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Cholangitis/cholangiohepatitis, mucocele, cholelithiasis, extrahepatic biliary obstruction
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What is the function of the biliary system?
To transport, store, and release bile for fat digestion and excretion of bilirubin, cholesterol, and toxins.
What are the major components of the extrahepatic biliary system?
Right and left hepatic ducts → common hepatic duct → cystic duct → gallbladder → common bile duct → duodenum (major papilla).
What is the primary stimulus for bile release from the gallbladder?
Cholecystokinin (CCK) released after a fatty meal.
What are the two broad categories of biliary disease?
Inflammatory (cholangitis/cholangiohepatitis) and obstructive (cholelithiasis, mucocele, EHBO).
What are the three forms of feline cholangitis/cholangiohepatitis?
Neutrophilic, lymphocytic, and chronic (mixed/lymphoplasmacytic).
What is the primary difference between the three forms of feline cholangitis/cholangiohepatitis?
The type of inflammatory cells and the suspected underlying pathogenesis.
What is neutrophilic cholangitis (NC) most commonly caused by?
Ascending bacterial infection from the duodenum via the common bile duct.
What bacteria are most often isolated from neutrophilic cholangitis?
E. coli, Enterococcus, Clostridium, Bacteroides
What is the typical signalment for NC?
Middle-aged to older cats with concurrent inflammatory bowel disease or pancreatitis (“triaditis”).
What are common clinical signs of NC?
Fever, vomiting, anorexia, icterus, and lethargy.
What are lab abnormalities of NC?
Elevated ALT, ALP, GGT, bilirubin; sometimes leukocytosis.
How is NC diagnosed?
Ultrasound (bile duct/gallbladder thickening) + cytology or culture from bile aspirate (cholecystocentesis).
What is the main treatment for NC?
Broad-spectrum antibiotics (ampicillin + enrofloxacin or metronidazole) for 4–6 weeks
What other drugs are indicated for NC?
Ursodiol (if ducts patent), SAMe, vitamin E, and fluids/nutrition.
What is the prognosis for NC?
Good to excellent if treated early.
What characterizes lymphocytic cholangitis (LC)?
Lymphoplasmacytic inflammation and portal fibrosis with minimal bacteria.
What is the suspected cause of LC?
Immune-mediated or chronic post-infectious inflammation.
What age of cats is affected by LC?
Usually older cats (>10 years).
What are the clinical signs of LC?
Chronic or intermittent anorexia, vomiting, icterus, weight loss, sometimes ascites.
What lab pattern is typical with LC?
Persistent moderate increases in ALT, ALP, GGT, and bilirubin; hypoalbuminemia if chronic.
What is seen on imaging of LC?
Irregular liver margins, bile duct dilation, and enlarged gallbladder.
How is LC diagnosed?
Biopsy with portal lymphocytic inflammation and fibrosis; sterile bile culture.
What is the main treatment of LC?
Prednisolone (1–2 mg/kg/day) tapered over months; ursodiol, antioxidants, ± chlorambucil in refractory cases.
What is the prognosis of LC?
Variable; fair if early, guarded if cirrhosis or portal hypertension develops.
What is the basic cause, acute/chronic, and basic treatment for neutrophilic vs lymphocytic cholangitis?
neutrophilic: bacterial, acute, antibiotics
lymphocytic: immune, chronic, steroids
What is cholangiohepatitis?
Inflammation of both bile ducts and hepatic parenchyma.
What typically causes cholangiohepatitis (mixed form)?
Extension of chronic cholangitis or bacterial infection reaching hepatic lobules.
What are typical biopsy findings of cholangiohepatitis?
Portal inflammation with lymphocytes, plasma cells, neutrophils; bile duct proliferation; variable fibrosis.
How is cholangiohepatitis treated?
Combination therapy: antibiotics + corticosteroids + ursodiol + antioxidants.
What is the prognosis for cholangiohepatitis?
Depends on chronicity; fair with appropriate therapy.
What is a gallbladder mucocele (GBM)?
Cystic distention of the gallbladder with inspissated mucus and bile.
What species is most affected by GBM?
Dogs, especially Shetland Sheepdogs, Cocker Spaniels, Border Terriers.
What are the risk factors for GBM?
Endocrinopathies (Cushing’s, hypothyroidism), hyperlipidemia, and certain drugs (trilostane).
What is the proposed pathogenesis of GBM?
Abnormal mucus secretion and impaired gallbladder emptying → bile concentration → cystic mucosal hyperplasia.
What is the characteristic ultrasound appearance of GBM?
“Kiwi fruit pattern” – organized stellate or striated echogenic bile.
What are the clinical signs of GBM?
Vomiting, anorexia, abdominal pain, icterus, lethargy; sometimes collapse if rupture occurs.
What lab findings are typical for GBM?
Marked ALP/GGT elevation, moderate ALT/AST increase, hyperbilirubinemia, neutrophilia.
What are potential complications to GBM?
Gallbladder rupture, bile peritonitis, or extrahepatic obstruction.
What is the treatment of choice for GBM?
Cholecystectomy (surgical removal of gallbladder).
What preoperative therapy is important prior to cholecystectomy?
Vitamin K, broad-spectrum antibiotics, fluid/electrolyte stabilization.
When is medical management appropriate for GBM?
Only if incidental GBM with no biliary obstruction — use ursodiol, antioxidants, and monitor with ultrasound.
What is the prognosis with GBM?
Excellent with elective cholecystectomy before rupture; poor if peritonitis occurs.
What are gallstones/choleliths composed of?
Cholesterol, calcium bilirubinate, or mixed bile salts.
What predisposes to cholelith formation?
Chronic biliary infection, stasis, altered bile composition.
Which species are more affected with choleliths?
Dogs > cats.
What are the typical clinical signs of choleliths?
Often incidental; when obstructive: vomiting, icterus, abdominal pain.
How are choleliths diagnosed?
Radiographs (some radiopaque), but ultrasound most sensitive.
What is the medical management for small non-obstructive choleliths?
Ursodiol (15 mg/kg/day) and antibiotics if infection suspected.
What is the treatment for obstructive or recurrent choleliths?
Surgical removal (cholecystotomy or cholecystectomy).
Concept: Choleliths are ______ so always address underlying infection or stasis.
often secondary
What is extrahepatic biliary obstruction (EHBO)?
Complete or partial obstruction of bile flow between the hepatic ducts and duodenum.
Which species is EHBO seen most commonly?
This is most commonly seen in cats
What are common causes of EHBO?
Pancreatitis (most common in dogs), GB mucocele, cholelith, neoplasia, duodenal foreign body.
What are clinical signs of EHBO?
Progressive jaundice, vomiting, anorexia, abdominal pain.
What laboratory findings are characteristic for EHBO?
High ALP and GGT, moderate ALT, hyperbilirubinemia (conjugated).
What imaging findings suggest EHBO?
Distended gallbladder, dilated bile ducts, hyperechoic pericholecystic fat.
What diagnostic test confirms obstruction?
Ultrasound ± bile duct contrast cholangiography or CT.
Why is biopsy avoided in obstructed animals EHBO?
High risk of bile leakage and peritonitis.
What is the main treatment of EHBO?
Surgical decompression or removal of obstruction (cholecystectomy or choledochotomy).
What supportive therapy is needed pre-op prior to EHBO removal?
Vitamin K, antibiotics, fluids, antioxidants.
What postoperative complications may occur with EHBO?
Sepsis, leakage, or recurrence of obstruction.
What is the prognosis for EHBO?
Good if treated before rupture; guarded if rupture or cholangitis occurs.