Acute mesenteric ischaemia

An 82-year-old woman with atrial fibrillation arrives at 04:00 with three hours of the worst central abdominal pain of her life — and a soft, non-tender abdomen. The registrar's lactate is 1.8 and he is reassured. He should not be: this is exactly the patient, exactly the examination and exactly the biomarker trap in which this disease kills two out of three people. Every step of her night is mapped below, with the numbers attached.^[1][9][5]

Definition and the four subtypes

Acute mesenteric ischaemia (AMI) is caused by sudden interruption of blood supply to the intestine, leading to cellular damage, intestinal necrosis and, commonly, death if untreated.^[1] The classification that drives every downstream decision is aetiological. Historically: mesenteric arterial embolism about 50%, arterial thrombosis 15–25%, mesenteric venous thrombosis 5–15%, and non-occlusive mesenteric ischaemia (NOMI) most of the rest.^[1] The contemporary shift is itself an exam point: WSES 2022 reports embolism down to about 25% of cases (modern anticoagulation for atrial fibrillation), thrombosis up from a historical 20–35% to about 40% (ageing atherosclerotic populations), and NOMI at about 25% and rising with the critically ill.^[1] Tamme's meta-analysis of 163 studies confirms the pooled picture: occlusive arterial disease constitutes 68.6% of all AMI, with similar proportions of embolism and thrombosis.^[5]

Each subtype has a fingerprint. The embolic patient has atrial fibrillation in nearly 50% of cases and a prior arterial embolus in about a third; the onset is abrupt.^[1] The thrombotic patient occludes an atherosclerotic SMA origin, often after a chronic mesenteric ischaemia prodrome of postprandial pain, weight loss and food fear — the history that tells you the lesion will not yield to simple embolectomy.^[1] The NOMI patient is the cardiac-failure or septic ICU patient on vasopressors, whose SMA vasoconstricts in a low-flow state without any occluding lesion.^[1] The venous patient presents more indolently — nausea, vomiting, cramping pain, gastrointestinal bleeding in 10% — on a background of thrombophilia.^[1][6]

Epidemiology — rare, elderly, lethal

^{[5] [1]}

AMI is uncommon — 0.09–0.2% of all acute emergency-department admissions — but it is a disease of the elderly, and the demographics are exponential: the incidence at 80 is roughly tenfold that at 60, and in patients aged 75 and over AMI is a more prevalent cause of acute abdomen than appendicitis.^[1] Mortality exceeds 50% where the disease goes unrecognised, and WSES's framing is that delay in diagnosis is the dominant factor behind mortality rates of 30–70%.^[1] The pooled short-term mortality in Tamme's analysis was 59.6%, improving from 68.7% in patients treated before 2000 to 55.0% in those treated from 2000 onwards — real progress, from a dreadful baseline.^[5] The subtype gradient matters for counselling: venous AMI carries the best prognosis (24.6%), NOMI the worst alongside unrevascularised arterial disease (58.4%), while successfully revascularised occlusive arterial AMI comes down to 33.9%.^[5]

Pathophysiology — mucosa first, then the cascade

Intestinal ischaemia begins at the metabolically vulnerable mucosa and progresses transmurally; early loss of the mucosal barrier permits bacterial translocation and septic complications, which is the rationale for immediate broad-spectrum antibiotics (1C).^[1] In occlusive disease the event is mechanical — an embolus lodged in the SMA (typically just distal to the middle colic origin, which is why the proximal jejunum may be spared) or thrombosis of an atherosclerotic origin. In NOMI the mechanism is functional: SMA vasoconstriction with low splanchnic flow, precipitated by hypovolaemia, cardiac failure, sepsis and vasoconstrictive drugs.^[1] In venous thrombosis the obstruction is outflow: congestion, submucosal oedema and haemorrhagic infarction behind a thrombosed superior mesenteric vein.^[6]

Two downstream phenomena complete the picture. First, reperfusion injury: release of toxic products after resection and restored flow induces inflammatory processes that can produce multiorgan failure even in the absence of necrotic bowel — the reason these patients go to ICU, not the ward, whatever the abdomen looks like at closure.^[1] Second, viability uncertainty: no intraoperative tool reliably declares bowel viable or dead at first look, which is the intellectual basis of the second-look laparotomy.^[1][22]

Clinical presentation

The classic early presentation is excruciating abdominal pain with an unrevealing examination — WSES's strong recommendation is that severe pain out of proportion to physical findings should be assumed to be AMI until disproven (1C), and that the key to early diagnosis is a high level of clinical suspicion.^[1] More than half of AMI patients undergo imaging with no prior suspicion of the diagnosis, so the radiologist, not the surgeon, is often the first person in a position to save the bowel.^[6]

The late presentation is the lethal one: when physical findings suggest an acute intra-abdominal catastrophe, bowel infarction has already occurred, and survival in this comorbid population falls dramatically. Peritonitis secondary to bowel necrosis mandates surgery without delay (1C).^[1] Between those poles sit the subtype fingerprints from the definition section — and the trap that the elderly, the sedated ICU patient and the NOMI patient present without any classic picture at all.^[1]

The biomarker trap — lactate and D-dimer

WSES is blunt: there are no laboratory parameters sufficiently accurate to conclusively identify the presence or absence of ischaemic or necrotic bowel, though lactate, leukocytosis and D-dimer may assist (2B) — and no accurate biomarker has been identified at all.^[1] Know the three datasets cold.

Lactate. More than 90% of AMI patients have leukocytosis and about 88% have metabolic acidosis with elevated lactate — but that is prevalence in established disease, not diagnostic performance.^[1] Cudnik's meta-analysis pooled lactate at sensitivity 86% but specificity 44%: it misses one in seven and cries wolf constantly.^[7] Collange's controlled multicentre study is the kill shot: matched ICU patients with and without AMI had statistically indistinguishable lactates on days 0 and 1, with discrimination AUCs of 0.57 and 0.60 — no better than a coin flip; the authors conclude lactate should not be used to diagnose AMI, though it still grades severity.^[9] What lactate does carry is prognostic weight: WSES quotes an elevated level (above 2 mmol/L) associated with irreversible ischaemia at a hazard ratio of 4.1, and Otto's multivariable analysis kept lactate among the independent mortality predictors.^[1][26]

D-dimer. The useful negative. Pooled sensitivity 96% with specificity 40% in Cudnik's analysis — a rule-out, not a rule-in; WSES cites a series in which no patient with a normal D-dimer had intestinal ischaemia.^[7][1]

Investigations — CTA without delay

Computed tomography angiography should be performed without delay in any patient with suspicion for AMI — WSES's only 1A recommendation in this disease. Delay in diagnosis is the dominant driver of the 30–70% mortality, and every 6 hours of delay in diagnosis (in practice, delay to CTA) doubles mortality.^[1] Plain X-ray is explicitly not recommended for evaluating intestinal ischaemia.^[1]

The accuracy figures form a consistent triad across eras: WSES quotes sensitivity 93% with specificity 100% (PPV 100%, NPV 94%); Cudnik's meta-analysis pooled CT at sensitivity 94% and specificity 95% (positive LR 17.5, negative LR 0.09) and concluded only CT angiography has adequate accuracy to establish the diagnosis in lieu of laparotomy; Reintam Blaser's 2025 radiology meta-analysis put CTA at sensitivity 92.0% and specificity 98.8% — markedly better than non-angiographic CT protocols (75.8%/90.5%).^[1][7][8] The protocol is biphasic or triphasic: pre-contrast images for vascular calcification, hyper-attenuating thrombus and intramural haemorrhage, then arterial and venous phases for thrombus in the mesenteric vessels, abnormal bowel-wall enhancement and embolism or infarction of other organs.^[1][28]

Reading the bowel, not just the vessel. The CTA signs that mark irreversible, transmural ischaemia are intestinal dilatation and wall thickening, reduction or absence of visceral enhancement, pneumatosis intestinalis and portal venous gas — especially in combination.^[1] Six radiological findings predict bowel necrosis: bowel-loop dilatation, pneumatosis, SMV thrombosis, free intraperitoneal fluid, portal vein thrombosis and splenic vein thrombosis.^[1] Among the non-vascular features, absent or reduced bowel-wall enhancement carries the best prognostic value (specificity 90.1%), and dilatation beyond 25 mm raises suspicion of necrosis in arterial AMI.^[8][6]

Differential diagnosis

The differential of the elderly patient with severe pain and a soft abdomen is, in practice, the differential of "things that kill quietly": ruptured abdominal aortic aneurysm, inferior myocardial infarction, pancreatitis, and the perforated viscus that has not yet declared itself. CTA answers most of these in one acquisition — which is the operational reason suspicion goes to CT rather than to a plain film or a lactate.^[1] Two framing facts keep AMI on the list: over 75 it is a more prevalent cause of acute abdomen than appendicitis, and more than half of cases are imaged without the diagnosis having been suspected.^[1][6] Once CTA shows vascular impairment with bowel injury and no other cause, the subtype patterns discriminate themselves — arterial occlusion with decreased wall enhancement, venous thrombosis with hypoattenuating wall thickening and submucosal oedema, NOMI with ischaemic bowel in the face of patent mesenteric vessels.^[6][1]

Management

The immediate bundle

Once the diagnosis is made or strongly suspected: fluid resuscitation with crystalloid and blood products (1B) with early haemodynamic monitoring, electrolyte correction, nasogastric decompression, and immediate broad-spectrum antibiotics (1C) for at least 4 days in the stable immunocompetent patient — ischaemia breaches the mucosal barrier and infection risk outweighs stewardship concerns here.^[1] Full-dose anticoagulation is started in everyone, regardless of subtype or operative plan: unfractionated heparin is effective and easy to manage, particularly with acute kidney injury.^[1] The international ICU study (370 patients, 33 centres) gives the bundle its outcome data: early full-dose anticoagulation was associated with 30-day survival of 53.5% versus 41.7% without (NNT 8), with no increase in haemorrhagic complications.^[27]

Revascularization — endovascular first, and the honesty paragraph

WSES: endovascular revascularization procedures are the primary option in arterial occlusion when sufficient expertise is available (1C) — while acknowledging that no randomised trial has compared open with endovascular approaches.^[1] The technique follows the lesion. Acute embolic SMA occlusion without peritonitis: aspiration embolectomy with thrombolytic treatment should be considered; there are no data showing superiority of open over endovascular treatment, though roughly 40% of endovascular cases go on to unplanned surgery.^[1] Atherosclerotic thrombotic occlusion at the SMA origin needs a different tool: stenting — at laparotomy, a retrograde open mesenteric (ROMS) or percutaneous approach can stent the origin, and surgical bypass (antegrade from the supracoeliac aorta, or retrograde from the infrarenal aorta or common iliac; single-vessel SMA revascularization is usually sufficient) is now seldom needed.^[28][1] For the patient in extremis, or where the skillset is absent, temporary SMA shunting should be considered to spare bowel while help arrives.^[1]

The comparative evidence must be quoted with its selection bias attached. Murphy's systematic review found 30-day mortality of 15–39% for endovascular versus 33–50% for open revascularization, with bowel resection in 14–28% versus 33–63%.^[11] But the Japanese JROAD-DPC analysis (746 revascularised patients) found in-hospital mortality statistically identical (22.5% endovascular versus 21.4% open), as were resection rates.^[12] The AMESI prospective substudy shows why: mortality was 2.9% in the endovascular-effective group, 41.2% where endovascular treatment was insufficient as monotherapy, and 45.8% in the surgical group — but no approach had an independent effect on mortality once severity was considered.^[13] Reintam Blaser's management meta-analysis reached the same conclusion by meta-regression: the endovascular advantage in crude analyses may be abolished by adjusting for illness severity.^[10] The examinable synthesis: choose by the patient's condition, the lesion and the available expertise — not by ideology — and say the selection-bias caveat out loud.^[13][10]

Laparotomy, resection and the viability problem

Peritonitis mandates surgery without delay (1C): bowel infarction has already occurred, and the goals at laparotomy are to re-establish blood supply where possible, resect frankly necrotic bowel and preserve everything marginal for reassessment.^[1] The operative dilemma is that no reliable tool predicts transmural necrosis at first look — clinical assessment by an experienced surgeon remains central, and marginal bowel is better left for a second look than either resected wholesale or anastomosed in doubt.^[28][22]

Damage control and the second look

WSES recommends damage-control surgery with temporary abdominal closure as an important adjunct when intestinal resection is required — it allows reassessment of bowel viability and manages severe abdominal sepsis (1B) — and calls damage control the surgical modality of choice in the critically ill AMI patient.^[1] Most patients are diagnosed only when transmural infarction has already developed, which is exactly when revascularization, resection, open abdomen and second look become necessary to salvage them.^[22]

The prospective evidence for the two-stage strategy is Brillantino's 85-patient series: at second look (48 h), 21% of the damage-control group required further resection for progressing ischaemia — bowel that would have been left or anastomosed at a one-stage operation — while anastomotic dehiscence fell from 23.4% with primary anastomosis to 5.3% with the two-step approach, and ileostomy from 19.1% to 2.6%, with no mortality penalty.^[23] Freeman's small ANZ series carried the same message two decades earlier: mortality was associated with attempting emergency operative revascularisation and with not performing a second look; every damage-control patient survived.^[25]

The counterweight is Hatchimonji's NSQIP analysis (5,514 emergency laparotomies for mesenteric ischaemia): open abdomen was associated with an adjusted OR of 1.58 for mortality — but not in the subgroup undergoing revascularization — and 10.8% of patients closed primarily still required reoperation.^[24] Read together: the open abdomen is a tool for the sickest and for revascularised bowel of doubtful viability, not a routine; and one in ten primarily closed abdomens earns its way back to theatre regardless.^[24][23]

NOMI — treat the pump, vasodilate the artery

The central principle of NOMI management is treatment of the precipitating cause: fluid resuscitation, optimising cardiac output and eliminating vasopressors where possible; prevention by maintaining abdominal perfusion pressure is the real cure.^[1][28] Adjunctive treatment includes systemic anticoagulation and catheter-directed infusion of vasodilators — most commonly papaverine into the SMA.^[1] The evidence is observational and must be labelled as such: WSES cites papaverine infusion reducing mortality and a Japanese nationwide study (161 treated versus 1,676 controls) associating vasodilator therapy with significantly lower in-hospital mortality and less abdominal surgery — in a selected, milder cohort; the same group's later surgical-subgroup analysis (928 NOMI patients operated on admission day) found postoperative vasodilators made no difference (30.9% versus 27.5% mortality).^[1][20][21] Infarcted bowel in NOMI is resected promptly (1C); peritonitis or perforation mandates exploration.^[1][21]

Mesenteric venous thrombosis — the anticoagulation-first subtype

MVT has a distinctive appearance on CTA, and when it is found in a patient without peritonitis, non-operative management should be considered (1B): the first-line treatment is anticoagulation — immediate unfractionated or low-molecular-weight heparin — and early heparin use is associated with improved survival; systemic thrombolysis is rarely indicated.^[1][18] Progression to peritonitis changes everything: explorative laparotomy, resection of frankly necrotic bowel only (anticoagulation may improve the picture over 24–48 hours), anastomosis deferred to second look, and full-dose intravenous heparin resumed at the end of the first operation — protamine can reverse it instantly if bleeding threatens.^[1][18] Patients who fail to improve on anticoagulation without peritonitis may go to endovascular therapy in expert centres, and Yang's stepwise intestinal-stroke-centre series (43 patients; thrombolysis in 84%, damage control in 47%, selective second look in 23%) achieved 30-day mortality of 11.6% with 90.7% recanalization.^[18][19] Two follow-through obligations: switch to oral anticoagulation once intestinal function recovers (DOACs increasingly used), and screen for inherited and acquired thrombophilia whenever there is no strong permanent trigger such as intra-abdominal cancer.^[18]

The intestinal stroke centre — what organised care buys

WSES cites the evidence that occlusive AMI treated in intestinal stroke centres with a multidisciplinary approach improves outcomes (1C): the team is emergency surgeon, vascular surgeon, interventional radiologist and intensivist, working to keep time to reperfusion as short as possible.^[1] The French results define the benchmark: Roussel's revascularised cohort achieved 2-year survival of 89.2% with 30-day mortality of 6.9% and bowel resection in only 24% (median 43 cm); Najdawi's endovascular series reached 88% technical success with 55% needing nothing further after the procedure; and the 5-year SURVI ICU experience (133 patients, 78.9% revascularised) reported 28-day mortality of 33.1% — against a historical 60–70%.^[14][15][17]

Special populations

The elderly. The exponential incidence curve makes AMI the great mimic of geriatric acute abdomen — commoner than appendicitis over 75 — with atypical, muted presentations and the worst mortality; age is also one of the SURVI mortality factors (with admission lactate and intestinal necrosis: all three present, 75% 28-day and 100% one-year mortality).^[1][17]

The critically ill and vasopressor-dependent. This is the NOMI patient: cardiac failure, sepsis, haemodialysis and high-dose vasoactive drugs are the reported associations, and NOMI is itself a cause of secondary worsening in septic shock. The management is haemodynamic before it is surgical.^[1]

The anticoagulated AF patient. Modern anticoagulation is reshaping the disease: embolism has fallen from 50% to about 25% of cases as warfarin and DOACs spread, so a breakthrough embolic AMI in an anticoagulated patient deserves a review of adherence and dosing.^[1]

The chronic mesenteric ischaemia prodrome. Postprandial pain, weight loss and food fear in the months before collapse identify the atherosclerotic thrombotic patient — the history that predicts an SMA-origin lesion needing stenting or bypass rather than embolectomy.^[1][28]

Complications and prognosis

The early killers are septic multiorgan failure from translocated bacteria and reperfusion injury — WSES warns that MOF can follow resection and restored flow even without residual necrotic bowel — and the complications of the open abdomen itself (prolonged ventilation; the NSQIP mortality association).^[1][24] The late burden is intestinal: short bowel syndrome and intestinal failure after massive resection — 59.8% of SURVI's ICU survivors had intestinal failure, though only 18.3% still required parenteral nutrition at one year — and WSES acknowledges the ethical decision the surgeon faces when infarction involves most of the small bowel.^[17][19][1]

Prognosis in one paragraph: untreated, mortality exceeds 50%; pooled short-term mortality is 59.6% overall but 33.9% when occlusive arterial disease is actually revascularised; subtype matters (MVT 24.6%, NOMI 58.4%); and the independent predictors of death are leukocytes, lactate, bilirubin, creatinine, aetiology and portomesenteric venous gas (HR 23).^[1][5][26] The survivors' obligations: lifelong anticoagulant or antiplatelet therapy for the majority (1B), surveillance imaging after revascularization (duplex at 1, 6 and 12 months, then annually), and the lifestyle and medication review that the aetiology dictates.^[1]

Revision summary

• Four subtypes, shifting mix: embolism 50%→25%, thrombosis up to 40%, NOMI 25%, venous 5–15%; each has a fingerprint history.^[1]
• Pain out of proportion is AMI until disproven (1C); peritonitis means infarction already (surgery without delay, 1C).^[1]
• Lactate cannot exclude (86%/44%; Collange AUC 0.57–0.60); D-dimer is the rule-out (96% sensitive).^[7][9]
• CTA without delay (1A): 92–94% sensitive, 95–98.8% specific; every 6 h of delay doubles mortality; plain film has no role.^[1][8]
• Bundle: resuscitate, antibiotics immediately (1C), full-dose heparin in everyone (30-day survival 53.5% vs 41.7%, NNT 8).^[1][27]
• Revascularize by subtype: endovascular first where expertise exists (1C), embolectomy for embolism, stent/ROMS or bypass for the SMA-origin thrombus, shunt in extremis — and quote the selection-bias caveat, not the crude mortality gap.^[1][13]
• Damage control: resect frankly necrotic bowel only, temporary closure, second look at 24–48 h — dehiscence 5.3% vs 23.4% one-stage; but open abdomen is for the sickest and the revascularised, not routine (NSQIP OR 1.58).^[23][24]
• NOMI: fix the cause, papaverine selected and observational; MVT: anticoagulation first (1B), laparotomy for peritonitis, thrombophilia screen.^[1][18]
• Stroke centres are the benchmark: 89.2% 2-year survival (Roussel), 28-day mortality 33.1% (SURVI); survivors need lifelong anticoagulation and surveillance.^[14][17][1]

Explain short bowel syndrome and intestinal failure after massive resection (SURVI: intestinal failure in 59.8% of ICU survivors, 18.3% on parenteral nutrition at 1 year; Yang SBS 13.95%).^[19] Quote mortality by era and subtype (Tamme; Cudnik 47% operative; SURVI 28-day 33.1%/1-year 46.6%; three risk factors → 75%/100%).^[17]

References28ShowHide

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