12-year-old spayed female Hound Mix

• A scant volume of mildly echogenic peritoneal effusion is located in the abdomen.
• The stomach contains a moderate amount of fluid but has normal wall layering. The duodenum and an elongated segment of jejunum contain numerous and often coalescing distally shadowing hyperechoic foci embedded within their walls, consistent with severe locally extensive ulcerations. In the affected jejunum, some of the ulcerative lesions may be full thickness, as some gas foci appear to extend to the serosal margins of the intestinal wall. No gas foci are located within the peritoneum immediately adjacent to the intestinal ulcerations and no free gas is observed elsewhere in the abdomen. The ulcerated duodenal and jejunal walls are also moderately circumferentially thickened with partial wall layering effacement. The ICJ and colon are normal.
• The pancreas is moderately diffusely thickened (right pancreas: 1.6 cm), with a mildly heterogenous parenchyma. The pancreatic margins are slightly irregular and moderately hyperechoic fat surrounds the pancreas.
• The left medial iliac lymph node is moderately enlarged (12 mm). The right medial iliac lymph node is normal in size, measuring 5 mm in thickness.
• The left inguinal lymph node is severely enlarged (2.7 cm) and heterogenous, in addition to being surrounded by severely hyperechoic fat that distally attenuates the ultrasound beam. •
• The ventral abdominal subcutaneous tissues are severely diffusely thickened, with thin linear hypoechoic striations coursing through hyperechoic fat.

1. Severe locally extensive small intestinal ulcerations (duodenal and jejunal) with associated enteritis and peritonitis. Several of the intestinal ulcerations appear full thickness or nearly full thickness. There is no evidence of pneumoperitoneum.
2. Scant volume of mildly echogenic effusion. This may represent a septic effusion, sterile inflammatory effusion, neoplastic effusion, or hemorrhage.
3. Pancreatitis.
4. Severe left inguinal and moderate left medial iliac lymphadenopathy. Both neoplastic infiltration and reactivity are considered.
5. Severe diffuse thickening and edema of the ventral abdominal subcutis.

The peritoneal effusion was sampled and was consistent with a non-septic, protein rich transudate. Serial AFAST examinations were performed after the comprehensive abdominal ultrasound to monitor the peritoneal effusion. The patient was already on multiple gastrointestinal protectants (ondansetron, sucralfate, and misoprostol), however after the ultrasound, famotidine was increased from 0.5 mg/kg IV q12h to a continuous rate infusion (8 mg/kg/day). Due to concerns for potential gastrointestinal translocation, treatment with broad spectrum antibiotics was also initiated (Unasyn 28.7 mg/kg IV q8h; Baytril 14.4 mg/kg IV q24h; Metronidazole 14 mg/kg IV q12h). During hospitalization, the patient became progressively anemic (presumably secondary to GI bleeding) and had a progressive band neutrophilia. The ventral abdominal bruising and edema was also progressive, and she was painful on examination. Due to poor prognosis, humane euthanasia was elected.

A gross necropsy was performed, which confirmed a large (12 x 6 cm) left inguinal swelling. Cytology of this lesion was consistent with a mast cell tumor with regional edema and hemorrhage, suggestive of degranulation. Ulcerative enteritis of the small intestine was confirmed. There was no evidence of small intestinal rupture, however a 30 cm long segment of the small intestinal wall was severely thinned with adjacent fibrinous omental adhesions, demonstrating that the intestinal wall was severely compromised. Steatonecrosis of the adipose tissue both in and around the pancreas supported concurrent acute pancreatitis.

Discussion

Abdominal ultrasound was able to provide an antemortem diagnosis of severe ulcerative enteritis, which helped guide patient therapies and diagnostics. Gastrointestinal ulcers have been sonographically described as a focal wall thickening containing a crater-like or linear defect of gas.1-3  Gastrointestinal ulcers in patients with mast cell neoplasia is a well-documented phenomenon, occurring secondary to hyperhistaminemia.4,5  Gastrointestinal ulceration secondary to inhibition of prostaglandin synthesis by either NSAIDS or corticosteroid usage has also been well described.1-3,6 In this case, multiple risk factors for ulcerative enteritis were present. This patient’s ulcerative lesions may have been secondary to underlying mast cell disease, receiving both a corticosteroid and an NSAID within a 24-hour period, chronic NSAID usage, or a combination of all of the above. In the duodenum, ischemic damage secondary to the patient’s pancreatitis is also plausible.