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Many faces of acute bowel ischemia: overview of radiologic staging
Insights into Imaging volume 12, Article number: 56 (2021)
Acute bowel ischemia (ABI) can be life threatening with high mortality rate. In spite of the advances made in diagnosis and treatment of ABI, no significant change has occurred in the mortality over the past decade. ABI is potentially reversible with prompt diagnosis. The radiologist plays a central role in the initial diagnosis and preventing progression to irreversible intestinal ischemic injury or bowel necrosis. The most single imaging findings described in the literature are either non-specific or only present in the late stages of ABI, urging the use of a constellation of features to reach a more confident diagnosis. While ABI has been traditionally categorized based on the etiology with a wide spectrum of imaging findings overlapped with each other, the final decision for patient’s management is usually made on the stage of the ABI with respect to the underlying pathophysiology. In this review, we first discuss the pathologic stages of ischemia and then summarize the various imaging signs and causes of ABI. We also emphasize on the correlation of imaging findings and pathological staging of the disease. Finally, a management approach is proposed using combined clinical and radiological findings to determine whether the patient may benefit from surgery or not.
There is a correlation between pathologic staging and radiologic findings of ABI.
Reversibility–irreversibility of ABI spans a temporal continuum with areas of overlap.
Understanding the pathophysiology of ABI can help for better management.
Management should be based on the latest stage identified.
Acute bowel ischemia (ABI) is defined as bowel injury associated with sudden interruption of blood supply to small or large intestine in an either segmental or diffuse pattern . Despite low incidence (accounting for only 0.09–0.2% of emergency departments admissions ), this is a life-threatening condition with mortality rate reaching 60–80%, even with surgical intervention . In spite of advances in detection and therapeutic options, no significant change has occurred in the mortality of ABI over the past decade . Furthermore, with increasing mean life expectancy, bowel ischemia has turned into one of the most ominous disorders of elderly patients in the clinical practice .
Clinical presentation, physical examination and laboratory findings are generally non-specific and do not reliably differentiate bowel ischemia from other abdominal emergencies without imaging . Patients with ABI may present with abdominal pain out of proportion to examination, rebound tenderness, epigastric bruit, vomiting and diarrhea, most of which happening in the late stages of the disease . Elevation of serum lactate levels could be also a late finding in the course of disease. This is true for other laboratory findings including neutrophilic leukocytosis, high anion gap metabolic acidosis, lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) .
Duration of insufficient blood flow is the most important prognostic factor which makes timely diagnosis and surgical intervention the cornerstones of improved outcome . Although X-ray (abdominal or upright chest) and abdominal ultrasound play a vital role in the first-line diagnostic workup of acute abdomen, they usually yield non-diagnostic results in case of ABI . Abdominal x-ray can show pneumoperitoneum, caused by bowel perforation in advanced stages of ABI, or even in some instances may show pneumatosis intestinalis in late in the disease course. Abdominal X-ray can also depict bowel distention as a non-specific finding caused by paralytic ileus in early stages of ABI. Abdominal ultrasound might be useful to assess intraperitoneal free fluid or portal venous gas in advanced ABI. Doppler study may also infrequently reveal arterial or venous occlusion in larger vessels.
With a 93% sensitivity and 96% specificity, multidetector computed tomography (MDCT) scan is widely utilized as the first-line imaging choice to confirm and localize ABI, determine its severity and exclude mimickers . MRI is not a common choice for diagnosing ABI in acute clinical settings, and due to its better visualization of thrombosis, inflammatory processes and adhesion bands, it is more frequently used in evaluation of chronic bowel ischemia .
ABI tends to develop through different stages with distinctive diagnostic features at each stage . CT scan plays an important role in appropriate triage of patients and early diagnosis of disease at the reversible stage. Thus, radiologists play a key role in the initial diagnosis by determining the location, extent of the disease and identifying the underlying cause, potentially preventing ABI progression to irreversible intestinal injury or bowel necrosis .
This review will address various causes and imaging signs of bowel ischemia with emphasizes on correlation of imaging findings and pathological staging of the disease. Finally, a management approach is proposed using combined clinical and radiological findings.
Intestinal ischemia develops when blood perfusion is disproportionate to the metabolic demands of the organ. Collateral circulation can protect the bowel from substantial damage when up to 75% of bowel perfusion is lost for 12 h ; however, complete perfusion loss of more than 4–6 h results in significant bowel injury . Therefore, the initial hours are a golden time to achieve a favorable outcome with prompt intervention. ABI has diverse etiologies that could be divided into: arterial, venous, non-occlusive and mixed type . Familiarity with each category will help radiologists take a proactive approach in early diagnosis of these emergent conditions (Fig. 1).
A solid understanding of vascular anatomy and territories is crucial to identify the areas that are particularly susceptible to infarction from global ischemia. The abdominal aorta gives off three major branches responsible for the arterial blood supply of gastrointestinal tract, namely celiac artery (CA), superior mesenteric artery (SMA) and inferior mesenteric artery (IMA), which perfuse foregut (from the oral cavity to the proximal part of the duodenum, D1), midgut (from the mid-duodenum, D2, to the proximal two-thirds of the transverse colon) and hindgut (from the distal one-third of the transverse colon to the upper portion of the anus), respectively  (Fig. 2). This accounts for the conventional anatomic pattern with other anatomical variations exist .
The mesenteric venous drainage includes superior mesenteric vein (SMV) and inferior mesenteric vein (IMV), grossly mirroring the arterial system and running alongside the corresponding arteries. IMV drains blood from rectosigmoid and left colon; meanwhile, SMV drains right and transverse colon, ileum and jejunum. Subsequently, SMV and splenic vein (SV) join together to form the portal vein. IMV can drain into splenic vein (SV), SMV or their confluence . In case of any arterial or venous occlusion, plenty of venous collateral pathways exist.
Absence or underdevelopment of vascular connections between two neighboring colonic vascular territories is regarded as “Watershed” areas. Junction of SMA and IMA at the colon’s splenic flexure is known as “Griffith’s point” . There is an additional watershed area in the rectosigmoid junction between IMA branches and hypogastric arteries known as “point of Sudeck” . These watershed areas are typically affected the most in hypoperfusion state .
Understanding the pathologic basis of ABI can help to estimate the probability of reversibility and choose the optimal treatment option. The gastrointestinal tract is made up of four layers, which include mucosa, submucosa, muscularis and serosa, from inner to outermost layer. ABI is categorized into 3 stages based on the involvement of each layer.
In stage I or the early stage, the damage is only confined to the mucosal layer . The early stage of ischemia is typically followed by the release of certain mediators (cytokines, platelet-activating factor and tumor necrosis factor), which leads to an inflammatory response, resulting in further damage of the intestinal wall . These changes are reversible and are not extended to the outer layers. This phase has the best prognosis and can heal completely with timely intervention.
Stage II or the intermediate stage is described as presence of specific pathologic changes (edema, erosion, hemorrhage and necrosis) in submucosa and muscularis propria . There are two enteric nervous plexuses in these layers. Meissner’s plexus lies in submucosa and mainly controls secretion and local blood supply, whereas Myenteric or Auerbach’s plexus is located between the longitudinal and circular layers of the muscularis propria and is responsible for the peristaltic movement of the bowel. Injury to these neural plexuses leads to a reduced blood flow, impaired motor function and results in loss of peristalsis and muscles tone . Fibrotic stricture of bowel eventually forms as the late outcome if perfusion restores (Figs. 3, 4).
Stage III, the late stage, is manifested by transmural bowel necrosis and is developed if blood supply is not eventually restored . Epithelial changes and alterations in cellular function in stage III lead to increased capillary permeability and therefore bacterial translocation . Subsequently, efficient hepatic detoxification is impaired and toxins release into the systemic blood circulation. Consequently, progressive multiorgan failure develops . It should be noted that bowel ischemia accompanied by reperfusion injury may lead to the disruption of mucosal barrier followed by bacterial invasion, septic shock and multiorgan failure, which may cause death without transmural necrosis . This phase is clinically presented with fever, bloody diarrhea and shock. The permanent end-stage bowel damage in this stage accounts for the highest mortality rate and unfavorable prognosis. Therefore, surgical intervention is mandatory . Schematic illustration of pathologic stages in ABI is shown in Fig. 5.
CT scan protocol
CT images are acquired in supine position from diaphragmatic dome to pubic symphysis covering the entire length of gastrointestinal tract. The protocol consists of unenhanced, arterial and portal venous phases for optimal visualization of hemorrhage, splanchnic vessels and bowel wall. Using unenhanced CT alone is inadequate and results in a delayed diagnosis as well as increased mortality . Following the injection of 2 ml/kg bolus of 350 mg iodine/ml contrast material at the speed of 3–5 ml/s, the scans are obtained in arterial (30 s delay) and portal (65 s delay) phases. For multidetector CT scanners, collimation of 0.5–2.5 mm, detector pitch of 0.9–1.5 and slice thickness of 2.5 mm are used . However, construction of thinner contiguous slices is recommended for multiplanar reformation and CT angiography.
Pre-contrast imaging is necessary as some important features of ischemia, like vascular wall calcification, hyperattenuating thrombosis and intramural hemorrhage, might be overlooked in post contrast images (Fig. 6). Oral contrast usage is not routinely recommended for patients suspicious for ABI because of potential delay and obscuration of intraluminal hemorrhage. Furthermore, adynamic ileus secondary to ABI prevents appropriate passage of oral contrast to distal bowel . Biphasic CT scan has also been shown to be adequate for diagnosis of ABI with high sensitivity and specificity [33,34,35,36,37,38].
Early imaging diagnosis of ABI is often challenging since each individual CT finding is non-specific when observed separately. These include altered bowel wall thickness, attenuation or enhancement along with increased luminal diameter, mesenteric fat engorgement and mesenteric fluid . The late findings suggestive of bowel necrosis include pneumatosis intestinalis, portal venous gas and pneumoperitoneum . CT scan findings have been shown to correlate with pathologic staging and can help to predict the chance of reversibility . Table 1 summarizes radiologic findings of ABI based on etiology and stage.
Early stage: Bowel wall may be unchanged or thickened at stage I. Edema in submucosa and muscularis propria results in hypoattenuated thickened bowel wall, which is the most common imaging feature with a sensitivity of 38–86% and a specificity of 38–72% [41, 42]. Increased vascular permeability at this stage leads to contrast extravasation and mucosal hyperenhancement, especially in portal venous phase . This mural stratification secondary to the enhancing mucosal and serosal layers with a hypoattenuating layer in between leads to the characteristic “Target” or “Halo” appearance . On the other hand, disruption of arterial blood flow can cause mural hypoenhancement, known as “Pale ischemia,” which has a sensitivity of 62% and a specificity of 96% [39, 40]. Because there is no nerve injury at this stage, bowel lumen maintains normal diameter. Another common appearance is the hyperattenuating wall or “White” pattern. This could be due to intramural hemorrhage at pre-contrast images or increased mural enhancement during reperfusion on post-contrast scans . Reduction of both arterial inflow and venous outflow also results in congestion and prolonged wall enhancement, “shock bowel” . Differentiating a normal enhancing wall from a hyperattenuating wall caused by intramural hemorrhage is impossible without the pre-contrast images. Increased wall thickness, mesenteric fat stranding and ascites are other CT scan findings that are evident in reperfusion injuries, with a high sensitivity but low specificity [41, 45].
Intermediate stage Deeper extension of ischemia in stage 2 leads to paralytic ileus and luminal dilatation induced by nervous plexus involvement . This finding has a sensitivity of 39–67% but is relatively non-specific, with a specificity ranging from 29 to 81% [34, 35, 41, 45]. Absence or minimal enhancement in the thickened bowel wall causes the “Grey” pattern at this stage; however, this pattern could also be seen with normal or even thin bowel wall segment [39, 40, 47]. The “Grey pattern” feature has a sensitivity of 40% and a specificity of 88% .The late sequel of this stage could be fibrotic stricturing following reparative changes .
Late stage In the late stage of arterial occlusion, transmural destruction of nerves and muscular layer leads to dilated, fluid or gas filled loops with extremely thinned wall, creating “Paper thin wall” appearance . Transmural necrosis also causes fluid translocation from intraluminal space to the mesenteric folds, causing mesenteric fat stranding and interloop free fluid as consequences. An additional well-recognized feature for this stage is the “Gas” pattern. This pattern is created as a rim of air bubbles or multiple small separated gas bubbles with circumferential distribution dissect wall layers . Transmural infarct and perforation can lead to translocation of intraluminal gas to the peritoneal cavity (pneumoperitoneum). Overview of enhancement patterns in each stage is shown in Fig. 7. It should be noted that different patterns of enhancement may occur simultaneously in a single patient (Fig. 8).
Arterial etiologies are the most prevalent causes of ABI, accounting for 60–70% cases . Arterial embolus and thrombosis are the most important subtypes.
Mesenteric arterial emboli (MAE) account for approximately half of all ABI cases . Arterial emboli typically originate from the heart, mainly caused by atrial fibrillation, structural abnormality or ischemic heart disease . SMA is more frequently affected than CA and IMA due to the larger diameter and sharper branching angle (~ 45º) . Considerable narrowing of the SMA immediately after the branching of the middle colic artery creates a vulnerable location for lodging embolus that leads to isolated ischemia of jejunum, ileum and proximal colon with the duodenum and transverse colon usually being spared . The lodgment is also depending on the size of the embolus, with larger emboli tending to occlude proximal mesenteric arteries, resulting in greater extent of ischemia and poorer prognosis . On the contrary, smaller emboli are usually trapped in distal branches causing a limited intestinal involvement with better prognosis . Emboli may also cause end-organ infarctions including lower extremities, spleen, kidneys and brain  (Fig. 9).
Mesenteric arterial thrombosis (MAT) is responsible for 20–35% of ABI cases . Patients generally have long-standing atheroma, or previous stenosis, and have a more indolent course of clinical symptoms . On the unenhanced phase, notable mural calcification of mesenteric arterial branches is usually evident, especially near the ostium and proximal parts of the vessel  (Fig. 10). Atherosclerotic changes are typically apparent in other organs including cerebral, renal, coronary and peripheral arteries . The process of ischemia starts when the gradual narrowing reaches a critical level. Then, location and severity of obstruction and development of collaterals determine evolution to bowel necrosis.
CT scan findings for both arterial embolus and thrombosis have great similarities. Low-attenuation filling defect on CT angiography or high attenuation intravascular substance on an unenhanced CT scan is a direct sign for arterial embolus or thrombosis, which can lead to “pale ischemia” and cause “paper-thin” bowel wall . The signs of atherosclerotic changes in the affected artery help differentiate these two entities.
Although arterial bowel ischemia has a much higher incidence in the elderly men over 70 years old , in younger individuals, thrombotic microangiopathies, antiphospholipid antibody syndrome, dissection and vasculitides may contribute to this type of ABI  (Figs. 11, 12). In such cases, unusual sites of the gastrointestinal tract including stomach, duodenum and rectum might be involved.
Mesenteric venous thrombosis (MVT) accounts for 5–15% of ABI cases with the youngest peak age of onset and significantly better prognosis when compared to the arterial category (41.7% vs. 73.9% mortality rate) . Although it can be primary on some occasions, the secondary type caused by underlying conditions and hypercoagulability state is much far more common, accounting for 80% of ABI cases [28, 60]. It is typically seen in young females taking hormonal contraceptives . Thrombosis often affects SMV and appears as a filling defect in the portal phase of contrast enhanced CT scan. Sometimes thrombosis could also be depicted as hyper attenuating material in the lumen of mesenteric vein. Combination of vascular findings and bowel wall abnormalities in CT scan resulted in a sensitivity of 96% and a specificity of 90–94% for diagnosis of mesenteric venous ischemia by CT scan [62,63,64].
In the early stage, the bowel wall is frequently thickened . This finding is more prominent than cases of isolated mesenteric arterial occlusion and is the result of reduced venous outflow and maintained high-pressure arterial inflow, which leads to high hydrostatic pressure and intramural edema . “Target” appearance is more common compared to arterial ABI [28, 43]. Wall thickening also can fall out as a result of intramural hemorrhage or superimposed infection may also contribute to the wall thickening in MVT. In veno-occlusive ABI, exudative fluid also accumulates in the intraluminal space of ischemic bowel and results in “completely fluid filled, gasless, dilated loop” . This rarely occurs in arterial form, thus helps in differentiating these entities. Extraluminal seepage of fluid causes mesenteric haziness and ascites . It should be noticed that the degree of wall thickening and ascites is not always proportional to the intensity of bowel wall damage  (Fig. 13). Eventually, with persistence of venous outflow occlusion, arterial inflow diminishes leading to decreased or absent wall enhancement showing “Gray” pattern on CT . The findings of the intermediate and late stages are similar to arterial cases (Figs. 14, 15).
Salim et al. demonstrated that small bowel wall edema was the independent risk factor associated with bowel resection in a prospective study on 102 patients with mesenteric venous thrombosis . In a study by Vietti Violi et al. on follow-up of 20 patients with acute mesenteric venous thrombosis, most cases (80%) evolved toward the chronic form with vein stenosis or occlusion and development of collateral veins. It has been reported that patients with short, isolated central mesenteric venous thrombosis in a larger vein might present higher probability of complete radiologic recovery . Higher rate of recanalization in patients with portal or mesenteric vein thrombosis was also observed by Condat et al. compared to patients with more extensive and distal thrombosis .
Non-occlusive mesenteric ischemia (NOMI) is responsible for almost 20% of ABI cases  and is caused by nonocclusive reduction of arterial blood flow. Hemodynamic instability followed by mesenteric arterial vasoconstriction is the main cause , usually seen as a part of systemic hypotensive state associated with impaired sympathetic response in elderly or critically ill patients with concomitant multiorgan damage . CT scan findings have significant overlap with other ABI entities or bowel disorders including infectious and inflammatory diseases of bowel, making the diagnosis even more challenging . The difficulty of early assessment, advanced age, comorbidities and generalized poor physical state are the reasons for the less than 50% survival rate in this subtype .
Generalized vasospasm may be obvious as narrowing of IVC, aorta and mesenteric vessels resulting in decreased enhancement of affected bowel segments and occasionally other organs (liver, spleen and pancreas) . Bowel wall thickness ranges from unchanged in earliest stages to markedly thinned in an advanced stage [40, 74]. Radiologic and pathologic findings indicating ischemic staging are the same as other entities (Figs. 16, 17). Four radiological signs had been suggested by Siegelman et al. in 1974 for description of mesenteric vasospasm based on conventional angiography : (1) narrowing in the origins of multiple branches of the SMA, (2) irregularities in intestinal branches as alternate dilatation and narrowing, “the string of sausages sign” , (3) spasm of the mesenteric arcades, (4) impaired filling of intramural vessels. Another suggested sign of NOMI has been contrast reflux into the abdominal aorta at angiography . Nakamura et al. reported that diameters of SMA and SMV have been significantly smaller in 11 NOMI cases than 44 controls on CT scan and SMV diameter was a more significant parameter than SMA diameter. Whether these results could be considered as diagnostic criteria remain to be investigated because the so-called smaller SMV sign has also been reported in other etiologies like acute SMA occlusion .
During the hypoperfusion state, colon is more vulnerable to ischemia than the small intestine . The anatomic and physiologic characteristics of the mesenteric circulation contribute to particular vulnerability of right colon in classical NOMI. Compared to the left colon, the right colon frequently lacks a well-developed and consistent marginal collateral network. The vasa recta of right colon are usually longer and originating further away from the bowel. Dominant involvement of right colon in NOMI could also be explained by the possibility of "mesenteric steal" from more proximal branches of SMA circulation when perfusion is compromised [79, 80]. Progression of damages occurs in almost a similar manner to small bowel ischemia from mucosa to serosa .
Mixed (strangulation) and other miscellaneous causes
Strangulated bowel is usually emanating from closed-loop obstruction and is responsible for 10% of ABI cases . It is described as a twisted C or U-shaped segment of small intestine with both proximal and distal parts obstructed and blood flow compromised, in which the affected segment is dilated, thin walled and fluid filled . Adhesion, hernia and volvulus can also be associated with closed-loop obstruction (Fig. 18, 19) . At earlier stages, arterial input is preserved due to its higher pressure but with taking time both arterial inflow and venous drainage usually get diminished . Signs and staging of ischemia in strangulated bowel are the same as other entities. Some specific features of closed-loop obstruction include radial distribution of intestinal loops and the “beak” sign or triangular loops, caused by fusiform tapering of fluid-filled bowel loops [39, 82]. The closed-loop mechanism in combination with reduced bowel wall enhancement and diffuse mesenteric haziness has been shown to predict strangulation accurately in adhesive small bowel obstruction . Higher risk of ischemia is seen in matted or multiple adhesive bands than single adhesive bands. Zinc et al. have suggested that the beak sign and fat notch sign are associated with the presence of a single adhesive band which can help to personalize patient’s treatment, for example by choosing the laparoscopic approach when non-operative treatment fails . The positive predictive values for a single adhesive band were 92% and 100% for the beak sign and the fat notch sign, respectively  (Figs. 20, 21).
Mixed arterial and venous ischemia are also infrequently seen in association with other conditions including trauma, chemotherapy, irradiation, drug induced, corrosive injury, lead poisoning, iatrogenic, etc.  (Figs. 22, 23, 24, 25, 26, 27, 28).
The main goal of management is to achieve a prompt diagnosis, specify the best treatment option and reduce mortality in these patients. ABI is a cardiovascular emergency which entails strict management rules identical to those created for acute myocardial or cerebrovascular ischemia . With immediate management, mortality rate is less than 10%, but this figure increases to 50–60% with moderate delay (6–12 h) and reaches 80–100% with a delay more than 24 h . These results clearly emphasize the close correlation between evolution of necrosis and increasing mortality. Therefore, restoration of the blood flow to the ischemic parts or revascularization is the fundamental principle for surgical and endovascular treatments in all stages. It is worth noting that the morphology of an ischemic bowel can be deceiving and even a severely ischemic bowel can be viable after revascularization . Nevertheless, surgical resection of the necrotic segments is usually inevitable in irreversible stage .
The management of ABI is summarized as “3Rs,” Resuscitation, Rapid diagnosis and Revascularization . Invasive hemodynamic monitoring, supportive care, serial assessment of electrolyte level and acid–base status and follow-up imaging are the best approaches in stage I and stage II in which there is no sign of necrosis [3, 6]. Patients should be kept “nil by mouth” which can protect them against ischemic exacerbation and reduce probability of emergency surgery. Systemic anticoagulation therapy with continuous infusion of unfractionated or low molecular weight heparin should be administered as part of early medical therapy especially in cases of veno-occlusive disease, unless there is a contraindication [51, 92]. Broad spectrum antibiotics are also part of initial therapy, especially in critically ill patients . In patients with NOMI, correction of precipitating cause in addition to administration of vasodilators is fundamental . Surgery is established as the best approach in patients with late stage bowel ischemia as revascularization, assessment of organs’ viability and resecting necrotic segments are achievable with surgery .
It is noteworthy that reversibility–irreversibility of the bowel spans a temporal continuum with areas of overlap (Fig. 29). In the co-occurrence of stages, management should be based on the latest stage identified. Nuzzo et al. in a prospective cohort of 67 patients with ABI identified three predictive factors of irreversible ischemic injury requiring resection as: (a) organ failure, (b) serum lactate levels > 2 mmol/l and (c) bowel dilation > 2.5 cm at the time of diagnosis. Having 1, 2 and 3 of these factors increased rate of irreversible necrosis to 38, 89 and 100%, respectively. They have suggested that these predictive factors could be useful in emergency setting to decide whether a surgical treatment is mandatory . According to the radiologic, clinical and laboratory findings, a proposed algorithm for management of ABI regardless of etiology is shown in Fig. 30 to determine whether the patient may benefit from surgery. Needless to say, that the goal of surgery is re-establishment of blood supply, resection of non-viable bowel and preservation of viable bowel. According to this algorithm, patients in early stage should be monitored or reimaged, while intermediate stage depends on the clinical and laboratory factors to decide whether the patient needs to be monitored or referred to surgical or vascular intervention. The late stage necessitates rapid laparotomy and/or revascularization.
Some non-ischemic conditions may have overlapping imaging features. Most notably, pneumatosis intestinalis may be found in any mechanical mucosal injury, increased mucosal permeability, infections, corticosteroid usage, organ transplantation, inflammation, certain pulmonary conditions with alveolar rupture and pneumatosis cystoides coli [96, 97]. Differentiation of this benign type of pneumatosis from its ominous counterpart as a sign of bowel necrosis might be challenging (Figs. 31, 32).
Bowel wall ischemia is sub-classified into three pathologic stages depending on the degree of mural involvement (mucosal, submucosal and trans-mural). There are imaging clues that indicate the severity of bowel wall involvement and suggest the pathologic stage. Bowel ischemia may be classified by etiology into the following categories: arterial, venous, non-occlusive mesenteric ischemia (NOMI), mixed arterial/venous and miscellaneous (rare). Imaging provides valuable information regarding the inciting cause. Both the reversibility and imaging stages of ischemia have considerable overlap; however, the management should be based on the latest stage identified. The imaging findings should be interpreted in the context of the clinical picture (serum lactate level, peritoneal signs, multiorgan failure, etc.) and management decisions should ultimately be guided clinically. Decision regarding whether the patient needs surgery or not is the most important question from clinician, which is usually unrelated to the etiology of the ABI since any cause of bowel ischemia may eventually results in a single outcome that is bowel necrosis. Therefore, focusing on the predictive factors of bowel necrosis rather than etiology can better help on the management of ABI cases.
Availability of data and materials
Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
Acute bowel ischemia
Inferior mesenteric artery
Inferior mesenteric vein
Mesenteric arterial emboli
Mesenteric arterial thrombosis
Multidetector computed tomography
Mesenteric venous thrombosis
Non-occlusive mesenteric ischemia
Superior mesenteric artery
Superior mesenteric vein
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Davarpanah, A.H., Ghamari Khameneh, A., Khosravi, B. et al. Many faces of acute bowel ischemia: overview of radiologic staging. Insights Imaging 12, 56 (2021). https://doi.org/10.1186/s13244-021-00985-9
- Acute bowel ischemia
- Radiologic staging
- Pathologic correlation