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 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.