Gastric actinomycosis constitutes a rare but treatable cause of gastric outlet obstruction. When encountered clinically, it is a difficult diagnosis to make before obtaining a surgical specimen, as exemplified by the following case. A 49-year-old Egyptian male with a history of hypertension and ventral hernia repair presented to the emergency room with a complaint of postprandial vomiting for 6 months that progressed from a coffee-ground appearance to bilious. The patient also reported a 45-pound weight loss during this time. He denied any use of nonsteroidal anti-inflammatory drugs. He had been incarcerated for 3 months in a federal penitentiary. On physical exam, the patient was afebrile with stable vital signs. Physical exam was significant for the presence of normal bowel sounds with mild epigastric tenderness on palpation. His abdomen was nondistended with no guarding, rebound, or hepatosplenomegaly. There was no stool in the vault on rectal exam. The remainder of his exam was unremarkable. Laboratory studies showed a white blood cell count of 6,900 cells per microliter with 55% segmented cells and hemoglobin of 17.4 g per deciliter. Chemistries showed evidence of metabolic alkalosis, mild prerenal azotemia, and normal liver studies. Abdominal radiograph was normal. Computed tomography of the abdomen and pelvis with contrast revealed a dilated stomach with the remaining bowel loops normal in caliber. An upper endoscopy performed the day following admission showed a thickened gastric outlet possibly secondary to edema versus a mass. Biopsies were obtained that showed intestinal metaplasia and chronic gastritis. The patient was initially treated conservatively with a clear liquid diet and a proton pump inhibitor twice a day. When his symptoms did not improve, he again underwent upper endoscopy with an unsuccessful balloon dilatation of the pyloric channel. Following 2 more weeks with little clinical improvement, the patient underwent a distal gastrectomy with Bilroth I reconstruction. Pathology of the surgical specimen showed necrosis, abscess, and sulfur granules consistent with Actinomyces infection. The patient was started on 24 million units of intravenous penicillin every day for 6 weeks, to be followed by a planned course of 10 months of oral penicillin. The patient's symptoms had resolved by the end of his intravenous penicillin course. This case illustrates both the diagnostic difficulties and the effective response to therapy of this rare gastric infection. An extensive review of the literature revealed 28 other cases of gastric actinomycosis, with numerous reports of infection throughout other regions of the gastrointestinal tract. Less than 10% of the reviewed cases included a diagnosis of actinomycosis made pre-operatively. In both our case and the reviewed cases, the diagnosis was only made with histopathologic evaluation of a surgical specimen. Although this diagnosis is typically delayed, the recognition of actinomycosis is crucial as this is a directly treatable cause of gastric outlet obstruction.
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