An 8-year-old 36.3-kg (79.9-lb) spayed female Rottweiler was referred because of recurrent bouts of anorexia and vomiting. The dog had a prolonged history (> 3 months) of intermittent bouts of anorexia, vomiting, and lethargy and a recent history (< 48 hours) of worsening clinical signs. Results of serial biochemical analyses conducted by the referring veterinarian indicated persistent and progressively high activities of alkaline phosphatase and serum concentrations of total bilirubin and triglycerides. The dog also had a long-term history of idiopathic epilepsy treated with phenobarbital, the dosage of which during the 2 months before the referral examination had been increased from 2.5 mg/kg (1.1 mg/lb), PO, every 12 hours to 3.1 mg/kg (1.4 mg/lb), PO, every 12 hours because of increased frequency of seizures.
On referral examination, the dog was bright, alert, and responsive but markedly icteric, with yellow mucous membranes, sclerae, and pinnae. The remainder of findings from the physical examination were within reference limits. Results of a CBC indicated neutrophilia (12.43 × 103 neutrophils/μL; reference range, 2.1 × 103 to 11.2 × 103 neutrophils/μL), lymphopenia (0.44 × 103 lymphocytes/μL; reference range, 0.78 × 103 to 3.36 × 103 lymphocytes/μL), and thrombocytosis (457 × 103 platelets/μL; reference range, 129 × 103 to 395 × 103 platelets/μL). Results of serum biochemical analyses indicated hypoalbuminemia (2.2 g/dL; reference range, 2.7 to 3.7 g/dL), total hypocalcemia (total calcium, 9.0 mg/dL; reference range, 9.3 to 11.5 mg/dL), hyponatremia (136 mmol/L; reference range, 145 to 153 mmol/L), hypochloremia (96 mmol/L; reference range 109 to 118 mmol/L), hypokalemia (3.3 mmol/L; reference range, 3.6 to 5.3 mmol/L), and cholestasis characterized by hypercholesterolemia (934 mg/dL; reference range, 143 to 373 mg/dL), hyperbilirubinemia (total bilirubin, 29.1 mg/dL; reference range, 0 to 0.3 mg/dL), and high activity of alkaline phosphatase (8,231 U/L; reference range, 8 to 139 U/L). All other hematologic results, including those for a coagulation panel, were within reference limits.
Given the concern for marked cholestasis, abdominal and thoracic CTa (64 detector row) with nonselective angiography was performed (Figure 1). The pancreas appeared thickened and had irregular margins. In the body of the pancreas, there were 3 fluid-attenuating (6- to 10-HU) round-to-lobular structures with contrast-enhancing rims. The largest of these structures was approximately 1.6 cm in diameter. The remainder of the pancreas had diffuse, mild contrast medium enhancement. The mesentery surrounding the pancreas was ill-defined because of fluid- to soft tissue–attenuating wispy striations confluent with the pancreas. The cystic and common bile ducts were distended, reaching a maximum diameter of 9 mm; however, an area of no distention was observed where the common bile duct neared the body of the pancreas and peripancreatic fat stranding (Figure 2). The intrahepatic bile ducts and the intraparenchymal pancreatic duct in the left lobe and body of the pancreas were diffusely distended up to 7 and 5 mm in diameter, respectively. The remainder of findings on CT were clinically normal.
Dorsal reconstructed (A) and transverse (B) plane postcontrast CT images of the cranial aspect of the abdomen of an 8-year-old 36.3-kg (79.9-lb) spayed female Rottweiler evaluated for anorexia and vomiting. Fluid-attenuating (6- to 10-HU) round-to-lobular structures with contrast-enhancing rims (arrows; A and B) are evident in the body of the pancreas, consistent with abscess formation in the pancreas. The remainder of the pancreas has diffuse, mild contrast medium enhancement, and the mesentery surrounding the pancreas is ill-defined because of fluid- to soft tissue–attenuating wispy striations confluent with the pancreas. Images are displayed in a soft tissue window (window width, 500 HU; window level, 70 HU), with 2-mm slice thicknesses. In each image, the dog's right is to the left, and the white line depicts the level of the orthogonal view. B—Obtained at the level of T13.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Dorsal reconstructed (A) and transverse (B) plane postcontrast CT images of the cranial aspect of the abdomen of an 8-year-old 36.3-kg (79.9-lb) spayed female Rottweiler evaluated for anorexia and vomiting. Fluid-attenuating (6- to 10-HU) round-to-lobular structures with contrast-enhancing rims (arrows; A and B) are evident in the body of the pancreas, consistent with abscess formation in the pancreas. The remainder of the pancreas has diffuse, mild contrast medium enhancement, and the mesentery surrounding the pancreas is ill-defined because of fluid- to soft tissue–attenuating wispy striations confluent with the pancreas. Images are displayed in a soft tissue window (window width, 500 HU; window level, 70 HU), with 2-mm slice thicknesses. In each image, the dog's right is to the left, and the white line depicts the level of the orthogonal view. B—Obtained at the level of T13.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Dorsal reconstructed (A) and transverse (B) plane postcontrast CT images of the cranial aspect of the abdomen of an 8-year-old 36.3-kg (79.9-lb) spayed female Rottweiler evaluated for anorexia and vomiting. Fluid-attenuating (6- to 10-HU) round-to-lobular structures with contrast-enhancing rims (arrows; A and B) are evident in the body of the pancreas, consistent with abscess formation in the pancreas. The remainder of the pancreas has diffuse, mild contrast medium enhancement, and the mesentery surrounding the pancreas is ill-defined because of fluid- to soft tissue–attenuating wispy striations confluent with the pancreas. Images are displayed in a soft tissue window (window width, 500 HU; window level, 70 HU), with 2-mm slice thicknesses. In each image, the dog's right is to the left, and the white line depicts the level of the orthogonal view. B—Obtained at the level of T13.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Dorsal (A), oblique dorsal (B), and oblique transverse (C) plane postcontrast CT images of the cranial aspect of the abdomen of the dog in Figure 1. The cystic and common bile ducts (white arrows; A and B) are markedly distended; however, there is severe narrowing of the common bile duct (black arrows) at the level of the pancreatic body. There are wisps of soft tissue attenuation (fat stranding) in the area of peripancreatic fat around the narrowed portion of the common bile duct, compatible with regional peritonitis secondary to pancreatitis. Images are displayed in a soft tissue window (window width, 500 HU; window level, 70 HU), with 2-mm slice thicknesses. In each image, the dog's right is to the left. A—The image is at the level of the cystic and common bile ducts. B—The image is at the level of the common bile duct and pancreatic body. C—The image is at the level of T13.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Dorsal (A), oblique dorsal (B), and oblique transverse (C) plane postcontrast CT images of the cranial aspect of the abdomen of the dog in Figure 1. The cystic and common bile ducts (white arrows; A and B) are markedly distended; however, there is severe narrowing of the common bile duct (black arrows) at the level of the pancreatic body. There are wisps of soft tissue attenuation (fat stranding) in the area of peripancreatic fat around the narrowed portion of the common bile duct, compatible with regional peritonitis secondary to pancreatitis. Images are displayed in a soft tissue window (window width, 500 HU; window level, 70 HU), with 2-mm slice thicknesses. In each image, the dog's right is to the left. A—The image is at the level of the cystic and common bile ducts. B—The image is at the level of the common bile duct and pancreatic body. C—The image is at the level of T13.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Dorsal (A), oblique dorsal (B), and oblique transverse (C) plane postcontrast CT images of the cranial aspect of the abdomen of the dog in Figure 1. The cystic and common bile ducts (white arrows; A and B) are markedly distended; however, there is severe narrowing of the common bile duct (black arrows) at the level of the pancreatic body. There are wisps of soft tissue attenuation (fat stranding) in the area of peripancreatic fat around the narrowed portion of the common bile duct, compatible with regional peritonitis secondary to pancreatitis. Images are displayed in a soft tissue window (window width, 500 HU; window level, 70 HU), with 2-mm slice thicknesses. In each image, the dog's right is to the left. A—The image is at the level of the cystic and common bile ducts. B—The image is at the level of the common bile duct and pancreatic body. C—The image is at the level of T13.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Extrahepatic biliary obstruction secondary to pancreatitis and concurrent abscess formation was suspected; however, neoplastic infiltrate had not been ruled out. Fine-needle aspiration of the pancreas was performed, and cytologic examination revealed cellular changes consistent with nonseptic, suppurative inflammation and necrosis. Samples for anaerobic and aerobic bacterial cultures were submitted and yielded no growth. Therefore, treatment for pancreatitis was initiated, including ondansetron (0.50 mg/kg [0.23 mg/lb], IV, q 12 h), famotidine (1.0 mg/kg [0.45 mg/lb], IV, q 12 h), ampicillin-sublactam (22 mg/kg [10 mg/lb], IV, q 8 h), a single dose of dexamethasone (0.065 mg/kg [0.030 mg/lb], IV, once), and IV fluid therapy with a balanced electrolyte solution. A nasogastric tube was placed, through which a blend of hypoallergenic dietb and water was administered at a rate of 30% resting energy requirements over a 24-hour period (10.0 kcal/kg/d [4.5 kcal/lb/d]). Given the possible contribution of phenobarbital to pancreatitis, the dog was transitioned to levetiracetamc (60.0 mg/kg [27.3 mg/lb], IV, once, followed by 20.0 mg/kg [9.1 mg/lb], IV, q 8 h) and phenobarbital was discontinued.
After 24 hours of treatment, only marginal improvement was detected in the dog's clinical status and in findings on repeated serum biochemical analyses. The dog remained anorexic and had functional ileus; however, its serum total bilirubin concentration had decreased from 29.1 to 23.1 mg/dL. Given the lack of improvement, we discussed with the owner treatment options, such as continued medical management, repeated percutaneous cholecystocentesis decompression, temporary PCD catheter, cholecystoenterostomy, or choledochal tube stent, and the decision was to move forward with placement of a temporary PCD catheter.
The dog was anesthetized and positioned in left lateral recumbency. The right lateral caudal aspect of the thorax and cranial aspect of the abdomen were sterilely prepared and draped. With ultrasonographic (8- to 5-MHz convex probe)d guidance, the gallbladder was located, and an optimal transhepatic route was selected in the ventral third of the 11th intercostal space on the right side, caudal to the caudal extent of the lungs, as defined by ultrasonographic reverberation artifact and the glide sign. Following administration of local anesthesia (0.5% lidocaine hydrochloride [5 mg total], SC), a skin incision was made and a 14-gauge, 5.2-inch-long over-the-needle cathetere was passed through the right 11th intercostal space, immediately cranial to the rib. Ultrasonography indicated that this path crossed approximately 2 cm of the right medial lobe of the liver, then into a distended intrahepatic bile duct. Bile was aspirated and collected for cytologic examination and quantitative bacterial culture. Then, through this same catheter, ioversolf contrast medium (3 mL; 350 mg iodine/mL) was injected for positive-contrast cholangiography (Figure 3). A straight-tip, stiff guidewireg (diameter, 0.035-inch; length, 145 cm) was passed through the catheter, down the intrahepatic bile duct, and into the gallbladder. The catheter was then removed over the wire. A 6F locking-loop drainage catheterh was advanced over the wire and into the gallbladder. The locking-loop suture was tightened, and the catheter was pulled taut to the body wall and attached to a 3-way stopcock. Patency was confirmed by first aspirating bile, then repeating positive-contrast cholangiography (ioversol, 3 mL). Through this catheter, approximately 150 mL of bile was removed, decompressing the biliary system. The catheter was flushed with 6 mL of sterile saline (0.9% NaCl) solution. A cruciate suture combined with retention sutures along the first 2 cm of tubing and a secondary encircling suture were placed with 3-0 nylon suture materiali to secure the cholecystostomy tube to the skin. Total procedural time, including surgical preparation of the dog and placement of the PCD tube, was 45 minutes. The dog was recovered from anesthesia without complication.
Fluoroscopic intraoperative positive-contrast cholangiographic image obtained after a distended intrahepatic bile duct (arrow) in the dog in Figures 1 and 2 was accessed with a 14-gauge, 5.2-inch-long over-the-needle catheter (arrowhead) and injected with contrast medium. The ventral aspects of the 13th ribs (asterisks), just dorsal to the costochondral junction, are evident in the lower left of the image. The dog's head is toward the right of the image, and dorsal is toward the top of the image.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Fluoroscopic intraoperative positive-contrast cholangiographic image obtained after a distended intrahepatic bile duct (arrow) in the dog in Figures 1 and 2 was accessed with a 14-gauge, 5.2-inch-long over-the-needle catheter (arrowhead) and injected with contrast medium. The ventral aspects of the 13th ribs (asterisks), just dorsal to the costochondral junction, are evident in the lower left of the image. The dog's head is toward the right of the image, and dorsal is toward the top of the image.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
Fluoroscopic intraoperative positive-contrast cholangiographic image obtained after a distended intrahepatic bile duct (arrow) in the dog in Figures 1 and 2 was accessed with a 14-gauge, 5.2-inch-long over-the-needle catheter (arrowhead) and injected with contrast medium. The ventral aspects of the 13th ribs (asterisks), just dorsal to the costochondral junction, are evident in the lower left of the image. The dog's head is toward the right of the image, and dorsal is toward the top of the image.
Citation: Journal of the American Veterinary Medical Association 257, 5; 10.2460/javma.257.5.531
After surgery, the dog continued to receive supportive care for pancreatitis and EHBO. Every 6 hours, bile fluid was drained from the PCD catheter and readministered through the nasogastric tube, which was also used to administer bolus feedings of the blenderized diet. Bile volume was quantified for each aspiration and steadily declined from 56 mL/h (1.4 mL/kg/h [0.6 mL/lb/h]) to 9 mL/h (0.2 mL/kg/h [0.1 mL/lb/h]) during hospitalization. When evaluated 22 hours after PCD catheter placement, the dog's serum total bilirubin concentration had decreased to 7.7 mg/dL, compared with 23.1 mg/dL preoperatively. Within 24 hours after PCD catheter placement, the dog was eating regularly and had increased intestinal peristaltic sounds on abdominal auscultation.
Three days after surgery, the volume of bile aspirated through the PCD catheter over a 24-hour period was < 0.6 mL/kg/h (0.27 mL/lb/h). Although, to our knowledge, no validated reference range for bile production in dogs existed, the volume of bile aspirated from the patient over a 24-hour period was less than the bile flow rate reported for a group of research dogs during a 24-hour period,1 and the lower rate in the dog of the present report was attributed to a partially patent common bile duct.
The dog was discharged, and the owner was instructed on how to aspirate the PCD catheter and continue to aspirate it every 12 to 24 hours at home. The dog dislodged the nasogastric tube 3 days after hospital discharge; therefore, readministration of aspirated bile was discontinued. A brief ultrasonographic examination 3 weeks after hospital discharge revealed that neither the gallbladder nor common bile duct was distended, despite > 24 hours without PCD catheter aspiration; therefore, aspirations were discontinued.
The PCD catheter remained in place for approximately 5 weeks to allow formation of a mature fistulous stoma tract. The dog was then returned for recheck examination, sedation, and positive-contrast fluoroscopic cholangiography, which confirmed patency of the common bile duct. Thus, the PCD catheter was removed. Abdominal ultrasonography revealed mild thickening of the pancreas (compatible with clinically improved pancreatitis) and scant free fluid at the previous PCD catheter site. No major complications occurred during the course of treatment; however, 1 minor complication of bile leakage at the PCD catheter and a 3-way stopcock juncture occurred but resolved with replacement of the stopcock. Results of follow-up serum biochemical analyses 7 months after surgery were completely within reference limits.
Discussion
In dogs, common causes of EHBO include pancreatitis, gallbladder mucoceles, choleliths, cholecystitis, and neoplasia, with pancreatitis and neoplasia being most common.2 Surgery is commonly performed to relieve biliary obstruction but is associated with high morbidity and mortality rates. Survival to hospital discharge varies from 41% (12/29) to 72% (43/60),2–4 with only 50% (6/12)5 of dogs also undergoing surgery for pancreatitis surviving to hospital discharge.
In human medicine, preoperative biliary drainage through PCD catheters or choledochal stents has been used since as early as 1978.6–10 Additionally, although PCD has preoperative value, it may also be used as a replacement for conventional surgery in select patients,7,11 including those with disease processes that can be medically managed (eg, pancreatitis or cholangitis) or those who could benefit from minimally invasive palliation (eg, patients who are ill or medically unstable or have aggressive neoplasia). Further, interventional procedures to establish biliary drainage with use of radiography and PCD catheter placement before or instead of cholecystectomy are frequently used and have improved patient outcome, compared with surgery alone.12
In veterinary medicine, although EHBO secondary to pancreatitis will resolve spontaneously in most patients given enough time, surgical correction has historically been implemented to relieve the obstruction in patients when their clinical status warrants it. The most common surgical procedures to correct EHBO are cholecystectomy and cholecystoduodenostomy, with an overall mortality rate of 28% (17/60) during hospitalization.5 The high mortality rate for the dogs of that study5 likely reflected the severity of underlying pathological changes requiring surgical intervention and secondary systemic effects. Systemic consequences of EHBO include acute tubular necrosis, coagulopathy, decreased wound healing, systemic and portal endotoxemia and bacteremia, continued gastrointestinal bacterial translocation, systemic inflammatory response syndrome, sepsis, and disseminated intravascular coagulation.5 It is therefore reasonable to consider that reducing these effects in animals before or instead of invasive surgery (eg, cholecystectomy and cholecystoduodenostomy) may reduce mortality rates of affected animals. Prospective studies assessing the value of PCD catheter placement during presurgical stabilization of animals with EHBO are warranted.
Ultrasonographically guided percutaneous cholecystostomy was attempted experimentally without fluoroscopy in 1983 but was unsuccessful in 4 of the 5 dogs; however, for 3 of the 4 dogs for which the procedure was unsuccessful, failure was attributed to decreased gallbladder size after cystic duct ligation.13 A study14 that compared laparoscopic transperitoneal, ultrasonographically guided transperitoneal, and ultrasonographically guided transhepatic methods of placing cholecystostomy tubes in 20 cadaveric dogs shows success rates of 100% (5/5), 0% (0/5), and 60% (3/5), respectively. Case reports describe the use of therapeutic PUC in 3 dogs with EHBO and pancreatitis15 and choledochal stenting in dogs and cats.4,16,17 Good outcomes were reported15 for all 3 dogs treated with PUC, including substantial improvement in serum bilirubin concentration following the procedure and recovery of 2 of the 3 dogs without more invasive surgical intervention. In 1 of those 3 dogs, PUC was performed multiple times, which suggested that this dog might have been a candidate for a continual method of draining the gallbladder, such as a PCD catheter as described in the dog of the present report. Treatment with internal drainage through surgically placed choledochal stents is associated with mortality rates similar to those for biliary diversion surgery.16 In another study,4 biliary stents were placed with endoscopic retrograde cholangiopancreatography in 9 dogs, no deaths were reported, and success was observed in 1 of the 2 client-owned dogs and 5 of the 7 research dogs; however, the procedure requires expert operator experience with the technique and advanced instrumentation that was not available at our institution.
Outcome for the dog of the present report exemplified successful use of a PCD catheter for treatment of EHBO secondary to pancreatitis in a dog. We also described novel replacement of bile during external biliary drainage in the dog. It has been suggested that an absence of intestinal bile results in a substantial but self-limiting increase in the intestinal gram-negative aerobic bacterial population, which may account for bacterial translocation in the early stages of biliary obstruction. Systemic endotoxemia is a risk for patients with biliary obstruction, and systemic sepsis could occur, especially in patients with concurrent factors such as immunologic depression and physical disruption of gut barrier function that may promote bacterial translocation.18 Relatedly, a study19 indicates that a short period of internal biliary drainage is a useful strategy in restoring Kupffer cell function, which helps in negating systemic endotoxemia and consequent complications of biliary obstruction. Because of this, several investigators in human medicine have advocated for oral administration (including by feeding tube) of bile in affected patients to allow for normal physiologic use of the bile. Benefits of bile replacement treatment during EHBO include restoration of intestinal microbiota and intestinal barrier function and integrity.20
Use of PCD to treat the dog of the present report had no major complications. Complications reported in human medicine include bile peritonitis, bleeding, hypotension, vagal reaction, catheter dislodgement, cholangitis, and acute respiratory distress.7,21 A minor complication did occur in the dog of the present report and consisted of transient bile leakage at the junction of the catheter and the 3-way stopcock. This likely could have been avoided if a different, commercially available PCD catheter had been used.
A study22 of 6 human patients shows the recommended duration for biliary drains to be left in place ranges from 2 to 120 days. This range reflects the various treatment purposes intended (eg, preoperative decompression, adjunct to medical treatment, or palliation) and maturation of a catheter site stoma tract to prevent leakage of bile. A study14 in which the PCD catheter tract was evaluated 9 and 25 days postoperatively indicates that maturation is not complete at 25 days. Although this suggests that a PCD catheter needs to be kept in longer than 25 days, more research is warranted regarding the average duration needed for a mature catheter tract to be formed.
When external biliary drainage is used, a consideration is whether external drainage will be converted to internal drainage. For instance, in human medicine, when patients present with acute biliary obstruction, the first treatment option is typically internal drainage by endoscopic retrograde cholangiopancreatography; however, when this is not possible, percutaneous drainage is performed and then may be converted to internal drainage. Several factors, including the clinical scenario and duration of anticipated need for drainage, would be considered. In the dog of the present report, we anticipated that the obstruction would be self-limiting and that the dog would recover if it survived the event of biliary obstruction. Therefore, we felt that internal conversion would not have been warranted.
Given the single treated dog of the present report, we could not draw conclusions on the repeatability, safety, or widespread applications of PCD in veterinary medicine. It was unknown whether the dog of the present report would have had the same success without intervention, and findings of early resolution of clinical signs (eg, chronic anorexia and hyperbilirubinemia) and promising long-term results (normalization of hepatobiliary parameters at 7 months) for the dog of the present report warrant further investigation of the use of PCD in veterinary patients with EHBO.
Ultrasonographically guided transhepatic PCD catheter placement provided fast resolution of EHBO secondary to pancreatitis in the dog of the present report. We believe that this minimally invasive, interventional radiographic procedure has the potential to decrease morbidity and prevent death in select patients, compared with traditional surgical options, and that additional research is warranted regarding clinical utility, safety, and long-term results of this procedure in veterinary patients, particularly those that have transient causes of EHBO, are too unstable to undergo more invasive biliary diversion techniques, or have biliary diseases that could benefit from palliation alone.
Acknowledgments
The authors declare that there were no conflicts of interest.
Presented in abstract form at the 2019 Annual Conference of the Veterinary Interventional Radiology and Interventional Endoscopy Society, Squaw Valley, Calif, May 2019.
ABBREVIATIONS
| EHBO | Extrahepatic biliary obstruction |
| PCD | Percutaneous cholecystostomy drainage |
| PUC | Percutaneous ultrasonographically guided cholecystocentesis |
Footnotes
Aquilion 64, Toshiba America Medical Systems Inc, Tustin, Calif.
ProPlan Veterinary Diets HA Hydrolyzed Canine Formula, Purina, St Louis, Mo.
Keppra, AuroMedics Pharma LLC, Windsor, NJ.
SonoSite Edge II ultrasound with C11x probe, Fujifilm, Bothell, Wash.
BD Angiocath, Becton, Dickinson and Co, Franklin Lakes, NJ.
Optiray 350, Guebert LLC, Villepinte, France.
Amplatz Super Stiff guidewire, Boston Scientific Corp, Marlborough, Mass.
SUB nephrostomy tube, Norfolk Vet Products Inc, Skokie, Ill.
Ethilon, Ethicon Inc, Somerville, NJ.
References
1. Boyer JL. Bile formation and secretion. Compr Physiol 2013;3:1035–1078.
2. Fahie MA, Martin RA. Extrahepatic biliary tract obstruction: a retrospective study of 45 cases (1983–1993). J Am Anim Hosp Assoc 1995;31:478–482.
3. Amsellem PM, Selm HB, MacPhail CM, et al. Long-term survival and risk factors associated with biliary surgery in dogs: 34 cases (1994–2004). J Am Vet Med Assoc 2006;229:1451–1457.
4. Berent A, Weisse C, Schattner M, et al. Initial experience with endoscopic retrograde cholangiography and endoscopic retrograde biliary stenting for treatment of extrahepatic bile duct obstruction in dogs. J Am Vet Med Assoc 2015;246:436–446.
5. Mehler SJ, Mayhew PD, Drobatz KJ, et al. Variables associated with outcome in dogs undergoing extrahepatic biliary surgery: 60 cases (1988–2002). Vet Surg 2004;33:644–649.
6. Nakayama T, Ikeda A, Okuda K. Percutaneous transhepatic drainage of the biliary tract: technique and results in 104 cases. Gastroenterology 1978;74:554–559.
7. Ferrucci JT, Mueller PR, Harbin WP. Percutaneous transhepatic biliary drainage: technique, results, and applications. Radiology 1980;135:1–13.
8. Mueller PR, van Sonnenberg E, Ferruci JT. Percutaneous biliary drainage: technical and catheter-related problems in 200 procedures. AJR Am J Roentgenol 1982;138:17–23.
9. Lammer J, Neumayer K. Biliary drainage endoprostheses: experience with 201 placements. Radiology 1986;159:625–629.
10. Dick BW, Gordon RL, LaBerge JM, et al. Percutaneous transhepatic placement of biliary endoprostheses: results in 100 consecutive patients. J Vasc Interv Radiol 1990;1:97–100.
11. Ito K, Fujita N, Noda Y, et al. Percutaneous cholecystostomy versus gallbladder aspiration for acute cholecystitis: a prospective randomized controlled trial. AJR Am J Roentgenol 2004;183:193–196.
12. Simorov A, Ranade A, Parcells J, et al. Emergent cholecystostomy is superior to open cholecystectomy in extremely ill patients with acalculous cholecystitis: a large multicenter outcome study. Am J Surg 2013;206:935–940.
13. McGahan JP, Phillips HE, Nyland T, et al. Sonographically guided percutaneous cholecystostomy performed in dogs and pigs. Radiology 1983;149:841–843.
14. Murphy SM, Rodriguez JD, McAnulty JF. Minimally invasive cholecystostomy in the dog: evaluation of placement techniques and use in extrahepatic biliary obstruction. Vet Surg 2007;36:675–683.
15. Herman BA, Brawer RS, Murtaugh RJ, et al. Therapeutic percutaneous ultrasound-guided cholecystocentesis in three dogs with extrahepatic biliary obstruction and pancreatitis. J Am Vet Med Assoc 2005;227:1782–1786.
16. Mayhew PD, Richardson RW, Mehler SJ, et al. Choledochal tube stenting for decompression of the extrahepatic portion of the biliary tract in dogs: 13 cases (2002–2005). J Am Vet Med Assoc 2006;228:1209–1214.
17. Mayhew PD, Weisse CW. Treatment of pancreatitis-associated extrahepatic biliary tract obstruction by choledochal stenting in seven cats. J Small Anim Pract 2008;49:133–138.
18. Clements WD, Parks R, Erwin P, et al. Role of the gut in the pathophysiology of extrahepatic biliary obstruction. Gut 1996;39:587–593.
19. Clements WD, McCaigue M, Erwin P, et al. Biliary decompression promotes Kupffer cell recovery in obstructive jaundice. Gut 1996;38:925–931.
20. Kamiya S, Nagino M, Kanazawa H, et al. The value of bile replacement during external biliary drainage: an analysis of intestinal permeability, integrity, and microflora. Ann Surg 2004;239:510–517.
21. vanSonnenberg E, D'Agostino HB, Goodacre BW, et al. Percutaneous gallbladder puncture and cholecystostomy: results, complications, and caveats for safety. Radiology 1992;183:167–170.
22. Eggermont AM, Laméris JS, Jeekel J. Ultrasound-guided percutaneous transhepatic cholecystostomy for acute acalculous cholecystitis. Arch Surg 1985;120:1354–1356.
