Abstract
Objective
Inferior mesenteric artery aneurysms (IMAAs) are extremely rare, and their natural history and treatment outcomes are poorly understood.
Methods
We performed a retrospective review of consecutive patients with IMAAs treated at a multistate health system between November 2005 and August 2025. Demographics, etiology, imaging features, treatment, and outcomes were analyzed.
Results
There were 15 patients (11 male; mean age, 66 ± 15 years), and all these patients were diagnosed on computed tomography angiography. Presentation was with nonspecific abdominal pain in nine patients (88%), symptomatic chronic mesenteric ischemia in one patient (6%), and shock owing to rupture in one patient (6%). The most common etiology was segmental arterial mediolysis (SAM) (n = 9 [60%]), followed by atherosclerosis (n = 6 [40%]). Ten patients (67%) were managed nonoperatively, and in these patients the mean IMAA diameter was 0.9 ± .4 cm. Over a median imaging follow-up of 42 months (range, 10-170 months), size remained stable with a mean IMAA diameter of 0.9 ± 0.4 cm. Surgical intervention was required in five patients (33%; mean IMAA diameter, 2.1 ± 0.4 cm). All three patients (20%) with atherosclerosis and celiomesenteric occlusion had an IMAA of >1.5 cm, consistent with poststenotic jet flow phenomenon. Indication for repair included IMAA enlargement to >2 cm, with symptomatic chronic mesenteric ischemia in one patient (6%). Procedures performed included aneurysm resection with aorta to IMA bypass with Dacron graft (n = 1), supraceliac aorta to celiac and superior mesenteric artery bypass with IMA aneurysmorrhaphy, and endovascular repair (covered stent placement, n = 1). In two patients (13%), the celiac and superior mesenteric artery were patent, and the IMAA was ligated (diagnosis at presentation with shock owing to IMAA rupture, etiology unknown; colectomy for recurrent diverticulitis and SAM with a 1.6-cm IMAA). There were no major postoperative complications or aneurysm-related death. At a median clinical follow-up of 50 months, two patients had died with a cause of death unrelated to IMAA.
Conclusions
Inferior mesenteric aneurysms secondary to SAM are usually smaller at presentation and have a benign course. IMAA associated with celiomesenteric occlusion experience progressive enlargement owing to jet phenomenon hemodynamics and require repair. Repair is required for rupture or when the aneurysm diameter reaches ≥1.5 cm if the celiac and superior mesenteric artery inflow are intact.
Keywords: Inferior mesenteric artery aneurysm, Celiomesenteric occlusion, Aneurysm, Rupture risk, Endovascular repair, Post-stenotic dilation, Hemodynamic mechanism
Article Highlights.
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Type of Research: Clinical cohort study
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Key Findings: Among 15 patients with inferior mesenteric artery aneurysms, 67% were managed nonoperatively with stable size (mean 0.9 cm) over 42 months. Five patients (33%) underwent intervention (mean 2.1 cm). All aneurysms ≥1.5 cm with celiomesenteric occlusion enlarged and required repair (P = .029). No aneurysm-related mortality occurred.
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Take Home Message: Inferior mesenteric artery aneurysms <1.5 cm are typically stable, especially in segmental arterial mediolysis, whereas aneurysms ≥1.5 cm associated with celiomesenteric occlusion demonstrate progressive enlargement and warrant repair.
Inferior mesenteric artery aneurysms (IMAA) are exceedingly rare, representing <1% of all visceral artery aneurysms.1, 2, 3 Most are incidentally detected on cross-sectional (mostly computed tomography [CT]) imaging performed for unrelated indications, and their natural history and management remain poorly defined. The pathogenesis of IMAA varies and includes atherosclerosis, segmental arterial mediolysis (SAM), and less commonly infection or connective tissue disorders.4, 5, 6, 7, 8, 9
The IMA plays a critical collateral role in mesenteric circulation, particularly in patients with occlusive disease of the celiac or superior mesenteric arteries.10, 11, 12, 13 In this setting, increased flow through the IMA and its branches can result in poststenotic dilation and aneurysm formation.1 This hemodynamic mechanism, also referred to as the jet flow phenomenon, has been described in isolated case reports.1,14
Existing literature on IMA aneurysms is limited to single-patient reports or small series, with variable etiologies and no consensus on indications for intervention.2,15 Reported management strategies range from observation to open or endovascular repair, often guided by size, symptoms, or associated visceral occlusive disease.15,16 The threshold for repair, particularly in small, asymptomatic aneurysms, remains uncertain.
The aim of this study was to review the presentation, etiology, management, and outcomes of patients with IMAAs treated within a multistate health system over a 20-year period and to identify imaging and clinical features associated with the need for repair. To our knowledge, this study includes the largest cohort to specifically evaluate the relationship between celiomesenteric occlusive disease and IMAA progression.
Methods
We performed a retrospective review of consecutive adult patients diagnosed with IMAAs between November 2005 and August 2025 across a multistate integrated health system and reviewed their electronic medical records. This retrospective study was reviewed by the institutional review board of the participating health system and deemed exempt from formal review, with a waiver of informed consent, in accordance with applicable regulations.
Patient selection and definitions
An IMAA is defined as a focal dilation ≥1.5 times the expected vessel diameter or >7 mm in maximum dimension.17 Inclusion criteria included all patients with radiographically confirmed IMA aneurysm on contrast-enhanced CT angiography, regardless of etiology or presentation. IMAA diameter was measured on multiplanar CT angiography images using an outer wall to outer wall technique at the maximal dimension. Aneurysm morphology (fusiform or saccular), branch involvement, and association with other visceral aneurysms were recorded.
Clinical presentation, imaging characteristics, treatment strategy, and outcomes were analyzed and studied in two groups based on etiology. Because this was a retrospective cohort, there was no pre-established diagnostic or surveillance protocol. However, all patients underwent extensive clinical and radiographic evaluation for inflammatory vasculitides (such as polyarteritis nodosa and Behçet disease), connective tissue disorders, mesenteric venous disease, and neurofibromatosis, were excluded based on clinical features, serology (C-reactive protein/vasculitis workup) and imaging, as decided by the treating physicians.
Group I was nonatherosclerotic attributed to SAM. The diagnosis of SAM was based on characteristic findings on contrast-enhanced CT angiography, including fusiform or dissecting aneurysms, arterial beading, focal dissections, or arterial irregularity involving visceral arteries in a nonatherosclerotic distribution.18 These findings occurred in the absence of CT evidence of mural calcification, plaque formation, concentric wall thickening, or perivascular inflammatory changes.
Group II were those with atherosclerosis: IMAA had wall calcification, plaque formation, or other evidence of arterial occlusive disease. In group II, the presence of celiac or superior mesenteric artery occlusion or stenosis was recorded.
Follow-up imaging was individualized based on aneurysm size, etiology, symptoms, and treating physician preference.
Stable aneurysm size was defined as a change of <5 mm on serial imaging. For patients managed nonoperatively, follow-up imaging intervals and serial aneurysm diameters were documented. For those undergoing operative or endovascular repair, details of the procedure, graft type, and intraoperative findings were reviewed. Outcomes analyzed included aneurysm growth, rupture, postoperative complications, and aneurysm-related mortality. Survival was calculated based on the last clinical follow-up.
Statistical analysis
Data were managed and stored in an Excel database and analyzed using SAS 9.1 software (SAS Institute). Results were reported as mean ± standard deviation for continuous variables and as counts with percentages for categorical variables. The differences between groups were analyzed using the Student t test or Mann-Whitney U test for continuous variables and Pearson or Fisher's exact test for categorical variables. A P value of <.05 was considered statistically significant. A Kaplan-Meier analysis was used to estimate long-term survival.
Results
There were a total of 15 patients (11 male, 4 female; mean age, 66 ± 15 years). Thirteen patients were Caucasian, one patient was Hispanic, and race/ethnicity was unknown in one patient. Presentation was with nonspecific abdominal pain (n = 9 [60%]); one patient (7%) presented with symptomatic chronic mesenteric ischemia, and one patient (7%) presented with shock owing to aneurysm rupture. Four additional patients were asymptomatic (27%), with aneurysms identified incidentally on imaging performed for unrelated indications. Comorbidities included hypertension (n = 10), diabetes mellitus (n = 2), hyperlipidemia (n = 9), and smoking (n = 7). All patients were diagnosed on CT angiography (Table I). No congenital or developmental mesenteric arterial variants were identified on imaging; associated vascular findings reflected acquired aneurysmal disease or occlusive pathology.
Table I.
Comparison of clinical and imaging characteristics in 15 patients with inferior mesenteric artery aneurysm (IMAA) based on etiology
| Characteristic | SAM (n = 9) | Atherosclerosis (n = 6) | Total (n = 15) | P value |
|---|---|---|---|---|
| Age, years | 59 ± 13 | 73 ± 12 | 66 ± 15 | .054 |
| Male sex | 7 (77) | 4 (66) | 11 (73) | .7 |
| Symptomatic presentation | ||||
| Nonspecific abdominal pain | 8 (89) | 1 (17) | 9 (60) | .006 |
| Chronic mesenteric ischemia | 0 (0) | 1 (17) | 1 (7) | – |
| Rupture/shock | 1 (11) | 0 (0) | 1 (7) | – |
| Comorbidities | ||||
| Hypertension | 5 (56) | 5 (83) | 10 (67) | .363 |
| Diabetes mellitus | 1 (11) | 1 (17) | 2 (13) | 1.00 |
| Hyperlipidemia | 5 (56) | 4 (67) | 9 (60) | .7 |
| Smoking history | 4 (44) | 3 (50) | 7 (47) | .841 |
| Mean IMAA diameter, cm | 1 ± 0.4 | 1.5 ± 1 | 1.3 ± 0.6 | .246 |
| IMAA range, cm | 0.5-1.5 | 0.5-2.5 | 0.5-2.5 | – |
| Aneurysm morphology | ||||
| Saccular | 0 (0) | 0 (0) | 0 (0) | – |
| Fusiform | 8 (89) | 6 (100) | 14 (93) | 1.00 |
| Location | ||||
| Proximal | 8 (89) | 6 (100) | 14 (93) | 1.00 |
| Distal | 0 (0) | 0 (0) | 0 (0) | – |
| Celiac/SMA occlusion | 0 (0) | 3 (50) | 3 (20) | .029 |
| Other visceral aneurysms | 3 (33) | 2 (33) | 5 (33) | 1.00 |
| Management strategy | ||||
| Nonoperative | 7 (78) | 3 (50) | 10 (67) | .324 |
| Intervention | 2 (22) | 3 (50) | 5 (33) | .324 |
SAM, Segmental arterial mediolysis; SMA, superior mesenteric artery.
Values are mean ± standard deviation or number (%).
Boldface entries indicate statistical significance.
In this series, etiology consisted of SAM or atherosclerosis, there were no other vasculitides or mycotic etiology reported.
Group I: SAM
Nine patients (60%) had IMAAs attributed to SAM. Aneurysms in this subgroup were smaller at presentation mean IMAA diameter 1.0 ± .4 cm, fusiform in morphology, and involved the proximal IMA in eight patients. In the SAM subgroup, three of nine patients demonstrated dissecting aneurysms on CT angiography, identified by characteristic imaging features. None of the patients had associated celiac or superior mesenteric artery stenosis or occlusion. Three patients (34%) had a concurrent common hepatic and superior mesenteric artery aneurysm. Operative intervention (IMA ligation) was performed in two patients (one at presentation with shock owing to rupture and another during colectomy for unrelated etiology). In the patient in the SAM cohort who underwent operative intervention, histopathology of the aneurysm wall tissue was nondiagnostic. The size at rupture was not documented; there was no aneurysm-related mortality. Management was nonoperative in seven of the nine patients (78%), and serial imaging follow-up was available in all. Imaging surveillance consisted of serial contrast-enhanced CT angiography at 6- to 12-month intervals (average of five CTs per patient). The median follow-up was 48 months (range, 10-114 months), during which aneurysm size remained stable (final mean diameter, 1.0 ± 0.4 cm).
Group II: Atherosclerosis
Six patients (40%) had IMAAs attributed to atherosclerosis. Aneurysms in this subgroup were larger at presentation, with a mean IMAA diameter of 1.5 ± 1.0 cm and fusiform morphology; the proximal IMA was involved in six patients. There were three patients in this subgroup with an IMAA of <1.5 cm (0.5, 0.5, and 1.3 cm); all three had a patent celiac or superior mesenteric artery.
All three patients with larger aneurysms (2.0, 2.4, and 2.5 cm) had concurrent celiomesenteric occlusions. Radiologically confirmed stenosis of the IMA proximal to the aneurysm was present in all three patients with celiomesenteric occlusion. Two patients demonstrated progressive enlargement: a 2.0-cm aneurysm increased by 1.0 cm over 84 months, and a 2.4-cm aneurysm enlarged by 0.6 cm over 4 years (Fig 1). All three patients with atherosclerosis and celiomesenteric occlusion had an IMAA of >1.5 cm, consistent with poststenotic jet flow phenomenon (Fig 1). Two patients (34%) in this subgroup had a concurrent visceral artery aneurysm.
Fig 1.
Serial computed tomography angiography (CTA) images in two asymptomatic patients with atherosclerosis and celiomesenteric occlusion with inferior mesenteric artery aneurysm (IMAA) enlargement to >2 cm owing to poststenotic jet flow phenomenon. (A) Open repair with aorto-IMA bypass using 10-mm and (B) endovascular repair with 8 × 38-mm iCast and 10 × 5-mm Viabahn covered stents.
Patients with SAM were more likely to present with nonspecific abdominal pain compared with those with atherosclerotic IMA aneurysms (89% vs 17%; P = .006). Celiac or superior mesenteric artery occlusion was more common in the atherosclerosis group (50% vs 0%; P = .029). IMAA secondary to SAM was did not show progressive enlargement owing to altered hemodynamics (post stenotic jet phenomenon), explaining their smaller size and relative stability. Surgical intervention was required in three patients (20%; mean IMAA diameter, 2.1 + 0.4 cm) (Table II). Indication for repair included IMAA enlargement to >2 cm in two patients (Fig 1), with one symptomatic chronic mesenteric ischemia in one patient. Procedures performed included aneurysm resection with aorta to IMA bypass with Dacron graft (n = 1), supraceliac aorta to celiac and superior mesenteric artery bypass with IMA aneurysmorrhaphy and endovascular repair (covered stent placement; n = 1). There were no postoperative complications and no IMAA-related deaths. Median clinical follow-up was 18 months (range, 12-108 months). Three patients with atherosclerosis and patent celiac or superior mesenteric arteries (20%) were managed nonoperatively; in these patients, the mean IMAA diameter was 0.8 ± 0.4 cm. Over a median imaging follow-up of 85 months (range, 24-170 months), size remained stable at a mean IMAA diameter of 0.8 ± 0.4 cm, and no mortality was reported.
Table II.
Comparison of clinical and imaging characteristics in 15 patients with inferior mesenteric artery aneurysm (IMAA) based on intervention status
| Variable | No intervention (n = 10) | Intervention (n = 5) | P value |
|---|---|---|---|
| Age, years | 64 ± 13 | 67 ± 18 | .840 |
| Male sex | 6 (60) | 5 (100) | .242 |
| Hypertension | 5 (50) | 5 (100) | .121 |
| Hyperlipidemia | 6 (60) | 3 (60) | 1.000 |
| Diabetes mellitus | 2 (20) | 0 (0) | 1.000 |
| Smoking history | 3 (30) | 4 (80) | .121 |
| Mean aneurysm diameter, cm | 0.9 ± 0.4 | 2.0 ± 0.6 | .011 |
| Etiology: SAM | 7 (70) | 2 (40) | 1.000 |
| Etiology: Atherosclerosis | 3 (30) | 3 (60) | .576 |
| Celiac/SMA occlusion present | 0 | 3 (60) | .022 |
| Symptomatic | 7 (70) | 4 (80) | 1.000 |
| Aneurysm morphology (fusiform) | 10 (100) | 5 (100) | 1.000 |
| Multiple visceral aneurysms | 4 (40) | 1 (20) | .606 |
SAM, Segmental arterial mediolysis; SMA, superior mesenteric artery.
Values are mean ± standard deviation or number (%).
Boldface entries indicate statistical significance.
Discussion
The Society for Vascular Surgery practice guidelines advise individualized management for IMAA owing to rarity; there are no specific size guidelines for repair.18 Our data provide insights into the natural history and management of IMAAs. The underlying etiology and associated hemodynamic factors are related to aneurysm formation and expansion. Therefore, they are critical in determining the need for intervention. Similar to other visceral artery aneurysms, IMAAs occur more often in men in their sixth decade.19 Atherosclerosis is considered to be the most common etiology.1 However, in our series, IMAA was more commonly associated with SAM. The majority of IMAAs are symptomatic, and overall, presentation with rupture is rare.
Atherosclerotic IMAAs in our cohort were more commonly associated with celiac and superior mesenteric artery stenosis or occlusion, suggesting a hemodynamic mechanism of poststenotic dilation. Increased flow through the IMA owing to compensatory collaterals generate increased shear stress and turbulent jet flow at the vessel wall, predisposing patients to a fusiform phenomenon is well-described in other visceral and peripheral arteries, where poststenotic aneurysmal dilation occurs distal to a high-grade stenosis.20 In this series, all IMAAs associated with celiomesenteric occlusion that measured ≥1.5 cm demonstrated either progressive enlargement or required intervention (Table II), whereas aneurysms <1.5 cm remained stable on long-term imaging follow-up. We also performed a detailed scoping review, and based on 74 patients in 70 publications; there are no reports of ruptured IMAAs that were noted as measuring <1.5 cm.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17,19, 20, 21, 22, 23, 24 Although the largest reported IMAA size was 9.1 cm, fatal rupture is reported at 2.0 cm.4,22, 23, 24
Based on these observations, repair should be considered for asymptomatic IMAA at a size of 1.5 cm, especially if the celiac and superior mesenteric arteries are occluded and if there is evidence of progressive enlargement. Repair is required for rupture, or when aneurysm diameter reaches ≥1.5 cm if celiac and the superior mesenteric artery inflow are intact. Early diagnosis and elective repair are critical, with lower associated morbidity and mortality rates compared with emergency intervention after rupture.12,17
SAM is a rare, nonatherosclerotic, noninflammatory arteriopathy that most commonly affects medium-sized visceral arteries and is characterized by arterial dissections, aneurysms, and vessel irregularity. In contemporary practice, the diagnosis of SAM is established primarily on the basis of characteristic contrast-enhanced CT angiographic findings; histopathological confirmation is often inconclusive, as in our patient, or not available. Typical imaging features include fusiform or dissecting aneurysms, focal arterial dissections, arterial beading with alternating stenosis and dilation, and involvement of multiple visceral arteries in a nonatherosclerotic distribution, in the absence of mural calcification, concentric wall thickening, or perivascular inflammatory changes (Fig 2). In the present series, SAM was diagnosed using these established radiographic criteria.18,25,26 The single ruptured IMA aneurysm in this series presented acutely without prior imaging, and, although the etiology could not be established definitively, the absence of atherosclerosis or celiomesenteric occlusive disease suggests a nonatherosclerotic process such as SAM, which has been reported to present with spontaneous rupture.27
Fig 2.
Contrast-enhanced computed tomography angiography (CTA) in an asymptomatic 73-year-old man demonstrating inferior mesenteric artery aneurysm (IMAA) related to segmental arterial mediolysis (SAM) associated with similar changes in celiac artery as well.
In our cohort, SAM-related aneurysms arise from nonatherosclerotic medial degeneration and are not dependent on altered hemodynamics, explaining their smaller size and relative stability. Conservative management with serial imaging is feasible for IMAAs that measure <1.5 cm. These findings highlight the importance of evaluating inflow vessels when assessing IMAAs, because the presence of proximal occlusive disease identifies a subgroup at greater risk for aneurysm enlargement and potential rupture. Aneurysm growth is not related specifically to smoking or the presence of aortoiliac or peripheral aneurysms. This series did not include any IMAAs with underlying vasculitis. IMAAs can be rarely associated with vasculitis and require multidisciplinary treatment.21 Rarely, these may regress after treatment with steroids and not require surgical intervention.6
Intervention is also dependent on the patency of the celiomesenteric circulation and individualized based on aneurysm size, patient comorbidities, and the extent of proximal and distal atherosclerotic vascular involvement. Ligation or embolization is safe and effective if the celiac and superior mesenteric arteries are patent but is fatal if performed in the presence of celiomesentreic occlusion.11
Surgical repair can be performed with aneurysm resection and IMA bypass using Dacron/polytetrafluorethylene conduits or IMA reimplantation. When considering open repair, revascularization of the superior mesenteric artery is preferable, but if this procedure adds significant complexity, intervention for the IMA alone is reasonable. The long-term outcomes after intervention for IMA aneurysms seem favorable, with low rates of reintervention or late aneurysm-related mortality. Endovascular repair with covered stent placement may also be safe and effective based on aneurysm morphology. One limitation of this study is that the overall sample size is small, reflecting the rarity of IMAA. Second, follow-up imaging intervals and modalities were limited, and the series did not have any mycotic aneurysm or aneurysm related to other vasculitis. However, with <100 cases reported in literature, this series remains the largest of this condition, so we do not find that these are major limitations.
Conclusions
We recommend intervention for an IMAA with celiomesenteric occlusion to prevent rupture, or at a size of 1.5 cm if the superior mesenteric and celiac arteries are patent. The natural history of a IMAA associated with IMA stenosis (poststenotic dilatation) as well as celiomesenteric occlusion is continued or more rapid growth owing to the jet flow hemodynamics, a phenomenon analogous to gastroduodenal aneurysms. Early endovascular intervention on celiac or superior mesenteric artery occlusion or IMA stenosis to change the flow dynamics and decrease the risk of growth could be considered in this rare condition.
Author contributions
Conception and design: ZO, JB, TW, IS
Analysis and interpretation: NB, JB, IS
Data collection: EA, AV, CB
Writing the article: EA, NB, JB, AV, CB, IS
Critical revision of the article: ZO, JB, TW, IS
Final approval of the article: EA, NB, JB, AV, CB, ZO, JB, TW, IS
Statistical analysis: Not applicable
Obtained funding: Not applicable
Overall responsibility: IS
Funding
None.
Disclosures
None.
From the Society for Clinical Vascular Surgery
Footnotes
The editors and reviewers of this article have no relevant financial relationships to disclose per the Journal policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest.
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