A 41-year-old man with a history of alcoholism for 10 years and sober for the last 3 years, recurrent alcoholic pancreatitis, and no known liver disease, presented with several episodes of hematemesis and abdominal pain for 2 days.

Esophagogastroduodenoscopy (EGD), performed 3 years earlier for abdominal pain, had revealed no esophageal varices, gastric varices, portal hypertensive gastropathy, or other GI lesions.

Physical examination revealed a blood pressure = 100/60 mm Hg, pulse = 60 beats/min, no jaundice, no stigmata of chronic liver disease, a soft abdomen with mild epigastric tenderness but no rebound tenderness, no abdominal bruit, and no pulsatile abdominal mass.

Rectal examination revealed gross melena.

Laboratory tests revealed hemoglobin = 12.5 g/dL, platelets = 301,000/mL, INR (international normalized ratio) = 1.0, blood urea nitrogen = 20 mg/dL, and creatinine = 1.1 mg/dL.

Serum aspartate aminotransferase = 21 IU/L, alanine aminotransferase = 16 IU/L, total bilirubin = 0.6 mg/dL, alkaline phosphatase = 64 IU/L, albumin = 4.4 gm/dL, and lipase = 32 U/dL.

The hemoglobin declined acutely to 9.3 g/dL.

Abdomino-pelvic computerized tomography (CT), with intravenous contrast, revealed a 5-cm wide, irregular, pancreatic/peripancreatic mass, compressing both the lesser curvature of the stomach and the SV (Fig.1A, B), a normal portal vein, and normal liver parenchyma.

The SV compression was pathophysiologically significant as indicated by proximal SV dilatation.

EGD revealed in the proximal stomach a fine, reticular, pale-white, polygonal, mucosal, network in a snakeskin pattern, and characteristic of portal hypertensive gastropathy that was actively oozing; extensive coffee-ground, blood clots in the stomach; small gastric cardial and fundal varices without stigmata of recent hemorrhage (SRH); and no esophageal varices (Fig.​2).

The extrinsic mass produced a large, round bulge extending into the lumen of the proximal gastric body along the lesser curvature (Fig.2).

Magnetic resonance cholangio-pancreatography (MRCP) revealed a 5-cm wide, enhancing, vascular mass likely arising from the LGA and located between the gastric lesser curvature and distal pancreatic body; compressing the stomach; compressing the middle SV; and resulting in large collateral veins draining the SV into the superior mesenteric vein (Fig.3A, B).

Abdominal ultrasound with Doppler studies demonstrated large, turbulent arterial flow into this vascular mass, suggesting a large PA (Fig.4).

Visceral arteriogram showed a 5.3 × 2.2-cm-wide PA supplied by an LGA branch (Fig.5A), which was embolized and occluded with microcoils (Fig.5B).

Eight weeks later, the patient had a stable hemoglobin level with no further GI bleeding.

Abdomino-pelvic CT angiography demonstrated the PA had markedly decreased in diameter, contained numerous microcoils, and had no blood flow ​(Fig.1C).