After studying this module the student should be able to:
1. Acute Hepatitis / Hepatocellular Necrosis
Causes: infectious agents (viruses in some species), toxins (xylitol in dogs, aflatoxins), drugs (acetaminophen in cats), ischemia, immune-mediated hepatitis.
Signs: anorexia, vomiting, depression, fever, icterus, coagulopathy, hepatic encephalopathy in severe cases.
Diagnostics: elevated hepatocellular enzymes (ALT, AST in small animals), hyperbilirubinemia, prolonged clotting times (PT/aPTT), hypoglycemia, hepatic ultrasound, cytology/biopsy.
Treatment: remove toxin/cause, supportive care (fluids, plasma for coagulopathy), hepatic protectants (S-adenosylmethionine/SAMe, N-acetylcysteine in some toxicities, ursodeoxycholic acid in cholestatic disease), antibiotics if secondary infection, nutritional support, treat complications (encephalopathy, DIC).
2. Cholangitis / Cholangiohepatitis / Ascending Bacterial Cholangitis
Definition: Inflammation of intrahepatic bile ducts ± adjacent liver parenchyma; common in cats (cholangitis complex).
Signs: anorexia, vomiting, icterus, fever, RUQ pain.
Diagnostics: cholestatic enzyme elevations (ALP, GGT), hyperbilirubinemia, ultrasound (bile duct dilation, thickened walls), cytology of bile, bile culture, liver biopsy.
Treatment: broad-spectrum antimicrobials guided by bile culture, ursodeoxycholic acid to improve bile flow and reduce cholestasis, supportive care, address predisposing causes (IBD, pancreatitis, biliary obstruction).
3. Hepatic Lipidosis (Fatty Liver)
Common in: cats (primary hepatic lipidosis), also occurs in ruminants in negative energy states (fatty liver in dairy cows), ponies/miniatures with hyperlipaemia.
Pathogenesis: rapid fat mobilization and impaired hepatic lipid export leads to triglyceride accumulation in hepatocytes → hepatic dysfunction.
Signs: anorexia, icterus, vomiting, lethargy, weight loss.
Diagnostics: marked hyperbilirubinemia, elevated liver enzymes, ultrasound to suggest fatty change; diagnosis confirmed by cytology/biopsy.
Treatment: aggressive nutritional support (enteral feeding tube in cats), correct underlying cause, antiemetics, hepatoprotectants.
4. Portosystemic Shunts (PSS)
Types: congenital (single extrahepatic or intrahepatic shunts) or acquired (multiple shunts secondary to portal hypertension).
Pathophysiology: portal blood bypasses hepatic detoxification → hepatic encephalopathy, poor growth, microhepatia.
Signs: stunted growth, behavioral changes, hepatic encephalopathy (seizures, ataxia), ammoniacal breath, urinary stones (struvite/urate), poor haircoat.
Diagnostics: low BUN, hypoalbuminemia, elevated bile acids or ammonia; imaging (Doppler ultrasound, nuclear scintigraphy) and contrast portography.
Treatment: medical management for encephalopathy (protein restriction, lactulose, antibiotics like neomycin/metronidazole), surgical attenuation/ligation of shunt when appropriate (e.g., ameroid constrictor), prognosis better for congenital single shunts if corrected.
5. Chronic Hepatitis and Cirrhosis
Causes: persistent infectious, immune-mediated, toxic, or metabolic insults leading to fibrosis.
Signs: progressive weight loss, ascites, coagulopathy, hepatic encephalopathy, intermittent jaundice.
Diagnostics: mixed hepatocellular and cholestatic enzyme patterns, ultrasound (nodular liver, ascites), biopsy showing fibrosis/cirrhosis.
Treatment: supportive, address underlying cause (immunosuppression for immune-mediated hepatitis), manage complications (diuretics for ascites, plasma for coagulopathy), prognosis guarded.
6. Hepatic Neoplasia
Primary (hepatocellular carcinoma, cholangiocarcinoma) or metastatic disease (common).
Signs: non-specific (anorexia, weight loss, abdominal distension), sometimes palpable mass.
Diagnostics: ultrasound, CT if available, cytology/biopsy, liver function testing.
Treatment: surgical resection when feasible, palliative care, prognosis variable.
7. Infectious & Parasitic Hepatopathies
Fascioliasis (liver fluke) in sheep, cattle — causes cholangitis, chronic wasting, anemia.
Leptospirosis can cause hepatic and renal damage in multiple species.
Bacterial hepatitis (e.g., Clostridial species) may cause severe necrosis.
Viral hepatitis (species-specific) in select species.
Diagnostics: fecal sedimentation (flukes), serology/PCR for infectious agents, biopsy.
Treatment: antiparasitics (triclabendazole for fluke), antimicrobials, supportive care.
8. Toxins Causing Hepatic Injury
Examples: aflatoxins, xylitol (dog), amanita mushrooms, certain drugs (acetaminophen in cats), copper toxicity (sheep, Bedlington terriers).
Approach: identify and remove exposure, decontamination if recent, treat supportively, consider chelation (e.g., D-penicillamine for copper) for specific toxins.
1. Acute Pancreatitis
Pathogenesis: premature activation of pancreatic proenzymes (trypsin) within the pancreas → autodigestion, acute inflammation, edema, hemorrhage; may trigger systemic inflammatory response syndrome (SIRS).
Predisposing factors: dietary indiscretion, high-fat meals (dogs), endocrinopathies (hypertriglyceridemia, diabetes), certain medications/toxins, abdominal trauma, idiopathic. In cats, pancreatitis is often chronic and associated with triaditis (concurrent cholangitis and inflammatory bowel disease).
Signs: anorexia, vomiting (dogs more likely), abdominal pain, depression, fever; in cats signs are often vague (anorexia, lethargy). Severe cases show shock, coagulopathies, and respiratory compromise.
Diagnostics: pancreatic lipase immunoreactivity (PLI, e.g., cPL/fPL) — species-specific tests; routine bloodwork (may see neutrophilia, anemia, hypocalcemia, elevated liver enzymes), abdominal ultrasound (enlarged hypoechoic pancreas, peripancreatic fluid), radiographs to rule out GDV/obstruction. Peritoneal fluid analysis may help. Definitive diagnosis via histopathology (rarely performed).
Treatment: primarily supportive: aggressive IV fluids, analgesia (opioids), antiemetics, early enteral nutrition when possible (small, frequent feeds or feeding tube), control of complications (antibiotics only if secondary infection suspected or confirmed), monitor for SIRS/organ dysfunction. Nutritional and lipid control for hypertriglyceridemia. Prognosis variable depending on severity and complications.
2. Chronic Pancreatitis
Pathology: repeated or persistent inflammation → fibrosis, loss of exocrine tissue, possible islet damage.
Signs: intermittent vomiting, chronic diarrhea, weight loss, poor appetite; may lead to EPI or diabetes mellitus over time.
Diagnostics: history, imaging, PLI may be variably elevated, fecal tests for maldigestion; biopsy is definitive.
Treatment: long-term management includes low-fat diets where appropriate, analgesia for chronic pain, enzyme supplementation if EPI develops, manage endocrine sequelae.
3. Exocrine Pancreatic Insufficiency (EPI)
Causes: chronic pancreatitis, pancreatic acinar atrophy (especially in German Shepherd dogs), post-surgical loss of pancreatic tissue.
Signs: weight loss despite good appetite, voluminous pale/frothy feces, steatorrhea, poor haircoat.
Diagnostics: TLI (trypsin-like immunoreactivity) low in EPI; fecal fat and elastase tests may assist. Response to enzyme replacement is diagnostic and therapeutic.
Treatment: pancreatic enzyme replacement (powdered enzyme mixed with food), dietary management (highly digestible diets, avoid high fat in dogs), treat small intestinal bacterial overgrowth if present, vitamin and micronutrient supplementation (fat-soluble vitamins).
4. Pancreatic Neoplasia
Adenocarcinoma, insulinoma (islet cell tumor) — more common endocrine tumor in dogs (insulinoma causes hypoglycemia).
Signs: non-specific for exocrine tumors; insulinomas present with episodic hypoglycemia, weakness, seizures.
Diagnostics: imaging (ultrasound, CT), insulin/glucose testing for insulinoma, cytology/biopsy.
Treatment: surgery where possible, medical management for insulinoma (prednisone, diazoxide) and palliative chemotherapy; prognosis often guarded.
History & physical exam
Appetite changes, vomiting/diarrhea, abdominal pain, jaundice, neurologic signs (hepatic encephalopathy), pruritus (cholestasis in some species), body condition, icterus, abdominal distension, signs of systemic disease.
Bloodwork
Hepatic enzymes: ALT (hepatocellular, dogs), AST (less specific), ALP and GGT (cholestasis - ALP inducible by steroids in dogs), bilirubin (conjugated/unconjugated), albumin (synthetic function), BUN (reduced with hepatic dysfunction), glucose (hypoglycemia with severe hepatic failure), coagulation profile (PT/aPTT) for coagulopathy.
Pancreatic tests: species-specific PLI (canine/feline), TLI (EPI), amylase/lipase (less specific in many species).
Other: CBC (inflammation, anemia), electrolytes (hypokalemia, hypocalcemia), bile acids (pre/postprandial bile acids for hepatic function), ammonia levels for encephalopathy (species and sample handling dependent).
Imaging
Abdominal ultrasound: first-line for liver size, architecture, nodules, biliary dilation, pancreatitis signs (enlargement, hypoechoic areas), peritoneal fluid.
Radiography: evaluate mass effect, mineralization, peritoneal gas.
Advanced imaging: CT/MRI for surgical planning or better anatomical detail.
Sampling
Abdominocentesis: assess peritoneal fluid (sepsis, hemorrhage).
Bile sampling: cytology and culture to identify ascending cholangitis.
Liver biopsy: percutaneous ultrasound-guided, laparoscopic, or surgical wedge — gold standard for definitive diagnosis and staging.
Fine needle aspirate (FNA): cytology useful but may miss diffuse disease.
General
Stabilize: fluids, correct electrolytes, manage shock.
Identify & remove cause (toxins, obstructive lesions).
Provide organ-specific supportive care (nutritional support, analgesia, antiemetics, hepatoprotectants).
Monitor for and treat complications early (coagulopathy, encephalopathy, sepsis).
Liver-specific management
Hepatic encephalopathy: restrict dietary protein (short term), lactulose (acidifies colonic contents and traps ammonia), oral antibiotics (neomycin/ metronidazole) to reduce urease-producing bacteria, treat precipitating causes (constipation, GI bleeding, infection).
Coagulopathy: vitamin K supplementation if cholestasis or rodenticide suspected; plasma transfusion for active bleeding.
Cholestasis: ursodeoxycholic acid, cholagogue agents, address obstruction.
Hepatoprotectants: SAMe, silymarin (milk thistle), N-acetylcysteine for acetaminophen toxicity (species specific).
Surgery: biliary obstructions, shunt attenuation, resection of focal lesions.
Pancreas-specific management
Pancreatitis: aggressive IV fluids (to maintain perfusion of pancreas), analgesia (opioids are first line), antiemetics, early enteral nutrition (once the patient is stable; avoid prolonged NPO in many cases), avoid high fat diets in dogs predisposed, monitor for SIRS and organ dysfunction, rarely surgical intervention for complications (necrosis, abscess).
EPI: lifelong enzyme replacement and dietary adjustments.
Insulinoma: surgical excision when possible; medical stabilization for hypoglycemia with diet, glucocorticoids, diazoxide.
Small animals (dogs & cats)
Dogs: acute pancreatitis (often dietary/hyperlipidemia related), chronic hepatitis, copper-associated hepatitis in certain breeds, PSS (congenital in small breeds), hepatocellular carcinoma, leptospirosis (liver & kidney).
Cats: cholangitis/cholangiohepatitis, hepatic lipidosis (common severe condition after anorexia), pancreatitis (often chronic and part of triaditis with IBD and cholangitis), cholestatic disease often subtle.
Equine: Liver disease less commonly primary; suspected causes include bacterial/viral hepatitis (rare), toxicoses (e.g., pyrrolizidine alkaloids causing chronic liver fibrosis), and hepatic lipidosis in ponies (hyperlipaemia). Colic often from intestinal issues rather than primary hepatic disease.
Ruminants (cattle, sheep, goats)
Fascioliasis (liver fluke): chronic parasitic cholangitis, weight loss, anemia, bottle-jaw.
Acute toxic hepatopathy (plants, mycotoxins), rumenitis with secondary liver abscesses (e.g., Fusobacterium necrophorum), copper toxicity, and Johne’s primarily intestinal but can affect hepatic function indirectly. Displaced abomasum is a ruminant gastric disease with metabolic consequences that may secondarily affect liver function.
Swine: Hepatitis (infectious and toxic), hepatic lipidosis rarely, parasitism; note production herd implications.
Avian & Exotics: Hepatomegaly and hepatic disease are common presentations; causes include infectious diseases, nutritional (fatty liver), toxins. Pancreatic disease less well described but can occur.
Prognosis varies widely: acute, reversible injuries treated early often have good outcomes; chronic cirrhosis or advanced neoplasia carry a guarded to poor prognosis.
Emphasize importance of timely care in suspected hepatic or pancreatic disease due to risk of rapid deterioration (e.g., acute pancreatitis with SIRS, hepatic necrosis).
Discuss long-term management needs (dietary changes, lifetime medications like enzyme supplements or lactulose) and potential costs of diagnostics/treatment.
Bile acids are sensitive tests for hepatic function (useful for PSS screening) but must be interpreted in context.
ALT is relatively liver-specific in small animals; AST is less specific (muscle). In large animals, these enzymes have different distributions—interpretation must be species-appropriate.
Hypoglycemia in neonates and severely ill animals can indicate hepatic insufficiency—check glucose early.
In pancreatitis, don't rely solely on serum amylase/lipase — use species-specific PLI/TLI and imaging.
Liver biopsy is the diagnostic gold standard for many hepatic conditions; plan coagulation assessment beforehand.
Cats often show vague signs for both hepatic and pancreatic disease—high index of suspicion is required.
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