A 70-year-old male presented to our medical center with one episode of “black tarry stools” in the morning. Three weeks prior to this admission, the patient underwent esophagogastroduodenoscopy (EGD), which revealed a 6-mm, clean-based ulcer at the gastroesophageal junction without active bleeding. Colonoscopy, performed during the same visit, was significant for mild diverticulosis and small nonbleeding hemorrhoids. He had a medical history of chronic active alcohol abuse, prior gastrointestinal bleeding, hypertension, diabetes mellitus type 2, and non-small-cell lung cancer (T2N0M0; status post-lobectomy, 18 years ago). The patient had been consuming 3-4 drinks of liquor daily; however, he was non-smoker and drug-free. He was under therapy with oral iron sulfate, metformin, pantoprazole, enalapril, and multivitamins. Review of the systems was significant for fatigue, malaise, and confusion. His vitals included blood pressure 137/81 mm Hg, heart rate 108 beats per minute, temperature 36.9°C, respiratory rate 16 per minute and oxygen saturation 100% on room air. On physical examination, he was in no acute distress but appeared lethargic. The cardiopulmonary examination was inconclusive for abnormalities. The abdomen was soft and non-tender without organomegaly.\nHe underwent extensive diagnostic workup. The details of his laboratory studies are provided in Table .\nChest radiograph showed left-sided thoracotomy with chronically elevated left hemidiaphragm but no airspace opacity, effusion, or pneumothorax. He was started on intravenous proton-pump inhibitor therapy for upper gastrointestinal bleeding. Subsequently, EGD showed nodular, edematous and erythematous mucosa with petechial hemorrhages in the gastric fundus and body, with questionable prominence of underlying vasculature (Figure ).\nThe endoscopy was inconclusive for an active bleeding focus; duodenum appeared normal. He also received one unit of packed red blood cells. During the course of hospitalization, he continued to experience black-colored stools. His hemoglobin demonstrated a gradual downward trend, prompting the need for a second endoscopic evaluation. On day 7 of admission, repeat EGD revealed frank fresh blood along with blood clots in the proximal body of the stomach. The clots were irrigated, suctioned, and removed with Roth net. A pinpoint area under one of the removed clots was actively oozing, which mimicked a Dieulafoy’s lesion; primary hemostasis was achieved with a combination therapy using epinephrine injection, cautery, and hemoclip application (Figure ).\nOn day 10 of admission, laboratory studies showed an acute elevation of liver enzymes (alanine transaminase 1096 IU/L; aspartate aminotransferase 123 IU/L; alkaline phosphatase 47 IU/L; and total bilirubin 1.3 mg/dL). Drug-induced liver injury and obstructing lesion were considered plausible. Computed tomography (CT) with pancreatic imaging protocol revealed a large 4.2 x 2.9-cm pseudoaneurysm, likely arising from the gastroduodenal artery, located in the head of the pancreas, with evidence of moderate intrahepatic ductal dilatation and portal vein obstruction. Given the large size with compressive features of the surrounding structures, embolization of the pseudoaneurysm utilizing 11 coils with thrombin/Gelfoam injection was performed (Figure ).\nA two-day post-procedure abdominal ultrasound showed an increase in the size of the pseudoaneurysm, measuring 5.6 x 5.8 cm. Interventional radiology then repeated the embolotherapy with thrombin injection. In the next few days, he continued to report both melena and bright red blood per rectum, but his hemoglobin remained stable. On day 19 of admission, third EGD was performed, which was unremarkable for an active bleeding spot. His hemoglobin started to drop but another endoscopic evaluation was not recommended as last EGD was unremarkable. Therein, a bleeding scan showed an equivocal left-flank bleeding focus, not suggestive of a lower gastrointestinal collection, but possibly a small bowel focus with low-grade extravasation. Subsequently, his hemoglobin dropped to 6.3 g/dL, with no signs of overt gastrointestinal hemorrhage. On day 27 of admission, abdominal paracentesis ruled out hemoperitoneum and CTA abdomen showed possible hemorrhage in the left flank outside the gastrointestinal tract, possibly due to an infarcted spleen.\nAfter a discussion with surgery and gastroenterology teams, a repeat EGD with a side-viewing duodenoscope was planned. It initially demonstrated an extremely small blood-oozing spot from the ampulla of Vater. The blood extravasation increased shortly after first pinpointing the source. Over the next few seconds, the blood started to ooze at a rapid rate. In the next one minute, frank intermittent bleeding through the ampulla of Vater into the duodenum was identified (Figure ).\nThese findings were consistent with hemosuccus pancreaticus, likely due to the bleeding from the pseudoaneurysm of the gastroduodenal artery. After the precise etiology establishment, surgical intervention was considered due to prior failed attempts of embolization. However, there was a high risk of perioperative mortality given the patient’s comorbid conditions, poor clinical and performance status and complexity of the anatomical location of pseudoaneurysm. Therefore, a conservative approach was preferred by the patient and his family. On the other hand, he continued to experience intermittent hemorrhage requiring blood transfusions with episodes of hemodynamic instability. An urgent embolization of the pseudoaneurysm was planned. However, the patient and his family refused to undergo therapeutic procedures. The patient continued to worsen clinically over the next few days but he wished not to be resuscitated. He died in a couple of days following hemodynamic instability.
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.