by congestive heart failure, shock, liver trauma, or post-cardiac surgery, resulting in cardiogenic or hypovolemic shock, particularly associated with post-shock hepatic reperfusion injury. The clinical manifestations resemble acute hepatitis, with persistently and significantly elevated alanine aminotransferase (ALT) levels, but without evidence of viral hepatitis infection or hepatotoxic drug exposure.

bubble_chart Pathogenesis

The pathogenesis involves xanthine oxidase-mediated generation of oxygen free radicals in the liver and complement activation.

bubble_chart Pathological Changes

Central necrosis of hepatic lobules, or even involvement of the entire hepatic lobule, may occur with congestion. The exact incidence remains unclear.

bubble_chart Clinical Manifestations

1. Manifestations of underlying diseases

This condition is commonly seen after cardiac surgery, especially in cases involving multiple valve replacements with prosthetic valves, acute myocardial infarction, and left ventricular failure caused by grade III arrhythmias, as well as grade III infections and sepsis. It is occasionally observed in cases of massive upper gastrointestinal bleeding occurring on the background of chronic liver disease. The aforementioned factors can all lead to a significant reduction in hepatic blood supply, with little relation to hepatic congestion.

2. Acute hepatitis-like manifestations

Ischemic hepatitis may also present with symptoms such as loss of appetite, discomfort and pain in the right upper quadrant, jaundice, and hepatomegaly. However, the more characteristic and common features are markedly elevated serum ALT and AST (aspartate aminotransferase) levels, which can reach more than 10 times the normal value, rising within 1–3 days of onset and rapidly returning to normal within 8 days. Concurrent increases in blood bilirubin, alkaline phosphatase, and lactate dehydrogenase (LDH) may also occur. Since LDH elevation can also stem from myocardial infarction, a significant rise in the LDH isoenzyme (LDH₅

bubble_chart Diagnosis

The diagnosis of this disease should meet the following criteria:

1. Significant and persistent elevation of ALT and AST within 3 days after grade III hypotension;

2. Exclusion of recent acute myocardial infarction;

3. Absence of serological markers for hepatitis virus infection, and exclusion of liver damage caused by toxins and chemicals.

bubble_chart Prognosis

Most patients can recover, which may be related to the intact reticular framework of the hepatic lobules after necrosis, serving as a template for hepatocyte proliferation. This condition rarely leads to liver failure. The mortality rate is usually determined by the underlying primary disease.

bubble_chart Differentiation

1. Acute sexually transmitted disease toxic hepatitis

This disease can be diagnosed by detecting serum hepatitis markers in patients, such as antigens or antibodies of hepatitis A, B, C, or even D viruses, or nucleic acid molecules (PCR method). However, it is somewhat difficult to diagnose ischemic hepatitis in virus carriers. In patients with ischemic hepatitis, aminotransferases (ALT, AST) often rise rapidly within 48 hours of onset and return to normal within 5–10 days, whereas the changes are slower in viral hepatitis. LDH is significantly elevated in ischemic hepatitis, whereas in viral hepatitis, it is only grade I elevated or not elevated at all. Liver biopsy and pathological examination can help differentiate the two.

2. Acute myocardial infarction

This disease can also cause changes in serum enzymes, but its typical colicky pain symptoms and dynamic electrocardiographic changes make it easy to distinguish from ischemic hepatitis. If necessary, testing for creatine phosphokinase isoenzyme (CPK-MB) and LDH₁

The treatment of this disease should focus on maintaining appropriate cardiac output. Aggressive and powerful diuresis can further reduce blood volume, worsen liver ischemia, and promote hepatocyte necrosis, which warrants attention. Dopamine can increase liver blood flow and has a cardiotonic effect, making it a viable option. Other drugs for preventing and treating shock/reperfusion liver injury are still in the experimental stage.