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A 9 year old spayed female mixed breed dog presented to Cornell University Hospital for Animals after being referred for pancreatitis, free gas in the abdomen, and a possible liver abscess. A week prior to the start of her clinical signs, the patient had presented to her primary care veterinarian for a broken toenail and received a four day course of Previcox (firocoxib). The referring veterinary hospital performed serial abdominal ultrasounds in which severe pancreatitis, a questionable liver abscess, and free gas and fluid were seen. The last scan revealed the patient had developed splenomegaly and she was referred to Cornell due to concern of a potential splenic venous thrombus. On presentation, the dog was quiet, alert, and responsive, however, on abdominal palpation, she assumed a kyphotic posture and appeared nauseated. Abdominal radiographs revealed free fluid and gas in the abdomen, at which point her care was transferred to the Soft Tissue Surgery Service. A CT scan revealed an abnormal mass with fluid to gas intensity on the patient’s right medial liver lobe, as well as a markedly thickened region of the pylorus of her stomach. Her abdominal lymph nodes were diffusely enlarged, and her liver had multiple regions of hyperintensity. Based on imaging, gastric perforation became the top differential and an exploratory laparotomy was performed. In surgery, a gastric perforation was discovered in the region of the pylorus, which was surrounded by numerous omental adhesions and adhesions to the right medial liver lobe. A Billroth I technique was elected to treat the perforation, as well as a partial lobectomy of the right medial liver lobe. The patient did well postoperatively, and was managed in ICU for five days. At her two week recheck, the dog had done well at home, but had a markedly decreased appetite and lost 10 pounds. Her four week recheck was significantly better; the patient had regained 6 pounds and was eating her normal presurgical amount of dog food. At last communication, the dog was still doing well at home. Histopathology on the tissues resected at the time of surgery determined the lesions seen were not part of a neoplastic process, and that the changes of the pylorus and right medial liver lobe were a consequence of a perforated gastric ulcer. While it cannot be proven, based on the history and timeline of events in this case, it was assumed that the patient’s gastric perforation was induced by the administration of firocoxib, a COX-2 selective NSAID, that occurred just prior to her presentation at Cornell. This report will describe pertinent clinical and diagnostic findings, the surgical technique elected and associated complications, as well as the role of COX-2 in maintaining healthy gastric mucosa.

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Billroth I, perforation, ulcer, NSAIDs, firocoxib


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