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 55-year-old male diagnosed case of ethanol-related chronic pancreatitis presented with frequent episodes of melena associated with paroxysms of abdominal pain. He was given blood transfusions elsewhere for severe anemia. As patient had persistent GI bleeding with repeated drop in hemoglobin, he was referred for further evaluation and management. On clinical examination, he had profuse sweating, hypotension, tachycardia, severe pallor and mild tenderness in the epigastrium. His laboratory investigations revealed hemoglobin of 7.1 g% and hematocrit of 22%, mild renal failure and increased serum triglycerides. Contrast-enhanced computed tomography of the abdomen showed evidence of chronic calcifying pancreatitis (). Esophagogastroduodenoscopy with a standard scope and colonoscopy were normal. Repeat esophagogastroduodenoscopy with a standard scope after an episode of melena showed active bleeding from the ampulla (). Angiographic study could not localize the site of bleeding. Endoscopic ultrasound showed chronic pancreatitis with a heterogeneous inflammatory lesion in the body of the pancreas (). As the bleeding source could not be localized and the patient had ongoing melena and drop in hemoglobin, emergency exploratory laparotomy was performed after initial hemodynamic stabilization. Pancreas was seen adherent to splenic vessels and hilum. There was evidence of splenic vein rupturing into the main pancreatic duct. Distal pancreatectomy with splenectomy was performed. The patient had an uneventful recovery postoperatively. Postoperative histology demonstrated chronic calcifying pancreatitis (), lymphnodes with reactive hyperplasia and congested spleen (). He was discharged in a hemodynamically stable condition and there was no further recurrence of GI bleeding after 6 months of follow up.