Case Study

Gallbladder perforation and splenic necrosis in a 7 year old FS Jack Russell Terrier dog

A 7-year-old FS Jack Russell Terrier dog with a history of regulated hypothyroidism, was presented for vomiting, lateral recumbency, and showing abdominal pain following ingestion of a ham bone. Additional history that the owner reported was that the patient had been showing polyuria/polydipsia prior to the incident. On physical examination the patient was laterally recumbent and very painful. CBC showed polycythemia, and low band neutrophils. On blood chemistry mildly elevated BUN, mildly elevated creatinine, and lipasemia; severely elevated ALT activity, and elevated cPLI were evident.

A 7-year-old FS Jack Russell Terrier dog with a history of regulated hypothyroidism, was presented for vomiting, lateral recumbency, and showing abdominal pain following ingestion of a ham bone. Additional history that the owner reported was that the patient had been showing polyuria/polydipsia prior to the incident. On physical examination the patient was laterally recumbent and very painful. CBC showed polycythemia, and low band neutrophils. On blood chemistry mildly elevated BUN, mildly elevated creatinine, and lipasemia; severely elevated ALT activity, and elevated cPLI were evident. A hemorrhagic diathesis was present on coagulation panel. Blood pressure was 145/80. The patient was treated with I.V. fluids, hetastarch, morphine/ketamine drip, fresh frozen plasma, antibiotics, and placed in an oxygen cage. On survey abdominal radiographs bony fragments were evident in the gastrointestinal tract. The patient was sedated, given an enema, and a large piece of bone was produced. After 42 hours on therapy the patient developed dyspnea, which, on survey thoracic radiographs was suggestive of fluid overload. Lasix was administered, which resulted in resolution of the dyspnea. Recheck blood chemistry showed, hypoproteinemia, elevated ALP activity, hyperglycemia, improved azotemia, and normalization of cPLI. Physical examination after 72 hours of supportive care found the patient BAR and ambulatory, not interested in food, and extreme pain upon palpation of the right mid-abdomen. Syringe feedings were started, which were well tolerated with no vomiting. However, the following morning the patient was less bright and more painful in the abdomen.

DX

Gallbladder perforation and splenic necrosis

Sonographic Differential Diagnosis

Gallbladder perforation, cholecystitis, localized bile peritonitis suspected. Likely concurrent inflammatory hepatopathy. Minor potential for hepatic neoplasia such as lymphoma.

Image Interpretation

Images 1 & 2, Videos 1 & 2: The liver is swollen and mildly heterogeneous with increased portal markings. The distinctive echogenic ill-defined hyperechoic fat adjacent to the gallbladder and localized free fluid is suggestive for GB perforation, or at least inflammation and localized blood or exudate. When a GB perforates it often collapses and appears essentially “normal”, “unremarkable” or only thickened from mural inflammation. The lack of GB dilation owing to loss of content into the adjacent space can be misleading in these cases. This presentation is particularly important if the patient demonstrates pain upon imaging the region (+ Murphy Sign). This patient had a + Murphy sign. Video 3: Close-up video of the GB demonstrates a loss of wall integrity and interruption of the linear detail of the wall in the 3 o`clock position. The accumulated fluid is present adjacent to this loss of GB integrity strongly suggestive for localized bile peritonitis. Ill defined echogenic reactive fat is typical for local inflammation. Image 4: partially collapsed GB with loss of wall detail in the 3 o`clock position bordered by echogenic ill-defined hyperechoic fat suggestive for adhesion or inflammation. Images 5 & 6. Lateral abdominal radiographs demonstrate simple uniform hepatomegaly without other specific findings.

Outcome

The patient thrived postoperatively with no complications.

Clinical Differential Diagnosis

multi-organ pathology: acute pancreatitis, acute hepatitis/cholecystitis – viral/bacterial/toxic, intestinal obstruction, intestinal perforation with peritonitis