Non-occlusive mesenteric ischaemia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

NOMI is intestinal ischaemia caused by inadequate splanchnic oxygen delivery and mesenteric vasoconstriction without an acute occluding thrombus. It occurs with low cardiac output, hypovolaemic or septic shock, vasoconstrictive treatment, cardiac surgery, renal replacement therapy, severe burns and raised intra-abdominal pressure. Pre-existing asymptomatic mesenteric stenosis may reduce reserve, but major arteries can remain patent. The ileocolic territory and right colon may be affected as well as small bowel.

Diagnosis is deliberately multimodal. Sedation removes pain and tenderness, so distension, feeding intolerance, gastrointestinal bleeding, worsening acidosis or escalating organ support may be the only clues. Lactate reflects systemic hypoperfusion and can be normal early. CTA should include arterial and venous phases and thin slices: reduced bowel enhancement, thickening, pneumatosis and portal venous gas without significant SMA occlusion support NOMI. Treatment occurs simultaneously—restore perfusion, treat the precipitant, involve surgery, give early antibiotics and decide whether bowel is viable. Catheter vasodilators are selective rescue, not an alternative to resecting necrosis.

Key points

Suspect NOMI in a shocked or critically ill patient with abdominal distension, pain, bleeding, feed intolerance or otherwise unexplained deterioration, even if the patient is sedated.
Obtain urgent contrast CTA in arterial and venous phases with thin slices; major mesenteric arteries may be patent while the bowel fails to enhance.
No single lactate or D-dimer measurement confirms or excludes NOMI. Only after cause correction, when bowel remains potentially viable and there is no peritonitis, perforation or clear necrosis, may an expert centre consider SMA catheter vasodilators under protective heparinisation; laparotomy overrides catheter rescue when bowel is non-viable.
Correct the cause immediately: restore effective circulating volume and cardiac output, treat sepsis, review avoidable vasoconstrictors and measure intra-abdominal pressure when relevant.
Give early broad-spectrum intravenous antibiotics in acute mesenteric ischaemia because mucosal failure permits bacterial translocation; no single stable national regimen covers every ICU exposure, allergy, renal function and operative finding, so select, culture-review and de-escalate through the severe-intra-abdominal-infection pathway.
Peritonitis, perforation or worsening with suspected necrosis requires prompt laparotomy, resection of clearly non-viable bowel and planned reassessment when viability is uncertain.
Selected patients without irreversible bowel injury may be considered for SMA catheter vasodilators under protective heparinisation in an expert centre.
Intra-arterial papaverine dosing in ESVS is study-derived, evidence is low, and sudden systemic hypotension is possible; it is not a routine ward prescription.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Low cardiac output

Heart failure, myocardial infarction and post-cardiac-surgery states reduce splanchnic oxygen delivery and provoke compensatory mesenteric vasoconstriction.

Shock and volume loss

Sepsis, haemorrhage, burns, hypovolaemia and dialysis-related hypotension reduce effective circulating volume and divert flow away from the intestine.

Pressure and medicines

Abdominal compartment syndrome mechanically impairs perfusion, while catecholamines, vasopressin, digoxin or cocaine may intensify mesenteric vasoconstriction.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Splanchnic vasoconstriction
Compensatory narrowing of patent mesenteric vessels preserves central circulation at the expense of mucosal flow, particularly during prolonged shock.
2
Mucosal barrier failure
Early mucosal hypoxia disrupts barrier integrity, permits bacterial translocation and progresses from reversible injury toward full-thickness necrosis.
3
Reperfusion injury
Restored flow releases inflammatory mediators and metabolites from injured bowel, potentially worsening capillary leak, acidosis and multiorgan failure.
4
Reduced reserve
Pre-existing mesenteric atherosclerosis may be asymptomatic until low flow removes collateral reserve, even without a new complete arterial occlusion.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Masked ICU presentationRed flag

A ventilated patient may show only distension, feed intolerance, maroon stool, rising support needs or new organ failure; absence of reported pain is meaningless.

Low-flow context

Septic, cardiogenic or hypovolaemic shock, recent cardiac or aortic surgery, dialysis-related hypotension and severe burns create the typical physiological setting.

Vasoconstrictor burden

High or rising catecholamine exposure, vasopressin and digoxin can worsen splanchnic perfusion, although essential vasopressors cannot simply be stopped without restoring circulation.

Peritoneal transitionRed flag

Guarding, rebound, rigidity, perforation or sudden deterioration indicates likely transmural infarction and moves management from rescue assessment to urgent surgery.

Patent-vessel paradox

CTA may show patent coeliac and superior mesenteric arteries alongside severe bowel injury; this discordance is characteristic of a non-occlusive mechanism.

Red flags requiring action

Peritonism, perforation, pneumoperitoneum or clinical collapse indicates likely transmural necrosis and demands urgent operative exploration.
Shock with new abdominal distension, gastrointestinal bleeding, feed intolerance or unexplained organ failure should trigger NOMI suspicion even without reported pain.
Absent bowel enhancement, pneumatosis or portal venous gas on CTA with no significant SMA occlusion is a high-risk non-occlusive pattern.
Rising vasopressor requirements, low cardiac output, severe hypovolaemia or abdominal compartment syndrome perpetuates mesenteric vasoconstriction and tissue hypoxia.
A normal early lactate does not exclude intestinal ischaemia; waiting for a biomarker threshold can sacrifice viable bowel.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

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 biphasic CT angiographyFirst step
Why
Assess bowel viability and exclude arterial embolism, thrombosis and mesenteric venous thrombosis.
Interpretation and limitations
Look for reduced enhancement, thickening, dilatation, pneumatosis, portal venous gas and free fluid despite patent major vessels. Do not let AKI alone delay a life-saving scan.
02
Serial lactate, blood gas and full blood count
Why
Track global hypoperfusion, acidosis, inflammation and treatment response.
Interpretation and limitations
Abnormal trends increase concern, but a single normal value cannot exclude NOMI and an elevated lactate cannot identify bowel viability by itself.
03
Haemodynamic assessment
Why
Identify low cardiac output, hypovolaemia, sepsis and excessive vasoconstrictor dependence that sustain mesenteric hypoperfusion.
Interpretation and limitations
Use repeated bedside perfusion assessment and appropriate monitoring; a normal blood pressure on high-dose vasopressors does not prove adequate gut flow.
04
Bladder pressure for intra-abdominal pressure
Why
Detect intra-abdominal hypertension or abdominal compartment syndrome in an at-risk patient.
Interpretation and limitations
Raised pressure with new organ dysfunction can require decompression; ESVS recommends urgent laparotomy when NOMI and abdominal compartment syndrome coexist.
05
Operative assessment with planned second look
Why
Determine viability when peritonitis or imaging suggests infarction and preserve uncertain bowel where possible.
Interpretation and limitations
Resect clearly necrotic segments, use damage-control principles in unstable patients and reassess borderline bowel after resuscitation rather than over-resecting once.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Arterial embolic AMI

Atrial fibrillation or cardiac embolic source with a discrete SMA filling defect indicates occlusive embolism requiring a revascularisation strategy.

Arterial thrombotic AMI

Known postprandial symptoms and calcified ostial multivessel disease strongly suggest acute thrombosis developing on chronic mesenteric atherosclerosis.

Mesenteric venous thrombosis

Venous filling defects, bowel oedema and prothrombotic risk indicate venous congestion; anticoagulation is central when peritonitis is absent.

Critical illness ileus

Ileus causes distension and feed intolerance but should not produce convincing bowel hypoenhancement, pneumatosis or portal venous gas in a deteriorating patient.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Worked caseDeterioration during septic shockFirst stepA sedated patient on increasing vasopressors develops distension, feed intolerance, acidosis and rising lactate.

1Recognise the high-risk NOMI pattern and examine for distension, bleeding and peritoneal signs while alerting critical care, radiology and surgery; do not wait for pain or a diagnostic lactate.
2Perform immediate arterial and venous phase CTA and simultaneously restore effective volume, optimise cardiac output, treat sepsis, stop enteral feeding, decompress the stomach and review avoidable vasoconstrictors.
3CTA bowel hypoperfusion with patent major vessels supports NOMI; peritonitis, perforation or non-viable bowel mandates urgent laparotomy and resection.
4Without irreversible injury, continue cause correction and discuss expert angiography with intra-arterial vasodilator under protective heparinisation; the evidence and regimen are specialist-dependent.
5Verify response through haemodynamics, lactate trend, abdominal findings and repeat imaging or operative second look; apparent arterial patency alone is not recovery.

02Immediate branchPeritonitis or perforationClinical or radiological evidence indicates transmural infarction, perforation or an acute peritoneal abdomen.

1Continue resuscitation, broad-spectrum intravenous antibiotics and organ support while proceeding to exploration without delay.
2Resect frankly non-viable bowel, preserve segments of uncertain viability when safe and use damage-control surgery for severe physiological derangement.
3Plan a second look in the appropriate operative window, monitor for ongoing shock and address abdominal compartment syndrome or continuing low flow.

03Selective rescueCatheter-directed vasodilationNOMI persists despite cause correction, bowel is not clearly infarcted and an expert mesenteric team judges catheter treatment proportionate.

1Confirm that immediate surgery is not indicated and obtain angiographic evidence compatible with vasoconstriction when proceeding.
2ESVS allows consideration of intra-arterial papaverine or prostaglandin in the SMA under protective heparinisation; monitor continuously for hypotension and bleeding.
3EscalationEscalate promptly to surgery if pain, peritoneal findings, organ failure or imaging worsens because vasodilation cannot reverse established necrosis.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Relieves severe mesenteric vasoconstriction in selected NOMI when bowel is potentially viable and correction of the precipitating low-flow state is insufficient.

Intra-arterial papaverine (specialist catheter rescue; no standard licensed UK NOMI regimen identified)

In an angiography suite, ESVS describes a study-derived 80 mg papaverine bolus directly into the superior mesenteric artery followed by 30–60 mg/hour for 24–72 hours. A current eMC search returned no papaverine SmPC, and no standard licensed UK intra-arterial NOMI regimen was identified; do not infer that every papaverine product or use is categorically unlicensed. The interventional, vascular, critical-care and pharmacy team must verify the available product and legal route, then select preparation, duration and protective heparinisation and stop for harm or lack of response.

Evidence is low and comparative dose studies are absent. Continuous arterial-pressure and rhythm monitoring is essential because sudden systemic hypotension can be fatal; assess bleeding risk, hepatic handling, line complications and the separate heparin indication. Never delay laparotomy for peritonitis, perforation or necrotic bowel.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Transmural infarction

Persistent hypoperfusion progresses from early mucosal injury to full-thickness bowel necrosis, perforation, diffuse peritonitis and overwhelming sepsis.

Short bowel syndrome

Extensive intestinal resection can leave inadequate absorptive length, requiring prolonged parenteral nutrition and coordinated specialist intestinal-failure care.

Abdominal compartment syndrome

Oedema and resuscitation raise intra-abdominal pressure, further impairing gut and renal perfusion in a self-amplifying cycle.

Multiorgan failure

Shock, bacterial translocation and reperfusion inflammation can drive renal, respiratory, hepatic and circulatory failure even after bowel treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Trend mean arterial pressure, cardiac output or other perfusion measures, vasopressor dose, urine output, lactate and acid-base status during resuscitation.
Repeat abdominal examination frequently and monitor distension, gastrointestinal bleeding, feed intolerance and organ support needs, including in sedated patients.
After catheter vasodilation, monitor invasive pressure, rhythm, access site, bleeding and angiographic or clinical perfusion response continuously.
After bowel surgery, monitor for ongoing necrosis, short-bowel risk, abdominal compartment syndrome, sepsis and the need for a planned second look.
Review antibiotic indication, cultures and duration daily; de-escalate to microbiology and operative findings rather than continuing unexamined broad coverage.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Patent is not perfused

CTA can show an open SMA while arteriolar vasoconstriction and low flow starve the bowel. Vessel patency answers a different question from tissue oxygen delivery.

Lactate is late and global

Lactate may rise from shock elsewhere and can remain normal early in bowel ischaemia. It is useful as a trend, not a gatekeeper to CTA.

Pressure can steal flow

Abdominal compartment syndrome reduces mesenteric perfusion mechanically; more fluid without measuring pressure can worsen the cycle and delay decompression.

Vasopressors are a balance

Essential vasopressors maintain systemic perfusion but may worsen mesenteric constriction. Correct volume and cardiac output, then use the lowest effective vasoconstrictor burden.

Rescue is not source control

Papaverine may relax vessels but cannot restore dead bowel. Peritoneal signs or perforation always override enthusiasm for catheter therapy.

11Common pitfallsFrequent interpretation and management errors.

01
Excluding NOMI because the SMA is patent misunderstands the definition and delays treatment.
02
Waiting for severe hyperlactataemia misses the early salvage window and confuses systemic shock with bowel-specific diagnosis.
03
Stopping vasopressors abruptly without correcting circulation can worsen global and mesenteric perfusion.
04
Using catheter vasodilators in peritonitis delays resection of necrotic bowel.
05
Avoiding CTA solely because creatinine is raised can trade a manageable contrast risk for missed lethal intestinal infarction.

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