Small Animal Section: No. 16

THE LIVER BIOPSY AND HEPATOPATHOLOGY

1    The role of the pathologist evaluating liver biopsies.

Note : To relate to the clinical findings and prognosis it is imperative that all the appropriate information be supplied during biopsy submission.

2    Morphological findings

     2.1 Hepatocellular degeneration (Vacuolar hepatopathy) :

Cloudy swelling & hydropic degeneration follow on inflammatory–, toxic-, metabolic- & anoxic insults, glycogen accumulation as well as bile acid induced cell damage resulting from  cholestasis. Cushing’s disease, chronic infections, peritonitis, chronic dental disease, pyelonephritis, numerous chemical toxins or therapeutic agents, endocrine diseases, etc are some disorders  to consider.

     2.2 Hepatic lipidosis :

Small fat vacuoles indicate acute cell injury while large vacuoles are more common with nutritional metabolic fatty hepatosis. The pathogenesis of hepatic lipidosis is idiopathic in adult cats, metabolic in diabetes mellitus & acute starvation, toxic induced in aflatoxicosis and secondary to disorderly fat metabolism in Schauzer & sheepdog hyperlipidaemia. Micro-vesicular intracyto-plasmic lipid accumulation occur in Niemann-Pick storage disease.

     2.3 Hepatocellular necrosis (necrobiosis)

Cell death during life.  Acute viral and drug induced injuries may cause individual shrunken acidophilic  apoptotic cells (Councilman bodies). Increased apoptosis is also found with some hepatotoxins and chronic hepatitis.

Acute,severe hepatic insult due to bacterial endotoxaemia will cause coagulative liver necrosis during septicaemic diseases. Lytic necrosis follows on neutrophil infiltration and release of lysosomal enzymes as seen with acute pancreatitis.

Centrilobular (periacinar) zonal necrosis occurs due to hypoxia (persistent anaemia),shock as well as with right-sided heart failure. Cyanotic induration (periacinar fibrosis) follows on chronic right heart failure. Certain hepatotoxins target the centrilobular areas and cause acute necrosis. Paracentral necrosis develops as an ischaemic lesion due to occlusion of a terminal portal venule in intravascular coagulation. Massive necrosis, usually toxic hepatosis, is more common in the left lobe due to blood flow. Biopsies from both left and right lobes should therefore be taken. Necrosis may cause collapse the reticular framework of the liver (reticular staining) and results in post necrotic scarring (collagen staining). Severe bridging necrosis and/or fibrosis has been correlated to shorter survival times and a less favourable prognosis.

Focal necrosis can result from bile infarcts  while piecemeal necrosis occures where small islands of hepatocytes become entrapped in the peri-portal inflammatory reaction. Piecemeal necrosis does not have prognostic significance per se.

   2.4  Inflammation

Neutrophils indicate active/acute disease while lymphocytes and macrophages become apparent in the portal tracts during chronic hepatitis. The degree of inflammation and necrosis is used for assessing/grading the severity of the hepatitis while the magnitude of fibrosis determine the stage of the disease. Cholangitis / cholangiohepatitis syndrome of adult cats possibly develops due to ascending infection (mostly enterobacterial) along the biliary tree with inflammation centred around portal bile ducts. Lymphocytic portal hepatitis represents a chronic immune mediated condition in old cats. Chronic lymphocytic portal hepatitis appears to be a distinct entity in old cats that may have an auto-immune pathogenesis. It does not progress to biliary cirrhosis.

    2.5  Chronic hepatitis, fibrosis and cirrhosis

Chronic hepatitis is an end stage hepatitis of a heterogenous group of inflammatory / necrotizing conditions such as in familial predispositions (viz. Bedlington terrier, cocker spaniel, Doberman pincher, Labrador retriever, West Highland terrier, Standard poodle), infectious conditions (infectious canine hepatitis, Leptospirosis etc.), drug induced (anticonvulsants, carprofen etc.), lobular dissecting hepatitis and idiopathic chronic hepatitis. Histopathology can determine the extent of hepatic fibrosis, bridging, type of inflammation, adjacent piecemeal parenchymal necrosis, chronic irreversible fibrosis and cirrhosis.

    2.6  Regeneration / Nodular hyperplasia

Hepatocytes have high regenerative capacity hence the common multifocal nodular hyperplasic regeneration. Nodular proliferative hyperplasia is found in older dogs without fibrosis and collagen stains should differentiate this from scarring or chronic cirrhosis

    2.7  Porto systemic shunts (PSS)

Chronic PSS is characterized by hepatocellular atrophy with inappropriate numbers of arterioles and bile duct like portal proliferation. Iron accumulation (Perl’s stain) and lipogranulomas are also common in this condition. Congenital PSS can be differentiated from acquired PSS by the absence of small portal venules, distended intrahepatic portal veins, hepatoportal fibrosis & immaturity of the animal.

    2.8  Extra-medullary haemopoiesis, cholestasis & pigmentations 

Haemopoiesis is normal in neonatal livers and found during chronic anaemia, chronic extra hepatic inflammation and chronic hepatic disease. Cholangiolar proliferation may follow on a variety of hepatic insults including cholestasis. Babesiosis and extra-hepatic bacterial infection are common causes for cholestasis. Copper toxicosis in Bedlington & West Highland terriers is an inherited copper susceptibility where progressive liver failure, hepatic fibrosis & intracytoplasmic ferric iron and copper pigments are found (Perl’s & Rubeanic acid stains respectively).

    3.Special stains

For further information contact:

VetPath Veterinary Pathologists
PO Box 8464, Pretoria 0001
Tel: (012) 529 8345/6
e-mail: info@vetpath.co.za

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Copyright © 2004 Bill Robb & Associates
Last modified: Friday June 25, 2004