Patients should be in the supine position, and images should be obtained from the liver dome to the pubic symphysis. Proposed CT parameters are shown in Table 1. Multiplanar reformations should be routinely rendered.

An unenhanced acquisition is recommended. When added to contrast-enhanced CT, it helps identify features of ischemic intestinal injury, namely, spontaneous hyperattenuation of the bowel walls and decreased or absent bowel wall enhancement. Therefore, it improves sensitivity, diagnostic confidence, and interobserver agreement [18]. However, the unenhanced acquisition should always be associated with a contrast-enhanced acquisition because unenhanced CT alone has been associated with a delay in diagnosis and increased mortality of AMI [14]. Virtual unenhanced imaging can be performed with spectral CT [19]. Comparison of conventional CT and dual-energy acquisitions has been evaluated only in an experimental swine model. Nevertheless, the results showed that dual-energy CT significantly improves visualization of decreased segmental bowel wall enhancement [20]. This should be balanced by the somewhat low probability of AMI in suspected cases [15, 16].

IV contrast injection is essential for visualizing both splanchnic vessels and bowel loops. Care should be taken to inject enough iodine (2 mL/kg of contrast medium with a concentration of 350 mg I/mL) at a high rate (> 4 mL/s) to obtain good arterial peak enhancement and maximal enhancement of the bowel wall. Oral contrast agents are not recommended, because they decrease the contrast between the bowel wall and the lumen, hampering image analysis. Moreover, they increase the duration of CT and can cause beam-hardening artifacts, which can alter visualization of small vessels. Finally, contrast propagation is often slow owing to the ileus [21–24].

An early arterial phase acquisition is extremely important for visualizing arterial vessels. Not only does it help identify vascular anomalies, especially when they are distal, but also it is of great value for treatment planning, despite the increase in radiation dose. Images should be obtained by bolus tracking or the bolus-triggered method with the enhancement threshold set at 120 HU. A fixed-delay acquisition (20–25 seconds) is not recommended because of increased risk of missing peak arterial enhancement in patients in poor hemodynamic condition. Portal venous phase acquisitions should be performed 50 seconds after arterial phase acquisitions to prevent early or late acquisition due to hemodynamic changes. The split bolus technique with two contrast boluses separated by a timed delay allowing a single-phase acquisition has been found to have good diagnostic value, afford diagnostic confidence, and reduce radiation exposure and interpretation times [25]. Thus, the split bolus technique can be considered an alternative technique, although it has never, to our knowledge, been compared with the multi-phasic protocol. Use of a portal venous phase alone has been found to decrease interob-server reliability [26, 27].

Fear of contrast-induced kidney injury should not be a contraindication to contrast enhancement when managing potentially life-threatening conditions such as AMI. Although chronic renal insufficiency and arterial AMI share risk factors, only 5% of patients with arterial AMI have been found to have chronic renal insufficiency before admission [17]. IV hydration is recommended for patients at high risk of contrast-induced kidney injury, but the amount of contrast medium should not be decreased. Moreover, although it is important to prevent patients from excessive radiation doses, because of the extremely poor short-term prognosis of AMI, attempts to avoid excessive radiation should not be allowed to result in poor acquisitions.

Arterial emboli—Arterial emboli cause approximatively 40–50% of cases of AMI [28]. Emboli usually originate in the heart or aorta and cause occlusion of arteries, especially the SMA, which is one of the most vulnerable arteries because of its small branching angle from the aorta [29]. In most patients blood flow is preserved in the proximal branches of the SMA and jejunal arteries, and the emboli lodge approximatively 6–8 cm beyond the ostium near the orifice of the middle colic artery [30] (Fig. 1). Pain is more severe and sudden in these cases than those with other causes. The vessel cutoff sign, which is a sharp ending of contrast material with a filling defect in the distal branches associated with enlargement of the SMA, is generally seen on contrast-enhanced CT studies if emboli are occlusive (collaterals are insufficient). A rare but indeterminate feature is diminished venous return seen as a reduction in the diameter of the superior mesenteric vein (SMV), which results in a reversed vessel diameter ratio when it is associated with enlargement of the SMA (SMV diameter / SMA diameter < 1) [2]. High attenuation of the SMA may also be seen on unenhanced images. Nonocclusive emboli can be found and are seen as eccentric luminal or central filling defects with a preserved opacified rim (ring sign). Only small branches may be affected [31] if the emboli are small with a possible decrease in diagnostic performance. Infarcts in other organs—kidneys, spleen, liver, and lower limbs—may be suggestive of nonocclusive emboli.

Arterial thrombosis—Arterial thrombosis of a previously stenotic mesenteric artery occurs in approximatively 20–35% of patients and is the leading cause of AMI in patients older than 70 years old [29]. Underlying chronic mesenteric ischemia is present in as many as 80% of patients but is misdiagnosed in most cases. Typical signs of chronic mesenteric ischemia are postprandial abdominal pain, fear of eating, and weight loss. Patients generally have atherosclerosis and cardiovascular, cerebrovascular, and peripheral arterial disease. Rupture of an atherosclerotic plaque leads to local exacerbation with acute-on-chronic mesenteric ischemia [32]. The occluded vessel presents with plaques (calcified or noncalcified). The site of thrombosis is generally proximal, near the ostium [33], and ischemia is often extended but depends on collaterals (Fig. 1).

Arterial dissection and vasculitis—Arterial dissection occurs in less than 5% of patients with AMI [28]. In most patients SMA dissection is the result of aortic dissection. A linear intraluminal filling defect, representing the flap separating true from false lu-mens, is seen on contrast-enhanced CT studies (Fig. 1). Most cases of arterial dissection are not complicated by AMI, especially if the false lumen is patent.

Other, rarer causes, such as segmental arterial mediolysis (SAM) or fibrous dysplasia may occur [34, 35]. The prevalence of SAM is unknown, and this recently described entity may be largely underdiagnosed. However, AMI is rarely associated with SAM, even if the SMA is the most frequent artery involved [36, 37]. Vasculitis may involve large, medium, and small vessels. Lesions of large and medium vessels are rarely a cause of AMI. They appear as diffuse vessel wall thickening with perivascular fat stranding. Small-vessel vasculitis may be more frequently involved. The lesions mainly appear as segmental small-bowel wall thickening with normal large vessels.

Nonocclusive mesenteric ischemia—Nonocclusive mesenteric ischemia (NOMI) is the most lethal form of AMI [4]. Its prevalence is highly dependent on the population studied and ranges from 6% [26] to 47% [15] of all cases of AMI. The pathogenesis is still poorly understood, and NOMI is one of the most challenging diagnoses to make. ICU patients with low cardiac output or hypovolemia and underlying atherosclerosis are particularly affected. Low-flow states activate the renin-angiotensin-aldosterone system and accentuate splanchnic vasoconstriction and SMA resistance, which further decreases regional blood flow [38]. The vasospasm may be reversed if the decrease in flow is rapidly corrected. In experimental AMI and sepsis models, however, splanchnic vasoconstriction that lasts more than approximatively 30 minutes becomes irreversible even if blood flow is restored through the SMA [38–40].

CT may show a flattened inferior vena cava, narrow veins [33], diffuse irregularities or stenoses of the SMA and SMA branches (“string of sausages” sign), and impaired filling in the intestinal arcades and intramural vessels [41, 42]. No evidence of underlying thromboembolic disease is found. The diameter of the SMA is reported to be smaller in NOMI without a reperfusion process [41, 43–45] than in occlusive forms of AMI (Fig. 2). A study comparing SMA diameters in 55 patients with NOMI with findings of previous contrast-enhanced abdominal CT performed for other reasons showed a mean decrease in diameter of approximatively 2 mm [45]. The measurement must be made at precisely the same point for this feature to be suggestive. We recommend measuring SMA diameter distal to the middle colic artery. Because NOMI generally occurs in hospitalized patients in poor general condition, previous abdominal CT images for SMA diameter comparison may often be found in the PACS.

Mesenteric venous thrombosis represents approximatively 5–20% of cases of AMI [29, 46, 47]. Patients are more frequently women, and thromboses occur in younger patients (4th decade). Approximatively one-half of patients have a history of deep vein thrombosis or pulmonary embolism [48]. The pain is nonspecific and subacute and progresses over 2–4 weeks. Clotting is by far the most frequent cause of nonmechanical mesenteric vein obstruction.

Prothrombic states resulting from systemic conditions account for most causes: cancer, myeloproliferative neoplasms, genetic coagulopathy or thrombophilia, and nephrotic syndrome [29, 49–52]. Occlusion generally affects the small and distal veins first and then progresses to the larger trunk, as found in a dog model of gradual occlusion of the SMV [53]. Thrombosis from other local conditions, such as inflammatory or infectious bowel disease, pancreatitis, and portal hypertension [54], may rarely cause mesenteric ischemia due to slow retrograde distal progression, which allows collaterals to develop [54, 55]. Isolated SMV thrombosis is generally not sufficient to cause ischemia [56].

Thrombus location and extension and adequate collateral circulation are important factors for predicting ischemia. If distal branches are compromised [50] and collaterals are inadequate when the thrombosis occurs, local elevation of blood pressure occurs, as does bowel wall edema and ultimately a decrease in arterial inflow. It has been suggested [50] that the more distal the thrombosis, the fewer are the collaterals and the greater is the risk of ischemia (Fig. 3). Acute thrombi exhibit spontaneous hyperattenuation on unenhanced images and are associated with enlargement of the vein (by displacement of the venous wall). This finding appears as a luminal filling defect with well-defined peripheral rim enhancement of the venous wall. The latter is highly specific (> 90%) [27, 57–59]. However, chronic occlusion appears as narrowed and atrophic vessels [33]. Inferior mesenteric venous thrombosis and venous colon ischemia are extremely rare [56].

Wall thickness—The normal thickness of the wall of an optimally distended segment of small bowel ranges from 1 to 5 mm, but this depends on the degree of distention. Comparing bowel wall thickening between similarly distended segments is important because walls are thinner when distended [60]. The increased permeability of damaged vessels causes mural edema (usually reversible) and results in bowel wall thickening. The sensitivity of this feature ranges from 38% to 88% and the specificity from 38% to 72% [61–63]. The variability occurs because of the heterogeneity of the populations studied and because wall thickening is observed in various nonischemic conditions [64]. In AMI of venous causes, this feature is more frequent than in other causes because of mural hemorrhage or edema due to venous stasis [31, 65].

Bowel wall thinning is typically encountered in cases of arterial occlusion with the bowel wall typically having a paper-thin appearance caused by loss of tissue volume, loss of intestinal muscle tone, and destruction of intramural nerves (adynamic ileus). It can be difficult to differentiate a thin wall from decreased or absent bowel wall enhancement. Specificity is reported to be high (88%) with low sensitivity (40%) and poor interreader agreement [63]. Bowel wall thinning is an early and suggestive feature in NOMI [66] without reperfusion.

Bowel wall attenuation on unenhanced images—A spontaneous increase in bowel wall attenuation on unenhanced images has high specificity (90–98%) and excellent interobserver agreement [26, 27] but low sensitivity (5–18%) for the diagnosis of AMI. This sign may be a result of hemorrhagic infarction caused by blood extravasation from damaged vessels during reperfusion but also of venous thrombosis leading to a destructive increase in the inner pressure of the wall. Normal bowel wall attenuation usually ranges from 10 to 20 HU. Increased attenuation from bowel ischemia is better visualized by comparing abnormal segments with an adjacent normal segment [67].

It is important to differentiate intramural hemorrhage from a reperfusion process. The latter has been described as an increase in wall attenuation on contrast-enhanced images. The former is identified on unenhanced images with limited or no change in attenuation after contrast administration. It is also important to remember that spontaneous wall hyperattenuation, especially when it is marked, can mimic wall enhancement on contrast-enhanced images. This shows the importance of acquiring unenhanced images first, to prevent misinterpreting contrast-enhanced bowel attenuation as normal when it is absent or decreased [68].

Wall enhancement on contrast-enhanced images—Assessment of bowel wall enhancement plays an extremely important role in the diagnosis of AMI. Decreased bowel enhancement is a major feature because it is a sign of the decreased blood inflow to the bowel wall [47] (Figs. 4–6). Absence of enhancement is rarely seen because the collateral supply is extensive. This feature has specificity and sensitivity ranging from 50% to 100% and 18% to 92%, respectively [27, 57, 58, 62, 63, 69]. This variability is associated with moderate interobserver agreement [70] (estimated κ = 0.52 in the study by Copin et al. [26]) and can be explained by its purely subjective (and in most studies visual) definition and by the frequent use of a suboptimal CT protocol without unenhanced acquisitions [26]. Jang et al. [71] suggested that a more quantitative approach using ROIs for the assessment of bowel wall enhancement is reliable and associated with better performance. Nevertheless, most teams still use a visual approach.

Increased enhancement is mainly seen in patients with hypovolemic shock and therefore in certain cases of NOMI. Paradoxic mucosal hyperenhancement with submucosal edema defines bowel shock, in which sympathetic stimulation triggers splanchnic vasoconstriction and leads to reduced bowel perfusion. The permeability of the bowel is damaged by poor oxygen provision, which causes interstitial leakage of contrast material, mucosal enhancement, and submucosal edematous wall thickening [72, 73]. The target sign, corresponding to hypoenhancing submucosa between the hyperenhancing mucosa and muscularis propria or serosa, is reported in arterial occlusion with reperfusion (Fig. 5), NOMI, and venous ischemia but also nonischemic diseases, such as Crohn colitis [33, 74]. Figure 7 summarizes the spectrum of bowel wall changes in mesenteric ischemia.

Dilated fluid-filled bowel loops (defined by a small-bowel diameter > 25 mm) are common in AMI (50–91% of patients) [13, 26, 75, 76] and are caused by either irreversible transmural ischemia or reflex interruption of bowel peristalsis, which causes fluid exudation into the bowel lumen [47]. The reported sensitivity (39–67%) and specificity (29–81%) of bowel dilatation are highly variable [27, 57, 58, 62, 63, 77, 78]. This feature is reported to be less prevalent in venous occlusion and NOMI than in arterial occlusion [79]. If vessel anomalies are not carefully sought in the presence of bowel dilatation, AMI can be confused with mechanical obstruction (small-bowel obstruction with closed-loop mechanism is the main differential diagnosis in that case) or simple ileus [47].

Pneumatosis is a highly specific feature when AMI is suspected (reported specificity, 81–100%) [57, 62, 63, 75, 80]. This sign is defined by the presence of gas bubbles in the bowel wall as a result of mucosal injury with gas dissecting through the layers of the bowel wall, extending through the superior or inferior mesenteric vein then into the portal venous system. Pneumatosis can be confounded with gas trapped between the bowel wall and residual fluid in the lumen, but this false pneumatosis is almost exclusively gravity dependent. Nevertheless, pneumatosis not only is associated with AMI but also may be found in inflammatory or infectious bowel, connective tissue disease, and iatrogenic mucosal injury (targeted chemotherapeutic or immunotherapeutic agents). It also can be caused by increased intraluminal pressure, as with asthma [81]. When extensive and not associated with symptoms, pneumatosis intestinalis is likely to be benign and not ischemic (Fig. 8).

Both ascites and mesenteric fat stranding are related to transudation caused by a reper-fusion process, elevated mesenteric venous pressure, or superinfection of the ischemic bowel (in delayed forms). Mesenteric fat stranding is usually seen in venous or arterial AMI. In NOMI, fat stranding is generally found in the presence of a reperfusion process [23]. These signs have good sensitivity but low specificity [27, 57, 58, 62, 63, 77, 78].

Most authors divide ischemic colitis into two separate entities: right ischemic colitis and left ischemic colitis (or nonright ischemic colitis). Whether the transverse colon should be included in one of these two entities continues to be a subject of debate [82–84]. Right ischemic colitis has a poorer prognosis than left ischemic colitis and is associated with a threefold higher rate of vessel occlusion [83, 84]. It is considered part of AMI. Left colic ischemia, however, is mainly a result of micro-vascular disease, and the inferior mesenteric artery is patent [84]. In as many as 90% of patients, right ischemic colitis is segmental [80]. Therefore, any feature of right colitis should prompt cautious analysis of the patency of the SMA and its distal branches. Extradigestive infarction due to emboli is found in 50% of patients with SMA occlusion; it mainly involves the kidneys or the spleen [45]. These findings are sometimes obvious and increase confidence in the diagnosis, especially when bowel anomalies are not suggestive.

Pneumoperitoneum is a consequence of bowel perforation and can therefore be considered a sign of transmural necrosis when AMI is confirmed. The prognostic value of pneumatosis intestinalis is still a subject of debate. Wang et al. [69] found pneumatosis in 59% of cases of surgically confirmed late necrotic mesenteric ischemia (compared with 5% in nonnecrotic AMI). Duron et al. [86], however, found that as many as 47% of patients who still had viable bowel presented with pneumatosis, indicating that this feature may be observed in ischemic but not yet necrotic bowel. Importantly, when pneumatosis has a bandlike appearance and when it is associated with portal venous gas, the probability of bowel necrosis is high [87, 88].

Nuzzo et al. [9] found that bowel loop dilatation was strongly associated with necrosis and was present in 64% of cases of pathologically confirmed transmural necrosis in AMI. This was probably the consequence of irreversible damage to the deeper muscle layers [47]. Finally, absence of wall enhancement or the presence of spontaneous hyperattenuation of the wall also suggests necrosis, but the value of this feature must be determined [9].

A reported 95% of patients with venous AMI treated with anticoagulation therapy do not need any additional endovascular or surgical treatment [89]. The estimated 30-day survival rate is greater than 80% and is highly influenced by the cause. When small-vein thrombosis is present, collaterals may be insufficient or inadequate, and patients are more likely to undergo surgical resection [90].