Extrahepatic biliary duct obstruction secondary to duodenal foreign bodies in 2 dogs

Abstract

Two dogs, a 5-year-old neutered male boxer dog and a 2-year-old neutered male Australian cattle dog, were evaluated for vomiting and inappetence. Both dogs were icteric on physical examination, and had hyperbilirubinemia, elevated liver enzymes, and inflammatory changes on diagnostic blood analysis. A proximal duodenal obstruction causing extrahepatic biliary duct obstruction (EHBDO) was suspected in both cases after diagnostic imaging was performed. Exploratory laparotomy confirmed duodenal foreign bodies in both cases. This case report defines duodenal foreign body as a differential diagnosis for EHBDO in dogs.

Case descriptions

Case 1

A 5-year-old neutered male boxer dog was referred to the Western College of Veterinary Medicine (WCVM), Saskatchewan, because of a 3-day history of vomiting, inappetence, abdominal pain, and icterus. A foreign body was suspected by the owner. The barium study performed by the referring veterinarian showed the passage of barium into the small intestines, with delayed gastric emptying.

On presentation the dog weighed 27.4 kg, with a body condition of 3 out of 9. The mucous membranes were icteric, with prolonged capillary refill time. Abdominal discomfort was noted. The remainder of the physical examination findings was within normal limits. The clotting time (PT and PTT) was within normal limits. Complete blood (cell) count (CBC) revealed mild erythrocytosis [9.22 × 10¹²/L; reference interval (RI): 5.80 to 8.50 × 10¹²/L], consistent with dehydration. Mild neutrophilia (14.38 × 10⁹/L; RI: 3.00 to 10.00 × 10⁹/L) with a moderate left shift (2.95 × 10⁹/L bands; RI: 0 to 0.10 × 10⁹/L) and mild toxic change were noted, consistent with active inflammation. Serum chemistry showed a 3-fold increase in amylase (3370 U/L; RI: 343 to 1375 U/L), and a greater than10-fold increase in lipase (5016 U/L; RI: 25 to 353 U/L). Hypercholesterolemia (13.62 mmol/L; RI: 2.70 to 5.94 mmol/L), hyperbilirubinemia (167.1 nmol/L; RI: 1.0 to 4.0 nmol/L), marked elevation in alkaline phosphatase (ALP, 4966 U/L; RI: 9 to 90 U/L), gamma-glutamyl transferase (GGT, 115 U/L; RI: 0 to 8 U/L), and alanine aminotransferase (ALT, 5467 U/L; RI: 19 to 59 U/L) were detected. Differential diagnoses included cholestasis due to extrahepatic biliary duct obstruction (EHBDO) (including choledocholith, foreign body, granuloma or tumor), pancreatitis or lipase-producing tumor. Diagnostic imaging was performed.

Abdominal ultrasonography showed sludge in the gallbladder, a large amount of gas, fluid, and hyperechoic content in the stomach that caused distal acoustic shadowing, consistent with retained barium from previous positive contrast upper gastrointestinal series. A homogeneously echogenic foreign body with a curvilinear interface was identified in the pyloric antrum that caused complete distal acoustic shadowing (Figure 1). The common bile duct could not be identified due to distal acoustic shadowing from content in the stomach. Although shadowing in the pyloric antrum suggested the presence of a gastric foreign body, other diseases such as gastric hyperplasia, neoplasia, or intussusception could not be ruled out due to the artifact from the barium. A thoracic radiograph series taken to rule out metastatic diseases showed a mild interstitial pattern, most likely from atelectasis.

Figure 1.

Ultrasound image of the pylorus in transverse section, showing a homogeneously echogenic foreign body within the lumen, causing marked distal acoustic shadowing.

An abdominal computed tomography (Toshiba 16 slice CT, 2.0 mm slices in soft tissue window; Toshiba Medical systems, Tustin, California, USA) was performed the following day to further evaluate the hepatobiliary system and gastrointestinal tract. A spiral-shaped soft tissue-attenuating structure was noted in the region of the pyloric antrum and proximal duodenum, spanning the pyloroduodenal junction. On transverse-oriented images, this feature had a target-like appearance (Figure 2). There was a small amount of mineral attenuating material within the gastric antrum and proximal descending duodenum. Small gas foci were present within and around the feature in the pyloroduodenal junction. The gastric wall and the descending duodenal wall appeared to be mildly thickened. The common bile duct was severely enlarged and measured up to 26 mm in diameter (Figure 3). The cystic duct was also enlarged and tortuous. The gallbladder appeared to be mildly enlarged. Positive contrast (iohexol Omnipaque; GE Healthcare, Chicago, Illinois, USA), 2 mL/kg body weight (BW) was administered IV (left cephalic vein). On the post-contrast images, the intrahepatic bile ducts were dilated and hypoattenuating relative to adjacent vasculature (Figure 4). The hepatic parenchyma was otherwise normal. There were also slight and non-specific enlargements of the hepatic, medial iliac, and mesenteric lymph nodes. These findings suggested biliary obstruction at the duodenal papilla.

Figure 2.

Transverse CT image (pre-contrast) of the cranial abdomen showing a spiral-shaped soft tissue-attenuating structure (arrow) in the region of the pyloric antrum.

Figure 3.

Transverse CT image (pre-contrast) of the cranial abdomen showing a severely enlarged common bile duct (arrow), which measured up to 26 mm in diameter. The portal vein (triangle) and the pancreas (asterisk) are shown.

Figure 4.

Transverse CT image (post-contrast) of the liver. The intrahepatic bile ducts (arrow) were dilated and hypoattenuating compared to adjacent contrast-enhanced vasculature.

An exploratory laparotomy was planned. The dog was pre-medicated with hydromorphone (Hydromorphone Hydrochloride; SteriMax, Oakville, Ontario), 0.1 mg/kg BW, IV, and anesthesia was induced with propofol (Propofol; Baxter Corporation, Mississauga, Ontario), 2.4 mg/kg BW, IV. During surgery, the common bile duct, gall bladder, and hepatic ducts were observed to be significantly enlarged, and the gallbladder could not be expressed. The pancreas was diffusely hyperemic and focally bile-stained. No evidence of bile duct rupture was noted. A foreign body was found in the proximal duodenum, in the region of the major duodenal papilla. The descending duodenum was moderately inflamed and mildly bile-stained. A 5 to 6 cm transverse enterotomy was performed on the antimesenteric border over the foreign body. A 10 × 6 cm foreign object (part of a Kong toy) was removed, after which the gallbladder was easily expressed. The enterotomy site was closed with 3-0 PDS (Polydioxanone; Ethicon, Markham, Ontario) in a simple interrupted pattern and leak tested with Fluorescein-tinted saline solution. A 1-cm³ nodule, in the left lateral liver lobe was removed and submitted for histopathology, which showed cholangiohepatitis.

The dog recovered from surgery and anesthesia uneventfully. Serum chemistry obtained 3 d after surgery showed resolution of the amylase and lipase elevations. Downward trending of cholesterol (6.42 mmol/L; 2.70 to 5.94 mmol/L), total bilirubin (22.9 nmol/L; 1.0 to 4.0 nmol/L), ALP (3052 U/L; 9 to 90 U/L), GGT (56 U/L; 0 to 8 U/L), and ALT (717 U/L; 19 to 59 U/L) were also noted. The dog was discharged 4 d after surgery with tramadol (Tranadol HCl; Attix Pharmaceuticals, Toronto, Ontario), 4 mg/kg BW, PO, q8h prescribed for pain control. He recovered uneventfully at home.

Case 2

A 2-year-old neutered male Australian cattle dog was referred to the WCVM because of a 3-day history of vomiting and a 2-day history of diarrhea. A CBC performed by the referring veterinarian showed neutrophilia (24.58 × 10⁹/L; RI: 3.00 to 10.00 × 10⁹/L) with a moderate to severe left shift (4.66 × 10⁹/L bands; RI: 0 to 0.10 × 10⁹/L) and mild toxic change. Stress lymphopenia (0.31 × 10⁹/L; RI: 1.20 to 5.00 × 10⁹/L) was also noted. Serum biochemistry showed mild hypochloremia (87 mmol/L; RI: 105 to 120 mmol/L), azotemia (creatinine 139 nmol/L; RI: 41 to 121 nmol/L), and hypercholesterolemia (14.38 mmol/L; RI: 2.70 to 5.94 mmol/L). Severe elevations in liver values were also seen, including hyperbilirubinemia (170.6 nmol/L; RI: 1.0 to 4.0 nmol/L), high ALP (4634 U/L; RI: 9 to 90 U/L), GGT (170 U/L; RI: 0 to 8 U/L), and ALT (2285 U/L; RI: 19 to 59 U/L). A T4 test was also performed and was within normal limits.

On presentation, the dog weighed 27.5 kg with a body condition score of 5/9. He was febrile with a temperature of 40.5°C, and his oral mucosa, sclerae, and inner pinnae were icteric. He was tense and painful on abdominal palpation.

Abdominal ultrasonography showed a curvilinear structure causing strong distal acoustic shadowing within the proximal duodenum (Figure 5). This structure measured approximately 24 mm × 42 mm and was irregular. The duodenal segment orad to this structure was mildly dilated and fluid-filled. The intestinal segment aborad to the structure was normal in size. The gallbladder was mildly distended, and a moderate amount of echogenic, gravity-dependent debris was noted within the lumen. The common bile duct was moderately dilated, measuring 8.7 mm in diameter. The liver parenchyma was unremarkable, and the rest of the abdomen appeared normal. No free abdominal fluid was seen. A proximal duodenal foreign body causing EHBDO was strongly suspected.

Figure 5.

Transverse ultrasound image of the duodenum showing a curvilinear structure causing strong distal acoustic shadowing.

The dog was premedicated with fentanyl (Fentanyl; Sandoz Canada), 3 μg/kg BW, IV, and induced with propofol (Propofol; Baxter Corporation) (4 mg/kg BW, IV). An exploratory laparotomy was performed. A foreign body was found within the proximal duodenum just aborad to the pylorus. The duodenum appeared to be moderately bruised in the region where the foreign body was located. A single enterotomy was performed on the antimesenteric border and aborad to the location of the foreign body, and the foreign body (a rubber pacifier) was removed. The enterotomy was closed with 4-0 PDS (Polydioxanone; Ethicon, Markhan, Ontario, Canada) in a simple interrupted pattern. Gallbladder and common bile duct patency was confirmed via manual expression. The rest of the abdominal organs appeared normal.

Two days after surgery a CBC showed persistent neutrophilia (19.85 × 10⁹/L; RI: 3.00 to 10.00 × 10⁹/L) with a mild left shift (0.47 × 10⁹/L bands; RI: 0 to 0.10 × 10⁹/L) and slight toxic change. Hypercholesterolemia (8.83 mmol/L; RI: 2.70 to 5.94 mmol/L), hyperbilirubinemia (26.6 nmol/L; RI: 1.0 to 4.0 nmol/L), elevated ALP (1800 U/L; RI: 9 to 90 U/L), GGT (69 U/L; RI: 0 to 8 U/L), and ALT (696 U/L; 9 to 90 U/L) were found on serum chemistry, but all parameters were trending downward compared to their values on presentation. Clinically the dog was also improving, and he was discharged 3 days after surgery, with pain medication [tramadol (Tranadol HCl; Attix Pharmaceuticals, Toronto, Ontario, Canada)], 4 mg/kg BW, PO, q8h prescribed.

The dog returned 5 d later for recheck blood analysis and abdominal ultrasonography. Neutrophilia (16.64 × 10⁹/L; RI: 3.00 to 10.00 × 10⁹/L) with a mild left shift (0.46 × 10⁹/L bands; RI: 0 to 0.10 × 10⁹/L) and slight toxic change were found on CBC. Hyperbilirubinemia (13.0 nmol/L; RI: 1.0 to 4.0 nmol/L), high ALP (1165 U/L; RI: 9 to 90 U/L), GGT (44 U/L; RI: 0 to 8 U/L), and ALT (346 U/L; RI: 19 to 59 U/L) continued to trend downward. On repeat abdominal ultrasonography, the common bile duct measured 5.2 mm, which was still dilated but was reduced compared to the previous measurement. No duodenal distension was noted, and the wall thickness was normal. A focal area of mild duodenal wall discontinuity was seen adjacent to the duodenal papilla. This was most likely the site of the recently performed enterotomy. There was mild medial iliac lymphadenopathy, likely reactive change due to the recent abdominal surgery. The dog continued to improve clinically and recovered uneventfully.

Discussion

Extrahepatic biliary duct obstruction (EHBDO) in dogs has been reported secondary to intramural, extramural, or intraluminal obstruction from a variety of etiologies. Intramural obstructions are from thickening or mass effect that originate from the wall of the biliary tract. Extramural causes are due to mass effects in organs adjacent to the biliary system and causing compression onto the biliary ducts. Intraluminal obstructions are from obstruction within the lumen, most commonly from choledocholiths (1). Differential diagnoses for EHBDO include neoplasia (lymphoma, bile duct and pancreatic adenocarcinoma, duodenal gastrinoma, biliary cystadenoma) (1–6), fibrosis and strictures from pancreatitis and peritonitis (7), cholelithiasis (1), malformations (extrahepatic biliary atresia, congenital choledochal cyst, pancreatic pseudocyst, polycystic liver disease) (5,6,8,9), infection with Toxocara (3), and small intestinal volvulus (1). To our knowledge, EHBDO secondary to a duodenal foreign body has not been reported in dogs. Two case reports have been published in cats (10,11). In one of the cases, a duodenal foreign body (an ear plug) caused obstruction at the major duodenal papilla (11), similar to the current 2 cases. In the other case, an intraluminal foreign body within the common bile duct (2 pieces of grass awns) caused obstruction of the biliary tract (10). In comparison, the foreign bodies in the 2 cases herein were in the duodenum, causing obstruction at the level of the major duodenal papilla, without migrating up the biliary duct. Nonetheless, the clinical presentation was similar.

With acute and complete EHBDO, animals often present with lethargy, intermittent fever, episodic vomiting, and prompt development of icterus (3). Acholic feces and the absence of urine urobilinogen may develop within the first week if the obstruction is complete (3). Bleeding tendencies may develop within 21 d, although this appears to be more common in cats than dogs (3). Mucosal ulceration at the pyloric-duodenal junction has been reported and can lead to significant blood loss and clinical anemia (3,4). The clinical presentations of our 2 cases were consistent with acute EHBDO secondary to gastrointestinal obstruction.

Hyperbilirubinemia occurs within 4 h of complete EHBDO (3,10). As bile outflow is compromised in the biliary tree, altered hepatocyte membrane permeability, and hepatocellular damage are reflected in serum elevation of ALT and AST (3,12). Serum ALP and GGT levels increase within 8 to 12 h of obstruction and are substantial within a few days (3). Hypercholesterolemia is often seen and reflects impaired cholesterol elimination (3). With chronicity, biliary cirrhosis can develop and may result in declining cholesterol levels (3,12). A hemogram may reveal neutrophilic leukocytosis (3). A regenerative anemia can also be present and is thought to reflect gastrointestinal bleeding. A non-regenerative anemia may develop with chronicity (3). No anemia was noted in either of our cases, but other clinicopathological findings were consistent with EHBDO.

Abdominal radiographs are often unrewarding in cases of EHBDO. Hepatomegaly, mass effect, or loss of focal serosal detail may be observed, depending on the underlying etiology, but radiographic signs are variable and non-specific (13,14). Abdominal ultrasonography is usually diagnostic for EHBDO. Retrograde dilation of the biliary tree from the point of obstruction is often seen (15). Progressive dilation of the common bile duct and hepatic ducts occurs within 3 days, with dilation of lobar and interlobar ducts seen by 7 d (15). Multiple, tortuous, irregular anechoic branching structures within the hepatic parenchyma, without Doppler signal, are usually noted (15). Sonographically, the diameter of the common bile duct in a normal dog is reported to be less than 3 mm (16). However, there is no cut-off measurement of the common bile duct that is diagnostic of EHBDO because the degree of dilation is highly correlated to the degree and chronicity of the obstruction (15). While ultrasound may disclose the general location of obstruction, it often cannot determine the underlying cause, and biopsies are frequently required for definitive diagnosis (6). In the second of our 2 cases, the sonographic findings were highly suggestive of a duodenal foreign body, but in the first case, interpretation of abdominal ultrasound was hindered by barium artifact, so CT was sought for further clarification prior to surgery. Computed tomography is valuable for diagnosis of hepatobiliary disease when superimposition of other organs or bowel gas is of concern, especially in large, deep chested dogs in which only intercostal sonographic windows may be available. Additionally, CT allows for a complete assessment of the biliary tree, liver, and pancreas, and thus serves as a potentially more sensitive imaging modality compared to ultrasound for diagnosis of hepatobiliary diseases (13,14).

Confirmation of EHBDO requires surgical exploration for inspection and potential biopsy of the liver and biliary structures, as well as for biliary decompression (3). Biopsy by percutaneous needle or laparoscopy is not recommended in EHBDO as these methods do not facilitate biliary decompression and risk laceration of the distended bile ducts (3). Gross inspection usually reveals the location and cause of obstruction, but palpation may be needed to diagnose obstructions within the lumen (3). The gallbladder can be compressed gently to determine if there is restricted bile outflow (3). In some cases, a duodenotomy, cholecystotomy, or choledochotomy may be necessary to verify the site of obstruction and to allow decompression (17). The overall reported mortality rate for extrahepatic biliary tract surgery is 22% to 64% (6,18). One of the most common causes of EHBDO in small animals is pancreatitis (6). In most cases the obstruction resolves spontaneously as the pancreatitis subsides, thus negating the need for surgical intervention (7). Periductal fibrosis and stricture are potential complications of acute pancreatitis (7). Surgical biliary decompression in this case is controversial (7), as concurrent pancreatitis increases mortality to 50% when the animal undergoes surgery (18,19). Therapeutic percutaneous ultrasound-guided cholecystocentesis has been described with an overall complication rate of 2.7%, and bile peritonitis occurring in 0.7% of cases (20,21). Fortunately, in our 2 cases the EHBDO was resolved after removal of the duodenal foreign bodies, and no biliary decompression surgery was required.

Prognosis for EHBDO is highly dependent on the underlying disease. If surgery is deemed necessary, long-term complications can include hepatic abscesses, acquired portal systemic shunts, and chronic pancreatitis (18). Both dogs in these 2 cases had a full recovery due to the curable underlying cause and the absence of postoperative complications.

Based on our report, obstruction of the duodenal papilla secondary to a proximal duodenal foreign body should be considered as a differential diagnosis for EHBDO in dogs. CVJ