Acute Mesenteric Ischaemia
Acute mesenteric ischaemia is the sudden decrease in blood supply to the bowel, resulting in bowel ischaemia and, if not promptly treated, rapid gangrene.
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|
|AMAE||50%||Cardiac causes* or abdominal / thoracic aneurysm|
|NOMI||20%||Hypovolemic Shock, Cardiogenic Shock|
|MVT||<10%||Coagulopathy, Malignancy, or Inflammatory Disorders|
*Cardiac causes include arrhythmias (e.g. AF), post-MI mural thrombus, or prosthetic heart valve
Rarer causes for acute mesenteric ischaemia include Takayasu’s arteritis, fibromuscular dysplasia, polyarteritis nodosa, and thoracic aorta dissections
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.
Traditionally, mesenteric ischaemia presents with a generalised abdominal pain, out 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 present in around 75% of cases.
On examination, the abdomen is often unremarkable* and the patient may find it difficult to localise the pain. However, remember late stage bowel ischaemia and necrosis can present as bowel perforation. Importantly, take note of any potential embolic sources, such as AF, heart murmurs, or signs of previous valvular replacement surgery.
*A history of AF or other cardiovascular disease increase the likelihood towards this diagnosis, and other points in the history to consider are previous DVT or PE or hypercoaguable states (e.g. active neoplasia or anti-phospholipid syndrome)
Mesenteric ischemia should always be considered in cases of severe 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 obstruction, and symptomatic AAA
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.
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, ischemia 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
Any suspicion of a bowel perforation warrants an initial AXR and erect CXR; if there is significant suspicion, then a CT abdomen with contrast is indicated.
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 immediately. 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.
The patient will have a significant acidosis and is at a high risk of developing multiorgan failure, therefore early ITU input to optimise the patient is necessary. Taking a patient to theatre for potential bowel resection without the support of ITU is likely to be futile.
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 under sedation, planned for potential relook laparotomy in 24-48 hours; the majority of patients will end up with a (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 around 50-80%, even if the diagnosis is made and treatment performed; those that survive may have short gut syndrome.
- 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