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Abstract

Acute mesenteric ischemia (AMI) is an abdominal emergency characterized by a sudden decrease in blood flow to meet the metabolic demands of bowel. AMI is uncommon but associated with high morbidity and mortality. Imaging plays a decisive role in early diagnosis and management because the symptoms of AMI are often nonspecific without specific laboratory tests or serologic biomarkers for early diagnosis. AMI comprises distinct entities with unique pathophysiology, imaging features, and management strategies. The basic causal mechanisms underlying AMI are inadequate inflow (arterial occlusion), inadequate outflow (mesenteric venous occlusion), global hypoperfusion (nonobstructive mesenteric ischemia [NOMI]), and strangulating bowel obstruction. Identifying transmural necrosis is critical for all causes of AMI. The authors review the foundational anatomy and pathophysiology of AMI, its distinct imaging features, and a systematic approach to AMI with emphasis on up-to-date imaging findings predictive of transmural necrosis. They emphasize a pathophysiology-based approach to AMI rather than a semiology-based approach (ie, patterns and signs) because the imaging features, significance, and predictive value of the imaging findings vary based on the underlying cause of AMI, with arterial occlusive AMI and NOMI having worse prognosis than mesenteric venous AMI. The authors highlight the specific vascular, bowel, and extraintestinal findings for each type of AMI with emphasis on imaging predictors of transmural bowel necrosis and address points of confusion to equip interpreting radiologists with a foundational understanding of AMI.
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Figures

Figure 1. Different causes of AMI. (A) The causes can be distilled into four basic underlying causes: inadequate inflow (eg, arterial occlusion; embolism and thrombosis), inadequate outflow (eg, mesenteric venous occlusion), global hypoperfusion (eg, NOMI), and strangulating bowel obstruction. (Created with BioRender.com; M. Lee, 2025; https://BioRender.com/zo4o4kg.) (B) Illustration shows a visual summary of AMI by cause, highlighting the characteristic vascular and bowel findings. SMA = superior mesenteric artery, SMV = superior mesenteric vein. (Illustration by A.M.S.)
Figure 2. Normal vascular anatomy. The arterial image (top right) shows a practical standardized segmentation dividing the SMA into three segments: proximal SMA (S1): SMA origin to the origin of the inferior pancreaticoduodenal artery (IPDA), which is an important foregut collateral; middle SMA (S2): between the origin of the IPDA and the origin of the ileocolic artery (this segment includes the jejunal, right colic, and middle colic arteries); and distal SMA (S3): distal to the ileocolic artery. (Illustration by A.M.S.)
Figure 3. Gross and microscopic (histologic) examples of ischemic bowel disease. (A) Photograph from small-bowel resection shows dusky hemorrhagic mucosa. (B, C) Photomicrographs of early ischemic changes show superficial mucosal damage (arrows in B), congestion (arrowhead in B), hemorrhagic epithelial necrosis (arrowhead in C), and focal crypt preservation (arrows in C). (Hematoxylin-eosin [H-E] stain; original magnification, ×40 [B] and ×100 [C].) (D) Photomicrograph shows transmural infarction resulting from ischemia, which is typically due to acute vascular obstruction. Straight arrow = mucosa, arrowhead = submucosa, curved arrow = muscularis propria. (H-E stain; original magnification, ×20.)
Figure 4. Theoretical enhancement curves with example mesenteric ischemia protocols. Left: Biphasic protocols have dedicated separately acquired arterial and portal venous phases. Right: Split-bolus protocols use two contrast material boluses separated by a set timed delay with a single-phase acquisition, to best represent a time point at which arterial and portal venous enhancement is greatest. Time is shown in seconds. (Created with BioRender.com; M. Lee, 2025; https://BioRender.com/inccxel.)
Figure 5. Interpretive approach to AMI. (Created with BioRender.com; M. Lee, 2025; https://BioRender.com/hsjibr8.)
Figure 6. Arterial occlusive AMI in a 63-year-old woman with acute abdominal pain and concern for AMI. (A) Sagittal CT angiogram shows a low-attenuation embolus (arrow) beyond the SMA origin with classic pathognomonic sparing of the proximal SMA. (B) Three-dimensional reconstruction image shows abrupt vessel cutoff at the middle SMA (arrow), corresponding to the occlusive embolus.
Figure 7. Arterial occlusive AMI in a 60-year-old man who underwent explant of an infected aortobifemoral graft and who experienced acute-onset abdominal pain and distention and pain related to arterial embolism causing mesenteric ischemia. (A) Axial CT angiogram shows a low-attenuation occlusive embolus (arrow) in the middle SMA and multiple small right renal infarcts (circle). (B) Conventional angiogram shows the corresponding abrupt cutoff (arrow) in the middle SMA.
Figure 8. Arterial occlusive AMI in a 66-year-old woman with abdominal pain, acute mesenteric ischemia, and complete right renal infarct related to arterial emboli. (A–C) Axial (A, B) and coronal (C) CT angiograms show a nonenhancing right kidney indicative of infarction (arrow in A), mural thrombus in the aorta (arrowhead in A), extensive mesenteric arterial occlusion involving the middle SMA (circle in C), and corresponding hypoenhancing loops of distal jejunum and ileum (arrows in B and C). There is preserved enhancement in the proximal jejunum. Associated wall thickening of the loops of hypoenhancing bowel suggests an element of reperfusion injury. (D) Three-dimensional reconstruction image shows abrupt cutoff of the middle SMA (arrow). There is residual positive enteric contrast material in the colon from a prior study.
Figure 9. SMA thrombosis and AMI in a 77-year-old man. Sagittal (A) and axial (B, C) contrast-enhanced CT images in soft-tissue window (B) and lung window (C) show proximal arterial thrombosis and occlusion at the SMA origin in the setting of severe atherosclerosis (arrow in A). There is extensive transmural ischemia involving loops of small bowel throughout the central and left abdomen, with extensive small-bowel pneumatosis (arrows in C) and absent wall enhancement (arrowheads in B). There are normally enhancing loops of bowel (arrows in B) in the right abdomen.
Figure 10. SMA thrombosis and AMI in a 49-year-old man. Sagittal (A) and axial (B) contrast-enhanced CT images show proximal arterial occlusion at the SMA origin (arrowhead in A) with extensive thin-walled, nonenhancing, dilated and fluid-filled loops of bowel (arrows). Bowel dilatation should be recognized as a predictor of transmural bowel necrosis in the setting of arterial occlusive AMI, not misinterpreted as simple ileus.
Figure 11. Arterial occlusive AMI in a 55-year-old woman with a history of renal transplant and arterial thrombosis. Sagittal (A) and axial (B) contrast-enhanced CT images show a low-attenuation SMA thrombus (solid arrow) and background calcified atherosclerosis. There is associated nonenhancement of small-bowel jejunal loops in the left abdomen (circle in B). There is a sharp transition between enhancing or perfusing loops (dashed arrow) and nonenhancing loops. There is faint peritoneal enhancement (arrowhead in B) adjacent to the nonenhancing bowel.
Figure 12. Characteristic imaging features of AMI from arterial occlusion in an 83-year-old man with a history of atrial fibrillation and arterial embolus. (A–C) Axial CT angiograms show a clot filling defect in the middle SMA (arrow in A), with corresponding nonenhancing or hypoenhancing dilated and fluid-filled loops of distal jejunum and ileum with paper-thin imperceptible walls (ovals in B and C). There is a sharp transition (arrows in B and C) between enhancing or perfusing loops and nonenhancing or hypoenhancing ischemic loops. The paper-thin imperceptible wall is predictive of transmural necrosis. (D) Three-dimensional reconstruction image shows abrupt cutoff of the middle SMA (arrowhead).
Figure 13. MVT in a 37-year-old woman with back pain and exercise intolerance. (A, B) Axial (A) and coronal (B) contrast-enhanced PVP CT images show expansile low-attenuation thrombus in the SMV (solid arrows) with associated rim enhancement (dashed arrow in A), attributable to the enhancing vein wall and surrounding stranding. (C, D) Axial (C) and coronal (D) contrast-enhanced PVP CT images show small-bowel wall thickening, mural stratification, mesenteric edema, and small-volume interloop fluid (oval in C, circle in D) due to venous congestion and ischemia, which are readily apparent on PVP images. (E) Coronal contrast-enhanced CT image with positive enteric contrast material from routine outpatient CT performed 12 months later after anticoagulation shows collateral formation (arrowheads).
Figure 14. Hemorrhagic shock causing NOMI in a 79-year-old critically ill man. Coronal (A) and axial (B) contrast-enhanced CT images show a widespread discontinuous pattern of bowel ischemia, with segmental hypo- and nonenhancing bowel (solid arrow in B) affecting multiple vascular territories (small bowel and colon). The affected bowel is thin walled and fluid filled. Differential enhancement is most notable compared with the enhancing duodenum (dashed arrow in B). Multifocal renal infarcts (circles in B) are indicative of multisystem involvement. There is also renal hyperenhancement related to shock. The patient died 1 day later.
Figure 15. Hemorrhagic shock causing NOMI in an 83-year-old woman. (A–C) Coronal CT angiogram (A) and coronal (B) and axial (C) contrast-enhanced CT images show a patent but attenuated, irregular-appearing SMA (arrow in A). There is widespread bowel ischemia with segmental areas of hypo- and nonenhancing bowel affecting multiple vascular territories. The ischemic bowel is thin walled and fluid filled (oval in B, circle in C) and hypoenhancing compared with small bowel in the right abdomen. Multifocal renal infarcts (arrows in C) are indicative of multisystem involvement. (D) Coronal contrast-enhanced CT image from 3 days earlier shows nondilated normally enhancing loops of bowel. Comparison with imaging studies obtained before critical illness can be helpful for assessing interval change and findings of transmural necrosis. The patient died 3 days later.
Figure 16. CLO in a 77-year-old man. (A, B) Axial (A) and coronal (B) contrast-enhanced CT images show an obstructed, U-shaped, fluid-filled, sequestered loop of bowel in the pelvis with high-attenuation intraluminal contents (solid arrows), compared with adjacent proximal loops of bowel and associated mesenteric haziness and edema (dashed arrow). Intraoperatively, the closed-loop segment was hemorrhagic appearing and torsed around a single adhesive band in the pelvis. (C) Gross specimen photograph shows approximately 75 cm of resected infarcted bowel.
Figure 17. Closed-loop SBO in an 85-year-old woman with pelvic pain secondary to the SBO. Axial noncontrast (A) and contrast-enhanced (B) CT images of the abdomen show dilated fluid-filled loops of bowel in the pelvis. High-attenuation contents within the obstructed sequestered loop of bowel probably represent necrotic bowel with intraluminal hemorrhage. Lower-attenuation fluid contents are noted in the upstream loops of small bowel in the left pelvis. The attenuation of the intraluminal contrast material was unchanged between noncontrast and contrast-enhanced imaging. The patient was taken emergently to the operating room, where CLO and small-bowel necrosis were confirmed, with subsequent small-bowel resection.
Figure 18. SMA embolus in a 68-year-old man with esophageal cancer. (A) Axial contrast-enhanced CT angiogram shows thin nonenhancing loops of bowel (arrows) in the pelvis. (B) Follow-up axial contrast-enhanced CT image 3 weeks later shows wall thickening of the ischemic loops (oval), related to reperfusion injury.
Figure 19. AMI in a 72-year-old man with atrial fibrillation. (A–C) Axial soft-tissue window (A), axial lung window (B), and coronal (C) contrast-enhanced CT images show extensive pneumatosis (arrow in A, oval in B), portal venous gas (black arrow in C), free fluid, and foci of pneumoperitoneum (white arrow in C). (D) Gross specimen photograph shows 260 cm of necrotic bowel.

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