Clinical features of hepatobiliary disease vary depending on type, mechanism, severity, zonal distribution and extent of involved parenchyma, and chronicity.
Important Features of Acquired and Congenital Hepatobiliary Disorders
––––--ACQUIRED--------- | ––––-CONGENITAL--------- | ||||
|---|---|---|---|---|---|
Early signs | Major bile duct occlusion | Severe hepatic insufficiency | PSVA, PSS | Microvascular dysplasiaa (no PSVA, microscopic shunting) | Ductal plate malformation |
Vomiting | ± Vomiting | ± Vomiting | Abnormal behavior: lethargic | Liver ± small, low normal | Liver ± small, low normal size |
Diarrhea/constipation | ± Diarrhea/constipation | ± Diarrhea/constipation | ± Diarrhea/constipation | No clinicopathologic markers except ↑↑↑ bile acids | ± Liver lobe hypoplasia |
Weight loss | Weight loss | Weight loss | Weight loss | ± Gallbladder atresia/hypoplasia | |
Pyrexia | Pyrexia | ± Pyrexia | ± Pyrexia | Protein C: normal (usually) | Predisposed to cholangitis |
“Noisy enzymes” | Polydipsia | Polyuria/polydipsia | Polyuria/polydipsia | No hepatic encephalopathy | ± Pyrexia if cholangitis |
Normal bilirubinemia | Jaundice within 72 hours | Jaundice as disease advances | No jaundice | Variable liver enzymes: most common ↑ ALT, ↑ALP with inflammatory bowel disease | Variable enzymes: ↑ ALT, ↑ ALP ↑ with inflammatory bowel disease |
Clear to yellow urine | ↑ ALP & GGT | Variable ↑ ALP, AST, ALP, GGT | ↓ RBC, MCV, ↓ BUN, ↓ creatinine | ||
Normal bile acids | ↑ ALT & AST, ↑ cholesterol | Gradual decline in cholesterol ↓ cholesterol | Variable liver enzymes ↓ cholesterol | No jaundice unless severe cholangitis | |
Polyuria/polydipsia | Orange urine ± neg urobilinogen: unreliable | Clear to orange urine urobilinogen "+" ↑↑↑ bile acids bruising/bleeding tendencies | Ammonium biurate crystalluria Normal coagulation ↑↑↑ bile acids | No ammonium biurate crystalluria unless acquired portosystemic shunts form secondary to congenital hepatic fibrosis Rarely dogs have PSVA—no ascites | |
Bleeding tendencies: 7–10 days | Brown to melenic feces | ↓ Protein C (< 70%) often | |||
Acholic (pale) feces | Brown feces | Copper-colored iris: cats | |||
Melenic feces if GI bleeding | Green feces: ↑ stercobilin | Typically no ascites | |||
Gastrointestinal ulceration | Normal to microhepatica: dog | Young dogs: melena—parasites | |||
Hepatomegaly: firm; rounded borders | Hepatomegaly: cat | Microhepatica with “plump” kidneys | |||
Palpable gallbladder: cat if chronic: > 6 weeks ascites edema (rare in cats) | Gastroduodenal ulceration associated with portal hypertension ascites if: portal hypertension ascites if: portal hypertension: ↓ albumin fosters ascites acquired portosystemic shunts | ± Cryptorchid (small-breed dogs) ptyalism (cats) rare gastrointestinal ulceration: ↑ risk for hepatic encephalopathy portal hypertension: only if intolerant to shunt ligation, true portal atresia, or arteriovenous malformation ascites rare unless portal vein atresia or hepatic arteriovenous fistula edema does not occur | |||
HE: variable stupor, lethargy, depression pacing, head pressing rarely coma, seizures hyperammonemia: usually coincides with HE signs ammonium biurate crystalluria cystic/renal calculi urinary tract obstruction pollakiuria: urinary calculi | HE: common tooth eruption bleeding →↑ risk HE GI bleeding: parasites →↑ risk HE amaurosis, stupor, depression, head pressing pacing, aggression (esp cats), ptyalism seizures with prolonged prodrome hyperammonemia: usually coincides with HE ammonium biurate crystalluria: common with HE | ||||
Ammonium urate cystic calculi: less common renal calculi may present for urinary obstruction →↑ BUN → NH3 →↑ risk HE hematuria: due to urinary bladder calculi | |||||
aDoes not limit lifespan PSVA, portosystemic vascular anomaly. PSS, portosystemic shunt. ALP, alkaline phosphatase. GGT, gamma glutamyl transferase. MCV, mean corpuscular volume. HE, hepatic encephalopathy. | |||||
General features include anorexia, vomiting, diarrhea, weight loss, and fever.
With severe, diffuse injury or cholestatic disorders (disorders causing bile flow stasis), animals may develop jaundice (yellow discoloration of nonpigmented tissues due to accumulation of bilirubin), polyuria (dilute urine production) and polydipsia (excessive water consumption), coagulation abnormalities (bleeding tendencies), or abdominal distention due to ascites (accumulation of abdominal effusion secondary to intrahepatic sinusoidal hypertension or prehepatic portal hypertension).
