Editorial Type: Soft-Tissue Surgery
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Online Publication Date: 01 May 2002

The Surgical Treatment of Cholelithiasis in Cats: A Study of Nine Cases

DVM, Diplomate ACVS and
VMD, MS, Diplomate ACVS
Article Category: Other
Page Range: 290 – 296
DOI: 10.5326/0380290
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Nine cats that had surgical treatment for obstructive cholelithiasis were reviewed to evaluate clinical signs, diagnostic test results, and outcome after surgery. Common clinical signs included progressive vomiting (9/9), dehydration (9/9), anorexia (6/9), icterus (5/9), and lethargy (4/9). Five cats had a cholecystectomy performed, one cat had a cholecystotomy, and three cats had a biliary diversion procedure. Four of the cats that had a cholecystectomy had no recurrence of vomiting or anorexia. The majority of cats (7/9) had multiple choleliths, which were radiopaque and most commonly composed of calcium carbonate. Seven cats were diagnosed with cholangiohepatitis, and four of these cats did not need long-term medical therapy. Most cats (7/9) survived long term postsurgery (mean, 21 months; median, 24 months) without additional medical therapy, while the two cats with concurrent hepatic lipidosis died. Cholecystectomy appeared to have low morbidity with good clinical success.

Introduction

Cholelithiasis in cats is uncommon and rarely reported as a cause of obstructive biliary disease.1–9 There are several factors which may contribute to cholelith formation, including biliary stasis, altered bile composition, cholecystitis, dietary factors, and biliary parasitic or bacterial infections.10–14 Cholangiohepatitis is often associated with feline cholelithiasis and may be a predisposing factor in its pathogenesis.1315 The most commonly reported choleliths in dogs are composed of calcium bilirubinate, but cholelith analysis has rarely been done in cats.135689 The purpose of this study was to describe clinical signs, diagnostic test results, and outcomes of the surgical treatments in nine cats with obstructive cholelithiasis.

Materials and Methods

Medical records of nine cats that had biliary surgery for obstructive cholelithiasis were reviewed. Signalment, medical history, clinical pathology, diagnostic tests, surgical treatment, histopathology results, cholelith analysis, and outcome were evaluated. Telephone interview with the owner or referring veterinarian was used to obtain follow-up information of at least 12 months. The date and cause of death were also recorded if the cat had died.

Results

Signalment

The three breeds represented were domestic shorthair (n=7), Abyssinian (n=1), and Maine coon (n=1). There were six neutered male cats and three spayed female cats. The age at presentation ranged from 5 to 18 years, with a mean age of 12 years. The mean weight was 4.7 kg (range, 3 to 5.6 kg).

Historical and Physical Examination Findings

The most common clinical signs included progressive vomiting (9/9), dehydration (9/9), anorexia (6/9), icterus (5/9), and lethargy (4/9).

Laboratory Evaluation

All of the cats were negative for feline leukemia virus and feline immunodeficiency virus. Hematological and serum biochemical analyses were performed in all of the cats [Tables 1, 2]. The mean white blood cell count was 14.93 × 103 cells/μL (range, 7.2 to 25.0 × 103 cells/μL). Four cats had neutrophilia (>12.5 × 103 cells/μL) and a mean banded neutrophil count of 799 cells/μL (range, 624 to 3,500 cells/μL). Seven cats had a lymphopenia (<1.5 × 103 cells/μL), and one cat had an eosinophilia (>1.5 × 103 cells/μL). The mean hematocrit was 34% (range, 17.5% to 44.1%), but one cat was anemic (17.5%). A coagulation profile was performed in eight cats, and all fell within reference ranges. Abnormalities on serum biochemical analysis included azotemia in two cats (serum urea nitrogen concentration, >35 mg/dL; creatinine, >2.0 mg/dL) and hyperglycemia (>150 mg/dL) in six cats. Five cats also had increased serum cholesterol levels, with a mean of 266 mg/dL (range, 223 to 360 mg/dL).

Seven cats had an increased serum total bilirubin (mean, 6.6 mg/dL; range, 0.5 to 16.1 mg/dL). The alkaline phosphatase activity was elevated in five cats (mean, 420 IU/L; range, 139 to 1,205 IU/L). The serum alanine aminotransferase (ALT) was increased in eight cats (mean, 709 IU/L; range, 78 to 2,096 IU/L), while six cats had an elevation of the serum aspartate aminotransferase (AST) (mean, 368 IU/L; range, 99 to 573 IU/L). Four cats that had hyperbilirubinemia also had bilirubinuria.

Diagnostic Imaging

Abdominal radiographs were taken in six cats, and five of these cats had radiopaque choleliths [Figures 1A, 1B]. Abdominal ultrasonography was performed in eight cats. Biliary distention suspicious for extrahepatic obstruction was seen in all eight cats, and choleliths were identified in seven. None of the cats had specialized imaging studies, such as hepatobiliary scintigraphy or intravenous cholangiocystography.

Microbiology

All of the cats had bile or fragments of a cholelith submitted for aerobic microbial culture at the time of surgery. Four cats also had anaerobic cultures submitted. Three of the four anaerobic samples had no growth, but one sample was positive for Bacteroides fragilis (this cat also had a positive aerobic culture). A single bacteria species was isolated from the aerobic samples in five cats that included Acinetobacter spp., Staphylococcus epidermidis, Enterococcus faecalis, Streptococcus viridans, and Escherichia coli. Antibiotic susceptibility testing was obtained for each aerobic bacterial isolate. All five isolates were sensitive to aminoglycosides (i.e., gentamicin or amikacin), four were sensitive to fluoroquinolones (i.e., enrofloxacin or ciprofloxacin), three were sensitive to first-generation cephalosporins (i.e., cefazolin, cephalothin) or amoxicillin/clavulanic acid, and two were sensitive to ampicillin.

Surgical Treatment

All of the cats had a celiotomy and abdominal exploratory, in which a large, distended gallbladder and extrahepatic biliary system were found. The stones were located both within the gallbladder (choleliths) and the bile duct (choledocholiths). None of the cats had a ruptured gallbladder or evidence of a generalized peritonitis. The liver had an abnormal appearance in all of the cats, being friable and diffusely swollen in two cats and firm in the other seven cats. None of the cats had evidence of an abdominal mass or mass associated with the gallbladder or biliary system.

A cholecystectomy was performed in five of the cats in conjunction with a duodenotomy to assess the patency of the common bile duct prior to gallbladder excision. One cat had a cholecystotomy to remove multiple choleliths. The other three cats had either a cholecystoduodenostomy (n=2) or a cholecystojejunostomy (n=1). Two of the cats had an intraoperative gastrostomy tubea placed. All of the cats had liver tissue samples collected intraoperatively for histopathological evaluation. The gallbladders of six cats were also submitted for histopathology.

Cholelith and Histopathological Analysis

Seven cats had multiple choleliths, while two cats had a single cholelith. Compositions of three choleliths that were submitted for analysis by crystallography consisted of calcium carbonate (100%) in two cats and calcium carbonate (40%), calcium bilirubinate (55%), and cholesterol (5%) in one cat.

Six cats had cholecystitis based on histopathological evaluation of their gallbladder samples, characterized by lymphocytic-plasmacytic inflammation. Seven of the nine cats had a histological diagnosis of cholangiohepatitis, characterized by lymphocytic-plasmacytic periportal inflammation, bile ductule hyperplasia, and periportal fibrosis. Two cats also had liver samples consistent with hepatic lipidosis characterized by vacuolated hepatocytes with canalicular bile stasis.

Outcomes

Seven of the nine cats were alive or survived from 13 months to 27 months after surgery (mean, 21 months; median, 24 months) [Table 3]. Six of the surviving cats were discharged with treatment for cholangiohepatitis, consisting of various antibiotics (such as amoxicillin, enrofloxacin, or metronidazole) alone or in combination with prednisone. Four of the cats with cholangiohepatitis had treatment discontinued within 1 month postsurgery, because there were no clinical signs. Only two cats required long-term treatment with prednisone for their cholangio-hepatitis, and both of these cats also had inflammatory bowel disease (IBD). Four of the surviving cats needed a blood transfusion postoperatively because of anemia, and only one cat was anemic preoperatively. The two cats with concurrent hepatic lipidosis (based on liver histopathology) both died postoperatively. One of the two cats failed to fully recover from anesthesia and died within 6 hours from cardiopulmonary arrest, while the other cat was euthanized 2 days after surgery because of marked anemia and hepatoencephalopathy. Both of these cats had obstructive cholelithiasis based on preoperative abdominal ultrasonography, and one cat had a cholecystectomy performed while the other had a cholecystoduodenostomy. Neither of these cats had a necropsy performed.

Four of the seven surviving cats had a cholecystectomy performed and a mean follow-up time of 22 months (range, 15 to 26 months) [Table 3]. All of these cats were alive when lost to follow-up and were receiving no medical treatment. None of the surviving cats with a cholecystectomy had a recurrence of vomiting or anorexia. The cat that had a cholecystotomy survived 13 months postsurgery but needed continued treatment for cholangiohepatitis and IBD (diagnosed by referring veterinarian based on histopathology of endoscopic intestinal biopsies). This cat was eventually euthanized because of vomiting and anorexia that recurred due to progression of the cholangiohepatitis and IBD.

Two of the seven surviving cats had either a cholecysto-duodenostomy or a cholecystojejunostomy performed, and both of these cats also had cholangiohepatitis. At surgery, the cat with a cholecystoduodenostomy was also diagnosed with IBD, which was treated with various dietary modifications and prednisone. This cat was eventually euthanized (18 months postsurgery) because of the development of chronic renal disease and progressive kidney dysfunction. The cat with a cholecystojejunostomy did well for 27 months postsurgery when it presented for dyspnea. A laryngeal mass was found on examination, and a biopsy revealed laryngeal squamous cell carcinoma. The cat was subsequently euthanized because of progressive dyspnea and a poor prognosis.

Discussion

The majority of the cats in this study were older (>10 years), neutered males, whereas in dogs, it is the older, female, small-breed dogs that are more commonly affected with cholelithiasis.10 Most of the previously reported cats with choleliths were also male, but they were younger (<10 years).1–689

All of the cats in this study and those reported in the veterinary literature had a progressive history of vomiting, which is consistent with cholelithiasis in dogs and humans.1–81011 Anorexia and lethargy were common in the cats of this study, just as they are commonly reported in cats with clinical and experimentally induced, extrahepatic biliary tract obstruction.1–916 Most of the cats (5/9) in this study were also icteric on presentation, which is often the situation in dogs (45%).1011 These clinical signs can be attributed to cholestasis and biliary obstruction, with the majority of the cats having hyperbilirubinemia and an increased serum ALT, serum AST, and serum alkaline phosphatase activities. Fewer cats had a neutrophilia (4/9) when compared to dogs.10 Despite the potential deficiency of vitamin K-dependent coagulation factors associated with chronic biliary obstruction,13 the cats in this study had normal preoperative coagulation profiles. These cats may have had an incomplete obstruction or were presented before malabsorption of vitamin K was clinically significant. The anemia postoperatively in four of the seven surviving cats cannot readily be explained, because only one of these cats was anemic prior to surgery (the Abyssinian had a long history of immune-mediated hemolytic anemia), and there was no significant intraoperative hemorrhage. The anemia may have been related to liver dysfunction secondary to the cholangio-hepatitis or perhaps was dilutional secondary to over-hydration with fluids in surgery and immediately postoperatively.

Biliary ultrasonography was very useful in evaluating the cases in this study and helped facilitate the need for early surgical intervention, especially with the lipidotic cats. Ultrasonographic evaluation of the gallbladder and bile duct has been shown to be an accurate method to determine extrahepatic biliary obstruction,17–19 as in the cat (n=1) in which the cholelith was visible on the abdominal ultrasound and not the abdominal radiograph. It has been reported that a diagnosis of extrahepatic biliary obstruction can be made in cats when the bile duct diameter exceeds 5 mm.19 Radiopaque choleliths (5/6) were common in this study, just as they have been reported to be in dogs (48%).10 In both species, choleliths commonly contain mixtures of calcium which makes them visible on survey abdominal radiographs.17

The bacteria isolated were similar to those in dogs and were sensitive to aminoglycosides (5/5) or fluoroquinolones (4/5), but only 3/5 were sensitive to first-generation cephalosporins or amoxicillin/clavulanic acid.10 Ampicillin was used in the majority (6/9) of cats prior to surgery, and this may help to explain the low number of isolates sensitive to ampicillin due to the selection of resistant bacteria. Also, prior antibiotic use could have contributed to obtaining a negative culture. Anaerobic culture was not routinely performed, but anaerobic bacteria involving the biliary tree should be considered and appropriate antibiotic therapy instituted (such as metronidazole in combination with an aminoglycoside or fluoroquinolone).

With the exception of one of the lipidotic cats, all of the cats with a cholecystectomy had complete resolution of clinical signs and a mean follow-up time of 22 months. Cholecystectomy had a low morbidity and mortality in cats, just as it does in dogs.101420 Cholecystoduodenostomy or cholecystojejunostomy was performed when obstruction of the bile duct could not be relieved. Recurrence of cholelithiasis has been reported in a cat with a cholecystojejunostomy.8 Although none of the cats in this study (postoperative follow-up, 13 months to 27 months) had recurrence of choleliths, it may be a potential complication when a cholecystectomy has not been performed. The pancreatic duct may be inadvertently ligated while performing a cholecysto-duodenostomy or cholecystojejunostomy, which will lead to exocrine pancreatic insufficiency.21 Biliary diversion procedures may also lead to biliary cirrhosis and duodenal reflux if the surgically created stoma strictures or is too small.1421 Bile peritonitis associated with gallbladder rupture secondary to cholelithiasis or cholecystitis did not occur in the cats in this study, as it can occur in dogs.102223

The majority (7/9) of cats had multiple choleliths, just as dogs have multiple choleliths (66%).10 Pure calcium carbonate choleliths were the most common in this study, which have been rarely reported.9 One cat did have choleliths composed of a mixture of calcium carbonate, calcium bilirubinate, and cholesterol. These mixed choleliths are the most commonly reported choleliths in cats to date.13568 In contrast, the most common choleliths in dogs are composed of calcium bilirubinate.10 The difference in this study may be due to the small number of choleliths analyzed.

There was abnormal liver histopathology in all the cats, with seven having cholangiohepatitis and two having hepatic lipidosis. The two cats with concurrent lipidosis responded poorly after surgery and were the only cats that did not survive. It has been reported that the mortality rate of feline hepatic lipidosis is approximately 40% with aggressive nutritional therapy and can be up to 90% without aggressive nutritional support.24 Both of these cats died before aggressive treatment for their lipidosis could be started. While there was a small number of affected cats, the combination of cholelithiasis and hepatic lipidosis was associated with a high mortality rate. In this study, all of the cats with cholangiohepatitis survived long term (>12 months), which is similar to other studies.2526

Conclusion

While cholelithiasis is often an incidental finding, biliary obstruction secondary to cholelithiasis should be considered in cats with a history of vomiting, anorexia, and icterus. Obstructive cholelithiasis was easily diagnosed with biliary ultrasonography and helped to facilitate early surgical intervention. The majority (7/9) of cats had multiple choleliths most commonly composed of calcium carbonate, and all had abnormal liver histopathology. Cholecystectomy appeared to have low morbidity and mortality in this study, and most (7/9) of the cats survived long term (24 months) postsurgery unless there was concurrent hepatic lipidosis.

Ponsky PEG tube; C.R. Bard, Inc., Billerica, MA

Table 1 Select Preoperative Blood Cell Count Values From Nine Cats With Cholelithiasis

          Table 1
Table 2 Select Preoperative Liver Serum Biochemical Values From Nine Cats With Cholelithiasis

          Table 2
Table 3 Surgical Procedures and Outcomes in Nine Cats With Cholelithiasis

          Table 3
Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).
Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).Figures 1A, 1B—. Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).
Figures 1A, 1B Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).

Citation: Journal of the American Animal Hospital Association 38, 3; 10.5326/0380290

Copyright: Copyright 2002 by The American Animal Hospital Association 2002
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  <italic toggle="yes">Figures 1A, 1B</italic>
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Figures 1A, 1B

Lateral cranial (1A) and ventrodorsal (1B) abdominal radiographic view of a cat (case no. 7) with radiopaque choleliths located within the gallbladder (arrow).


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