NOMI, first described by Ende in 1958, is characterized by intestinal ischemia and necrosis resulting from circulatory disturbance despite the absence of organic obstruction in the mesenteric artery [1]. This condition arises due to decreased cardiac output and circulating plasma volume, leading to the activation of the renin angiotensin system. This leads to sustained hypoperfusion in the intestine, and sympathetic nerve stimulation causes mesenteric vessel spasms, contributing to the pathogenesis of NOMI [2]. NOMI accounts for approximately 20–30% of the cases of intestinal ischemia and has a mortality rate of 50–80%, mainly due to delayed diagnosis resulting from the lack of clinical symptoms [3, 4]. Furthermore, risk factors for NOMI include cardiac diseases, arteriosclerotic disease, cerebrovascular disease, diabetes mellitus, dialysis, burns, extracorporeal circulation, usage of certain drugs, and advanced age [5, 6]. Recognizing these risk factors and understanding the subtle clinical presentations of NOMI are crucial for early intervention and improved outcomes.

Heer et al. proposed three diagnostic criteria for NOMI: (1) absence of an obstruction in the mesenteric vessel supplying the bowel necrosis area, (2) segmental and discontinuous bowel ischemia and necrosis, and (3) histopathologic evidence of bowel hemorrhage and necrosis [7]. In the present case, although segmental ischemia was not observed, preoperative CT and intraoperative findings supported criteria 1 and 3, which are consistent with the NOMI diagnosis.

The surgical goals include assessing intestinal viability and resecting necrotic portions. Diagnosing gross intestinal necrosis is challenging, with clinical criteria having an accuracy of 57.7%.

In NOMI, where bowel ischemia progresses from the mucosa to all layers, accurate identification of salvageable bowel regions by intraoperative serosal observation [8] is challenging. Although intraoperative mucosal surface observation using a small bowel endoscope has been proposed [9], its practical implementation is complicated and is associated with a risk of mucosal damage. Conversely, the ICG fluorescence method (intravenous ICG solution, Diagnogreen®, Daiichi Sankyo, 2.5 mg/mL) offers a noninvasive and simple diagnostic approach for determining the extent of intestinal necrosis. ICG emits fluorescence under near-infrared light, which is captured by a dedicated charge-coupled device camera, allowing for the visualization of in vivo information, including blood and lymph flow [10]. This method enables the evaluation of the mucosal condition from the serosal surface, providing visualization to approximately 10 mm deeper than the tissue surface [11]. In a study by Ishizuka et al., ICG fluorescence was used to identify bowel necrosis in four of six NOMI cases that were undetectable to the naked eye [12], similar to the present case.

Intraoperative ICG fluorescence shows promise in the diagnosis of bowel necrosis; however, there are notable limitations. First, the package insert mentions shock as a potential side effect, although not significant. Second, the use of Diagnogreen is contraindicated for iodine-sensitive patients because of its iodine content. Third, ICG fluorescence is qualitative and does not quantify organ perfusion, which complicates the determination of the optimal perfusion threshold for bowel preservation [10]. In our case, a retrospective comparison of intraoperative ICG findings with postoperative histopathology enabled us to differentiate between edematous and necrotic intestinal mucosa based on ICG fluorescence intensity. However, it was difficult to determine the preservation potential based on reduced ICG fluorescence intensity alone. Therefore, all areas with decreased fluorescence were resected to avoid potential new ischemia. Fortunately, no postoperative evidence of ischemia in the remaining bowel was noted, thereby obviating the need for a second-look surgery. However, extensive bowel resection may be required in patients with widespread reduction of ICG fluorescence. In cases with severe hypoperfusion in an extensive area, a wide bowel resection cannot be avoided, as it could lead to short bowel syndrome. However, when the mild hypoperfusion area is extensive, determining the extent of resection is difficult. The basic flow is that the mild hypoperfusion area is preserved and re-evaluated at the second-look operation. However, if the patient’s general condition makes it difficult to perform a second-look operation, it may be necessary to resect the mild hypoperfusion area at the first surgery in preparation for short bowel syndrome. When the mild hypoperfusion area is not extensive, it may be possible to avoid the second-look operation by resecting the entire hypoperfusion area, as in this case. A PubMed search using NOMI and ICG as keywords revealed five cases, including this case. Three cases were anastomosed at the primary surgery, and the second look operation could be omitted (Table 2) [13,14,15,16]. According to Ishizuka et al., 83% was performed ICG test had no anastomotic intestinal problems [12]. Using ICG potentially led to this result because it can detect the ongoing ischemia with only ischemia on the mucosal surface and no change on the serosal surface. If ICG test is performed, the possibility of reischemia is low [12]. Moreover if all areas of reduced blood flow can be resected, a primary anastomosis may be considered. However, if the cause of hypoperfusion of the intestinal tract is clear and has not been corrected before surgery, or if the area showing ischemia on ICG examination is extensive and the resection of the entire area would result in short bowel syndrome, we should opt for second-look operation. In addition, it is possible that interpretations of the ICG study may differ because of different experience, however, we believe that such bias can be corrected by quantifying the ICG test. Thus, it is essential to gain experience by comparing intraoperative ICG fluorescence intensities with pathological findings.