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. ).
A 38-year-old male complaining of recurrent episodes of melena for the past 2 weeks was admitted to the emergency department of our hospital. Two days before the hospital visit, the patient had complained of the presence of blood in vomiting and had a history of recurrent complaints of upper abdominal pain often radiating to the back. His previous medical history revealed that he had suffered from chronic pancreatitis for 3 years before present admission, possibly due to alcohol abuse. He was resuscitated with the blood and intravenous fluid for melena during present admission. Ultrasonography (USG) whole abdomen revealed a moderately enlarged liver (18.5 cm × 12.3 cm) with heterogeneous echotexture, with a prominent portal vein, of size 1.3 cm; hepatic and splenic hilar collaterals were suggestive of portal hypertension. The presence of mild ascites was documented. Transabdominal USG showed echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci in the pancreas suggestive of fibrotic changes. There was evidence of irregular dilated main pancreatic duct with pancreatic and intraductal calculi. These features were consistent with chronic pancreatitis. The findings were suggestive of alcoholic liver disease with portal hypertension and chronic obstructive pancreatitis. After resuscitation, upper GI endoscopy was performed on two different occasions that showed bleeding from the second part of the duodenum with an abnormal tortuous vessel at the ampulla of Vater. This was diagnosed as hemosuccus pancreaticus, which might have caused the bleeding []. Serendipitously during the endoscopy, a worm was also found penetrating the mucosa of the duodenum. The worm was retrieved and referred to the laboratory for identification. It was a single intact live worm (size 12.3 mm × 0.3 mm) reddish pink, with head bent in the same direction of the body curvature with a spine at the posterior end []. The buccal capsule had six teeth (four hook-like on ventral surface and two knob-like on dorsal surface) []. The live worm was seen to lay eggs while examining under the microscope []. Three consecutive stool samples of the patients were examined. The stool sample was dark-colored, semi-solid in consistency without any parasitic elements. Wet mount examination of stool revealed nonbile-stained ova (60– 65 μm in length, 40– 45 μm in width) with transparent hyaline shell membrane containing blastomeres. The above morphological features of the worm and micrometry of the ova were consistent with Ancylostoma duodenale. For further confirmation and to exclude the probability of mixed infection with Strongyloides stercoralis, the modified Harada– Mori nematode larval culture method[] was performed, and larva of hookworm was retrieved after 1 week of incubation at ambient room temperature. However, duodenal biopsy could not be done to rule out this possibility.\nThe patient was a chronic alcoholic and had deranged liver functions. Other laboratory test revealed low hemoglobin (5.6 g/dL), elevated total leukocyte count (12,300/μl) with increased eosinophils (neutrophils - 54%, lymphocytes – 24%, eosinophils – 16%, and monocytes – 6%), hyperbilirubinemia (total serum bilirubin 12.5 mg% and conjugated bilirubin 11.7 mg%), alanine transaminase/aspartate transaminase (87.7/90 IU), serum alkaline phosphatase (827 IU/L), hypoalbuminemia (2.3 g%), and raised serum globulin (3.9 g%) with reversal of albumin:globulin ratio. Blood and urine cultures were bacteriologically sterile. Peripheral blood smear examination showed microcytic, hypochromic anemia, with the absence of any hemoparasites. The patient was planned for contrast-enhanced computed tomography (CECT) abdomen, but the course of illness was rapidly fatal, and he succumbed to the illness within 48 h of admission, hindering further investigative course. The cause of death was unexplained shock secondary to upper GI bleeding precipitated by chronic, alcoholic liver disease with chronic pancreatitis and portal hypertension.