Gallbladder (GB) rupture is a surgical emergency, due to potential bile leakage and the subsequent development of bile peritonitis (6,8). Although GB rupture can also occur due to abdominal trauma or intraoperative iatrogenic damage, in veterinary medicine, the primary etiology is the progression of GB diseases, such as GB mucocele, cholecystolithiasis, or cholecystitis (3,7,12,13,15). Bile peritonitis can cause inflammatory responses, hemolysis, tissue necrosis, and induce endotoxemia, leading to an increased risk of morbidity and mortality (10). Therefore, in cases in which gallbladder rupture is suspected, rapid diagnosis and prompt surgical intervention are essential. This case report describes the incidental finding of GB rupture in two dogs with elevated liver enzyme levels and small GBs without bile leakage, as typically observed with GB rupture.

Case 1

A 5-year-old spayed female Chihuahua weighing 3.5 kg was referred to the Veterinary Medical Teaching Hospital of Chungnam National University because of elevated liver enzymes detected during pre-anesthetic blood analysis before dental scaling at a local veterinary clinic. The patient had no specific clinical signs upon admission but had a history of vomiting one month prior to admission. Increased canine C-reactive protein (2.8 mg/L; reference range [RR] = 0.1-1 mg/L) and elevated liver enzymes including alanine aminotransferase (ALT) (677 U/L; RR = 10-125 U/L), alkaline phosphate (ALKP) (1,130 U/L; RR = 23-212 U/L), and gamma-glutamyl transferase (GGT) (32 U/L; RR = 0-11 U/L) were observed on serum biochemistry (Catalyst One Chemistry Analyzer; IDEXX Laboratories Inc.; Westbrook, USA). The serum total bilirubin level was within the normal range.

Abdominal radiography revealed a linear radiopaque structure measuring 4.1 mm in length within the right upper abdomen, which was consistent with the presence of cholecystoliths based on its anatomical location. The gallbladder (GB) was rounded and slightly small (10 × 12 mm) on abdominal ultrasonography (Fig. 1A). Echogenic sludge and multiple hyperechoic cholecystoliths were observed in the GB. Furthermore, the GB wall and adjacent structure, presumed to be the greater omentum, was hyperechoic. Computed tomography revealed a small GB measuring 10.8 × 5.2 × 9.2 mm (length × width × height), with multiple cholecystoliths measuring <2 mm inside (Fig. 2A). Additionally, the cystic duct was dilated to 5 mm, and the common bile duct (CBD) opening into the duodenum measured 4.5 mm in diameter, with no choledoliths observed (Fig. 2B). Based on these findings, the patient was diagnosed with cholecystolithiasis. Considering the potential risk of GB rupture or extrahepatic biliary tract obstruction (EHBO), cholecystectomy was planned.

Figure 1. Small-sized gallbladder on preoperative abdominal ultrasonography in case 1 (A) and case 2 (B).

Figure 2. Preoperative computed tomography in case 1: (A) small sized gallbladder (yellow arrow) with cholecystoliths. (B) Dilated distal common bile duct (white arrow) without choledoliths. Du, duodeneum; S, stomach; L, liver.

The dog was preoxygenated with 100% oxygen using a flow-by technique. Cefazolin sodium (22 mg/kg, IV; Cefazolin; Jonggeundang), maropitant (1 mg/kg, SC; Cerenia; Zoetis), and midazolam (0.2 mg/kg, IV; Midazolam Inj.; Bukwang) were administered as pre-medication. Induction was performed by slow administration of propofol (4 mg/kg IV; Anepol; Hana), followed by endotracheal intubation. Anesthesia was maintained using isoflurane (Ifran; Hana), and constant rate infusion of remifentanil (0.1-0.3 ug/kg/min; Remiva Inj.; Hana) was used for perioperative analgesia. When adequate depth of anesthesia was achieved, the patient was placed in dorsal recumbency for surgery. After midline celiotomy, severe adhesions were observed between the GB and adjacent tissues, including the liver, greater omentum, and diaphragm (Fig. 3A). The GB and adherent tissues were carefully dissected, and a small shrunken GB was observed. After confirming the patency of the CBD, cholecystectomy was performed, followed by sufficient abdominal lavage. A Jackson-Pratt drain was placed and the abdominal wall was routinely closed using the three-layer technique.

Figure 3. Intraoperative images (A, B) and resected gallbladder (GB) (C, D) in two dogs. (A) Ruptured GB adhered to surrounding tissues in case 1. (B) Severely dilated common bile duct (white arrow) in case 2 after cholecystectomy (white asterisk). (C) Perforated GB (yellow arrow) in case 1. (D) Perforated GB (yellow arrow) in case 2. D, diaphragm; Q, quadrate hepatic lobe; GB, gallbladder; P, pancerease; Du, duonedum.

Case 2

A 9-year-old castrated male Poodle weighing 5.3 kg presented with a primary complaint of jaundice and anorexia. The patient was lethargic upon presentation and had a history of vomiting > 10 times in the previous 3 days. Serum biochemical results revealed elevated AST (874 U/L; RR = 0-50 U/L), ALT (over, RR = 10-125 U/L), ALKP (3,500 U/L; RR = 23-212 U/L), and GGT (197 U/L; RR = 0-11 U/L). Serum total bilirubin was also increased (30 mg/dL; RR = 0.0-0.9 mg/dL).

No specific findings were observed on abdominal radiography. Abdominal ultrasonography revealed a small GB measuring 10 × 10 mm, with an irregular GB wall containing echogenic sludge (Fig. 1B). The entire extrahepatic biliary tract, including the CBD, showed dilatation of up to 8.3 mm. No choledocholiths obstructing the biliary tree were observed on ultrasonography. The patient was tentatively diagnosed with EHBO. Emergency cholecystectomy was performed to ensure biliary patency.

General anesthesia was administered using the same protocol as described in Case 1. Following midline celiotomy and an additional paracostal incision, a small GB and severe dilatation of the CBD were confirmed (Fig. 3B). The extensive adhesion between the GB and the quadrate hepatic lobe necessitated partial lobectomy to remove the GB. Additionally, retrograde choledochal catheterization and lavage were performed through an antimesenteric incision in the duodenum to ensure biliary patency. Abdominal lavage was also performed, followed by routine closure of the abdominal wall.

In both cases, a small perforation was observed in the resected GB (Fig. 3C, D). Cholecystoliths were identified within the resected GBs in both dogs. The elevated preoperative liver enzyme levels gradually improved postoperatively in both cases (Table 1). There were no specific complications related to cholecystectomy during the postoperative period, and the dogs were discharged without any complications on postoperative days two (Case 1) and five (Case 2).

Table 1 . Preoperative and postoperative serum biochemistry results in case 1 and case 2.

Parameter	Reference range	Case 1					Case 2
		Preoperative	POD-1	POD-4	POD-8		Preoperative	POD-2	POD-8	POD-12
AST	0-50 (U/L)	44	116	31	23		874	271	56	33
ALT	10-125 (U/L)	677	300	153	179		Over	635	93	43
ALKP	23-212 (U/L)	1,130	315	252	179		3,500	3,500	2,595	786
GGT	0-11 (U/L)	32	5	0	0		197	59	30	3
Total bilirubin	0.0-0.9 (mg/dL)	0.4	0.2	0.3	0.3		30.0	4.1	2.0	1.2

POD, postoperative day; AST, aspartate aminotransferase; ALT, alanine aminotransferase; ALP, alkaline phosphatase; GGT, gamma-glutamyl transferase..

Gall bladder rupture in dogs can occur due to various causes, although it is more commonly associated with GB disease than with trauma (4,9,14,17). Bile is sterile in normal dogs; therefore, theoretically, the acute phase of bile peritonitis caused by GB rupture is a non-septic condition (10,16). However, depending on the cause of GB rupture, septic bile peritonitis, which has a guarded prognosis compared with sterile bile peritonitis, can develop or progress (9,10,12). Patients suspected of having bile leakage or bile peritonitis are at risk of deterioration at any time. Therefore, prompt surgical intervention is recommended to help improve the prognosis.

The presentation of clinical signs in dogs with gallbladder rupture can range from asymptomatic to severe shock, and is likely associated with factors such as the volume of bile leakage and the presence of bacterial infection (8,9,11). Clinical manifestations are typically nonspecific and include lethargy, anorexia, vomiting, diarrhea, abdominal pain, distention, and jaundice (8,11). Notably, GB rupture should be suspected when abdominal radiography reveals decreased serosal detail, and discontinuity of the GB wall, hyperechoic structures adjacent to the GB, or free fluid accumulation in the abdominal cavity on abdominal ultrasonography (1,5,8). Diagnostic imaging is not infallible, as it lacks both sensitivity and specificity for the definitive diagnosis of GB rupture (1,6). Typically, analyzing the bilirubin concentration of the abdominal fluid obtained through abdominocentesis and comparing it to serum bilirubin levels is an effective method for diagnosing bile leakage resulting from GB rupture (2,8,9).

During the surgery, there was no evidence of bile leakage associated with GB rupture in both our cases. Small-sized GB were observed on abdominal ultrasonography in both dogs. Rupture of the GB is suspected to have resulted from cholecystitis induced by cholecystolithiasis. It is presumed that only a small amount of bile leakage occurred at the time of GB rupture, and that the perforated GB adhered to the surrounding tissues, such as the hepatic lobe, greater omentum, or diaphragm, during the acute phase, preventing continuous leakage and the development of bile peritonitis. In Case 1, there were no specific biochemical findings except for elevated liver enzyme levels. In Case 2, although the dog exhibited vomiting and jaundice, this was believed to be unrelated to the GB rupture and was attributed to EBHO.

Even in cases where there is no evidence or clinical signs related to bile leakage or bile peritonitis, the presence of elevated liver enzymes in biochemistry and a small-sized gallbladder observed on abdominal ultrasonography should raise the suspicion of gallbladder rupture.

Conceptualization: Moon CH, Jeong SM; Data curation: Moon CH, Kim HJ, Lee WJ; Formal analysis: Moon CH, Kim HJ; Funding acquisition: Jeong SM; Investigation: Moon CH; Supervision: Jeong SM; Writing - original draft: Moon CH; Writing - review & editing: Moon CH, Kwon YS, Jeong JM, Kim DH, Lee HB, Jeong SM.

This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (No. 2022R1F1A1071251).

The authors have no conflicting interests.