01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Acute mesenteric ischaemia is a sudden mismatch between intestinal oxygen supply and demand. Arterial emboli often lodge just beyond proximal superior mesenteric artery branches and spare the proximal jejunum; in-situ thrombosis usually arises on calcified ostial atherosclerosis and may follow a history of postprandial pain. Mesenteric venous thrombosis impedes venous outflow and causes oedema and haemorrhagic injury, while non-occlusive mesenteric ischaemia results from intense vasoconstriction and low cardiac output without a fixed obstruction. Mucosal injury progresses to barrier failure, bacterial translocation, transmural infarction, perforation and sepsis. Early abdominal findings may be deceptively mild, so diagnostic delay is the major preventable hazard.
The decisive test is an AMI-protocol CT angiogram, not a single laboratory result. The request must state the suspicion so the acquisition includes thin-slice arterial and portal-venous phases and the report addresses arteries, veins and bowel viability. Once diagnosed, treatment occurs in a centre able to combine endovascular and open vascular treatment with gastrointestinal surgery and critical care. Endovascular aspiration, thrombolysis or stenting may restore flow with less physiological stress in selected arterial occlusion, whereas laparotomy is mandatory for peritonitis and permits bowel assessment. Revascularisation and bowel surgery are one coordinated problem: restoring flow before resection can reveal salvageable intestine, and a planned second look avoids premature anastomosis or excessive resection.
Key points
- Suspect AMI from the clinical trajectory: abrupt severe pain, pain disproportionate to early examination, vomiting or diarrhoea, embolic risk, atherosclerosis, venous thrombosis risk or low-flow critical illness.
- Request urgent CT angiography with contrast in arterial and venous phases, slices no thicker than 1 mm and an optional non-contrast run; ESVS recommends this regardless of renal function because delay risks fatal bowel loss.
- After CTA classifies the mechanism, give systemic unfractionated heparin when indicated and bleeding risk permits; for thrombotic or embolic SMA occlusion, consider endovascular treatment first only where expertise is immediately available and no peritonitis mandates emergency laparotomy coordinated with revascularisation.
- A normal lactate, D-dimer or white-cell count does not exclude early AMI. Lactate elevation may reflect late tissue injury or another cause and cannot establish the diagnosis alone.
- Classify the mechanism because arterial embolus, arterial thrombosis on atherosclerotic disease, mesenteric venous thrombosis and non-occlusive low-flow ischaemia require different definitive treatment.
- For thrombotic or embolic superior mesenteric artery occlusion, ESVS 2025 advises considering endovascular revascularisation first line where expertise is immediately available; laparotomy remains necessary for peritonitis or non-viable bowel.
- When feasible, restore blood flow before judging resection margins. If bowel is removed after revascularisation, leave uncertain segments and anastomosis decisions for planned second-look laparotomy rather than sacrificing potentially viable bowel.
- Give immediate broad-spectrum intravenous antibiotics, restore perfusion without excessive crystalloid, correct electrolytes and acidosis, decompress the stomach, and use unfractionated heparin when anticoagulation is indicated and bleeding risk permits.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Arterial embolism
Cardiac or aortic emboli abruptly occlude the SMA, commonly with atrial fibrillation or recent myocardial injury.
Arterial thrombosis
In-situ thrombosis usually occurs at a calcified mesenteric origin after collateral reserve has already been reduced by chronic multivessel atherosclerosis.
Venous thrombosis
Mesenteric venous thrombus obstructs outflow, so rising capillary pressure produces bowel-wall oedema, haemorrhage and ultimately impaired arterial inflow.
Non-occlusive hypoperfusion
Low output and vasoconstriction reduce mesenteric flow despite patent major vessels, especially in critically ill patients.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Oxygen-supply failure
The metabolically active mucosa is injured first when arterial delivery falls or venous congestion prevents adequate capillary oxygen exchange.
- 2Barrier breakdown
Epithelial disruption leaks fluid into the lumen and permits bacterial products to enter the circulation, amplifying systemic inflammation and shock.
- 3Transmural infarction
Continued hypoperfusion extends injury through muscularis and serosa, producing non-viable bowel, perforation, peritonitis and septic multiorgan failure.
- 4Reperfusion injury
Restored flow may worsen oedema and oxidative injury, so physiological and bowel monitoring continue after technical success.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Abrupt severe central abdominal pain in atrial fibrillation or another embolic source, with minimal tenderness early, suggests SMA embolism. Later guarding, acidosis and shock signify progression rather than diagnostic reassurance.
Acute deterioration on a background of food fear, weight loss, diffuse vascular disease or prior mesenteric symptoms suggests thrombosis of a chronically stenosed ostial vessel; multivessel disease limits collateral rescue.
Pain may evolve over days and is associated with intra-abdominal inflammation, malignancy, thrombophilia or portal hypertension. CT venous-phase filling defect, mesenteric oedema and haemorrhagic bowel thickening are discriminating.
Consider in shock, severe heart failure, dialysis, sepsis or high-dose vasoconstrictor exposure. Findings may be patchy and no occlusion is required; treatment targets low flow and precipitating vasoconstriction.
Peritonism, haemodynamic instability, ileus, gastrointestinal bleeding and organ failure are late features. Absence of dramatic tenderness does not protect a frail, sedated or critically ill patient.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Urgent multiphase CT angiographyFirst step - Why
- First definitive test in every patient with suspected AMI who is being considered for active treatment; acquire contrast arterial and venous phases with at most 1 mm slices, optionally preceded by non-contrast CT.
- Interpretation and limitations
- Identify embolus or ostial thrombosis, vessel patency, venous thrombus, collateral flow and bowel enhancement. Reduced enhancement, dilation, pneumatosis, portal gas or perforation increases concern for irreversible injury. Perform regardless of renal function because missed AMI outweighs contrast-associated risk.
- 02
Arterial blood gas, lactate and serial physiology - Why
- Measure severity, perfusion and response to resuscitation without using a biomarker as a gate to imaging.
- Interpretation and limitations
- Metabolic acidosis or rising lactate supports advanced hypoperfusion but is neither sensitive nor specific. A normal early lactate cannot rule out AMI.
- 03
Full blood count, U&E, LFT, coagulation and group-and-save - Why
- Identify inflammation, haemoconcentration, renal injury, electrolyte disturbance, coagulopathy and readiness for intervention.
- Interpretation and limitations
- Leucocytosis and renal dysfunction support severity but are non-diagnostic. Results guide resuscitation, anticoagulation and operative planning; they must not delay CTA.
- 04
ECG and embolic-source assessment - Why
- Detect atrial fibrillation, myocardial ischaemia or another cardiac cause while urgent abdominal management proceeds.
- Interpretation and limitations
- Atrial fibrillation strengthens an embolic mechanism and guides later echocardiography and anticoagulation; sinus rhythm does not exclude embolism.
- 05
Operative bowel assessment - Why
- At laparotomy determine peristalsis, colour, mesenteric pulsation and perfusion after revascularisation; adjunct fluorescence may help but does not replace judgement.
- Interpretation and limitations
- Clearly necrotic bowel is resected. Equivocal segments are preserved where safe for planned second look, recognising vasopressors and shock can confound appearance.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Perforated viscus
A perforated ulcer, diverticulum or tumour also causes abrupt pain and peritonitis; CT localises free gas and the diseased viscus.
Acute pancreatitis
Epigastric pain and lipase elevation can overlap, but neither excludes AMI when vascular risk and disproportionate pain are present.
Bowel obstruction
Dilation and vomiting can result from ischaemic ileus; assess enhancement and vessels rather than stopping at obstruction.
Aortic catastrophe
Aortic dissection or rupturing aneurysm can mimic AMI and simultaneously obstruct mesenteric branches, so the full aorta needs CTA assessment.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Worked emergency caseSevere pain with little early tendernessFirst stepA patient with atrial fibrillation develops sudden central abdominal pain, vomiting and rising physiological concern despite a relatively soft abdomen.+
- 1Treat this mismatch as suspected AMI: resuscitate, give intravenous broad-spectrum antibiotics, notify vascular and gastrointestinal surgical teams and state AMI explicitly on the CT request.
- 2Obtain urgent thin-slice arterial-and-venous phase CT angiography regardless of renal function; do not wait for lactate, D-dimer or creatinine normalization.
- 3If CTA shows embolic SMA occlusion without peritonitis, consider immediate endovascular-first revascularisation in the 24/7 specialist service and verify restored flow clinically and angiographically.
- 4If peritoneal irritation persists or bowel viability is doubtful, proceed to laparotomy, resect only non-viable bowel and plan a second look when margins or reconstruction remain uncertain.
02Preferred arterial pathwayArterial occlusion and bowel rescuePreferredCTA demonstrates thrombotic or embolic SMA occlusion in a patient eligible for active treatment.+
- 1Begin resuscitation and antibiotics and use systemic unfractionated heparin when indicated and not contraindicated, because its short action and reversibility suit unstable patients and renal impairment.
- 2First lineWhere immediate expertise exists and there is no reason that laparotomy must come first, consider endovascular revascularisation as first-line therapy; select aspiration, thrombolysis, angioplasty or stenting by lesion and bleeding risk.
- 3Aim to revascularise before bowel resection so viability is assessed under restored perfusion, but perform emergency laparotomy without delay when peritonitis identifies likely infarction.
- 4After resection, avoid a primary reconstruction when physiology or bowel viability is uncertain and schedule second-look laparotomy, commonly within 24–48 hours.
03Alternative mechanismsVenous thrombosis or non-occlusive diseaseAlternativeCTA shows mesenteric venous thrombosis or patent vessels with a low-flow vasoconstrictive pattern.+
- 1For venous thrombosis without peritonitis, start therapeutic anticoagulation, usually intravenous unfractionated heparin initially in an unstable patient or renal impairment, and treat the provoking cause.
- 2For non-occlusive ischaemia, reverse shock and low cardiac output, reassess vasoconstrictors, optimise oxygen delivery and seek early interventional or surgical advice if bowel injury persists.
- 3EscalationEscalate either mechanism to laparotomy for peritonitis, perforation, worsening organ failure or radiological evidence of necrosis; anticoagulation does not salvage dead bowel.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Bowel necrosis and perforation
Irreversible full-thickness injury causes gangrene, leakage and peritoneal contamination; resection is required because reperfusion cannot restore dead bowel.
Sepsis and multiorgan failure
Necrotic intestine and lost barrier integrity drive bacteraemia, vasodilatory shock, acidosis and progressive respiratory, renal and circulatory failure.
Short-bowel syndrome
Loss of extensive small bowel reduces absorptive surface, causing diarrhoea, electrolyte loss, malnutrition and possible long-term parenteral nutrition dependence.
Recurrent occlusion
A persistent cardiac embolic source, stent thrombosis, graft failure or progressive plaque can abruptly interrupt restored mesenteric perfusion again.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Trend pain, abdominal examination, blood pressure, urine output, lactate, pH and organ support frequently; improvement in one measure cannot alone prove bowel viability.
- After revascularisation, monitor access sites, distal perfusion, recurrent pain, bleeding, reperfusion injury and vessel patency; persistent peritoneal signs still require laparotomy.
- At planned second look, reassess previously equivocal bowel and decide reconstruction only when perfusion and physiology are secure.
- Investigate the mechanism after rescue: continuous rhythm assessment and echocardiography for embolism, atherosclerotic risk review for thrombosis, and selective thrombophilia or malignancy assessment for unexplained venous thrombosis.
- Plan nutrition and short-bowel support early after extensive resection, but avoid delaying definitive reperfusion or source control for nutritional optimisation.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Kidney function does not veto CTA
ESVS explicitly recommends urgent contrast arterial-and-venous phase CTA regardless of renal function. Contrast risk can be managed later; diagnostic delay permits irreversible intestinal necrosis.
Lactate is a severity marker, not a rule-out test
The liver can clear portal lactate and early mucosal ischaemia may not raise systemic levels. Use trends for physiology while acting on clinical suspicion and CTA.
Mechanism directs treatment
An embolus, ostial atherosclerotic thrombosis, venous thrombosis and non-occlusive vasoconstriction can produce similar pain but need different revascularisation, anticoagulation or haemodynamic strategies.
Revascularisation changes the resection boundary
A dusky segment may recover after arterial inflow returns. Restoring flow first when feasible and using second look can preserve bowel length without retaining clearly necrotic intestine.
Endovascular first does not mean laparotomy never
The ESVS recommendation applies to thrombotic or embolic SMA occlusion and available specialist expertise. Peritonitis, perforation or ongoing doubt about bowel viability still demands operative inspection.
11Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for an elevated lactate or D-dimer delays the only decisive imaging test and misses early disease.
- 02
Ordering a routine portal-venous abdominal CT without stating suspected AMI can omit the arterial acquisition and obscure a treatable occlusion.
- 03
Avoiding contrast solely because creatinine is raised reverses the immediate risk hierarchy in a time-critical lethal condition.
- 04
Treating all AMI as arterial embolism misses venous thrombosis and non-occlusive disease, for which the definitive strategy differs.
- 05
Assuming successful angiography proves viable bowel misses persistent necrosis; abdominal findings and planned reassessment remain essential.