A 71–year–old woman with diabetes, hypertension and GERD presented with massive hematemesis and syncope. She was a former smoker who drank alcoholic occasionally. Seven months earlier she has mild pancreatitis without gallstones (edema marginating the pancreas and the second portion of duodenum without vascular abnormalities and lipase 165 U/L [114–286 U/L]). Her medicines included metformin, glipizide, telmisartan, pravastatin and omeprazole. She was pale, diaphoretic and had an initial blood pressure of 37/29 mm Hg with a pulse of 84. She was resuscitated and treated with crystalloids, blood, plasma, platelets, pantoprazole and octreotide. She required tracheal intubation for upper endoscopy, which revealed a 2 cm submucosal ulcerated lesion in the second portion of the duodenum with pulsatile oozing of blood. Therapeutic intervention was not thought to be safe or feasible, nor was she hemodynamically stable for emergency surgery. Liver and pancreatic enzymes were normal. Abdominopelvic computed tomographic angiography revealed a 3.4 cm pseudoaneurysm arising from the right hepatic artery, prominent reactive wall thickening of the duodenum, a 4.4 cm abdominal aortic aneurysm, and perigastric varices suspicious for portal hypertension. Transcatheter arterial embolization (TAE) of the right hepatic and distal common hepatic arteries was accomplished with a variety of coils and plugs with excellent results. Her course was complicated by a large NSTEMI (troponin 60 ng/mL) and bilateral leg DVT with pulmonary embolism requiring an IVC filter. She was discharge to inpatient rehabilitation on day 13.
Hepatic artery psuedoaneurysms (HPA) are a rare cause of life–threatening upper gastrointestinal (UGI) hemorrhage that can be difficult to treat. Predisposing conditions include blunt or penetrating abdominal trauma, pancreaticoduodenal or hepatic surgery, vasculitis, and periarterial inflammation due to pancreatitis or cholecystitis. Prompt diagnosis and intervention is critical to decrease the susbstantial mortality associated with HPA–associated bleeding into the stomach, duodenum or biliary tract.
This case highlights the rare complication of HPA with massive UGI hemorrhage due to preceding pancreatitis. TAE is the preferred initial intervention to manage unstable patients with life–threatening UGI hemorrhage due to hepatic and other visceral arterial aneurysms and pseudoaneurysms. Conventional surgery can be undertaken later, if required. TAE of the liver is usually well–tolerated due to the dual portal and systemic arterial blood supply. However, because of the underlying conditions associated with HPA, a number of these patients do not have patent portal veins. These individuals have a higher risk of hepatic ischemia, necrosis and abscess formation with TAE. In these patients one should strongly consider the placement of percutaneous endovascular balloon–expandable coronary stent–grafts in order to preserve the arterial blood supply to the liver.