PAN is a rare cause of vasculitis first described by Rokitansky in 1852 and published by Kussmaul and Maier in 1866 [4]. Primary etiology of PAN can be idiopathic; however, secondary causes have been linked to chronic Hepatitis B and C infection, Hairy Cell Leukemia, and Adenosine Deaminase 2 deficiency [5]. Due to the systemic deposition of immune complexes, PAN can present in a variety of forms. Multisystem involvement is common in this disease with the kidneys and GI system typically being affected. Other systems involved can include the liver, muscles, nervous, mesenteric vessels, and skin [6]. Therefore, other signs of PAN can include skin lesions, hypertension, neurologic dysfunction, myalgias, renal insufficiency, and abdominal pain. The lung is typically spared in PAN preventing the development of pulmonary symptoms.

Due to the rarity of the disease, clinical suspicion should be confirmed with a biopsy of the medium-sized arteries for histological analysis or angiography if biopsy cannot be performed [7]. Histological presentation of PAN is characterized by transmural inflammation of the arterial wall with fibrinoid necrosis and leukocytic infiltrates [8]. The inflammation of the arteries leads to thickening of the vessel wall and intimal proliferation causing luminal narrowing. Through this mechanism, the vessels are predisposed to thrombosis and the supplied tissue receives reduced blood flow leading to ischemia and necrosis. Over time, the wall of the vessels become weakened and promote aneurysm formation that may eventually lead to the rare complication of vessel rupture.

Visceral artery aneurysm is an extremely rare condition with a reported incidence of approximately 0.01–2% [9]. Previous cases in the literature have reported predominate locations were in the splenic artery (60%), hepatic artery (20%), celiac trunk (5.5%), superior mesenteric artery (4%), gastric and gastroepiploic arteries (4%), intestinal arteries (3%), and the pancreaticoduodenal arteries (2%). The etiology of visceral artery aneurysm is typically atherosclerosis occurring approximately 32% of the time, followed by medial degeneration (24%), abdominal trauma (22%), infection/inflammation (10%), and other causes such as connective tissue disorders, hyperflow conditions and vasculitis (12%) [10]. There have been very few documented cases of omental artery vessel aneurysm and rupture (Table 1). In addition, compiled with the rarity of its etiology due to PAN as seen in our case, there are even fewer reports in the literature of such a case.

Omental artery aneurysms are rare and are associated with a high risk of rupture necessitating prompt treatment. Due to its rarity definitive guidelines regarding indications for intervention or surgery have not yet been established. However, an open surgical approach has been most frequently reported. Kramman et al. reported an endovascular embolization approach that was successful 85% (11/13) of the time [18]. However, in more recent years, there has been a discussion of non-operative management with corticosteroids and cyclophosphamide, which decreases the aneurysm size and increases survival rates up to 80% [19, 20]. In our case, a combination of both open surgical resection and post-operative management with cyclophosphamide and corticosteroids were needed due to the nature of the patient’s urgent clinical presentation.