Mesenteric Ischaemia

Mesenteric ischaemia is inadequate intestinal perfusion sufficient to threaten bowel viability. It is a vascular syndrome rather than a single disease.

The clinically useful classification is:

• Acute arterial embolism, commonly involving the superior mesenteric artery
• Acute arterial thrombosis, usually superimposed on mesenteric atherosclerosis
• Mesenteric venous thrombosis
• Nonocclusive mesenteric ischaemia from profound low flow or vasoconstriction
• Chronic mesenteric ischaemia from progressive arterial stenosis

The most important distinction is acute versus chronic disease. Acute disease threatens bowel viability within hours. Chronic disease produces recurrent postprandial hypoperfusion and can suddenly thrombose, producing acute on chronic mesenteric ischaemia.

Acute disease classically causes severe abdominal pain disproportionate to initial physical findings. The abdomen may remain soft until transmural infarction causes peritonitis.

Clinical context suggests mechanism:

• Sudden severe pain with atrial fibrillation suggests arterial embolism.
• Acute pain following months of postprandial pain and weight loss suggests thrombosis of chronic atherosclerotic disease.
• Mesenteric venous thrombosis often causes a more progressive abdominal pain syndrome in a patient with malignancy, inflammatory disease or thrombophilia.
• Nonocclusive disease occurs in critically ill patients with shock, severe heart failure or major vasopressor exposure.

Chronic mesenteric ischaemia presents with postprandial pain, progressive food avoidance and weight loss. Diarrhoea or nausea may coexist. Absence of an abdominal bruit does not exclude it.

CT angiography: first line investigation whenever acute mesenteric ischaemia is suspected and the definitive anatomical investigation for chronic arterial disease. In acute disease, CT angiography should be obtained without delay. Every major delay to diagnosis worsens bowel loss and mortality.

Laboratory abnormalities are supportive rather than diagnostic. Leukocytosis, acidosis and raised lactate occur with advanced disease, but no laboratory test reliably excludes early intestinal ischaemia. Lactate above 2 mmol/L in the appropriate clinical setting is concerning for advanced injury but must not be used as a screening gate before CT angiography.

Treatment follows the mechanism.

Acute arterial occlusion: immediate resuscitation, systemic anticoagulation unless contraindicated, broad spectrum antibiotics and urgent revascularisation. Endovascular therapy is preferred where expertise is immediately available and there is no established peritonitis. Peritonitis requires laparotomy with bowel assessment and simultaneous or staged revascularisation.

Mesenteric venous thrombosis: therapeutic anticoagulation is first line when there is no peritonitis or infarcted bowel. Surgery is reserved for necrosis or perforation.

Nonocclusive disease: correct the low flow state, optimise cardiac output, reduce unnecessary vasoconstrictors and consider catheter directed mesenteric vasodilator therapy in appropriate centres. Necrotic bowel requires resection.

Chronic arterial disease: symptomatic disease requires revascularisation. Endovascular stenting is now generally preferred, with the superior mesenteric artery the priority target when only one vessel is treated.

The presence of peritonitis changes the entire pathway. It strongly suggests transmural infarction and mandates emergency abdominal exploration rather than prolonged vascular investigation.