Acute mesenteric ischemia (AMI) accounts for 60% to 80% of all cases of mesenteric ischemia and has a mortality rate between 59% and 93% [2–7]. AMI can be caused by arterial emboli, arterial or venous thrombosis and non-occlusive obstruction. In all causes, the sudden onset of intestinal hypoperfusion can lead to hypoxemia and intestinal hypoxia with irreversible bowel damage [3, 4]. Risk factors for developing AMI depend on the etiology: more often patients are older than 50 years and suffer from congestive heart failure, recent myocardial infarction, hypovolemia, hypotension or sepsis [2–6, 8]. Clinical presentation is nonspecific, often presenting as a sudden onset of severe abdominal pain, frequently out of proportion to what is found at physical examination. Accompanying symptoms and signs are nausea, vomiting and hypotension [2, 3, 5, 6, 8, 9]. The absence of specific signs upon physical examination can make the diagnosis of AMI very challenging and the clinical consequences of missed AMI can be catastrophic. A rapid diagnosis is the most important factor for prognosis, and urgent investigation of vessel patency should thus be done by abdominal CT or IADSA [2, 3, 5–7, 9]. During the work-up, the patient should be closely monitored and stabilized . Once the diagnosis has been made, ischemic bowel segments should be resected and the blood flow restored as soon as possible. Depending on the etiology of the acute ischemia, the restoration of blood flow can be achieved either surgically, using intra-arterial vasodilatation, embolectomy or bypass, or via medical revascularization with, for example, intravenous heparin [2, 3, 5, 8].
Chronic mesenteric ischemia (CMI) is a rare condition that accounts for only 5% of all intestinal ischemic events [1, 10, 11]. It is caused by atherosclerotic occlusion or severe stenosis of the mesenteric vessels in more than 90% of cases [1–3, 6, 8–13]. Ischemia occurs when the blood supply to the intestines is inadequate as a result of lesions affecting one or more of the three mesenteric arteries: the celiac artery, the superior mesenteric artery or the inferior mesenteric artery [3, 6, 10, 12]. In most patients, at least two of the three arteries are either completely obstructed or severely narrowed before symptoms of CMI occur [1–3, 6–8, 10, 11, 13]. However, CMI due to isolated occlusion of the celiac artery or the superior mesenteric artery has also been described [6, 9, 12]. Distal lesions carry a greater risk of symptoms than proximal lesions because they are less likely to develop collateral arteries [7, 12].
Risk factors for CMI are the same as those for atherosclerosis, namely hyperlipidemia, hypertension, diabetes and smoking [1, 2, 10, 11, 13]. Further, most patients are older than 60 years of age, and women are affected three times more frequently than men [2, 8–13].
As with AMI, clinical diagnosis is often difficult due to the vague symptomatology. Symptoms of CMI typically develop when there is a postprandial increase in blood flow demand. The most characteristic symptom is intestinal angina. This typical abdominal pain occurs within the first hour after ingestion of a meal. It is often located in the epigastric region or the mid-abdomen and is described by patients as dull and crampy. Diarrhea, nausea and vomiting are commonly present [1, 6, 8–13]. Most patients have significant weight loss caused by sitophobia [1, 6, 7, 9, 10, 12]. Physical findings are usually both aspecific and unremarkable and pain is frequently out of proportion to the objective findings on investigation. Sometimes a bruit can be heard over the epigastric region [1, 10, 11, 13].
Duplex ultrasonography, IADSA, CT angiography and magnetic resonance angiography can be used to detect intra-abdominal vascular disease [1, 2, 6–13]. The treatment goal in CMI is to relieve symptoms, improve nutritional status and prevent progression to acute ischemia [9, 10, 12, 13]. Open surgical revascularization is still considered the first choice for patients with CMI [3, 8, 13]. However, endovascular procedures are currently considered a viable alternative and are increasingly performed, and the medical literature has confirmed their feasibility and safety with an acceptable rate of patency [2, 3, 8, 10, 12, 13].
In the current case, confusion existed about the true etiology. There was a discrepancy between her symptomatology, namely intestinal angina, diarrhea and sitophobia suggesting CMI, and the diagnostic sign of an isolated occlusion of a branch of the superior mesenteric artery, which pointed towards the diagnosis of AMI. No reasonable explanation could be found for the symptoms of melena and fever. The AMI was caused by an arterial embolism, most likely due to atrial fibrillation. In this context we may conclude that this case is a late and unusual presentation of AMI. In our opinion, it is the size of the embolism that is responsible for the localization of the ischemic zone. The localization of this zone is a coincidence.
An extensive work-up was done as a consequence of the confusion. An upper gastrointestinal endoscopy and an enteroclysis were performed to indicate the severity, extent and location of the ischemic segment. However they proved unnecessary, as angiography was the most accurate imaging technique [1–13].
Revascularization by operative or endovascular procedures in this case was not possible because of the distal site of the occlusion. Resection of her small bowel segment was the only appropriate action. However, generally, revascularization procedures are mandatory [1, 3–13].
As far as we know, this is the first report presenting a case with segmental occlusion of the superior mesenteric artery causing AMI.