Clinical Review: Mesenteric ischaemia

Contributed by Dr Kenneth Fung, CT1 doctor, London Deanery, and Mr Joseph Dawson, specialist registrar in vascular and general surgery, North East Thames Deanery

IC is generally accepted as the most common bowel ischaemia (Photograph: SPL)
IC is generally accepted as the most common bowel ischaemia (Photograph: SPL)

Section 1: Epidemiology and aetiology
Mesenteric ischaemia describes a group of disorders characterised by a symptomatic reduction in blood supply to the GI tract. The term is used to refer to ischaemic conditions affecting the whole GI tract, whereas ischaemic colitis (IC) is specific to the colon.1

Mesenteric ischaemia occurs when there is an occlusion, stenosis or systemic reduction in blood flow in at least one of the three principal visceral arteries: coeliac axis (CA), superior mesenteric artery (SMA) and inferior mesenteric artery (IMA), with the SMA affected in 85% of acute cases.

Mesenteric ischaemia can be divided into acute mesenteric ischaemia (AMI) and the less common chronic mesenteric ischaemia (CMI).

Mesenteric ischaemia is relatively uncommon but incidence increases with age. It is more common in females (75% of CMI patients), and those with a history of coronary or peripheral vascular disease (50% of CMI patients).

The incidence of bowel ischaemia was reported as 1.09 per 100,000 person-years in a recent study using data from the General Practice Research Database.2 However, IC is accepted as the most common bowel ischaemia. CMI accounts for 5% of ischaemic bowel events.

Mesenteric ischaemia is predominantly an atherosclerotic occlusive disease (see table); risk factors and associations include MI, arrhythmia, cardiomyopathy, diabetes, hypertension, smoking, hypercholesterolaemia and peripheral arterial disease.

Intrinsic (arterial vasodilation) and extrinsic (hormonal and neural) mechanisms regulate normal mesenteric blood flow. In the acute setting, these mechanisms can compensate for a 75% reduction in blood flow for up to 12 hours by recruiting an extensive network of collaterals.

In AMI, prolonged under-perfusion of the gut leads to a loss of mucosal barrier protection, resulting in bacterial translocation with subsequent sepsis, multiorgan failure and death, unless timely intervention is achieved.

Causes of mesenteric ischaemia
  • Arterial embolism (50%)3
  • Cardiogenic (AF, left-sided thrombus)
  • Aortic wall atherosclerotic plaque (including iatrogenic)
  • Pre-existing lesion at artery origin (20%)
  • Inadequate mesenteric blood flow (low cardiac output, hypotension, hypovolaemia, vasoconstriction, inotropes)
  • Systemic coagulopathy (75%)                                   
  • Others (25%): malignancy, inflammatory disorders, portal venous stasis, infection, COC (5%)
RARE CAUSES (5%)   Takayasu’s arteritis, fibromuscular dysplasia, polyarteritis nodosa, thoracic aorta dissections
PROGRESSIVE ATHEROSCLEROSIS (90%) Pre-existing mesenteric arterial disease
NON-ATHEROSCLEROTIC (10%) Takayasu’s arteritis, systemic lupus erythematosus, radiation, cocaine, Buerger’s disease, aortic dissection, extrinsic coeliac artery compression by median arcuate ligament

Section 2: Making the diagnosis
Most cases are seen in elderly patients with cardiovascular risk factors, but mesenteric ischaemia can occur in younger patients with coagulopathies, vasculitis or cocaine use. It comprises a range of disorders typified by vague, non-specific symptoms, so a low threshold for investigation is necessary.

AMI may present non-specifically, but should be suspected in patients with acute severe abdominal pain out of proportion to clinical findings. Pain is usually periumbilical, lasts hours and can be associated with fever, nausea and diarrhoea.

Symptoms tend to have a more gradual onset in NOMI and venous thrombosis. Physical examination can reveal abdominal distension, tenderness, guarding and rectal bleeding.

CMI is difficult to diagnose and most patients are asymptomatic - at least two of the three arteries to the gut must be stenotic or occluded for symptomatic CMI to occur. Symptomatic CMI causes malnutrition and can progress to AMI.

Typically, patients present with progressive postprandial abdominal pain 15-60 minutes after eating, which lasts up to four hours. They may also have a fear of eating. However, classic symptoms are only present in half of patients. An abdominal bruit may be present.

The classic presentation of IC is mild to moderate abdominal pain becoming more generalised and frequent. It is usually left-sided because the 'watershed' region of the colon is around the splenic flexure where the collateral supply to the colon may be deficient.

Clinically, patients do not look unwell unless fulminant ischaemia is present.

Mesenteric ischaemia is managed in secondary care. Suspected AMI should be referred to the surgical team for urgent intervention.

Differential diagnoses of AMI include infective diarrhoea, inflammatory bowel disease and acute diverticulitis. CMI should be referred to gastroenterology or colorectal outpatients.

Differential diagnoses of CMI include peptic ulcer, gall stones, malignancy and chronic pancreatitis, and investigations may be required to exclude these first.

Initial investigations of suspected AMI include routine blood tests, arterial blood gas (metabolic acidosis and raised lactate) and stool culture. Chest and abdominal X-rays help to exclude bowel perforation and may demonstrate 'thumb-printing' of oedematous bowel wall.

Although mesenteric angiography is the gold standard, it is invasive, so is not used first-line, but often combined with endovascular treatment in established cases. Contrast enhanced CT-angiography (CT-A) has become the primary investigation of choice because its sensitivity for diagnosing AMI is >90%.5 Contrast-enhanced magnetic resonance angiography (CE-MRA) is an alternative. Non-specific changes may be seen on CT-A or CE-MRA in IC, necessitating sigmoidoscopy or colonoscopy to identify mucosa changes in the watershed areas, combined with biopsies.

Section 3: Managing the condition
Patients with suspected AMI are initially managed with a combination of oxygen, IV fluids, antibiotics and heparin.

Often, signs of peritonitis or perforation are present and a laparotomy is required to assess bowel viability and excise gangrenous segments. Primary anastomosis is not performed due to the risk of anastomotic breakdown and bowel ends are exteriorised with a view to anastomosis following a second look laparotomy 24-36 hours later.6 Bowel resection should be combined with visceral revascularisation if possible, to minimise further ischaemic damage.

Embolectomy and thromboembolectomy may be performed, depending on the site and nature of the occlusion, and mesenteric artery bypass may be required from the aorta or iliac arteries.

Interventional radiology has a role in the absence of peritonitis or perforation if symptoms are less than eight hours old.

Thrombolysis or angioplasty may be undertaken in the presence of anticoagulation.

Intra-arterial vasodilators such as papaverine and prostaglandin may be given to patients with NOMI via angiography catheter, and glucagon can be used IV to increase splanchnic blood flow. However, there is limited evidence regarding the timing and efficacy of thrombolysis and anticoagulation.

Mesenteric venous thrombosis usually presents late, requiring laparotomy and extensive bowel resection with an associated high mortality. Subsequent anticoagulation is recommended - recurrence rates are high.

Conservative management is indicated in most patients with IC but current literature supports surgical management when signs of peritonitis or fulminant IC are present.7 However, there is no consensus on the most appropriate surgical resection or the role of antibiotics, IV fluids, enteral feeding or total parenteral nutrition.

Medical therapy
CMI patients should receive best medical therapy including antiplatelets, antihypertensives and statins. Antispasmodic medications have been shown to reduce mortality and occurrence of acute venous thrombosis.5 Symptomatic patients may be considered for revascularisation by open surgery or radiological intervention.7

Although it has been suggested that up to 96% will benefit symptomatically from revascularisation,8 mesenteric revascularisation has a higher perioperative risk than other elective vascular procedures, with mortality rates reported up to 12%, and postoperative complication of >50%.

Reconstruction takes the form of a bypass graft from the aorta or iliacs to beyond the stenosis in the target mesenteric vessel.

Single or multivessel reconstruction can be performed, with a balance between reduced restenosis and recurrence versus prolonged surgery.

Endovascular options include percutaneous transluminal angioplasty (PTA) and stenting, associated with similar patency rates to open surgery with reduced morbidity and mortality.9

Stenosis of coeliac trunk and superior mesenteric artery (Photograph: SPL)

Section 4: Prognosis
The outcome in AMI has improved but remains poor due to delayed diagnosis, severe physiological insult, advanced age and significant comorbidities. Venous thrombosis has a better prognosis, with a mortality rate of 32% compared with 54% for embolic disease, rising to 70-80% for arterial thrombosis or NOMI.10

CMI has a good prognosis, with a five-year survival rate of 70%.1 Studies demonstrate graft patency up to 78% at five years with traditional surgical vascular bypass, while endovascular therapy is associated with medium-term success rates of >90%, but may require reintervention.5 IC has the best prognosis of all bowel ischaemia, but still carries an overall mortality of 22%.11

Despite the lack of clinical guidelines and evidence, most clinicians would prescribe warfarin to patients who had a mesenteric venous thrombosis. This is often continued for three to six months if thrombotic risk factors were temporary, but for life in the presence of persistent hypercoagulable states such as thrombophilia.

All patients with any form of mesenteric ischaemia should have their cardiovascular risk factors optimised, including smoking cessation, control of hypertension, hypercholesterolaemia and diabetes, and treatment of any underlying autoimmune disease.

The ischaemia resolves for most patients with IC, but some develop chronic segmental colitis or strictures.12 If strictures are asymptomatic, they can be observed clinically because they usually resolve in one to two years.13

Those patients who have undergone bypass grafts may be entered into a graft surveillance programme involving periodic scans.

Section 5: Case study
Mrs B was a 65-year-old smoker with a history of IHD, hypertension and hypercholesterolaemia. She initially visited her GP with a three-month history of abdominal pain which was worse after eating.

She was prescribed PPIs and told to return if there was no improvement. The PPIs did not help and an abdominal ultrasound was organised. This revealed several gall stones in the gall bladder and she was referred for surgery.

Following this consultation she was advised to follow a fat-free diet and an oesophagogastroduodenoscopy (OGD) was arranged. At follow-up, she said the dietary change had not helped her pain and she felt that this had caused her to lose weight.

The OGD was reported as normal and an elective laparoscopic cholecystectomy was performed. At her six-week follow-up, she still reported postprandial pain; this was put down to postoperative pain, for which she was prescribed analgesia.

Mrs B visited her GP two months later with continuing weight loss and pain. An urgent CT abdomen and pelvis was performed for occult malignancy. This revealed normal interabdominal organs, but extensive aortic calcification was noted, which extended into the superior mesenteric artery. She was referred to the surgical outpatients clinic, where a diagnosis of CMI was made.

A mesenteric CT-A was performed, revealing a tight coeliac stenosis, a short SMA occlusion and occluded IMA with an extensive established collateral network. Following consultation, intervention was offered, but preoperative cardiopulmonary exercise testing and cardiac perfusion studies suggested she was high risk for open surgery.

She therefore underwent PTA and stenting of her CA and SMA. The procedure was successful but Mrs B had a peri-procedure MI. However, she made a good recovery and the rapid symptomatic relief enabled her to eat.

At her two-month follow-up she had put on weight and the surveillance duplex revealed the stents were patent. She was treated with dual antiplatelet therapy for a year and remains on aspirin and simvastatin.

Section 6: Evidence base
Clinical trials

There are no RCTs comparing endovascular and open surgery in mesenteric ischaemia.

Case series would suggest that open reconstruction is appropriate in young, fit patients, whereas elderly patients with extensive comorbidities benefit from undergoing minimally invasive endovascular therapy.


Key text

  • Bhattacharya V, Stansby G. Postgraduate Vascular Surgery (first edition). Cambridge, Cambridge University Press, 2010.
  • Beard J, Gaines P. Renal and Intestinal Vascular Disease in Vascular and Endovascular Surgery (fourth edition). Oxford, Saunders, 2009.


This contains a good summary of presentation, investigation and management for patients.

The American College of Gastroenterology website provides an excellent overview of bowel ischaemia for patients and families.

Reflect on this article and add notes to your CPD Organiser on MIMS Learning


These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.

  • Make a register of your patients with a history of ischaemic bowel; ensure their cardiovascular risk factors are optimised.
  • Ask about intestinal angina when you review your patents with known coronary artery, cerebrovascular, or peripheral vascular disease.
  • Ask your patient participation group if they would like you to host a roadshow for your patients focusing on smoking-related diseases.

1. Brandt L, Boley S. Gastroenterol 2000; 118: 954-68.

2. Huerta C, Rivero E, Montoro M et al. Aliment Pharmacol Ther 2011; 33: 969-78.

3. Wilcox M, Howard T, Plaskon L et al. Dig Dis Sci 1995; 40: 709-16.

4. Lock G. Best Pract Res Clin Gastroenterol 2001; 15: 83-98.

5. Sreenarasimhaiah J. Best Pract Res Clin Gastroenterol 2005; 19: 283-95.

6. Berland T, Oldenborg W. Curr Gastro Reports 2008; 10: 341-6.

7. White C. Chronic mesenteric ischemia: Prog Cardiovasc Dis 2011; 54: 36-40.

8. Kihara T, Blebea J, Anderson K et al. Ann Vasc Surg 1999; 13: 37-44.

9. Renner P, Kienle K, Dahlke M et al. Langerbeck Arch Surg 2011; 396: 3-11.

10. Schoots I, Koffeman G, Legemate D et al. Br J Surg 2004; 91: 17-27.

11. Diaz Nieto R, Varcada M, Ogunbiyi O et al. Colorectal Dis 2011; 13: 744-7.

12. Sreenarasimhaiah J. BMJ 2003; 326: 1372-6.

13. Longo W, Ballantyne G, Gusbery R. Dis Colon Rectum 1992; 35: 726-30.

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