Acute Mesenteric Ischaemia

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Last updated: October 7, 2020
Revisions: 31

Last updated: October 7, 2020
Revisions: 31

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Acute mesenteric ischaemia is the sudden decrease in the blood supply to the bowel, resulting in bowel ischaemia and, if not promptly treated, death.

In this article, we shall look at the causes, clinical features and management of a patient with acute mesenteric ischaemia.


The common causes of acute mesenteric ischaemia can be classified into:

  • Thrombus-in-situ (Acute Mesenteric Arterial Thrombosis, AMAT)
  • Embolism (Acute Mesenteric Arterial Embolism, AMAE)
  • Non-occlusive cause (Non-Occlusive Mesenteric Ischemia, NOMI)
  • Venous occlusion and congestion (Mesenteric Venous Thrombosis, MVT)
Type Proportion of Cases Underlying Cause
AMAT 25% Atherosclerosis
AMAE 50% Cardiac causes* or thoraco-abdominal aneurysm
NOMI 20% Hypovolaemic shock, cardiogenic shock
MVT <10% Coagulopathy, malignancy, autoimmune disorders

*Cardiac causes include arrhythmias (e.g. atrial fibrillation), post-MI mural thrombus, or prosthetic heart valve

Rarer causes for acute mesenteric ischaemia include Takayasu’s arteritis, fibromuscular dysplasia, polyarteritis nodosa, and thoracic aortic dissections.

Risk Factors

The risk factors for acute mesenteric ischaemia depend on the underlying cause.

Specifically, however for AMAE, the main reversible risk factors are smoking, hyperlipidaemia, and hypertension, much the same as for chronic mesenteric ischaemia.

Clinical Features

Traditionally, mesenteric ischaemia presents with a generalised abdominal painout of proportion to the clinical findings, although it can often be more variable or subtle than this. The patient will typically complain of a diffuse and constant pain, with associated nausea and vomiting in around 75% of cases.

Abdominal examination will often reveal non-specific tenderness*, with no specific clinical signs. In later stages (especially if the bowel has perforated), patients will have features of globalised peritonism.

Importantly, take note of any potential embolic sources, such as atrial fibrillation or heart murmurs, that may provide a suggestion to the underlying cause

Figure 1 – Acute bowel ischaemia, resulting in bowel necrosis

Differential Diagnosis

Mesenteric ischaemia should always be considered in cases of acute abdomen, especially where there is no other obvious cause. Other causes of acute abdomen that may have similar presentations include peptic ulcer disease, bowel perforation, and symptomatic AAA


Laboratory Tests

An arterial blood gas (ABG) should be performed urgently, to assess the degree of acidosis and serum lactate, secondary to the severity of bowel infarction (however these can be normal, even in severe cases).

Routine blood tests that should be performed, including FBC, U&Es, clotting (especially if patient anti-coagulated), amylase*, and LFTs (if the coeliac trunk is affected, ischaemia of the liver may cause derangement), as well as a group and save.

*Whilst an amylase is commonly measured to exclude pancreatitis as a cause of the abdominal pain, counter-intuitively amylase also rises in mesenteric ischaemia, as well as ectopic pregnancy, bowel perforation, and diabetic ketoacidosis.


The definitive diagnosis of acute mesenteric ischaemia, for both arterial and venous mesenteric disease, requires a CT scan with IV contrast (as a triple phase scan, with thin slices taken in the arterial phase)

Arterial bowel ischaemia will initially show on CT imaging as oedematous bowel, secondary to the ischaemia and vasodilatation, before progressing to a loss of bowel wall enhancement* and then to pneumatosis.

*Oral contrast should be avoided in cases of mesenteric ischaemia due to difficulty in assessing for bowel wall enhancement

Figure 2 – CT Scan showing bowel ischaemia


Initial Management

Acute mesenteric ischaemia is a surgical emergency, requiring urgent resuscitation with early senior involvement. Ensure the patient receives IV fluids, a catheter inserted, and a fluid balance chart started. For confirmed cases, broad-spectrum antibiotics should be given, due to the risk of faecal contamination in case of perforation of the ischaemic (and potentially necrotic) bowel and bacterial translocation.

The patient will have a significant acidosis and is at high risk of developing multi-organ failure, therefore early ITU input to optimise the patient and for post-operative support is necessary.

Definitive Management

The location, timing, and severity of the mesenteric ischaemia, among other factors, will determine the surgical intervention performed:

  • Excision of necrotic or non-viable bowel, if not suitable for (or able to access) revascularisation
    • Post-operatively the patient should be on the intensive care unit, planned for potential relook laparotomy in 24-48 hours; the majority of patients will end up with either covering loop or end stoma and there is a high chance of short gut syndrome.
  • Revascularisation of the bowel, involving removal of any thrombus or embolism via radiological intervention; the decision for revascularisation is made depending upon the state of the patient, the bowel, and the angiographic appearance of the mesenteric vessels
    • This is preferably done through angioplasty due to the risk of aortic contamination in open surgery, however open embolectomy is possible either through the CT, SMA, IMA, or the aorta


The main risks from mesenteric ischaemia are bowel necrosis and perforation.

Mortality is between 50 to 80%, even if the diagnosis is made and treatment performed; those that survive may have short gut syndrome.

Key Points

  • Acute mesenteric ischaemia is most commonly caused by an embolus, yet may also be caused by a thrombus-in-situ, venous occlusion, or non-occlusive causes
  • Patients present with excessive pain, out of proportion to clinical findings with typically an otherwise unremarkable examination
  • Ensure to assess for potential sources of embolus
  • Definitive diagnosis is made via CT angiography
  • Surgical treatment involves either bowel resection or revascularisation, however mortality rates are >50% even in treated cases