- Liver biopsy
Generally 10% neutral buffered formalin. Non–formalin-fixed tissue may be needed for tests such as microbiological analysis or copper quantification studies.
Gross processing in autopsy
Make consecutive liver slices, such as in the sagittal or coronal plane.
Basic gross examination
- Inspect the color and texture of the surfaces, including external and cut surfaces. Potential pathologies:
- Look for any focal change in the liver volume, mainly any tumor. If found: Further information: Liver tumor
- Determine liver weight. The standard reference range for men is 970–1,860 g (2.14–4.10 lb) and for women 600–1,770 g (1.32–3.90 lb).
- Weight. If abnormally low or high, preferably include the reference range.
- Color and texture of cut surfaces
- Any focal change
Microscopic evaluation in autopsy
A minimal screening of autopsy specimens include:
- A severity grading of previously known liver diseases.
- Commonly, this includes to quantify any cirrhosis, at least if the patient had alcohol abuse.
Steatohepatitis with mild fibrosis (van Gieson's stain).
Histopathology of steatohepatitis with moderate fibrosis (van Gieson's stain).
- Further information: Cirrhosis
- Steatosis is also common:
- Signs of acute liver failure. Further information in section below.
- Signs of malignancy. If a tumor is found: Further information: Liver tumor
- Signs of congestive hepatopathy (indicating heart failure). Further information in section below.
- Signs of inflammation at least around the portal triads.
Acute liver failure
Acute liver failure has multiple etiologies, and hence various presentations. Regardless of etiology, the initial hepatic insult that leads to acute liver failure is “hepatitis” in the broadest sense, with extensive hepatocyte injury and necrosis. The initiating process may damage the liver by zonal necrosis (with a centrilobular or acinar zones 3 necrosis indicating mainly acetaminophen hepatotoxicity), or it may damage the liver by a diffuse hepatitis with necrosis and inflammation as exemplified by acute viral hepatitis A, B, or E infections or other drug hepatotoxicities.
Histopathology of acute hepatitis with lobular disarray and associated lymphocytic inflammation, acidophil acidophil body formation (arrow) and bilirubinostasis.
Massive hepatic necrosis: Liver cell dropout, residual hepatocytes and intact portal tract pattern.
- Acute hepatic congestion shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.
- Typical findings of chronic hepatic congestion are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.
Common normal findings
Hepatocyte 'lipofuscin, is of no real pathologic importance and does not warrant a mention in the report.
- At least if the patient had alcohol abuse, a quantification of cirrhosis.
- Optionally, even absence of hepatitis, malignancy, congestive hepatopathy and/or steatosis.
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