Cholecystitis

Cholecystitis is the inflammation of the gallbladder wall, which can be acute or chronic, and is often associated with biliary sludge, cholelithiasis, or bacterial infection. The condition may be classified as necrotizing, emphysematous, or eosinophilic, with potential complications including gallbladder mucocele, rupture, and peritonitis. The gallbladder serves as a reservoir for bile, which is produced by the liver and released into the duodenum to aid in fat digestion. Inflammation disrupts this function and can lead to systemic illness, particularly if infection or rupture occurs.

The primary etiologies include bacterial infections (commonly Escherichia coli, Enterococcus spp., Clostridium spp., Bacteroides spp., and Salmonella spp.), which may ascend from the intestinal tract or spread hematogenously. Biliary sludge and cholelithiasis can cause obstruction and stasis, predisposing to inflammation. In some cases, trauma, ischemia, or neoplasia (e.g., adenocarcinoma) may be inciting factors. Eosinophilic cholecystitis is suspected to be immune-mediated or allergic in origin. Parasitic infections (e.g., flukes) are rare but possible in endemic areas. Toxins and certain drugs (e.g., some antimicrobials) have been implicated in rare cases.

Cholecystitis is more common in dogs than cats. In dogs, middle-aged to older animals are typically affected, with no strong breed predisposition, although Shetland Sheepdogs and Cocker Spaniels may be overrepresented for gallbladder mucocele, which can predispose to cholecystitis. Cats are less commonly affected, but when present, it is often associated with cholangitis or pancreatitis (triaditis). There is no significant sex predilection. Geographic variation may reflect the prevalence of biliary parasites or specific infectious agents.

The pathophysiology involves bile stasis, which allows bacterial proliferation and toxin production, leading to mucosal irritation and inflammation. In acute cases, the gallbladder wall becomes edematous and congested, with neutrophilic infiltration. In chronic cases, fibrosis and lymphoplasmacytic infiltration occur. Necrotizing cholecystitis can lead to ischemia and gangrene, increasing the risk of rupture. Emphysematous cholecystitis is caused by gas-producing organisms (e.g., Clostridium spp.) and is a severe form. The inflammatory process can release cytokines and endotoxins into the systemic circulation, causing sepsis and multi-organ dysfunction. If the gallbladder ruptures, bile peritonitis ensues, which is life-threatening.

Predisposing factors include biliary sludge, cholelithiasis, hyperlipidemia, hypothyroidism, hyperadrenocorticism, and obesity. Concurrent gastrointestinal disease, such as inflammatory bowel disease or pancreatitis, can increase the risk. Immunosuppression, whether due to disease or medication, may predispose to bacterial cholecystitis. In cats, cholangitis and pancreatitis are common concurrent conditions. Age-related changes in bile composition and gallbladder motility may also contribute.

Clinical signs vary from subtle to severe. Common signs include vomiting, anorexia, lethargy, abdominal pain (often cranial abdominal), and fever. Icterus may be present if there is extrahepatic biliary obstruction. In chronic cases, intermittent vomiting and weight loss may be observed. In severe cases with rupture, signs of peritonitis (e.g., shock, severe abdominal pain, and abdominal distension) may develop. Some animals may be asymptomatic, particularly in chronic or mild cases.

Differential diagnoses include: 1) Cholangitis (inflammation of the bile ducts, often with similar clinical signs but different imaging findings), 2) Cholelithiasis (gallstones without significant inflammation, may be incidental), 3) Gallbladder mucocele (accumulation of mucus, can lead to obstruction and rupture), 4) Pancreatitis (can cause secondary biliary inflammation), 5) Hepatic disease (e.g., hepatitis, cirrhosis, which may cause icterus and elevated liver enzymes), 6) Gastrointestinal foreign body or obstruction (causing vomiting and abdominal pain), 7) Peritonitis (primary or secondary to other causes), 8) Neoplasia (e.g., gallbladder adenocarcinoma, which may mimic cholecystitis on imaging).

The diagnostic approach begins with a thorough history and physical examination. Baseline blood work (CBC, serum biochemistry, and electrolytes) and urinalysis are performed. If cholecystitis is suspected, abdominal ultrasound is the imaging modality of choice to assess gallbladder wall thickness, biliary sludge, choleliths, and pericholecystic fluid. If ultrasound is inconclusive, advanced imaging such as CT may be considered. Bile sampling via ultrasound-guided cholecystocentesis or during surgery is recommended for cytology and culture. Histopathology of the gallbladder wall is the gold standard for definitive diagnosis, but is often obtained at surgery. Additional tests may include coagulation profile, blood gas analysis, and specific biomarkers such as C-reactive protein (CRP) or serum amyloid A (SAA).

Hematology may show leukocytosis with a left shift, or leukopenia in severe sepsis. Serum biochemistry often reveals elevated liver enzymes (ALT, ALP, GGT), hyperbilirubinemia, and possibly elevated bile acids. Electrolyte imbalances (e.g., hypokalemia) and acid-base disturbances may occur. Urinalysis may show bilirubinuria. Coagulation abnormalities may be present due to vitamin K malabsorption or hepatic dysfunction. Specific biomarkers such as CRP and SAA are often elevated. Bile culture and cytology are essential for identifying bacterial infection and guiding antimicrobial therapy.

Radiography may show a soft tissue mass in the cranial abdomen, but is often unremarkable. Ultrasonography is the most valuable imaging modality, revealing a thickened gallbladder wall (>2-3 mm), biliary sludge, choleliths, pericholecystic fluid, and possibly a distended gallbladder. In emphysematous cholecystitis, gas echoes may be seen within the wall. CT can provide more detailed assessment of the biliary tree and surrounding structures. MRI is rarely used but may be helpful in complex cases. Endoscopic retrograde cholangiopancreatography (ERCP) is not commonly performed in veterinary medicine.

Cytology of bile obtained via cholecystocentesis may show neutrophils, bacteria, and cellular debris. Histopathology of the gallbladder wall reveals neutrophilic or lymphoplasmacytic inflammation, necrosis, fibrosis, and possibly mucosal ulceration. Special stains (e.g., Gram stain) can help identify bacterial organisms. In eosinophilic cholecystitis, eosinophilic infiltration is prominent.

Treatment depends on the severity and underlying cause. Medical management includes antimicrobial therapy (based on culture and sensitivity, but initially broad-spectrum), analgesics, antiemetics, and fluid therapy. Choleretics such as ursodeoxycholic acid (10-15 mg/kg PO q24h) may be used to promote bile flow. In cases of extrahepatic biliary obstruction or rupture, surgical intervention (cholecystectomy) is indicated. Supportive care includes nutritional support (e.g., feeding tube if anorexic), and management of complications such as sepsis or peritonitis. In severe cases, intensive care with monitoring of vital parameters is essential.

Prognosis is good for mild to moderate cases with prompt medical management. However, cases with gallbladder rupture, necrotizing cholecystitis, or sepsis have a guarded to poor prognosis. Mortality rates can be high in complicated cases. Chronic cases may have recurrent episodes. Negative prognostic indicators include severe systemic illness, coagulopathy, and delayed treatment.

Follow-up should include serial physical examinations, blood work (CBC, biochemistry, bile acids) to monitor liver function and resolution of inflammation. Repeat abdominal ultrasound may be performed to assess gallbladder wall thickness and resolution of biliary sludge. Antimicrobial therapy should be continued for at least 2-4 weeks, and re-culture may be indicated if clinical signs recur. Long-term management may include dietary modifications (low-fat diet) and ursodeoxycholic acid therapy.

Pearls: 1) Always consider cholecystitis in dogs with unexplained vomiting and elevated liver enzymes. 2) Ultrasound-guided cholecystocentesis is a valuable diagnostic tool but should be performed with caution due to risk of bile peritonitis. 3) Early surgical intervention is crucial if rupture is suspected. Pitfalls: 1) Do not rely solely on radiography; ultrasound is essential. 2) Avoid using corticosteroids without ruling out infection. 3) Do not delay surgery in cases of extrahepatic obstruction or rupture.

Antimicrobials: Amoxicillin-clavulanate (12.5-25 mg/kg PO q8-12h) or cefazolin (22 mg/kg IV q8h) for initial therapy; adjust based on culture. Metronidazole (10-15 mg/kg PO q12h) may be added for anaerobic coverage. Analgesics: Buprenorphine (0.01-0.02 mg/kg IV/IM q8-12h) or fentanyl CRI (2-5 mcg/kg/h). Antiemetics: Maropitant (1 mg/kg SC q24h) or ondansetron (0.5-1 mg/kg IV q12h). Choleretics: Ursodeoxycholic acid (10-15 mg/kg PO q24h). Fluid therapy: Balanced crystalloids (e.g., Lactated Ringer's) at maintenance or higher rates depending on hydration status. In cases of sepsis, consider vasopressors (e.g., norepinephrine CRI) and colloids. Adjust dosages in renal or hepatic impairment.

Studies have shown that bacterial cholecystitis is commonly associated with E. coli and Enterococcus spp., and that culture-guided antimicrobial therapy improves outcomes. A retrospective study by Center et al. (2013) reported that dogs with gallbladder mucocele had a high risk of rupture, and early cholecystectomy was recommended. Consensus guidelines from ACVIM (2019) on hepatobiliary disease recommend ultrasound as the primary imaging modality and cholecystocentesis for bile culture. Research on eosinophilic cholecystitis is limited, but it is considered immune-mediated and may respond to corticosteroids. Overall, prompt diagnosis and treatment are critical for favorable outcomes.