Mesenteric ischemia is intestinal ischemia from acute or chronic reduction of bowel blood flow. Acute mesenteric ischemia (AMI) is a surgical emergency — mortality reaches 60-80%. Most common causes are SMA embolism (50%), SMA thrombosis (25%), non-occlusive mesenteric ischemia (NOMI, 20%), and mesenteric venous thrombosis (5%). CTA shows filling defect or occlusion in SMA, decreased bowel wall enhancement, pneumatosis intestinalis, porto-mesenteric venous gas, and mesenteric whirl sign. Early diagnosis and emergent vascular intervention (embolectomy, thrombolysis, angioplasty) or surgical resection is life-saving.
Age Range
50-85
Peak Age
70
Gender
Equal
Prevalence
Uncommon
In mesenteric ischemia, reduced bowel blood flow causes cellular hypoxia and ATP depletion. Mucosa is affected first as the highest metabolic layer, and the countercurrent exchange mechanism at villus tips exacerbates hypoxia. Mucosal barrier breaks down — bacterial translocation and endotoxemia begin. In SMA embolism, the embolus is usually cardiac in origin (atrial fibrillation, left ventricular thrombus, valvular vegetation) and lodges 3-10 cm distal to the SMA origin — typically at the middle colic artery branch point. Therefore proximal jejunum is spared while ischemia develops from mid-jejunum distally. SMA thrombosis develops on ostial atherosclerotic background — some patients with chronic stenosis have developed collaterals (arc of Riolan, marginal artery) so ischemia severity varies. In NOMI, there is no mechanical occlusion — low cardiac output, vasopressor use, or splanchnic vasoconstriction causes perfusion insufficiency. In venous thrombosis, SMV occlusion causes venous congestion → bowel wall edema → transmural ischemia chain. On CT, ischemic bowel loses enhancement because contrast cannot reach the capillary bed. When transmural necrosis begins, pneumatosis intestinalis and porto-mesenteric venous gas develop — these findings indicate irreversible damage.
Complete loss of wall enhancement in ischemic bowel segment with paper-thin appearance — the most sensitive CT finding of complete perfusion loss from arterial occlusion. Creates stark contrast with enhancing normal surrounding bowel wall.
CTA shows filling defect (embolus) or complete occlusion (thrombosis) in SMA lumen. Embolus typically lodges 3-10 cm distal to SMA origin at middle colic artery branch point. Thrombosis extends from ostium proximally and usually on atherosclerotic background. Filling defect appears as hypodense area within the contrast-filled vessel lumen.
Report Sentence
CTA shows filling defect/occlusion in SMA ... cm distal to origin, consistent with acute mesenteric ischemia.
Decreased or absent wall enhancement in ischemic bowel segment — 'paper-thin wall' appearance. Normal bowel wall enhances homogeneously in portal venous phase (70-120 HU), while ischemic segment remains hypodense (20-40 HU) or shows no enhancement. Marked contrast difference with surrounding normal bowel delineates the ischemic boundary. Segment length depends on occlusion location and collateral status.
Report Sentence
Markedly decreased bowel wall enhancement in the ischemic segment, consistent with transmural ischemia.
Intramural gas in bowel wall (pneumatosis intestinalis) and gas in porto-mesenteric venous system — most serious findings of transmural necrosis. Pneumatosis in linear or cystic pattern. Portal venous gas appears as linear branching hypodense foci in liver periphery (subcapsular). These findings strongly correlate with mortality.
Report Sentence
Pneumatosis intestinalis and porto-mesenteric venous gas are present, consistent with transmural necrosis; emergent surgical evaluation required.
Filling defect or complete occlusion in SMV lumen — main finding of venous mesenteric ischemia. SMV thrombosis usually develops in settings of portal hypertension, hypercoagulability, pancreatitis, or intra-abdominal infection. Thrombus may extend to portal vein. Bowel wall thickening, mesenteric edema, and ascites accompany due to venous congestion.
Report Sentence
Filling defect in SMV lumen, consistent with venous mesenteric thrombosis and ischemia.
Bowel wall thickening (>3 mm small bowel, >5 mm colon) and edema in ischemic segment. Target sign: mucosa and serosa enhance while submucosa remains hypodense from edema. Mesenteric thickening and haziness accompany. These findings are more pronounced in venous ischemia as venous congestion increases wall edema.
Report Sentence
Bowel wall thickening and target sign pattern in the ischemic segment, consistent with ischemic edema.
Increased density in bowel wall (40-60 HU) on non-contrast CT — indicates intramural hemorrhage. Normal bowel wall is 20-30 HU. Hemorrhagic ischemia is more common in reperfusion injury or venous ischemia. Non-contrast scan before contrast series is critical to detect this finding.
Report Sentence
Increased bowel wall density on non-contrast CT, consistent with intramural hemorrhage.
Criteria
50% of AMI. Cardiac source embolus (AF, LV thrombus). Occlusion 3-10 cm distal to SMA origin. Proximal jejunum spared, ischemia from mid-jejunum distally.
Distinct Features
CTA: meniscus-shaped filling defect in SMA. Proximal SMA contrast-filled, no contrast distal to occlusion. Concurrent splenic, renal infarcts may accompany.
Criteria
25% of AMI. Ostial thrombosis on atherosclerotic background. Collaterals may have developed from chronic stenosis. Ischemia severity variable.
Distinct Features
CT: calcified atherosclerotic plaque and thrombus at SMA ostium. Other visceral arteries may show stenosis. Arc of Riolan and marginal artery may be enlarged as collaterals.
Criteria
20% of AMI. No mechanical occlusion — splanchnic hypoperfusion from low cardiac output, vasopressors, dialysis, sepsis. Highest mortality (70-90%) because diagnosis is delayed.
Distinct Features
CT: SMA patent but diffuse vasospasm in branches — irregular caliber narrowing. 'String of sausages' pattern: alternating normal and ischemic segments. Patchy bowel wall enhancement decrease.
Criteria
5% of AMI. SMV thrombosis — portal HT, hypercoagulability, pancreatitis, intra-abdominal infection. Subacute presentation common. Lower mortality (20-30%) than other types.
Distinct Features
CT: SMV filling defect, prominent bowel wall thickening (edema), target sign, mesenteric haziness, ascites. SMA patent on arterial phase.
Distinguishing Feature
Internal hernia: swirl sign and clustered loops without SMA/SMV occlusion. Mesenteric ischemia: primary vascular occlusion or perfusion insufficiency.
Distinguishing Feature
Adhesive SBO: mechanical obstruction but preserved wall enhancement (without strangulation). Mesenteric ischemia: loss of enhancement and vascular occlusion are distinguishing.
Distinguishing Feature
Infectious enteritis: bowel wall thickening with increased enhancement (hyperemia), no vascular occlusion. In ischemia, decreased enhancement and vascular occlusion are critical differences.
Distinguishing Feature
Closed-loop SBO: mechanical cause at obstruction point (band, hernia) with clear transition points. Primary mesenteric ischemia: vascular occlusion without mechanical obstruction and widespread ischemia.
Urgency
emergentManagement
surgicalBiopsy
Not NeededFollow-up
specialist-referralAcute mesenteric ischemia is a surgical emergency — mortality 60-80%. SMA embolism: emergent embolectomy or catheter-directed thrombolysis. SMA thrombosis: surgical bypass or endovascular stenting. NOMI: treat underlying cause + intra-arterial vasodilator (papaverine). Venous thrombosis: anticoagulation, thrombectomy if needed. Necrotic bowel resection mandatory. Second-look laparotomy at 24-48 hours to reassess necrosis margins.
Acute mesenteric ischemia has 60-80% mortality. Early diagnosis and rapid surgery are life-saving. CT angiography is the gold standard. Portal venous gas and pneumatosis indicate transmural necrosis and poor prognosis.