Gastric diverticula are the least common gastrointestinal diverticula. Patients can be diagnosed incidentally on EGD or present with variable symptoms such as abdominal fullness, anorexia, and perforation. Gastric diverticula can be acquired from malignancy, peptic ulcer disease, or prior surgery or be congenital. Treatment varies based on symptomatology ranging from conservative medical management with proton pump inhibitors to surgical treatment with open or laparoscopic resection. We present a case of a 73-year-old female with acquired gastric diverticulum presenting as a gastric outlet obstruction who was successfully treated with conservative medical therapy.

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A 41-kg, 12-hour-old Quarter Horse filly presented to the Boren Veterinary Medical Teaching Hospital for a 12-hour history of weakness and recumbency. The mare had a history of premature lactation and presumptive placentitis, which was treated with trimethoprim-sulfamethoxazole by the referring veterinarian. The filly was born at 315 days gestation; parturition was unattended. The filly was found recumbent and unable to stand. Before referral, the attending veterinarian administered 1 L of colostrum via nasogastric tube. Upon presentation to the veterinary teaching hospital, the filly was recumbent and lethargic with intermittent bouts of hyperresponsiveness. Rectal temperature was 94°F, heart rate was 132 beats per minute, and respiratory rate was 24 breaths per minute. A grade 3/5 systolic murmur was auscultated over the left heart base. Mucous membranes were hyperemic with a capillary refill time of approximately 2 seconds. Abrasions were present along the gingiva and around the eyes and muzzle. Petechiae were observed in both pinnae. The foal's distal limbs were cool and edematous, peripheral pulses were weak, and the coronets of all 4 feet were circumferentially dark red.Presumptive diagnoses of neonatal encephalopathy and sepsis were made. An IV jugular catheter was placed. Blood was collected for bacterial culture and sensitivity, CBC, fibrinogen concentration, serum biochemistry, and quantification of serum immunoglobulin G (IgG) concentration. The CBC disclosed immature (band) neutrophilia (558 bands/lL; reference range, <200 bands/lL) and toxic polymorphonuclear leukocytes. A biochemistry profile identified hypoproteinemia (3.8 g/dL; reference range, 5.6-8.0 g/dL) characterized by hypoglobulinemia (1.1 g/dL; reference range, 2.6-5.6 g/dL), azotemia (creatinine, 4 mg/dL; reference range, 1.2-2.0 mg/dL), hypoglycemia (37 mg/ dL; reference range, 70-120 mg/dL), hypernatremia (156 mEq/L; reference range, 130-146 mEq/L), hyperchloremia (112 mEq/L; reference range, 95-110 mEq/ L), and increased creatine kinase activity (40016 IU/L; reference range, 20-500 IU/L). Quantification of IgG a concentration was consistent with failure of passive transfer (IgG < 400 mg/dL). Neonatal sepsis score was calculated to be 18.1 Arterial blood gas sampling was not attempted because of limb edema and weak peripheral pulses. Blood pressure measured using an oscillometric blood pressure monitor b applied to the middle coccygeal artery yielded a mean arterial pressure of 70 mmHg.Initial medical treatment consisted of a plasma c transfusion (25 mL/kg), IV fluids (1 L bolus of 0.45% sodium chloride followed by 0.45% sodium chloride with 10% dextrose at 6 mg/kg/min), broad spectrum antimicrobials (ceftiofur, d 10 mg/kg IV q6h), dimethyl sulfoxide e (1 g/kg/d diluted to a 10% solution IV), thiamine (10 mg/kg IV q24h), and magnesium sulfate (25 mg/kg/h). After plasma c transfusion, quantification of serum IgG a concentration indicated persistent hypogammaglobulinemia (IgG, 400-800 mg/dL); an additional plasma c transfusion (25 mL/kg)...

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