A 39-year-old man was admitted to the hospital due to hematemesis and melena for 2 wk, with a new episode lasting 1 d.\nTwo weeks before admission, the patient had hematemesis and melena without obvious known causes. He vomited light red fluids 4-5 times/d and passed tarry stools 3-4 times/d; these events were accompanied by epigastric pain, abdominal distension, and fatigue. He had no dizziness or syncope. He was hospitalized at a local hospital where examinations showed a hemoglobin (Hb) level of 86 g/L. Esophagogastroduodenoscopy (EGD) showed fresh blood in the descending part of the duodenum but did not show a clear bleeding site. The patient was treated with blood transfusion, acid blockers, and intravenous (IV) fluid and discharged from the hospital after no recurrence of hematemesis or melena was observed.\nOne day before admission to our hospital, the patient vomited bright red blood once and was admitted to the local hospital. Bedside EGD showed no obvious bleeding in the upper gastrointestinal tract. During his hospitalization, the patient had repeated hematemesis and hematochezia 4-5 times/d accompanied by left upper abdominal pain and fatigue. His minimum Hb level was 42 g/L. After treatment with blood transfusion, IV fluid, acid blockers, and hemostasis, he was transferred to our hospital for emergency admission.\nThe patient had a history of chronic pancreatitis. He denied chronic diseases such as hypertension, coronary heart disease, and diabetes, a history of abdominal surgery and trauma, and a history of food and drug allergy.\nThe patient denied a history of smoking and drinking and any history of diseases in family members.\nOn admission, the patient had a body temperature of 37.2 °C, a pulse of 102 beats/min, a respiratory rate of 19 times/min, a blood pressure of 117/91 mmHg, and an oxygen saturation of 98%. The patient had manifestations of anemia and pale conjunctiva. His abdomen was soft with upper abdominal tenderness. No rebound tenderness was noted. No abdominal mass was palpable. No other obvious abnormality was noted.\nThe complete blood count on admission was as follows: White blood cell count, 8.00 × 109/L; red blood cell count, 2.34 × 109/L; Hb, 66 g/L; hematocrit, 0.192; platelet count, 108 × 109/L; total amylase, 198 U/L; D-dimer, 6060 µg/L; hypersensitive C-reactive protein, 40.1 mg/L; procalcitonin, 0.12 ng/mL; and serum albumin, 24 g/L (Table ). Coagulation function, alanine aminotransferase, aspartate aminotransferase, total bilirubin, alkaline phosphatase, glutamyl transpeptidase, urinalysis results, stool analysis, tumor marker expression, troponin I, and electrocardiogram results were all within normal limits.\nA noncontrast-enhanced computed tomography (CT) scan of the abdomen and pelvis showed pancreatic swelling, uneven density, vague edges, multiple spots of calcifications, and hyperintense opacities in the pancreatic head and body, indicating chronic pancreatitis and pancreatic head hemorrhage.\nSubsequent contrast-enhanced CT of the abdomen showed isointense, rounded opacities with a diameter of approximately 41 mm in the pancreatic head that were enhanced with contrast in the arterial phase and were closely related to the gastroduodenal artery, indicating pseudoaneurysm (Figure ). Furthermore, digital subtraction angiography performed via the celiac trunk showed the formation of pseudoaneurysms at the proximal gastroduodenal artery; the remaining blood vessels were unremarkable (Figure , Video 1A).
A 67-year-old Caucasian man was admitted with diffuse abdominal pain, vomiting, diarrhea, and 4 kg weight loss within a couple of weeks. He had a history of alcohol abuse but further medical history was negative. There was no significant abdominal tenderness, no abdominal palpable mass or flank-knocking tenderness. Laboratory studies showed mild anemia with a hemoglobin level of 10.0 g/dL. An abdominal ultrasound (US) scan showed a partially inverted flow in the portal vein with a small cirrhotic liver, ascites, and a small spleen. Abdominal computed tomography (CT) revealed a large pseudoaneurysm between the SMA and coeliac trunk with a diameter of 77 × 53 × 59 mm. Just below this pseudoaneurysm lay the pancreas with calcifications due to chronic pancreatitis. CT angiography revealed an arterioportal fistula between the pseudoaneurysm and portal vein. Due to this pseudoaneurysm, there was compression of the superior mesenteric vein. Ascites around the liver and spleen were seen, probably due to portal hypertension. There was an increase of the pseudoaneurysm diameter compared to the abdominal CT scan made 5 days earlier, with a maximal diameter of 81 mm (Fig. ). Digital angiography revealed a pseudoaneurysm arising from the proximal superior mesenteric artery with fistulization to the portal vein. The pseudoaneurysm was filled via a large defect in the top of the superior mesenteric artery (Fig. ).\nFrom a technical point of view, covered stenting of the SMA was preferred over embolization of the pseudoaneurysm. A 6 French LIMA sheath was placed in the superior mesenteric artery using a femoral approach. Next, a balloon-expandable covered stent (Bentley Begraft® diameter 8 mm, length 37 mm; Bentley, Hechingen, Germany) was deployed in the SMA. Control angiography showed refilling of the pseudoaneurysm via the common hepatic artery (CHA) through the right gastric and gastroduodenal arteries (Fig. ). Since there was no filling of the CHA from the coeliac trunk, it is probable that the CHA originated from the SMA as a normal variant and was separated from its origin, possibly due to the pancreatitis (Fig. ). After catheterization of the CHA via the left and then the right gastric artery, selective embolization was performed with a 2.7 Fr Progreat® microcatheter (Terumo Medical Corp., Somerset, NY, USA) using multiple Hilal microcoils (3, 4, and 5 mm wide and 3 and 6 cm long; Cook Medical, Bloomington, IN, USA), covering the origin of the GDA (Fig. ). The residual perfusion of the liver is only supplied by the right gastric artery from the left gastric artery.\nPostoperatively, the patient was given clopidogrel therapy for 6 weeks and lifelong acetylsalicylic acid.\nHe was discharged on the eighth postoperative day. Follow-up after 6 months revealed no recurrent abdominal symptoms. The pseudoaneurysm was no longer detectable on control CT angiography (Fig. ).