Acute Mesenteric Ischaemia

Acute mesenteric ischaemia is sudden interruption or severe reduction of intestinal blood flow sufficient to cause ischaemic injury and potentially bowel necrosis.

Major mechanisms are superior mesenteric arterial embolism, arterial thrombosis, mesenteric venous thrombosis and nonocclusive mesenteric ischaemia.

The disease is time critical. Untreated ischaemia progresses from mucosal injury to transmural necrosis, perforation, bacterial translocation, severe acidosis and multiorgan failure. Mortality remains high, particularly after infarction has developed.

Severe poorly localised abdominal pain disproportionate to the examination remains the classic early presentation and should be treated as mesenteric ischaemia until disproven in the appropriate patient.

Risk pattern is highly informative:

• Atrial fibrillation, recent myocardial infarction or cardiac embolic disease suggests superior mesenteric artery embolism.
• Diffuse atherosclerosis plus previous postprandial pain and weight loss suggests acute arterial thrombosis.
• Malignancy, thrombophilia, portal inflammatory disease or recent abdominal surgery suggests mesenteric venous thrombosis.
• Critical illness, cardiogenic shock, severe sepsis or high vasopressor requirement suggests nonocclusive disease.

Nausea, vomiting, diarrhoea or gastrointestinal bleeding may accompany the pain.

Development of focal guarding or generalised peritonitis usually signifies advanced transmural ischaemia or infarction and requires surgery without delay.

CT angiography immediately: defines the vascular lesion and bowel consequences. Do not wait for renal function normalisation when clinical suspicion is strong, because delayed diagnosis is substantially more dangerous than contrast exposure in this setting. WSES recommends CT angiography without delay in every suspected case.

Check full blood count, renal function, electrolytes, coagulation profile, blood gas and lactate. Crossmatch blood if laparotomy is likely.

Lactate is useful for severity and resuscitation monitoring but cannot exclude early disease. Advanced ischaemia can produce metabolic acidosis, hyperkalaemia and rising lactate.

Begin treatment while CT angiography and vascular or surgical teams are being mobilised.

Keep fasting, establish large bore IV access, correct hypovolaemia with balanced crystalloid and decompress the stomach with a nasogastric tube where distension or vomiting is significant. Avoid excessive crystalloid because bowel oedema and abdominal compartment pressure can worsen intestinal perfusion.

Give broad spectrum antibiotics early because mucosal ischaemia permits bacterial translocation. A practical regimen is:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, with renal adjustment.

Where this is unavailable, ceftriaxone 2 g IV every 24 hours plus metronidazole 500 mg IV every 12 hours provides community acquired Gram negative and anaerobic coverage.

Unless there is active bleeding or another major contraindication, initiate therapeutic unfractionated heparin. WSES recommends full dose anticoagulation before intervention, particularly because unfractionated heparin is rapidly titratable and suitable in renal failure.

A commonly used therapeutic regimen is:

Unfractionated heparin 80 units/kg IV bolus followed by 18 units/kg/hour IV infusion, then titrate using the institutional activated partial thromboplastin time or anti Xa protocol. The precise bolus may be omitted or modified when the patient is already anticoagulated or has high bleeding risk.

Arterial embolism or thrombosis without peritonitis: pursue immediate mesenteric revascularisation. Endovascular aspiration thrombectomy, thrombolysis or stenting is preferred where expertise is immediately available. Atherosclerotic ostial thrombosis generally requires angioplasty and stenting rather than simple embolic extraction.

Peritonitis or suspected bowel necrosis: proceed to emergency laparotomy. Resect only clearly nonviable bowel and restore mesenteric flow whenever feasible. Revascularisation before extensive bowel resection may salvage marginal intestine.

Questionable bowel should be preserved initially when possible. Following revascularisation, allow reperfusion and reassess colour, mesenteric pulsation and perfusion. When viability remains uncertain, leave bowel in discontinuity and perform a planned second look operation approximately 24 to 48 hours later.

Damage control surgery is appropriate with shock, severe acidosis, hypothermia, coagulopathy, gross bowel oedema or uncertain viability. Avoid committing a physiologically exhausted patient to a high risk primary anastomosis.

Mesenteric venous thrombosis without peritonitis is usually treated nonoperatively with therapeutic anticoagulation. Surgery is required if infarction, perforation or progressive peritonitis develops.

Nonocclusive mesenteric ischaemia: correct hypovolaemia and cardiac dysfunction, reduce vasoconstrictors where clinically feasible and treat the precipitating shock state. Catheter directed papaverine or other vasodilator therapy can be considered in specialist centres.

After revascularisation and bowel resection, monitor aggressively for reperfusion injury, acidosis, hyperkalaemia, renal failure and recurrent ischaemia. Document the exact remaining small bowel length because extensive resection may result in intestinal failure and short bowel syndrome.