Cholelithiasis

Outline

Overview
Signalment
Signs
Causes and Risk Factors

BASICS

Overview

Refers to calculi in the biliary tree
Relatively uncommon
The pathogenesis possibly involves retrograde bacterial infection from the small intestine. Ascending infection is thought to initiate a cholangitis/cholangiohepatitis, which may be a predisposing factor in cholelith formation
Plant material has occasionally been found in choleliths, further supporting retrograde invasion of bacteria and even ingesta from the duodenum as a predisposing factor of disease
Deconjugation of bilirubin diglucuronide by bacterial β-glucuronidase occurs with subsequent precipitation of calcium bilirubinate, and cementation by anionic glycoproteins is thought to result in the formation of calculi

Signalment

Most affected horses are 5–15 years old; cases of cholelithiasis have been reported in horses as young as 3 years
No breed or sex predilections
No reported geographic distribution

Signs

Intermittent colic
Icterus
Fever
Depression
Weight loss
Hepatic encephalopathy
Photosensitization

Causes and Risk Factors

The condition is sporadic
No clearly established risk factors have been identified

Diagnosis ⬆ ⬇

Outline

Differential Diagnosis
CBC/Biochemistry/Urinalysis
Other Laboratory Tests
Imaging
Other Diagnostic Procedures
Pathologic Findings

DIAGNOSIS

Differential Diagnosis

Other causes of chronic liver disease can be differentiated with US and biopsy
Mild, recurrent colic may be caused by gastrointestinal problems; however, most of these conditions are not accompanied by changes in serum liver enzymes or icterus. Right dorsal displacement of the large colon can result in mild colic, icterus, and increases in serum GGT and conjugated bilirubin

CBC/Biochemistry/Urinalysis

Markedly elevated hepatobiliary enzymes GGT (commonly 7–20 times normal), alkaline phosphatase, and bilirubin; mild to moderate increases in hepatocellular enzymes sorbitol dehydrogenase, glutamate dehydrogenase, and aspartate aminotransferase (2–4 times normal). Significantly elevated serum bile acids
Increase in the conjugated bilirubin fraction to >25% of the total bilirubin is common, but in approximately one-third of cases the conjugated/total bilirubin is <25%
CBC—neutrophilia
Fibrinogen and globulin—elevated (except in cases of common variable immunodeficiency)

Other Laboratory Tests

Prothrombin time and activated partial thromboplastin time—may be prolonged.

Imaging

US reveals increased hepatic echogenicity, hepatomegaly, distended bile ducts, and occasionally calculi are visualized. Choleliths seen in 50–75% of cases
Duodenoscopy may reveal a “bulge” at the level of the major duodenal papilla if obstruction is in the common bile duct

Other Diagnostic Procedures

Liver biopsy and aerobic and anaerobic bacterial culture of biopsy sample. Positive cultures are obtained in approximately 50% of cases.

Pathologic Findings

Hepatomegaly, periportal fibrosis, dilation of bile ducts, and inflammation. Concentric fibrosis is present around ducts in some cases with obstructing stones.

Treatment ⬆ ⬇

TREATMENT

Medical therapy
Choledocholithotomy or choledocholithotripsy should be considered in cases unresponsive to medical therapy

Medications ⬆ ⬇

MEDICATIONS

Drug(s) of Choice

Long-term antibiotic therapy ideally based on culture and sensitivity results from liver biopsy
Gram-negative enteric and mixed anaerobic bacteria are the most frequently isolated; antibiotics with good Gram-negative activity (enrofloxacin, third-generation cephalosporins, aminoglycosides, trimethoprim–sulfamethoxazole) and antimicrobials effective against enteric anaerobes (penicillin, metronidazole, chloramphenicol) should be selected
Ursodiol (ursodeoxycholic acid)—anti-inflammatory and choleretic agent
DMSO—solubilize calcium bilirubinate
IV fluids and anti-inflammatories

Follow-up ⬆ ⬇

Outline