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Review

Colonic Ischemia Following Major Vascular Surgery: A Literature Review on Pathogenesis, Diagnosis, and Preventive Strategies

1
Vascular and Endovascular Surgery Unit, Sant’Andrea Hospital of Rome, Department of Molecular and Clinical Medicine, “Sapienza” University of Rome, 00185 Rome, Italy
2
Vascular and Endovascular Surgery Unit, Sant’Andrea Hospital of Rome, Department of General and Specialistic Surgery, “Sapienza” University of Rome, 00185 Rome, Italy
*
Author to whom correspondence should be addressed.
Appl. Sci. 2025, 15(15), 8482; https://doi.org/10.3390/app15158482
Submission received: 23 June 2025 / Revised: 24 July 2025 / Accepted: 28 July 2025 / Published: 30 July 2025

Abstract

Colonic ischemia (CI) is a serious and potentially fatal complication after major abdominal vascular surgery. This literature review explores the pathogenesis, risk factors, diagnostic methods, and preventive strategies associated with CI, emphasizing the differences between emergency and elective treatments. Early diagnosis through clinical signs and instrumental diagnostics, such as sigmoidoscopy and computed tomography, is crucial. Preventive measures, including preoperative evaluation and perioperative management, are emphasized to reduce the incidence of CI. The results of different studies suggest that endovascular aneurysm repair (EVAR), both emergency and elective, has lower risks of ischemic complications than open surgical repair (OSR), as well as better survival for patients. Further research and standardized clinical guidelines are needed to improve patient outcomes and minimize CI severity.

1. Introduction

Colonic ischemia (CI) following major abdominal vascular surgery is one of the rarest but most lethal and often unrecognized complications. This condition arises from a temporary or permanent reduction in blood flow to the colon, resulting in tissue hypoperfusion and subsequent necrosis of the intestinal wall. The incidence of ischemic colitis remains significant in patients undergoing isolated aortic surgery or associated with peripheral revascularization for Peripheral Chronic Obliterative Arteriopathy, also known as Peripheral Artery Disease, and its pathogenesis is multifactorial [1]. The onset of CI is associated with longer hospital stays, increased complexity of care, and reduced long-term survival after aortic surgery [2]. The mortality rate is high, and so the early identification of this condition is crucial. It can be achieved by recognizing signs and symptoms and using appropriate instrumental diagnostics.
The incidence of colonic ischemia (CI) following major aortic surgery has remained relatively stable over the years, yet it continues to be a matter of debate, due to the heterogeneity in sample sizes and patient characteristics among different studies. The most notable recent finding is the significantly lower incidence of CI following endovascular aortic repair (EVAR) compared to open surgical repair (OSR). Conversely, Behrendt et al. reported an incidence of approximately 0.6% after EVAR, versus 3.7% following OSR (p < 0.001), due to the absence of aortic cross-clamping and reduced intraoperative blood loss, minimizing the likelihood of hypoperfusion and subsequent ischemia–reperfusion damage [3].
Moreover, the majority of the current literature focuses exclusively on either elective or urgent settings. This narrative review aims to synthesize the current body of evidence regarding this complication, including both urgent and elective settings, and focus on the understanding of risk factors, strategies for early diagnosis, and the development of tailored therapeutic approaches to optimize management.
The prognosis for these patients can be improved by optimizing risk factors, implementing perioperative and intraoperative strategies, and ensuring early diagnosis, with a consequent reduction in mortality rate.
A comprehensive literature search was conducted using PubMed to identify studies reporting on colonic ischemia (CI) in the context of major aortic surgery. The search included articles published from 2000 to 2025 and used the following MeSH search terms: “[colonic ischemia]”; “[bowel ischemia]”, “[vascular surgery procedure]”, “[rupted abdominal arotic aneurysm]”, “[abdominal surgery]”, and “[postoperative complications]”.
Only studies published in English were considered. Additional relevant articles published prior to this timeframe were included when identified through the reference lists of selected papers, based on their relevance to the topic.
Studies were screened based on their titles and abstracts, and full texts were reviewed for inclusion based on relevance to colon ischemia as a postoperative complication of elective or urgent aortic surgery, including both endovascular aortic repair (EVAR) and open surgical repair (OSR).

2. Anatomy and Pathophysiology

The splanchnic vascularization is provided by the following:
  • Celiac Trunk (CT): The first branch of the abdominal aorta and distributes blood to the upper abdominal organs, dividing into three branches: the left gastric artery supplies the proximal part of the stomach’s lesser curve and the distal part of the esophagus, the splenic artery supplies the proximal and middle parts of the stomach’s greater curve, stomach fundus, pancreas, and spleen, and the common hepatic artery supplies the liver, stomach pylorus, gallbladder, proximal part of the duodenum, pancreatic head, and distal parts of the stomach’s curves.
  • Superior Mesenteric Artery (SMA): Arises from the abdominal aorta and supplies the midgut. It provides blood to the distal portion of the duodenum, jejunum, ileum, cecum, ascending colon, and the proximal two-thirds of the transverse colon.
  • Inferior Mesenteric Artery (IMA): Arises from the abdominal aorta and supplies the hindgut. It vascularizes the distal one-third of the transverse colon, descending colon, sigmoid colon, and the upper part of the rectum.
  • Hypogastric Arteries (HAs): Also known as the internal iliac arteries, provide blood to the pelvic organs, gluteal region, and perineum, supplying the bladder, the reproductive organs, the rectum, and the medial compartment of the thigh.
All these arteries are interconnected through anastomotic arches:
  • The arch of Bühler: Results from the anastomosis between the superior (CT) and inferior (SMA) pancreaticoduodenal arteries.
  • The marginal arch of Drummond: Runs along the mesenteric insertion of the transverse and left colon and is composed of the middle colic artery (SMA) and the left colic artery (IMA).
  • The arch of Riolan: A collateral circle connecting the left colic artery (IMA) and the ascending branch of middle or right colic artery (SMA).
In the general population, there is great anatomical variability, and these anastomotic circles may not be fully developed. Approximately, in 5% of cases some of these anastomoses may be lacking, leading to a higher risk of CI [4].
This collateral arterial network performs a crucial compensatory role when one or two visceral vessels are occluded or significantly stenotic, helping to maintain visceral perfusion and prevent gastrointestinal ischemia. The presence of multiple arterial collateral circulations often limits the extension and severity of ischemic clinical manifestations. Conversely, the interruption of the IMA is generally well tolerated in both open and endovascular repair due to the extensive collateral network between the SMA and hypogastric arteries, provided these vessels are patent and free of significant disease.
Blood circulation in intermesenteric circulation can be bidirectional. In cases of ostial occlusion of the SMA, the arches of Drummond and Riolan are perfused in a caudo-cranial direction. Otherwise, in cases of infrarenal aorto-iliac occlusion, the blood flow goes in a cranio-caudal direction through the IMA, moving retrogradely through the colic arches (Drummond and Riolan) to revascularize the SMA via the middle colic artery. In some cases of aorto-iliac occlusion, mesenteric circulation contributes to the perfusion of the lower limbs through collateral vessels between the SMA, the IMA, and, through hemorrhoidal circulation, the hypogastric arteries, ultimately reconstituting collateral circulation at the femoral level.
However, there are some vulnerable points in this network particularly prone to the development of CI: Griffith’s point, located at the left colic flexure between the ascending left colic artery and the marginal artery of Drummond; Suddeck’s point, located at the origin of the last sigmoid artery in the region of the sigmoid colon [5]; and Reiner’s critical segment, a segment of the SMA between the region above the origin of the second intestinal artery and the middle colic artery and the region below the origin of the ileocolic artery (Figure 1).
In addition to anatomical variability, several comorbidities must be considered for their increased risk of CI following aortic aneurysm repair. These include previous thromboembolic events, heart failure with reduced left ventricular function, generalized atherosclerosis, sepsis, thrombophilia, renal failure, elderly age, and female sex [6].
Several studies have identified female sex as an independent predictor of postoperative intestinal ischemia compared to male sex. Previous literature reported that female patients have a 1.6-fold increased risk of developing intestinal ischemia following abdominal aortic aneurysm (AAA) repair (OR: 1.6, CI: 1.1–2.2). This may be attributed to the smaller caliber of arterial vessels and the increased fragility of the arterial wall typically observed in females. Additionally, proximal extension of the aneurysm increases the risk of colonic ischemia due to the potential involvement of visceral arteries and the need for suprarenal clamping, which may impair mesenteric perfusion and collateral flow. Additional factors such as prolonged surgery, higher blood loss, and vasopressor use further exacerbate splanchnic hypoperfusion [6,7,8]. More details are shown in Table 1.
Certain drugs have been found to promote the onset of CI, such as catecholamines, antibiotics, chemotherapy, diuretics, and immunosuppressive therapies [9].
To improve the understanding of incidence, additional risk factors, and preventive measures, it is necessary to distinguish postoperative CI following elective procedures from CI that occurred after emergency surgery for a ruptured abdominal aortic aneurysm (rAAA).

3. Colonic Ischemia After rAAA Repair

In case of an rAAA, postoperative complications tend to be numerous and more frequent compared to elective treatments, whether through open surgical repair (OSR) or endovascular aneurysm repair (EVAR). These complications include pulmonary disorders, cardiac events, renal failure, lower-extremity ischemia, wound complications, and colonic ischemia. The incidence of these complications is higher after OSR than emergency EVAR [10].
Specifically, CI following an rAAA is strongly associated with perioperative hypotension, hypovolemic shock, the use of high-dose catecholamines, possible reperfusion injury, and embolic events [11,12,13]. Omran et al. reported that a norepinephrine dosage > 64 µg/kg (RD 0.40, 95% CI: 0.25–0.55, p < 0.001) is a significant predictor of CI after an rAAA. Furthermore, ischemic colonic lesions were more frequently observed in patients with preoperative shock compared to those who were hemodynamically stable (20.7% vs. 4.2%, p < 0.05) [14]. Additionally, previous authors demonstrated that CI following EVAR is often attributed to systemic embolic events leading to bowel ischemia [15].
After the rupture of an AAA, a retroperitoneal hematoma may develop, and its severity is time-dependent. A retroperitoneal hematoma represents an abdominal space-occupying lesion, and the larger it is the greater the increase in intra-abdominal pressure, leading to the development of abdominal compartment syndrome. Moreover, the retroperitoneal hematoma contributes to the worsening of hypovolemia and hemorrhagic shock because of ongoing bleeding, coagulopathy, and the sequestration of liquids in the third space, necessitating resuscitation maneuvers with fluid therapy and transfusion of blood as well as blood components to stabilize the hemodynamic.
However, it is necessary to limit fluid administration to reduce the risk of intestinal edema and ascites, which can further increase intra-abdominal pressure and exacerbate the development of abdominal compartment syndrome. If this syndrome is not promptly recognized and treated, it could lead to multi-organ failure, due to CI caused by visceral hypoperfusion, venous return compression, and intestinal traction [16,17].
In the meta-analysis by Jalzadeh H. et al., 101 studies with a total of 52,670 patients were analyzed, revealing a 10% prevalence of clinically relevant CI. The incidence reported across the studies was 3.9% following EVAR and 10% after OSR, with a relative risk (RR) of 1.8 [12]. Mortality rates in the latter meta-analysis were highly variable, with some studies reporting mortality exceeding 50% in patients with confirmed ischemia.
The higher incidence of intestinal ischemia after OSR compared to EVAR is primarily due to the greater surgical trauma associated with the open technique, including direct aortic manipulation and prolonged clamping, which often compromise blood flow to the intestines. OSR is also linked to higher blood loss, longer operative times, and increased transfusion requirements, all contributing to hemodynamic instability and splanchnic hypoperfusion. Furthermore, the manipulation of the aorta can lead to microembolization, which may cause ischemia in the mesenteric branches. In contrast, patients undergoing EVAR typically have more stable clinical conditions and a favorable anatomy, while those requiring OSR are often more critical or have a complex anatomy, introducing a selection bias. Moreover, such a metanalysis, despite the methodological strength and large sample size, presents some limitations due to the heterogeneity between studies, including differences in patient characteristics, ischemia definitions, surgical techniques, and perioperative management. Additionally, the lack of a standardized definition of intestinal ischemia leads to the potential underestimation or overestimation of incidence. Lastly, some older studies included in the meta-analysis reflect outdated surgical practices and protocols; therefore, these results need to be taken with caution, and further studies are needed to evaluate them [14,15,16,17]. A previous study by M.M. Thompson et al. and a recent systematic review by Tsilimigras DI et al. have demonstrated a lower inflammatory response and less ischemia–reperfusion injury after EVAR compared to OSR, which may contribute to a reduction in microembolization, leading to CI [18,19].
Additionally, in the meta-analysis by Jalalzadeh H. et al., the reintervention rate was approximately half the CI prevalence, and patients who developed bowel ischemia (BI) after ruptured AAA repair had significantly higher morbidity and mortality, even in the absence of reintervention [12].
This divergence can be attributed to the high variability in the diagnostic methods and criteria across different studies, which are not standardized. Recent studies often identify many cases of non-clinically relevant CI. On the other hand, some studies present selection bias by reporting only those cases of CI that necessitate reintervention, with a consequent failure in reporting the overall prevalence of CI. This makes it difficult to draw a unanimous conclusion from the literature.
Regarding diagnostic criteria, several studies have demonstrated the high sensitivity of sigmoidoscopy in detecting CI following rAAA surgery [19,20,21,22] (Figure 2).
This heightened sensitivity has led to an increased incidence rate of CI, between 14% and 32%, without a corresponding increase in resection rates due to the conservative management of many mild or moderate ischemia cases.
The study by Jalalzadeh et al. demonstrated a negative predictive value (NPV) of endoscopically normal colonic mucosa, suggesting that the absence of endoscopic lesions allows for the clinically safe exclusion of transmural ischemia. In contrast, the presence of moderate to severe endoscopic abnormalities was associated with a positive predictive value (PPV) of 73%, indicating a high likelihood of transmural damage requiring surgical intervention [23]. However, recent studies have demonstrated that the specificity of sigmoidoscopy in identifying transmural ischemia that necessitates surgical resection is lower [23,24]. For this reason, recent European guidelines recommend considering sigmoidoscopy in case of high clinical suspicion of CI and not routinely after rAAA repair [25]. Additionally, some authors suggest the early consideration of exploratory laparotomy to optimize diagnosis and overall patient management [26,27].
Preventive Strategies: The following several measures are required to prevent CI after rAAA repair:
  • Preparatory Assessment: Careful analysis of the risk factors mentioned allows patients at increased risk to be identified before surgery. Accurate valuation of SMA and CT patency to consider endovascular or open revascularization in the case of stenosis or occlusion.
  • Hemodynamic Stability: Maintaining stable blood pressure and adequate perfusion during and after surgery reduces ischemic suffering due to severe hypotension.
  • Surgical Technique: in patients at increased risk, opting for EVAR over OSR may reduce the incidence of CI. EVAR is associated with less surgical trauma, absence of aortic cross-clamping and a reduced inflammatory response.
  • Intra-Abdominal Pressure Management: Early recognition and management of increased intra-abdominal pressure are essential to prevent multi-organ failure and CI.

4. Colonic Ischemia After Elective AAA Repair

CI after elective AAA repair is a rare but significant complication, with a reported incidence of 1–3% in OSR and 0.5–3% in EVAR [28,29]. Becquemin et al. found no significant differences between the two surgical approaches [30,31]. On the other hand, Moore et al. and Mehta et al. observed variations in bowel ischemia rates between OSR and EVAR, with rates of 2% and 0.6% in EVAR-treated patients, respectively, compared to 2.6% and 2% in those undergoing open repair [32,33]. However, these differences did not reach statistical significance due to small sample sizes.
The most recent study by Perry et al. analyzed a larger cohort and confirmed previous findings, reporting a similar risk of CI after EVAR at 0.5%, compared to 1.9% after OSR. This larger sample size reduced uncertainties associated with smaller series and identified the open surgical technique as an independent risk factor, with a 2.7-fold increased risk of ischemia compared to EVAR [34].
Regarding fenestrated endovascular aneurysm repair (FEVAR), ischemic complications involving the intestinal tract, though relatively uncommon, occur more frequently than with standard EVAR, as demonstrated by previous studies. This complication is mainly attributed to splanchnic hypoperfusion, rather than embolic events or direct vessel injury, which are rare occurrences [35]. Effective management may include endovascular interventions or revascularization of the SMA, either via retrograde extra-anatomic bypass (e.g., from the common iliac artery to the SMA) or antegrade aorto-mesenteric bypass, particularly when the affected aortic segment lies outside the stent graft landing zone. The current literature lacks sufficient data on the incidence and risk factors of CI following FEVAR in an urgent setting. Further studies are needed to better characterize this complication in such a clinical setting.
Despite the relatively low incidence, preventing this complication is essential due to its association with perioperative mortality, estimated to be approximately 50% even in elective treatment settings [36].
Careful preoperative assessment of splanchnic circulation is crucial to prevent colonic ischemia, particularly the evolution of SMA patency and the presence of a positive history for previous colonic surgery, which could compromise collateral blood flow. Regarding this topic, several studies in the literature have evaluated the consequences of intentional hypogastric artery interruption in both open and endovascular procedures. Earlier research, such as that by Wolpert et al. and Mehta et al., found no significant differences in outcomes for patients who had at least one hypogastric artery sacrificed [37,38]. However, more recent studies have identified hypogastric occlusion as an independent risk factor for ischemic complications, including intestinal ischemia [38,39,40,41].
In the study by Ultee et al., interruption of the hypogastric artery, whether by ligation or occlusion during open repair, or by embolization during EVAR, was significantly associated with an increased risk of postoperative intestinal ischemia (OR: 1.7, 95% CI: 1.0–2.8). Patients with bilateral occlusion exhibited an even higher risk [8].
A more recent analysis by Zhang J. et al. demonstrated significantly higher perioperative mortality in patients with compromised pelvic perfusion (5.5% vs. 3.1%; p < 0.001). Bilateral interruption of blood flow was associated with greater perioperative mortality compared to unilateral interruption (7.1% vs. 4.7%; p = 0.147) [42]. Therefore, maintaining hypogastric perfusion in patients at a higher risk of intestinal ischemia has a pivotal role. In cases of endovascular treatment, it could be achieved by using an iliac branch endograft that aims to preserve its vascularization, although it increases the complexity and the duration of the procedure [43].
In the case of open surgery, the necessity of surgical anastomosis on the common femoral artery due to the presence of an aneurysmal or occlusive disease of the common and/or external iliac arteries is considered another independent predictor of bowel ischemia, because it could limit the retrograde reperfusion of the hypogastric artery. These patients, who need a femoral anastomosis in the case of aortic surgery, typically present more advanced degrees of atherosclerosis of mesenteric vessels and a higher risk of (micro)embolization of atherothrombotic debris [41,44].
Particular attention is given to the management of the IMA. Ligation of the IMA is generally considered acceptable in the presence of adequate collateral circulation, if there is no critical obstructive disease in other splanchnic arteries and at least one HA remains patent. Therefore, surgical reimplantation of the IMA is not a standard practice and is reserved for patients at higher risk of postoperative intestinal ischemia [45,46].
Recent studies, such as those by Lee et al. and Jayaraj et al., have not demonstrated the significant supremacy of IMA preservation over ligation, with a lower incidence of intestinal ischemic complications observed only in selected patients [47,48].
Therefore, the accurate preoperative assessment of pelvic and bowel perfusion is essential in aortic surgery to minimize complications such as bowel or spinal ischemia, gluteal claudication, and impotence, and to improve postoperative outcomes.
Preventive Strategies: The following maneuvers can help prevent CI after elective AAA repair:
  • Accurate Preoperative Assessment of Splanchnic Circulation: Patency of the SMA, any previous colon surgery, and integrity of the HA.
  • Preservation of HAs: During surgical procedures, both open and endovascular, especially in patients at high risk of intestinal ischemia.
  • Management of IMA: Ligation of the IMA is generally acceptable in the case of the absence of critical obstructive disease in other splanchnic arteries and if the patency of at least one HA is maintained. Surgical reimplantation of the IMA is not a standard practice and is reserved for patients with a higher risk of postoperative CI.

5. Clinical Presentation and Instrumental Diagnosis

CI may manifest with different signs and symptoms depending on the severity of the ischemia. Often, the symptomatology may initially be non-specific and misdiagnosed. The most common clinical presentation includes abdominal pain and diarrhea with rectal hemorrhage, associated with worsening of the general clinical condition, often resulting in an initial increase of infection markers [49].
In most cases, the onset of this complication occurs within the first postoperative week [18]. In case of an rAAA, the diagnosis is even more complex due to the critical general condition of the patient, as a result of the possible onset of respiratory failure, cardiovascular instability, renal failure, and increased catecholamine requirements, irrespective of CI [25].
Morphologically, CI may involve only the mucosa with the possibility of complete healing, or the mucosa and the musculature leading to fibrosis, or it may be transmural, resulting in intestinal gangrene and subsequent perforation. The gangrenous form more often occurs after aortic surgery, whereas the non-gangrenous form occurs in 80% of cases of idiopathic ischemic colitis.
There are no specific laboratory tests for a certain diagnosis of CI. Increased infection markers and lactate levels are the most indicative parameters of possible CI, but normal values in the presence of specific symptoms do not exclude a diagnosis for CI [50].
Research into biomarkers for intestinal ischemia has identified several promising candidates, including intestinal fatty acid-binding protein (I-FABP), glutathione S-transferases (GSTs), and D-lactate. These biomarkers hold potential for the early diagnosis and assessment of intestinal injury, although none is sufficiently accurate to be used as an exclusive diagnostic tool [51].
I-FABP is a small cytoplasmic protein expressed in mature enterocytes located on the villi of the small intestine. In the case of mucosal injury, it is released into the circulation, making it a potential early indicator of intestinal ischemia. In a study by Shi H et al., patients with confirmed ischemia exhibited significantly elevated mean I-FABP levels (149.74 ng/mL) compared to non-ischemic patients (36.78 ng/mL). However, elevated I-FABP levels have also been observed in other gastrointestinal conditions, such as Crohn’s disease and celiac disease, which may affect its specificity [52].
Glutathione S-transferases (GSTs) are enzymes distributed throughout the intestinal tract that are released into the bloodstream following cellular injury, including ischemic damage. Circulating GST levels have been shown to correlate with the severity of histological injury. Although promising in experimental models, further clinical studies are needed to establish GSTs as reliable biomarkers for intestinal ischemia in humans [53].
D-lactate is produced by bacterial fermentation in the gastrointestinal tract and is normally present in the bloodstream at minimal levels. Intestinal ischemia can increase gut permeability, allowing D-lactate to enter the circulation. In the same study by Shi et al. [52], mean D-lactate levels in ischemic patients were significantly higher (52.73 μg/mL) compared to non-ischemic controls (15.58 μg/mL). However, elevated D-lactate levels can also occur in conditions associated with increased intestinal permeability or bacterial overgrowth, which may limit its specificity.
Given the limitations of individual biomarkers, combining multiple markers may improve diagnostic accuracy and offer a more comprehensive evaluation of intestinal integrity, supporting an earlier diagnosis of ischemia [54].
As previously reported, in the case of clinical suspicion (suggestive symptoms and supportive laboratory markers), the gold-standard diagnostic tool is the sigmoidoscopy, which can determine whether the ischemia is transmural or not [21]. In an emergency, examination of the distal portion of the colon is sufficient because ischemia affects the left hemicolon in more than 90% of patients [55].
Computed tomography (CT) imaging can provide indirect and additional clinical information, such as detecting thickening of the colonic wall, the presence of toxic megacolon, and reduced perfusion of the intestinal wall [56], while also excluding other intra-abdominal pathological findings [57] (Figure 3).
Although several intraoperative methods are available to assess intestinal perfusion, none can definitively predict the development of ischemia. Clinical evaluation during open surgery, based on bowel color and peristalsis, is often insufficient, prompting the use of more objective and quantitative techniques [58].
Doppler ultrasound can assess blood flow in mesenteric or marginal arteries, but its sensitivity is limited, with high rates of false negatives and positives. More advanced techniques, such as visible-light spectrophotometry (VLS) and near-infrared spectroscopy (NIRS), as well as measuring tissue oxygen saturation (StO2), can be useful. Lee et al. demonstrated that persistently low mucosal StO2, measured intraoperatively with VLS, may indicate early colonic ischemia [59]. However, a precise StO2 threshold predictive of ischemia has yet to be established, and variability in measurement algorithms and interference from intestinal contents (bile, stool, or food) remain critical challenges [60].
Fluorescence imaging using intravenous fluorescein or indocyanine green (ICG) dye has also been applied to visualize intestinal perfusion. ICG, in particular, allows for repeatable measurements due to rapid hepatic clearance, but requires specific equipment and is influenced by intestinal contents. Limiting thresholds for irreversible ischemia have not been yet standardized [61].
Optical coherence tomography (OCT) has emerged as a high-resolution, non-invasive tool for intraoperative intestinal viability assessment; however, this technique needs to be further validated [62].

6. Treatment

In the event of diagnosed CI, conservative treatment is reserved only for patients in whom necrosis is not transmural and clinical conditions remain stable, in the absence of organ failure. Specifically, monitoring in an intensive care setting is required, with close control of bowel evacuation, adequate infusion therapy, antibiotic coverage, and parenteral nutrition. The duration of parenteral nutrition typically depends on the time required for intestinal function to recover [49].
On the other hand, in the presence of highly suggestive clinical signs, an exploratory laparotomy may be necessary: findings of transmural intestinal ischemia and necrosis of the intestinal wall are clear indications for emergency surgery [63] (Figure 4).
Resection of the non-viable segment must be extensive and it should be ensured that anastomoses were performed on viable tissue to avoid a subsequent aortic graft infection, as well as failure of the intestinal anastomosis. When there is uncertainty regarding the viability of the remaining bowel, leaving the abdomen open can facilitate better blood flow by reducing IAP, and allowing for a second-look operation. Mortality rates among patients with this complication range from 41% to 53%, depending on whether the procedure was performed electively or in an emergency setting, and on the patient’s comorbidities [49].
Table 2 provides a concise overview of the main findings related to ischemic colitis following vascular surgery, as reported in the present review.

7. Conclusions

In patients undergoing major abdominal vascular surgery, one of the most severe complications is colonic ischemia, which, although rare, carries a high risk of postoperative morbidity and mortality. The multifactorial etiology of this condition, due to intraoperative variables, pre-existing comorbidities, and altered blood flow, underscores the necessity for an integrated and multi-disciplinary clinical approach. To reduce complications, the early diagnosis of CI achieved by clinical sign recognition, laboratory tests, and instrumental examinations with sigmoidoscopy and computed tomography is essential for proper and timely treatment and management.
This literature review highlights the importance of the preoperative assessment of intestinal vascularization, vigilant perioperative monitoring, and the selection of the most appropriate surgical technique for each patient in the prevention of ischemic colitis. Notably, for patients at a higher risk of colonic ischemia (CI), EVAR represents a valid alternative due to its lower incidence rates of ischemic complications compared to open surgery. In cases of transmural ischemia, conservative management, when feasible, and prompt surgical intervention are pivotal strategies to improve long-term survival.
Continued exploration of the pathogenetic mechanisms and preventive strategies may lead to significant advancements in reducing the incidence and severity of ischemic colitis. Future prospective studies and the implementation of standardized clinical guidelines will be essential in standardizing management protocols and optimizing outcomes in patients with this complication.

Author Contributions

Conceptualization F.R., P.S. and M.T.; methodology, F.R. and P.S.; data curation, P.S. and F.R.; writing—review and editing, F.R.; writing—review and editing, G.C.; supervision, P.S. and M.T.; drawing, E.R. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflict of interest.

Abbreviations

The following abbreviations are used in this manuscript:
AAAAbdominal Aortic Aneurysm
CIColonic Ischemia
CTCeliac Trunk
EVAREndovascular Aneurysm Repair
FEVARFenestrated Endovascular Aneurysm Repair
HAHypogastric Arteries
ICGIndocyanine Green
IMAInferior Mesenteric Artery
I-FABPIntestinal Fatty Acid-Binding Protein
NIRSNear-Infrared Spectroscopy
NPVNegative Predictive Value
OCTOptical Coherence Tomography
OROdds Ratio
OSROpen Surgical Repair
PPVPositive Predictive Value
rAAARuptured Abdominal Aortic Aneurysm
RRRelative Risk
SMASuperior Mesenteric Artery
StO2Tissue Oxygen Saturation
VLSVisible-Light Spectrophotometry
GSTsGlutathione S-Transferases
CT (imaging)Computed Tomography

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Figure 1. Splanchnic vascular anatomy illustrating the major abdominal arteries and their collateral networks. The celiac trunk, superior mesenteric artery, inferior mesenteric artery, and hypogastric arteries are shown, along with key arterial anastomoses: the arch of Bühler, the marginal artery of Drummond, and the arch of Riolan (providing collateral flow between the middle colic and left colic arteries). Critical watershed areas prone to ischemia, Griffith’s point, Sudeck’s point, and Reiner’s segment are also indicated.
Figure 1. Splanchnic vascular anatomy illustrating the major abdominal arteries and their collateral networks. The celiac trunk, superior mesenteric artery, inferior mesenteric artery, and hypogastric arteries are shown, along with key arterial anastomoses: the arch of Bühler, the marginal artery of Drummond, and the arch of Riolan (providing collateral flow between the middle colic and left colic arteries). Critical watershed areas prone to ischemia, Griffith’s point, Sudeck’s point, and Reiner’s segment are also indicated.
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Figure 2. CI visualized with sigmoidoscopy. (Courtesy of the Gastroenterology Unit of Sant’Andrea Hospital of Rome, IT.) (A) Mucosal damage located at the transverse colon, characterized by edema, erythema, and petechial hemorrhagic lesions. (B) Ischemic changes involving the colic splenic flexure, showing more pronounced mucosal discoloration and loss of vascular pattern.
Figure 2. CI visualized with sigmoidoscopy. (Courtesy of the Gastroenterology Unit of Sant’Andrea Hospital of Rome, IT.) (A) Mucosal damage located at the transverse colon, characterized by edema, erythema, and petechial hemorrhagic lesions. (B) Ischemic changes involving the colic splenic flexure, showing more pronounced mucosal discoloration and loss of vascular pattern.
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Figure 3. CT findings of CI. (A) Ileal air–fluid levels (B) Bowel wall pneumatosis.
Figure 3. CT findings of CI. (A) Ileal air–fluid levels (B) Bowel wall pneumatosis.
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Figure 4. (A) Intraoperative appearance of colonic ischemia, showing necrotic mucosa with the loss of vascular pattern, consistent with transmural ischemia. (B) Resection of non-viable tissue to prevent further complications using a surgical linear stapler. (Personal experience.).
Figure 4. (A) Intraoperative appearance of colonic ischemia, showing necrotic mucosa with the loss of vascular pattern, consistent with transmural ischemia. (B) Resection of non-viable tissue to prevent further complications using a surgical linear stapler. (Personal experience.).
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Table 1. Semi-quantitative analysis of the main risk factors potentially associated with the development of CI after major aortic surgery, highlighted from the articles included in the present review. Background color intensity corresponds to the estimated level of risk, from minimal (green) to critically increased (red). x: reported association between the listed risk factor and colonic ischaemia.
Table 1. Semi-quantitative analysis of the main risk factors potentially associated with the development of CI after major aortic surgery, highlighted from the articles included in the present review. Background color intensity corresponds to the estimated level of risk, from minimal (green) to critically increased (red). x: reported association between the listed risk factor and colonic ischaemia.
Risk
Factor
Relative Risk
Very Low
(Minimal or Negligible Risk)
Low
(Slight Increase in Risk)
Moderate
(Average or Baseline Risk)
High (Significantly Increased Risk)Very High
(Critically
Increased Risk)
Age < 70 yearx
Ruptured aneurysm x
EVAR treatment x
Male sexx
Renal failure x
Pulmonary history x
Hypertension x
Diabetes x
Proximal extension of the aneurysm x
Peripheral arterial disease x
Table 2. Main findings of the studies cited in this review.
Table 2. Main findings of the studies cited in this review.
StudyStudy TypeKey Findings
Jalalzadeh H et al. [12].Meta-analysisClinically relevant CI prevalence of 10%. Incidence of 3.9% post-EVAR and 10% post-OSR. EVAR associated with a lower relative risk of CI compared to OSR.
Tsilimigras DI et al. [19].Systematic reviewEVAR associated with reduced inflammatory response and less ischemia–reperfusion injury compared to OSR.
Perry et al. [34].Cohort studyCI incidence after EVAR was 0.5%, compared to 1.9% after OSR. Open surgical technique is an independent risk factor for CI.
Wolpert et al./Mehta et al. [38,39].Retrospective studiesInterruption of hypogastric artery blood flow showed no significant differences in outcomes; more recent studies indicate a risk of ischemic complications.
Lee et al./Jayaraj et al. [47,48].Recent studiesNo significant supremacy in preserving IMA versus ligation, except in selected patients.
Moore et al./Mehta et al. [32,33].Observational studiesVariability in bowel ischemia rates between OSR and EVAR, with no statistical differences due to small sample sizes.
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Ruggiero, F.; Colonna, G.; Taurino, M.; Romano, E.; Sirignano, P. Colonic Ischemia Following Major Vascular Surgery: A Literature Review on Pathogenesis, Diagnosis, and Preventive Strategies. Appl. Sci. 2025, 15, 8482. https://doi.org/10.3390/app15158482

AMA Style

Ruggiero F, Colonna G, Taurino M, Romano E, Sirignano P. Colonic Ischemia Following Major Vascular Surgery: A Literature Review on Pathogenesis, Diagnosis, and Preventive Strategies. Applied Sciences. 2025; 15(15):8482. https://doi.org/10.3390/app15158482

Chicago/Turabian Style

Ruggiero, Federica, Giulia Colonna, Maurizio Taurino, Elisa Romano, and Pasqualino Sirignano. 2025. "Colonic Ischemia Following Major Vascular Surgery: A Literature Review on Pathogenesis, Diagnosis, and Preventive Strategies" Applied Sciences 15, no. 15: 8482. https://doi.org/10.3390/app15158482

APA Style

Ruggiero, F., Colonna, G., Taurino, M., Romano, E., & Sirignano, P. (2025). Colonic Ischemia Following Major Vascular Surgery: A Literature Review on Pathogenesis, Diagnosis, and Preventive Strategies. Applied Sciences, 15(15), 8482. https://doi.org/10.3390/app15158482

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