Case Presentation: A 64-year-old male with a past medical history of coronary artery disease and hypertension presented with a one-month history of progressive exertional shortness of breath and chest pain. During this same period he also complained of persistently black but formed stools. Other than a daily baby aspirin, he did not use any Non-Steroidal Anti-Inflammatory Drugs. Physical examination was unremarkable except for pallor. Fecal occult blood testing was positive. The patient had a normocytic anemia with a hemoglobin of 4.3 g/dL, hematocrit of 15%, reticulocyte percentage of 4.9%, ferritin of 5.2 ng/mL, and a total iron binding capacity of 394 ug/dL. Troponin was elevated to 0.384 ng/mL and his electrocardiogram appeared non-ischemic without ST segment or T wave abnormalities. He was transfused with 2 units of packed red blood cells and was admitted for further workup of severe anemia likely secondary to a gastrointestinal bleed. Esophagogastroduodenoscopy revealed gastric varices and a red wale sign indicating recent bleeding. Bleeding varices in the context of normal AST, ALT, INR, and bilirubin, and no additional sequelae of cirrhosis prompted an evaluation of the cause of increased portal venous pressure. A computed tomography scan of the abdomen and pelvis revealed a 4.2 cm mass in the pancreatic tail encasing the splenic artery and vein. An endoscopic ultrasound with fine needle aspiration revealed pancreatic adenocarcinoma. Carbohydrate antigen 19-9 was 1 unit/mL and carcinoembryonic antigen was 1.3 ng/mL. The patient was stabilized and discharged home with outpatient follow up for staging and further management of pancreatic adenocarcinoma.
Discussion: Pancreatic adenocarcinoma classically presents with painless jaundice because most exocrine pancreatic cancers occur in the head of the pancreas and cause biliary duct obstruction. Pancreatic tail masses however often present with non-specific symptoms due to the lack of biliary duct obstruction. These symptoms include weight loss, non-specific pain, weakness, anorexia, nausea, and vomiting. Pancreatic tail masses often do not present until the mass becomes very large and there is locally advanced disease. Our patient’s pancreatic tail mass encased the splenic vein, causing portal hypertension and gastric varices. These gastric varices slowly bled and the patient started to experience chest pain due to myocardial demand ischemia from severe anemia (type II myocardial infarction). Gastric varices have a lower incidence but higher rebleeding and mortality rates when compared to esophageal varices. Although our patient’s tumor also encased the splenic artery, histologically confirmed splenic artery invasion does not have independent prognostic value for pancreatic cancer.
Conclusions: This unusual presentation of pancreatic cancer clearly demonstrates the pathophysiology of both type II myocardial infarction and gastric varices.
