Pancreatic pseudoaneurysms occur most commonly in the setting of recurrent pancreatitis wherein digestive pancreatic enzymes erode the pancreatic or other peripancreatic arteries [4]. The resulting pathology is a fragile, contained hematoma where the surrounding wall consists of produts of the clotting cascade, including fibrin and platelet crosslinks that are substantially weaker than the normal vascular structure [5,6]. Pseudoaneurysms can also occur in the setting of mechanical damage to the vasculature, typically following pancreaticobiliary surgery, transplantation, or trauma [4]. Our patient’s pseudoaneurysm was diagnosed when he presented to the hospital following blunt abdominal trauma sustained during a physical altercation, after he was discharged for an acute exacerbation of pancreatitis. His presenting symptoms were significant for nausea, right upper quadrant pain, epigastric pain, and left upper quadrant pain.

The statistical frequency of gastroduodenal pseudoaneurysms, like our patient’s, is 10-20% of all reported peripancreatic pseudoaneurysms and 1.5% of all reported visceral arterial pseudoaneurysms [7,8]. Pseudoaneurysm only occurs in 3.5-10.5% of pancreatitis cases in general [1]. Diagnosis of pancreatic pseudoaneurysms is typically made through incidental findings on abdominal or pelvic CT imaging; this modality is 67% sensitive for diagnosing a pancreatic pseudoaneurysm [9]. Literature is consistent in affirming CT angiography as the gold standard diagnostic modality for pancreatic pseudoaneurysms with the greatest sensitivity of 100% [9]. Less sensitive modalities include ultrasonography (50%) and upper endoscopy (20%) [9].

Gurala, D., et al. proposed a classification system based on the relative size of the originating rtery (including the capacity for surgical excision), communication to the gastrointestinal tract (GIT), and on the presence or absence of pancreatic juices [10]. Specifically, type I psuedoaneurysms occur in minor arteries that can be easily excised, while type II occurs in major arteries with minimal hemodynamic compromise if surgically removed. Type III are not amenable to surgical removal given their association with major arteries that cannot be excised. Further subclassification depends on the presence or absence of communication with the GIT. Type A pseudoaneurysms lack communication, and tend to produce lower volumes of hemorrhage leading to a confined hematoma. Note that with expansion into the retroperitoneal space, these can compress the bleeding site, leading to abdominal compartment syndrome. On the other hand, type B pseudoaneurysms maintain communications with the GIT, which tend to begin as minor, localized bleeding but are more likely to progress to fatal hemorrhage. Lastly, they are categorized based on the presence or absence of pancreatic juices, with implications regarding the likelihood of successful stent placement and viability. Type 1 pseudoaneurysms lack pancreatic secretions and are typically excellent candidates for endovascular stenting or embolization. Type 2 pseudoaneurysms are exposed to pancreatic juices, imparting a greater risk of enzymatic degradation including potential destruction of the stent or embolization agent, making endovascular approaches less viable. Ultimately, classification aims to simplify and guide management decisions on the basis of characteristics that may preclude specific management trajectories. Our patient’s pseudoaneurysm involved the gastroduodenal artery without communication to the GIT and with no evidence of pancreatic juices, and was thus classified as type IIA1. While both surgical and endovascular approaches were feasible courses of management in a hemodynamically stable patient, embolization would be less invasive and was performed on our patient in an effort to minimize the risk of surgical complications.