1–10.4% in autopsy statistics [4, 5]. The splanchnic vessels most commonly involved are the splenic (56%), hepatic (19%), superior mesenteric (8%) and gastric (5%) [1]. The incidence of a gastroepiploic artery rupture is rare, account for 4.5% of the overall splanchnic origins of idiopathic spontaneous intraperioneal bleeding [6, 7]. Spontaneous nonaneurysmal right gastroepiploic artery rupture (RGEA) is among the rarest [1]. None of the reviewed reports have dealt with, specifically, right gastroepiploic

artery rupture without aneurismal changes [1]. The previous enigmatic 20–30% of apoplexy with no identifiable source is now thought to be related to common vascular disease with arteriosclerosis and hypertension felt to represent risk factors [8]. The exact mechanism is unknown, but likely represents

weakness of the tunica media, predisposing #selleck products randurls[1|1|,|CHEM1|]# rupture in the face of abrupt increases in pressure. Pathology specimens regularly exhibit disruption of elastic lamellae [9, 10]. Unfortunately, we didn’t have any histopathology of the vessel wall to know the exact etiology of our patient’s disease; however we think that the data above is the main cause of her RGEA rupture especially that she has been treating hypertension for seven years and also because the surgical exploration didn’t reveal any evident aneurysm of the RGEA. Spontaneous hemorrhage can be seen with inflammatory erosive processes which explain the association with necrotizing arteritis DNA/RNA Synthesis inhibitor in polyarteritis nodosa and rheumatoid arthritis [8, 9]. This may explain that an aneurysmic stage does not necessarily precede the spontaneous rupture of a visceral artery [1]. The presentation and clinical progression of abdominal apoplexy frequently follows a rather predictable course. Before rupture, there may be a history of vague abdominal pain which

is the case of our patient. The symptoms are usually non specific. Physical examination before or soon after rupture is likely to be relatively normal although no one finding is pathognomonic. Hypotension may be present depending on whether the hemorrhage is contained or free intra-abdominal rupture exists. The presentation of acute hemoperitoneum is divided into three main Adenosine triphosphate phases: an early phase of mild-to-severe abdominal pain, a latent phase lacking any symptomatology, lasting from hours to days and a final phase of acute hemoperitoneum in which the patient experiences a rapid increase in the severity of the symptoms, especially the abdominal pain [1]. The diagnosis is generally made on laparotomy for haemodynamic instability which is the case of our patient. In less urgent cases, ultrasonography or CT scan with intra venous contrast can be used. In the hemodynamically unstable patient, FAST (focused assessment by sonography in trauma) examination may be useful to detect intra-abdominal hemorrhage. However, CT scan represents the most important imaging technic.