In a recent survey of HPVG, Kinoshita et al. reported a mortality rate of 39% among all 182 cases reported by 2001. HPVG occurs in different clinical scenarios, including bowel necrosis, digestive tract dilation, intraperitoneal abscesses, ulcerative colitis, Crohn’s disease, gastric ulcers, complications associated with endoscopic procedures, and intraperitoneal tumors. Most frequent cause of HPVG is mesenteric vascular occlusion and subsequent bowel necrosis. The mortality rate is high among cases of HPVG that is associated with bowel necrosis (75%), and emergency surgery is recommended for these potentially lethal cases . Given the high mortality rate of HPVG associated with bowel necrosis, the underlying disease might be an important factor that contributes to patient survival. The degree of bowel necrosis also seems to be associated with the mortality rate. Although NOMI is an important pathology associated with HPVG and it has the highest mortality rates when it is associated with different critical conditions, an increasing number of patients managed using conservative treatment have been reported . In 1958, Ende described the first cases of NOMI in 3 patients with heart-failure-associated low outputs . Recently, a variety of predisposing factors for NOMI have been reported, including heart failure/cardiogenic shock, aortic insufficiency, the administration of vasoconstrictive medications, and dialysis [11,13,15]. Although a relatively low level of mortality has been demonstrated among dialysis patients without bowel necrosis, NOMI has the poorest survival rate among the different mesenteric ischemia etiologies, primarily because of the severity of the comorbid conditions that precipitate reductions in mesenteric perfusion and diagnostic delays. NOMI is associated with 20–30% of all cases of acute mesenteric ischemia and has a mortality rate of 70–90%, which has changed little over time, it is associated with 20–30% of all cases of acute mesenteric ischemia. It leads to extensive irreversible intestinal necrosis for which the prognosis is very poor, despite the absence of organic obstructions in the principal arteries. Contrast-enhanced CT scanning reveals patent mesenteric vessels, but the intestinal wall shows a reduced level of enhancement, both of which are indicative of a diagnosis of NOMI, and surgical intervention might be required if the ischemic damage progresses. In this case, we were unable to perform contrast-enhanced CT because the patient had acute kidney injury due to septic shock. However, portal venous gas secondary to NOMI was strongly suspected, because the patient had septic shock with diffuse peritonitis, extended pneumatosis intestinalis on CT, and no evidence of vascular occlusion with segmental circulatory insufficiency during surgical exploration. Pathological investigations of delayed strictures of the small bowel caused by ischemia have reported that the membranous exclusion and ulcer formation are caused by bowel perfusion disorders. Inflammation and fibrosis then reach the sub-mucosal and sub-serosal layers and extend to incorporate the entire circumference of the bowel lumen [22,23]. In the current case, the same pathological findings were observed, and these formed part of the rationale for our diagnosis of a delayed intestinal stricture caused by NOMI.
NOMI can be treated surgically or non-surgically. Surgical treatment should be considered for patients with suspected bowel necrosis or peritonitis, and for those whose laboratory investigations reveal leukocytosis, elevated levels of liver enzymes, creatinine phosphokinase, serum urea, creatinine, and amylase, and acidosis . Presently, early angiography is performed on patients in whom mesenteric ischemia is suspected and there are no signs of sepsis or peritonitis. If NOMI without the evidence of bowel necrosis or peritonitis is diagnosed, vasodilators will be initiated, for example, prostaglandin E1 and nitroglycerin [11,13]. If gangrenous or transmural ischemic changes in the bowel are found during surgical exploration, resectional treatment is recommended. However, a bowel that is not infarcted but is of questionable viability should not be resected, and a second-look laparotomy is indicated in these cases . The risks and benefits associated with resectional and non-resectional treatments are yet to be determined. While non-resectional treatment could avoid the complications associated with laparotomy and intestinal resection, a delayed intestinal stricture as occurred in this case, might be a risk associated with non-resectional treatment. Bowel stenoses that present after non-surgical treatment have been reported in patients with blunt abdominal trauma [16,17], inflammatory bowel disease, tuberculosis , ischemic colitis [19,20], and in non-steroidal anti-inflammatory drug-related enteropathy . Pneumatosis that is accompanied by neonatal necrotizing enterocolitis has also been reported in 10–20% of the cases who present with delayed strictures [25-27]. A literature search performed on Medline (Ovid) and PubMed using the key words “non-occlusive mesenteric ischemia” and “stricture” or “stenosis”, from 1965 to 2013, uncovered only 2 cases , and no cases have been reported since the use of CT technology became routine.
Previously, NOMI was recognized as an acute phase critical condition that required early identification and appropriate surgical intervention. However, the possibility of delayed structural changes in the ischemic bowel of NOMI patients who are managed without resection of the involved bowel must be acknowledged, as has been demonstrated in the present case report.