Overview

• Cholecystitis = gallbladder (GB) inflammation.
• Choledochitis = large bile duct inflammation.
• Associate with cholelithiasis; GB mucocele (GBM); extrahepatic bile duct obstruction (EHBDO); or inflammation involving intrahepatic biliary structures.
• Severe GB inflammation can lead to rupture and subsequent bile peritonitis, necessitating combined surgical and medical treatments.
• Bile duct obstruction increases risk for biliary infection: enteric bacteria transmigrating the bowel wall, pass into the portal circulation, enter the liver, GB, and bile, dispersing endotoxins and bacteria initiating sepsis, and in some cases, bile and /or septic peritonitis.

Signalment

• Dog and cat
• No breed or sex predilection
• Necrotizing cholecystitis (dogs)-usually middle-aged or older animals.
• GBM: predisposition for dogs with hyper-lipidemia (e.g., endocrinopathies [hyperadreno-corticism, hypothyroidism, diabetes mellitus), pancreatitis, glucocorticoid administration, nephrotic syndrome, idiopathic hyperlipidemia (e.g., Shetland sheepdogs, miniature Schnauzer)-leads to cholestasis and cholecystitis; (see Gallbladder Mucocele).

Signs

• Choledochitis: vague signs, variable icterus.
• Sudden onset: inappetence, lethargy, vomiting, vague abdominal pain (may be postprandial with cholecystitis or GBM).
• Mild to moderate jaundice and fever common.
• Chronic postprandial discomfort/distress.
• Severe disease-shock due to endotoxemia, bacteremia, and hypovolemia.
• Soft tissue mass in right cranial abdomen palpable in small dogs and cats reflecting inflammation and adhesions of GB and pericholecystic tissues.

Causes & Risk Factors

• Impaired bile flow at cystic duct or GB, GB dysmotility, or ischemic insult to the GB wall may precede cholecystitis.
• Irritants in sludged bile (e.g., lysolecithin, prostaglandins, choleliths, liver flukes) or retrograde flow of pancreatic enzymes (cats) may initiate/augment GB or duct inflammation.
• Previous enteric disorders, trauma, abdominal surgery-may be contributing factors.
• Anomalous GB or duct development: choledochal cyst (rare, cats > dogs).
• Bacterial infection-common; retrograde invasion via ducts from intestine or hemato-genous dispersal from splanchnic circulation.
• Toxoplasmosis and biliary coccidiosis-rare.
• Necrotizing cholecystitis (dogs)-ruptured GB (common) and complicating cholelithiasis; E. coli and Enterococcus spp-common isolates.
• Emphysematous cholecystitis/choledochitis-rare, associates with diabetes mellitus, traumatic GB ischemia, acute cholecystitis (with or without cholelithiasis); common gas-forming organisms-Clostridia spp. and E. coli often cultured.

Differential Diagnosis

• Pancreatitis
• Focal or diffuse peritonitis
• Bile peritonitis
• Gastroenteritis causing biliary involvement
• Cholelithiasis
• Cholangiohepatitis
• Hepatic necrosis or abscessation
• EHBDO
• GBM
• Septicemia

CBC/Biochemistry/Urinalysis

• Variable leukocytosis with toxic neutrophils and inconsistent left shift
• High bilirubin; bilirubinuria
• High ALT, AST, ALP, and GGT activity
• Low albumin with peritonitis
• High cholesterol and bilirubin if EHBDO
• Hypercholesterolemia and/or hyperlipidemia (triglycerides): breed-related, endocrine, pancreatitis, nephrotic syndrome.

Other Laboratory Tests

• Abdominocentesis-inflammatory effusion; (see Bile Peritonitis)
• Bile culture (dogs)-E. coli, Enterococcus spp., Klebsiella spp., Pseudomonas spp., Clostridium spp, others
• Coagulation tests-abnormal if chronic EHBDO (vitamin K deficiency) or DIC in severe conditions with sepsis.

Imaging

• Abdominal radiography-may reveal loss of cranial abdominal detail with focal or diffuse peritonitis or effusion; ileus; radiodense choleliths; gas in biliary structures; radiodense GB (dystrophic mineralization due to chronic inflammation, porcelain GB, rare).
• Ultrasonography-fluid interface surrounding GB enhances wall image; diffusely thick GB wall, segmental hyperechogenicity and /or laminated wall in necrotizing cholecystitis; double-rimmed GB wall: acute cholecystitis, hepatitis, cholangiohepatitis, third-space fluid dispersal (hypoproteinemia, right heart failure, renal failure, pyelonephritis, abdominal effusion, iatrogenic fluid overload); GB lumen filled with amorphous echogenic stellate or finely striated pattern, resembling sliced kiwi fruit (“kiwi sign”) if GBM; GB rupture implicated by discontinuous GB wall, pericholecystic fluid or generalized effusion, and hyperechogenicity of surrounding tissue; failure to image GB: may implicate rupture or agenesis; mineralized GB wall may indicate dystrophic mineralization (Limey GB, sacculated GB or ducts due to malformation- Caroli's malformation); intrahepatic bile ducts difficult to visualize or prominent: ascending cholangitis (thick walls), or EHBDO (dilated ducts); pericholecystic fluid: necrotizing cholecystitis and surgical emergency.
• Choledochitis involving CBD: thick wall, intraluminal debris, extends into hepatic ducts.

Pathologic Findings

Gross appearance-erythematous GB; may appear green-black if necrotizing lesion; tenacious “inspissated” biliary material common with GBM; pigmented choleliths if infection; blood with hemobilia; CBD with thick wall, variable intraductal debris (e.g., biliary particulates, suppurative inflammation).

Drug(s)

• Antibiotics-before surgery; broad spectrum; surgical manipulations may initiate bacteremia; select antibiotics for enteric Gram-negative and anaerobic flora; refine treatment using culture and sensitivity results; good initial choice: triad combination of: metronidazole, ticarcillin (or clavamox) and a fluorinated quinolone. Reduce standard dose for metronidazole by 50% if cholestatic jaundice.
• Ursodeoxycholic acid-10–15 mg/kg PO daily divided BID with food, tablet form provides best bioavailability; requires decompression of EHBDO prior to treatment.
• Antioxidants: vitamin E ( -tocopherol acetate)-10 IU/kg (see Bile Duct Obstruction (Extrahepatic)); S-adenosylmethionine (SAMe) use enteric-coated bioavailable product; on empty stomach)-GSH donor (20 mg/kg PO q24h), 2h before feeding; non-bile acid dependent (GSH) choleresis (40 mg/kg PO q24h).
• Vitamin K₁-0.5–1.5 mg/kg SC or IM q12h for 3 doses; caution: never administer IV (anaphylactoid reaction); treat early to allow response before surgical manipulations.

Contraindications

Ursodeoxycholic acid-contraindicated in uncorrected EHBDO or bile peritonitis.

Patient Monitoring

• Physical examination and pertinent diagnostic testing-repeat every 2–4 weeks until abnormalities resolve.
• If septic-continue antibiotics until enzymes resolve.

Possible Complications

Anticipate a protracted clinical course with ruptured biliary tract or peritonitis.

Associated Conditions

• Cholelithiasis
• Ductal plate malformation
• EHBDO
• Gallbladder mucocele
• Bile peritonitis

Age-Related Factors

Congenital malformations of biliary structures do not predispose patients to cholecystitis but predispose to choledochitis.

Zoonotic Potential

Campylobacter and Salmonella may cause cholecystitis in dogs; advise owner if diagnosed

Abbreviations

• ALP = alkaline phosphatase
• ALT = alanine aminotransferase
• AST = aspartate aminotransferase
• DIC = disseminated intravascular coagulation
• EHBDO = extrahepatic bile duct obstruction
• GB = gallbladder
• GBM = gallbladder mucocele
• GGT = γ–glutamyltransferase
• GSH = glutathione

Author Sharon A. Center

Consulting Editor Sharon A. Center