Acute mesenteric ischaemia

• Acute mesenteric ischaemia is a sudden fall in blood flow to the small or large intestine, usually through the superior mesenteric artery, that progresses to bowel necrosis, sepsis and death unless blood flow is restored within hours.
• It is uncommon in emergency admissions (about 0.09 to 0.2%), but it is a leading cause of emergency intestinal resection and carries an untreated mortality of about 50%.^[1]
• The main mechanisms are superior mesenteric artery (SMA) embolism (about half of cases), non-occlusive mesenteric ischaemia (about one in five), arterial thrombosis on atherosclerosis (15 to 25%), and mesenteric venous thrombosis (5 to 15%).^[1]
• The classic clue is severe, poorly localised abdominal pain that seems out of proportion to the early physical findings, often with vomiting and later bloody diarrhoea.
• The diagnosis is made with CT angiography without delay; plain films and blood tests are adjuncts. Treatment is resuscitation, broad-spectrum antibiotics, heparin, and rapid revascularisation, with resection of dead bowel and often a planned second look.

By the end of this page you should be able to:

1. Explain the relevant mesenteric arterial and venous anatomy, and why the watershed areas are at risk.
2. Contrast the four causes by mechanism, typical patient, tempo and clinical clues.
3. Recognise acute mesenteric ischaemia early and request the correct imaging without waiting for plain films or laboratory results.
4. Interpret CT angiography findings, including the signs that mark irreversible bowel injury.
5. Plan the acute management pathway: resuscitation, antibiotics, anticoagulation, revascularisation by cause, resection of necrotic bowel and second-look surgery.
6. Explain why NOMI and mesenteric venous thrombosis are managed differently.
7. Recognise chronic mesenteric ischaemia and its progression to acute disease.
8. Describe the expected mortality and how it rises with every hour of delay.

The intestine has an enormous mucosal surface and a very high blood flow, about 20% of the cardiac output in the fasting state, which can rise by 100 to 150% for 3 to 6 hours after a meal. That postprandial hyperaemia is why a narrowed mesenteric artery becomes symptomatic after eating. The mucosa is injured first, starting at the villous tips and moving towards the serosa; this is why severe pain precedes peritonitis. Once the serosa is involved, peritonitis and irreversible necrosis are present.^[3]

Acute mesenteric ischaemia most often involves the small bowel supplied by the superior mesenteric artery; the large bowel is involved less often and usually in combination. Permanent loss of bowel length is the lasting harm: the surgical aim is to restore flow while it is still reversible and to resect only what is dead.

AMI is uncommon: the WSES 2022 guideline places its incidence at about 0.09 to 0.2% of all acute admissions to emergency departments. It increases exponentially with age, and it is a common cause of emergency intestinal resection rather than of all abdominal pain.^[1]

The prognosis is serious. If untreated, mortality is about 50%. With modern care, reported mortality still ranges from 30 to 70%, and delay in diagnosis is the dominant factor behind those figures. Mortality rates in the literature depend heavily on aetiology and on how quickly diagnosis is made.^[1]

See also "Prognosis and mortality" below for the time-dependence of outcome and the difference between endovascular and open revascularisation.

The three main unpaired arteries of the anterior aorta supply the gut from the lower oesophagus to the mid-rectum.

• Celiac trunk (coeliac axis), arising at the level of the first lumbar vertebra, gives the left gastric, splenic and common hepatic arteries and supplies the stomach, liver, spleen, pancreas and duodenal bulb.
• Superior mesenteric artery (SMA) arises just below the celiac trunk, descends in front of the duodenum and supplies the distal duodenum, jejunum, ileum and colon up to the splenic flexure.
• Inferior mesenteric artery (IMA) arises at the level of the third lumbar vertebra and supplies the descending colon, sigmoid colon and rectum to the pectinate line.

The important SMA branches are the inferior pancreaticoduodenal, middle colic, right colic, ileocolic and a series of jejunal and ileal branches. The IMA gives the left colic, sigmoid and superior rectal arteries.

The gut is protected by rich anastomoses, but these are not enough for sudden large-vessel occlusion.

• The pancreaticoduodenal arcades link the celiac territory to the SMA.
• The marginal artery of Drummond runs along the mesenteric border of the colon and links SMA branches (middle and right colic) with IMA branches (left colic).
• The arc of Riolan (meandering mesenteric artery) is a more central collateral channel between the superior and inferior mesenteric systems that dilates in chronic stenosis.

Watershed areas, where territories meet and anastomoses are weakest, are the first to infarct in low-flow states:

• Griffiths' point at the splenic flexure, between the SMA and IMA territories.
• Sudeck's point at the rectosigmoid junction, between the IMA and systemic (hypogastric) supply.

These same territories are the classic sites of ischaemic colitis. In acute large-vessel occlusion the dead segment is larger than a single watershed zone, but watershed anatomy explains why NOMI and shock preferentially damage the colon at these flexures.

The venous return follows the arteries. The superior mesenteric vein joins the splenic vein to form the portal vein, so mesenteric venous thrombosis can propagate into the portal system.

The etiology of AMI has changed over time: modern anticoagulation for atrial fibrillation and longer survival with atherosclerotic disease have altered the mix, with increasing proportions of arterial thrombosis on atherosclerosis. The WSES 2022 guideline reflects this shift: its background section attributes roughly half of cases to SMA embolism, 15 to 25% to arterial thrombosis and about 20% to NOMI, while its recent-trends section records embolism at about 25%, arterial thrombosis rising from 20 to 35% historically to about 40%, and NOMI at about 25%.^[1]

Shared risk factors include atrial fibrillation, recent myocardial infarction and other sources of cardiac thrombus, valvular disease, diffuse atherosclerosis and peripheral arterial disease, hypercoagulable states, portal hypertension, recent surgery (including cardiac surgery using cardiopulmonary bypass), severe dehydration, and critical illness with multiple organ failure.

AMI is broadly occlusive or non-occlusive. Within occlusive disease, embolism, thrombosis and venous thrombosis behave differently.

SMA embolism is the classic "surgical abdomen in an older person with atrial fibrillation". The embolus usually originates in the left atrium or ventricle, travels down the aorta and lodges in the SMA. Patients often have other clues to systemic embolism: a prior stroke or transient ischaemic attack, splenic or renal infarction, or an acutely ischaemic limb. Because venous return remains intact, the early bowel changes are less dramatic on CT than in arterial thrombosis, but the pace is fastest.

Thrombosis usually occurs on a pre-existing atherosclerotic plaque at the origin of the SMA, and it is often accompanied by celiac occlusion, so collateral supply fails at the same time. A detailed history matters: many of these patients have undiagnosed chronic mesenteric ischaemia with postprandial pain, food fear and weight loss. Vasculitis, mesenteric dissection and mycotic aneurysm are rarer causes of SMA thrombosis. Involvement of the ileocolic artery can produce necrosis of the proximal colon.

NOMI is best understood as a splanchnic low-flow syndrome rather than a blocked artery. Splanchnic vasoconstriction is triggered by systemic hypoperfusion, sometimes worsened by vasopressors. Common settings are heart failure, cardiopulmonary bypass, dialysis, major surgery, sepsis, dehydration and abdominal compartment syndrome. Because the vessels are patent, CTA shows ischaemia despite open arteries, and the distribution is often patchy. NOMI mortality is reported at 50 to 85%.^[1]

Mesenteric venous thrombosis accounts for less than 10% of mesenteric infarctions and for about 5 to 15% of AMI cases. Thrombosis reflects Virchow's triad: stasis, hypercoagulability and endothelial injury. In young patients, a substantial minority occurs without an obvious cause. Thrombus can extend into the portal and splenic veins, and venous congestion produces bowel wall thickening, oedema and haemorrhage on imaging rather than arterial cut-off. A portal vein thrombosis or unexplained infarction in a young adult should prompt a thrombophilia work-up and screening for malignancy.^[1]

The sequence is the same whatever the cause: hypoperfusion, mucosal ischaemia, loss of the mucosal barrier, bacterial translocation, transmural necrosis, perforation, peritonitis, sepsis and shock.

• Mucosa first. Villous tips are most metabolically active, so injury starts there. Loss of the barrier lets luminal bacteria and toxins cross before any sign of peritonitis.
• Pain before signs. Visceral afferents are stimulated by ischaemia and distension, so severe pain is felt while the parietal peritoneum is still unaffected.
• Irreversibility. Once the mural and serosal layers are involved, peritonitis appears and bowel can no longer recover.
• Reperfusion injury. Restoring flow to dead or dying gut adds oxidative and inflammatory injury, which is why second-look surgery is often needed.

The rate of progression depends on the cause. Embolic occlusion can kill a segment in hours, venous thrombosis may smoulder for days, and NOMI worsens in step with the underlying shock.

The classic presentation is severe, poorly localised abdominal pain that seems out of proportion to the physical findings early in the disease. In a study summarised by the WSES guideline, 95% of patients had abdominal pain, 44% nausea, 35% vomiting, 35% diarrhoea and 16% blood per rectum. Other symptoms include anorexia, haematemesis, melaena and obstipation. Patients with arterial thrombosis often describe a history of postprandial pain, weight loss or food fear from chronic mesenteric ischaemia, or previous revascularisation procedures.^[1]

• SMA embolism: sudden, dramatic, "worst ever" pain in an older person with atrial fibrillation or a recent myocardial infarction.
• Arterial thrombosis: may be sudden-on-chronic; pain is often progressive and accompanied by postprandial symptoms.
• NOMI: pain is generally more diffuse and episodic, with poor cardiac performance; the patient is often unconscious, ventilated or sedated, which makes diagnosis harder.
• MVT: often slower and less dramatic initially, with nonspecific gastrointestinal symptoms and abdominal distension; it may present days after the thrombus.

Bowel sounds may be normal, increased or absent; they are an unreliable sign.

Early on, the abdomen may be soft with only mild or disproportionate tenderness, even while the patient is in severe pain. As ischaemia progresses:

• focal or generalised peritonism appears;
• abdominal distension and guarding develop;
• fever, tachycardia and hypotension signal sepsis and shock;
• blood on rectal examination is a late sign.

Clinical signs of peritonitis are subtle in some patients and, when present, predict intestinal infarction. A high index of suspicion is the real diagnostic tool: the WSES guideline notes that the "classic" out-of-proportion presentation is becoming less common, while "acute-on-chronic" presentations are probably underdiagnosed.

• New severe, poorly localised abdominal pain in a patient with atrial fibrillation or recent myocardial infarction.
• Pain out of proportion with a soft abdomen and a raised lactate or metabolic acidosis.
• Any critically ill patient with new abdominal pain, distension, rising lactate or feeding intolerance.
• Postoperative abdominal pain with rising inflammatory markers, even days after discharge.
• Portal vein thrombosis or unexplained bowel infarction in a young adult.
• Hypotension or peritonitis in a patient with possible AMI.

The key differential is anything that produces sudden severe abdominal pain or acute peritonism. The features below are clues, not rules.

AMI is a clinical diagnosis supported by imaging; there is no single blood test that proves or excludes it. Delays are usually caused by repeating plain films or waiting for biomarkers rather than acting on clinical suspicion. The WSES 2022 guideline recommends CT angiography without delay in any patient with suspicion for AMI.^[1]

Plain abdominal radiographs have a limited role, especially early on: a negative film does not exclude AMI. They may later show sentinel loops, thumbprinting, pneumatosis intestinalis or portal venous gas. Contrast studies and non-angiographic CT can miss early disease.

Multidetector CTA with both arterial and venous phases is the investigation of choice. It should be performed as soon as AMI is considered, because the risk of missed ischaemia outweighs the risk of any delay in imaging. CTA:

• confirms or excludes mesenteric arterial occlusion;
• distinguishes embolic, thrombotic, non-occlusive and venous disease;
• assesses bowel viability and perforation;
• provides vascular mapping for open or endovascular intervention.

WSES 2022 cites a systematic review of diagnostic accuracy for CTA in acute mesenteric ischaemia with sensitivity about 93% and specificity about 100%, with very high positive and negative predictive values when interpreted by experienced readers.^[1] A more recent review (Gries 2024) reports 96 to 100% sensitivity and 94 to 100% specificity for a biphasic CT angiography protocol in the same disease.^[3]

Findings fall into two groups:

• Vascular: arterial cut-off or filling defect, venous thrombus, poor or absent visceral enhancement, collateral dilatation.
• Bowel (reversible): dilated loops, wall thickening, mesenteric stranding, ascites and hyperenhancement from reperfusion.
• Bowel (advanced, often irreversible): absent enhancement, pneumatosis intestinalis, portal or mesenteric venous gas, and free intraperitoneal air. Six radiological findings, including bowel loop dilatation, pneumatosis intestinalis, superior mesenteric vein thrombosis, free fluid, portal vein thrombosis and splenic vein thrombosis, predict bowel necrosis.

Pneumatosis intestinalis needs context: one large multicentre retrospective study found that about 60% of patients with this sign had benign disease. Interpret it with the clinical picture and other signs of infarction. In NOMI, CTA may demonstrate bowel ischaemia and free fluid despite patent mesenteric arteries.^[1]

• Duplex ultrasound has a limited role in acute disease, especially once the patient is critically ill or the bowel is distended. It may be helpful early in chronic cases and is used for surveillance after revascularisation.
• Magnetic resonance angiography is an established technique for evaluating the mesenteric vessels but is slow and less suitable in the acute setting.
• Conventional (catheter) angiography remains useful when endovascular therapy is planned, when the diagnosis remains uncertain after CTA, or when intervention can be performed in a hybrid operating theatre. It can be done intraoperatively.
• Laparoscopy or laparotomy is both diagnostic and therapeutic when peritonitis is present. Diagnostic laparoscopy has not been widely adopted for AMI, but laparoscopy can be used for a second look.

There is no accurate biomarker for intestinal necrosis. Normal or abnormal results should never replace CT angiography. Serum markers can corroborate suspicion:

• Leukocytosis: more than 90% of patients have an elevated white cell count.^[1]
• Metabolic acidosis with an elevated lactate: occurs in about 88% of patients. A lactate above 2 mmol/L is associated with irreversible intestinal ischaemia hazard ratio 4.1 (95% confidence interval 1.4 to 11.5; p under 0.01).^[1]
• D-dimer: reflects clot formation and lysis. No patient presenting with a normal D-dimer had intestinal ischaemia in the reported data; a D-dimer above 0.9 mg/L had specificity 82%, sensitivity 60% and accuracy 79%.^[1]

• D-dimer above 0.9 mg/L is therefore a useful adjunct, but nothing more.^[1]
• Elevated amylase occurs in roughly half of cases and is nonspecific.
• Blood cultures should be taken, but they do not change the first hour of management.

Other supportive markers (D-dimer, leukocytosis, acidosis) are weak individually; the strongest single investigation remains CTA.

AMI is managed by a multidisciplinary team: emergency physician, surgeon, intensivist, radiologist and, when needed, anaesthetist. Reperfusion must happen as soon as possible; the time-to-reperfusion interval should be as short as the patient's physiology and service organisation allow.

All patients need initial supportive care:

• Nil by mouth, nasogastric suction and bowel rest.
• Intravenous fluid resuscitation with correction of electrolytes and acid-base balance.
• Oxygen, analgesia and temperature and glucose control.
• Cardiac monitoring, treatment of atrial fibrillation and other precipitants.
• Stop or reduce vasoconstrictors if possible; improve perfusion.
• Careful anticoagulant management; full-dose anticoagulation before surgery (see below).

• Antibiotics: broad-spectrum intravenous antibiotics should be given immediately. Intestinal ischaemia destroys the mucosal barrier early and permits bacterial translocation, with a high risk of septic complications. Antibiotic therapy should be given for at least 4 days in immunocompetent, stable patients, with longer courses for signs of ongoing infection. As soon as possible the regimen should be narrowed according to culture results.^[1]
• Anticoagulation: full-dose anticoagulation should be initiated in all patients before surgery. Unfractionated heparin is effective and easy to manage, especially when acute kidney injury is present. Early heparin has been associated with improved survival in mesenteric venous thrombosis. Patients with atrial fibrillation need long-term anticoagulation for recurrent embolism prevention.

SMA embolism. Embolectomy, open or by endovascular aspiration, is a well-established definitive treatment, and thrombolysis (through the SMA) can be considered in patients with no signs of acute peritonitis. Evidence does not show superiority of open over endovascular management in acute embolic occlusion. Surgery is mandatory to assess bowel viability, and the laparotomy also allows aspiration embolectomy through the vessel.

SMA thrombosis. Thrombosis at the origin of the SMA, usually on atherosclerosis, generally requires either endovascular stenting or angioplasty, or surgical bypass. Bypass may be performed antegrade from the supraceliac aorta or retrograde from the infrarenal aorta or common iliac arteries. Single-vessel revascularisation of the SMA is usually sufficient acutely, even though the celiac and IMA may also be diseased. Temporary SMA shunting should be considered if the technical skillset is not available.

Non-occlusive mesenteric ischaemia. Neither NOMI nor mesenteric venous thrombosis typically requires arterial repair. The focus is to correct the underlying cause and improve mesenteric perfusion: treat the shock, sepsis or heart failure; optimise volume status; reduce or withdraw vasopressors where possible; and improve oxygen delivery. Infarcted bowel must still be resected. Direct vasodilator therapy is mentioned by several guidelines but is uncommon in practice. Catheter-directed infusion of papaverine (a vasodilatory and antispasmodic agent) into the SMA is the most commonly described intra-arterial agent, and early treatment with vasodilators has reduced mortality in small studies. Damage-control surgery is important because these patients are often physiologically exhausted.

Mesenteric venous thrombosis. The first-line treatment is anticoagulation, usually continuous unfractionated heparin. Systemic thrombolysis is rarely indicated. When clinical signs demand operative intervention, resect only obviously necrotic bowel using damage-control techniques, because anticoagulation may improve the clinical picture over the next 24 to 48 hours. Early heparin is associated with improved survival. Peritonitis still requires emergency surgery.^[1]

• Resect all non-viable gut. Intestinal viability is the most important factor influencing outcome. Non-viable, unrecognised intestine leads to multi-system organ dysfunction and death.
• Preserve viable bowel. Resection should be as limited as gross and adjunctive assessment (perfusion, Doppler, fluorescence) allows, with clear documentation of remaining bowel length in the operative note.
• Damage-control techniques. Temporary abdominal closure with a vacuum-assisted device or temporary dressing gives an easy route to a second look 24 to 48 hours later, which is often when the final extent of viability becomes clear. Intraoperative bowel oxygenation, myoelectric activity and perfusion assessment are available adjuncts.^[1]
• Second-look surgery. A planned second look is indicated when viability was doubtful at first operation, or when perfusion has been restored but the bowel still looks marginal. Second-look laparoscopy can avoid a full reopening in critically ill patients and can be performed at the bedside in intensive care, but in one reported series only about 20% of patients actually underwent a second-look laparoscopy, and the technique has not been generally adopted.^[1]

Some studies report less need for laparotomy, less bowel resection and significantly lower mortality with endovascular techniques compared with open surgery. A large database study from 2005 to 2009 recorded mortality of 24.9% after endovascular intervention versus 39.3% after open revascularisation. A pooled meta-analysis of nineteen observational studies estimated an odds ratio of 0.45 for bowel resection and for 30-day mortality with endovascular treatment. The ESVS 2017 guideline reported pooled 30-day mortality after treatment of 17.2% (367 of 2131 patients) with endovascular therapy versus 38.5% with open surgery.^[2]

Endovascular therapy is only appropriate when there is no peritonitis and no clear infarction. Most patients still need laparotomy to assess bowel viability, and many teams now use a hybrid approach: endovascular revascularisation first, followed by laparoscopic or open assessment of the bowel, or the reverse.

• Sepsis and septic shock from bacterial translocation and bowel necrosis.
• Perforation and diffuse peritonitis.
• Acute kidney injury and multi-organ failure.
• Short bowel syndrome after extensive resection, with long-term parenteral nutrition or intestinal transplantation being the only solution in the most severe cases.
• Strictures and fibrosis from ischaemic (non-transmural) injury discovered later.
• Recurrent thrombosis and embolism, particularly if atrial fibrillation is undertreated or predisposing prothrombotic states persist.
• Haemorrhagic complications of anticoagulation and reperfusion injury.

Mortality for AMI remains high world-wide: from about 50% untreated, to 30 to 70% even with modern care. Factors that worsen outcome include delay beyond 6 hours, peritonitis at presentation, extensive bowel necrosis, NOMI, advanced age, renal failure and multi-organ dysfunction. Every 6 hours of delay in CT angiography doubles mortality. There is good evidence that centres of excellence with high awareness, early imaging, a low threshold for revascularisation and strong postoperative care reduce mortality.^[1]

A non-acute-on-chronic "textbook" presentation is becoming less common; the acute-on-chronic thrombotic presentation is probably underdiagnosed, which means some AMI deaths are misattributed to sepsis, ileus or multi-organ failure.

Chronic mesenteric ischaemia (CMI, "intestinal angina") is atherosclerotic stenosis that does not yet cause infarction but produces a postprandial supply-demand mismatch: after eating, mesenteric blood flow must rise by 100 to 150% for 3 to 6 hours, and stenotic vessels cannot deliver. It is a major risk factor for AMI, because thrombosis usually occurs on this pre-existing disease.^[3]

Typical features:

• postprandial abdominal pain beginning after meals (often dull, cramping, epigastric or periumbilical) and lasting for hours;
• food fear, with the patient avoiding eating and losing weight (malnutrition and weight loss are common);
• early satiety, nausea, vomiting, diarrhoea or constipation and malabsorption;
• symptoms in a patient with diffuse atherosclerosis, often with other arterial disease (angina, cerebrovascular or peripheral vascular disease).

Patients presenting with symptomatic chronic mesenteric ischaemia are at high risk of in-hospital AMI, so a clear history should prompt early imaging.

Investigation of CMI uses duplex ultrasound at intervals (reported protocols include studies at 1 month, 6 months, 12 months, then annually after revascularisation), cross-sectional angiography and, when appropriate, endovascular repair. Symptomatic multi-vessel disease generally warrants revascularisation of more than one of the three major mesenteric vessels, by endovascular stenting or open bypass. This decision is usually made in a vascular centre.^[3]

• Older adults are the largest group; presentation is atypical and delays are common.
• Patients with atrial fibrillation need both acute revascularisation and long-term anticoagulation to prevent recurrence.
• Pregnancy and the puerperium raise suspicion for mesenteric venous thrombosis; imaging with CTA must be justified and tends to use CT with careful shielding, or MRI if available and the patient is stable.
• Immunocompromised and transplant patients may progress without typical pain and have higher infection risk.

Where CT angiography is not available, the diagnosis rests on a high index of clinical suspicion, plain abdominal radiographs (looking for thumbprinting, pneumatosis or portal venous gas), bedside ultrasound where operators are trained, and early laparotomy. A negative plain film never excludes AMI. Unfractionated heparin and broad-spectrum antibiotics are usually available and should be started promptly; revascularisation may consist of open embolectomy or bypass performed in the same operation as bowel assessment, since endovascular options are limited. Late presentation and absence of hybrid theatres mean mortality in low-resource settings is often higher. Centres that can agree on a referral and rapid-imaging pathway, even a simple telephone link to a CT-capable hospital, improve survival.

• WSES 2022 (World Society of Emergency Surgery, "Acute mesenteric ischemia: updated guidelines") recommends CT angiography without delay in any patient with suspicion of AMI (strong recommendation, high-quality evidence); full-dose anticoagulation with unfractionated heparin before surgery; broad-spectrum antibiotics immediately; and revascularisation tailored to the cause, with damage-control and second-look strategies.^[1]
• ESVS 2017 ("Management of the Diseases of Mesenteric Arteries and Veins") covers acute and chronic mesenteric ischaemia and mesenteric venous thrombosis, with evidence and consensus recommendations on imaging, revascularisation and follow-up that remain widely quoted.^[2]
• The two guidelines agree on CTA as the first investigation and on heparinisation before surgery; they differ in emphasis, with ESVS 2017 covering chronic and venous disease in more depth and WSES 2022 concentrating on the emergency.^[2]

• Acute mesenteric ischaemia is an uncommon but devastating vascular emergency (about 0.09 to 0.2% of emergency admissions) with untreated mortality around 50%.^[1]
• The four mechanisms are SMA embolism (~50% historically, about 25% in more recent series), NOMI (~20 to 25%), arterial thrombosis (15 to 25%, up to about 40% recently) and mesenteric venous thrombosis (5 to 15%).^[1]
• Severe, poorly localised pain out of proportion to early signs is the classic clue; nausea, vomiting, diarrhoea and bloody stool follow as the bowel infarcts.
• More than 90% of patients are leukocytotic, and about 88% have an elevated lactate, but neither sign is reliable for timing; lactate above 2 mmol/L predicts irreversible ischaemia with hazard ratio 4.1.^[1]
• CT angiography without delay is the diagnostic test of choice; a normal D-dimer makes intestinal ischaemia unlikely, and a D-dimer above 0.9 mg/L has specificity 82%, sensitivity 60% and accuracy 79%.^[1]
• Plain films cannot exclude disease; a negative film is meaningless.
• Resuscitation, nil by mouth, broad-spectrum antibiotics for at least 4 days and full-dose unfractionated heparin come first.^[1]
• Revascularise by cause: embolectomy/aspiration (embolism), stent or bypass (thrombosis), treat the shock and consider papaverine (NOMI), heparin (venous thrombosis).
• Resect only obviously dead bowel, document remaining length, and plan a second look at 24 to 48 hours when viability was doubtful.^[1]
• NOMI has the highest mortality and does not require arterial repair; mesenteric venous thrombosis responds to anticoagulation and rarely needs thrombolysis.
• Every 6 hours of delay in CT angiography doubles mortality; early referral and a low threshold for imaging save lives.^[1]
• Chronic mesenteric ischaemia (postprandial pain, food fear, weight loss) is the precursor lesion in many thrombotic cases and needs vascular follow-up.

Chronic mesenteric ischaemia is discussed briefly above. Atrial fibrillation is the most common embolic source and needs long-term anticoagulation. Short bowel syndrome follows massive resection. Peritonitis, septic shock and multiple organ dysfunction are the terminal complications. Ischaemic colitis, acute pancreatitis and strangulated small-bowel obstruction are the main differentials.

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