Acute mesenteric ischaemia

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

Acute mesenteric ischaemia is a final common pathway with four main mechanisms. An SMA embolus often causes abrupt pain in a patient with atrial fibrillation and may spare the vessel origin. Thrombosis occurs on chronic ostial atherosclerosis and may represent acute-on-chronic disease. Mesenteric venous thrombosis impairs outflow and causes oedema and haemorrhage. Non-occlusive mesenteric ischaemia occurs in shock, severe cardiac failure, dialysis or vasoconstrictor exposure despite no fixed occlusion.

Early examination can be deceptively soft because mucosal ischaemia precedes transmural peritonitis. Nausea, vomiting, urgent stool or blood may occur. As infarction develops, pain can briefly diminish while toxicity, guarding and shock worsen. Risk recognition and CTA therefore precede reliance on classic signs. Serum lactate reflects systemic balance and may be normal while a segment of gut is threatened.

Management joins diagnosis and treatment. CTA identifies vessel, bowel enhancement, pneumatosis, portal venous gas, mesenteric oedema and alternative causes. An arterial occlusion may undergo aspiration, thrombectomy, stenting or open embolectomy or bypass; venous thrombosis is primarily anticoagulated unless infarction demands surgery; non-occlusive disease needs correction of low flow and specialist vasodilator strategies. Second-look surgery avoids either leaving dead bowel or sacrificing potentially recoverable bowel.

Key points

Severe abdominal pain out of proportion to early examination is the classic clue, but older, sedated or critically ill patients may present with delirium, diarrhoea, bleeding or unexplained organ failure.
Arterial embolism is associated with atrial fibrillation or cardiac thrombus; arterial thrombosis with atherosclerosis; venous thrombosis with thrombophilia or inflammation; non-occlusive disease with low flow and vasoconstriction.
A normal lactate, pH or D-dimer cannot exclude early bowel ischaemia; laboratory abnormalities often mark advanced disease.
Request urgent CT angiography with arterial and portal-venous assessment and make the suspicion explicit; non-contrast CT or routine portal-venous imaging may miss the vascular diagnosis.
Do not delay clinically necessary contrast because kidney function is unknown when bowel survival is at stake; resuscitate and involve radiology.
Immediate care includes ABCDE, analgesia, careful crystalloid, broad antibiotics, nil by mouth and therapeutic anticoagulation unless contraindicated, alongside urgent operative and vascular planning.
Restore mesenteric blood flow as early as possible using endovascular, open or hybrid techniques, while resecting only clearly non-viable bowel and considering a second look.
Peritonitis, perforation or shock indicates infarcted bowel until proven otherwise and demands emergency laparotomy with critical-care support.

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

Arterial embolism

Cardiac emboli, particularly with atrial fibrillation or intracardiac thrombus, can abruptly occlude a previously patent mesenteric artery.

Arterial or venous thrombosis

Atherosclerotic arterial disease may thrombose at a narrowed origin, while mesenteric venous thrombosis is associated with inflammation, malignancy and thrombophilia.

Non-occlusive low flow

Shock, severe cardiac failure and vasoconstrictor exposure can reduce splanchnic perfusion without a fixed arterial blockage, especially in critically ill patients.

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

1
Perfusion failure
Arterial inflow loss, venous congestion or severe vasoconstriction deprives metabolically active bowel mucosa of oxygen, initially injuring the vulnerable mucosa.
2
Barrier breakdown
Mucosal injury causes oedema, haemorrhage and loss of epithelial integrity, permitting bacterial and toxin translocation into the circulation.
3
Transmural infarction
Persistent ischaemia extends through the bowel wall, causing necrosis, perforation, peritonitis, profound sepsis and irreversible organ failure.

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

Arterial embolic patternRed flag

Sudden severe diffuse pain with minimal early tenderness in a person with atrial fibrillation, recent infarction or embolic disease should trigger immediate CTA.

Acute-on-chronic thrombosisRed flag

A history of postprandial pain and weight loss followed by abrupt persistent pain suggests thrombosis of established mesenteric atherosclerosis.

Mesenteric venous thrombosisRed flag

More gradual pain, bowel-wall oedema or bleeding with thrombophilia, malignancy, pancreatitis, portal disease or inflammation suggests venous outflow obstruction.

Non-occlusive ischaemiaRed flag

A critically ill patient on vasopressors develops distension, feeding intolerance, acidosis or unexplained deterioration; abdominal pain may be absent.

Transmural infarctionRed flag

Peritonism, shock, severe metabolic acidosis, pneumatosis with poor enhancement, portal venous gas or perforation indicates advanced injury requiring immediate laparotomy.

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
CT angiography abdomen and pelvisFirst step
Why
Acquire arterial and portal-venous phases urgently to identify arterial or venous occlusion, non-occlusive vasospasm, bowel viability and alternative pathology.
Interpretation and limitations
A patent proximal artery does not exclude distal emboli or non-occlusive disease. Absence of late signs does not exclude salvageable early ischaemia.
02
Blood gas, lactate and metabolic profile
Why
Assess shock, acidosis, renal injury and serial response alongside FBC, coagulation, CRP, amylase and crossmatch.
Interpretation and limitations
Normal lactate cannot rule out early disease. Rising lactate and acidosis suggest advanced injury but are not specific.
03
ECG and embolic-source assessment
Why
Identify atrial fibrillation or myocardial ischaemia and plan echocardiography or cardiac imaging after immediate bowel treatment.
Interpretation and limitations
A cardiac source supports embolism and determines long-term prevention but should not delay CTA or revascularisation.
04
Thrombophilia and provoking-factor assessment
Why
After stabilisation, investigate malignancy, inflammatory disease, portal pathology, oestrogen exposure and selected thrombophilia in mesenteric venous thrombosis.
Interpretation and limitations
Acute thrombosis and anticoagulation alter some assays; haematology should time and interpret testing.
05
Operative bowel viability assessment
Why
Directly assess colour, peristalsis, mesenteric pulsation and adjunct perfusion in a patient with peritonitis or uncertain bowel survival.
Interpretation and limitations
Borderline bowel may recover after revascularisation and resuscitation; planned second look can preserve length.
06
Histology and resection specimen
Why
Confirm ischaemic injury and seek embolic, vasculitic, thrombotic or alternative pathology in removed bowel.
Interpretation and limitations
Histology often cannot identify the entire upstream mechanism; combine it with CTA and operative findings.

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

Acute pancreatitis

Severe epigastric pain with characteristic enzyme elevation supports pancreatitis, whereas vascular risk and CT angiographic occlusion or poor bowel enhancement favour mesenteric ischaemia.

Perforated viscus

Abrupt pain with free intraperitoneal gas and early peritonism suggests perforation; early mesenteric ischaemia may have extreme pain despite a soft abdomen.

Bowel obstruction

Colicky pain, distension and a mechanical transition point favour obstruction, though closed-loop obstruction can itself strangulate and produce secondary ischaemia.

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

01ImageSuspected early ischaemiaFirst stepDisproportionate pain or high-risk deterioration raises mesenteric ischaemia before peritonism.

1Use ABCDE, provide analgesia, obtain access and bloods, and call senior general and vascular surgery while requesting immediate CTA by name.
2Do not allow a normal lactate or unavailable creatinine to delay a life-saving scan; communicate cardiac, vascular and low-flow risks to radiology.
3Start broad antibiotics, nil by mouth and careful fluid resuscitation, and give therapeutic heparin unless bleeding or another contraindication is identified.
4Move directly from CTA to the endovascular, hybrid or open revascularisation plan.

02OperatePeritonitis or infarctionThere is perforation, peritonism, shock or convincing transmural non-viability.

1Proceed to emergency laparotomy with vascular or interventional input and critical-care resuscitation; do not await further biomarker change.
2Revascularise when feasible before final bowel assessment, control contamination and resect clearly necrotic segments.
3Use damage-control principles and a planned second look when viability remains uncertain or physiology is hostile.
4Contact an intestinal-failure centre early if extensive resection may be required.

03MechanismTailor definitive treatmentDefinitiveCTA establishes arterial embolus, arterial thrombosis, mesenteric venous thrombosis or non-occlusive disease.

1For arterial occlusion, select endovascular thrombectomy or stenting, open embolectomy or bypass based on anatomy, bowel state and local capability.
2For venous thrombosis without infarction, anticoagulate and treat the provoking factor; operate only when bowel compromise requires it.
3For non-occlusive disease, correct low cardiac output and hypovolaemia, minimise vasoconstriction where possible and use specialist catheter vasodilator treatment selectively.
4Establish long-term anticoagulant or atherosclerotic secondary prevention and review recurrence risk after survival.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Prevents thrombus propagation and is especially central in mesenteric venous thrombosis while definitive treatment proceeds.

Unfractionated heparin

Therapeutic intravenous bolus and infusion according to the local vascular protocol and coagulation monitoring, unless active bleeding or another contraindication exists.

Bleeding, HIT and monitoring error. Do not postpone revascularisation or laparotomy to achieve a laboratory target; reverse when emergency surgery requires.

Reduces bacterial translocation and treats contamination as the mucosal barrier fails.

Broad-spectrum intravenous antibiotics

Immediate local intra-abdominal sepsis regimen with Gram-negative and anaerobic cover, adjusted for renal function and cultures.

Antibiotics cannot restore perfusion. Narrow after source control and microbiology and monitor allergy, renal injury and C. difficile.

Corrects hypovolaemia and supports mesenteric perfusion during imaging and intervention.

Balanced crystalloid

Small reassessed boluses followed by goal-directed replacement using NICE CG174, urine and haemodynamics rather than an unbounded fixed volume.

Excessive fluid can worsen bowel oedema and abdominal pressure; cardiac failure and non-occlusive disease require critical-care haemodynamic expertise.

Relieves mesenteric arterial spasm in selected non-occlusive ischaemia alongside correction of systemic low flow.

Catheter-directed vasodilator

Interventional specialist regimen, such as papaverine where locally available, delivered selectively for non-occlusive vasoconstriction.

Hypotension, arrhythmia and catheter complications. It is not an empirical ward infusion and does not treat infarcted bowel.

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

Bowel necrosis and perforation

Untreated vascular compromise causes irreversible infarction, contamination and the need for extensive resection rather than bowel-preserving revascularisation alone.

Sepsis and multiorgan failure

Barrier failure and necrotic bowel drive shock, acidosis, renal injury and respiratory failure, with mortality rising once peritonitis develops.

Short-bowel syndrome

Extensive resection can leave inadequate absorptive surface, causing high-output losses, malnutrition and dependence on specialist intestinal-failure support.

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

Repeat abdominal findings, pain, perfusion, urine and lactate frequently through resuscitation and after revascularisation.
Monitor anticoagulation, platelets, haemoglobin and bleeding while recognising the need for rapid operative reversal.
Assess renal function and contrast exposure without allowing monitoring to obstruct urgent diagnosis.
After revascularisation, watch for reperfusion injury, compartment physiology, recurrent occlusion and ongoing bowel necrosis.
Use second-look surgery when planned and reassess nutrition or remaining bowel length after resection.
Establish telemetry and cardiac evaluation for embolic sources and secondary-prevention follow-up after the acute phase.
Document time of suspicion, CTA request, specialist contact and reperfusion because delay is a major modifiable risk.

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

Pain may improve when bowel dies

Loss of sensory function can reduce pain as transmural necrosis advances, so apparent relief with worsening physiology is ominous.

Lactate is not a gatekeeper

Hepatic clearance and limited segmental injury keep lactate normal early. Clinical probability should gate CTA.

CTA must include vessels

A non-contrast renal-colic scan or generic portal-venous study is not equivalent to an arterial and venous mesenteric protocol.

Revascularise before judging

Dusky bowel may recover after flow restoration. When safe, reperfusion before final resection and a second look preserve absorptive length.

NOMI has no clot to find

Low flow and intense vasoconstriction can infarct bowel despite patent major vessels, especially in critical illness.

11Common pitfallsFrequent interpretation and management errors.

01
Reassuring oneself with a normal lactate.
02
Ordering routine CT rather than CTA and omitting the suspicion.
03
Waiting for peritonism before involving vascular and general surgery.
04
Treating pain relief as recovery during worsening shock.
05
Giving anticoagulation but delaying necessary revascularisation.
06
Resecting borderline bowel before restoring flow when a second-look strategy is possible.