Mesenteric Ischaemia
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Direct answer
Pain out of all proportion to the physical examination — severe colicky or constant periumbilical pain with a soft, near-silent abdomen — is the signature of acute mesenteric ischaemia, most often an embolus into the superior mesenteric artery (about half of cases) in a patient with atrial fibrillation or recent myocardial infarction, less often SMA thrombosis on established atherosclerosis, non-occlusive ischaemia in shocked intensive-care patients, or mesenteric venous thrombosis in hypercoagulable states. Diagnosis is by CT angiography, which has replaced catheter angiography as first-line while remaining therapeutic through intra-arterial papaverine, thrombolysis or stenting. Treatment couples restoration of flow — embolectomy, thrombectomy or endovascular recanalisation — with resection of non-viable bowel, accepting a mandatory second-look laparotomy when viability is uncertain. Chronic mesenteric ischaemia, the "intestinal angina" of postprandial pain, food fear and weight loss, is revascularised by angioplasty-stenting or bypass.
What you must remember
- Cause hierarchy: SMA embolus roughly 50 per cent (atrial fibrillation, mural thrombus, valve lesions — emboli preferentially lodge just beyond the middle colic branch), SMA thrombosis about 20 per cent (atherosclerotic ostial disease with a collateral-rich but slower-onset picture), non-occlusive mesenteric ischaemia about 20 per cent (digoxin, vasopressors, dialysis hypotension), and venous thrombosis about 5-10 per cent (thrombophilia, cirrhosis, portal hypertension, oral contraceptives).
- The silent interval: agonising pain, then a deceptive quiescent few hours, then return of pain with distension, absent bowel sounds, peritonism and shock as transmural infarction declares itself — waiting for peritonism is waiting too late.
- Blood tests: raised lactate, metabolic acidosis with high anion gap, leucocytosis, hyperamylaesaemia and hyperphosphataemia are late markers; near-normal bloods never exclude early ischaemia.
- Imaging: CT angiography is the diagnostic standard; plain films show late nonspecific findings — dilated loops, thumbprinting from mucosal oedema, and pneumatosis or portal venous gas as very late signs. Catheter angiography remains both diagnostic and therapeutic (papaverine infusion for non-occlusive disease, thrombolysis for emboli).
- Watershed zones: the splenic flexure (Griffith's point, SMA-IMA junction) and the rectosigmoid (Sudeck's point, IMA-superior rectal junction) are the perfusion boundaries that ischaemic colitis classically strikes.
- Operative principles: embolus via brachial or SMA arteriotomy with Fogarty balloon embolectomy, assess bowel viability by colour, pulsation and peristalsis (fluorescein or Doppler adjuncts), resect the dead segments, and commit to a second-look laparotomy in 24-48 hours whenever viability is doubtful.
- Chronic disease triad: postprandial abdominal pain (patient stops eating — food fear), weight loss, and often a history of atherosclerotic disease elsewhere; duplex shows elevated peak systolic velocities at the SMA origin, and the diagnosis is clinical because stenosis alone is common in asymptomatic patients.
- Ischaemic colitis contrast: it usually affects the left colon, follows aortic surgery, dialysis or hypotension, presents with bloody diarrhoea, and is managed conservatively with fluids and antibiotics in most cases — surgery only for gangrene or stricture.
A worked vascular emergency
A 68-year-old man with atrial fibrillation, not on anticoagulation, develops sudden severe periumbilical pain and one vomit; the abdomen is soft with minimal tenderness, and he is sweating and tachycardic. Reasoning: pain out of proportion plus atrial fibrillation equals mesenteric embolus until proven otherwise. Pathway: resuscitate, start a heparin infusion, and obtain an urgent CT angiogram rather than waiting for lactate to rise or peritonism to appear. If the CT shows an occlusive embolus with viable-appearing bowel, options are open SMA embolectomy or endovascular aspiration/thrombolysis depending on centre capability; if it shows pneumatosis or free fluid with peritonitis, he goes straight to laparotomy — embolectomy plus resection of non-viable jejunum-ileum, primary anastomosis only if the patient is stable, and a planned second-look at 24-48 hours because the demarcation line of ischaemic bowel advances. After surgery, the embolic source is treated: anticoagulation for the arrhythmia, because the second embolus is commoner in the exam question than in the ward.
Where students slip
The commonest error is anchoring on "gastroenteritis" because early bloods and examination are normal — the classic stem describes severe pain with an unremarkable abdomen, and the tested next step is CT angiography, not observation and antiemetics. The second slip is confusing acute mesenteric ischaemia with ischaemic colitis: SMA disease gives small-bowel ischaemia with pain and minimal bleeding, while ischaemic colitis gives left-sided bloody diarrhoea after a hypotensive episode and is usually managed without surgery. Third, the second-look laparotomy is not a hedge but a commitment — deciding at 24-48 hours regardless of the patient's apparent progress, because intestinal viability cannot be reliably judged at the first operation.
Frequently asked questions
What is the most common cause of acute mesenteric ischaemia?
Embolic occlusion of the superior mesenteric artery, usually from the heart in atrial fibrillation or after myocardial infarction, accounting for about half of cases.
Which investigation is the diagnostic standard for acute mesenteric ischaemia?
CT angiography of the abdomen, which demonstrates the level of occlusion and bowel viability changes; catheter angiography is retained where intra-arterial therapy such as papaverine is planned.
Why is a second-look laparotomy performed after mesenteric revascularisation?
Because bowel viability cannot be reliably assessed intra-operatively, a planned re-exploration at 24-48 hours detects extension of infarction before it causes perforation and sepsis.
How does ischaemic colitis differ from acute mesenteric ischaemia?
Ischaemic colitis affects the colon — classically the splenic flexure and rectosigmoid watersheds — follows hypoperfusion, presents with bloody diarrhoea, and is usually treated conservatively, whereas SMA ischaemia presents with pain out of proportion and requires urgent revascularisation.
What is the triad of chronic mesenteric ischaemia?
Postprandial abdominal pain leading to food fear, weight loss from voluntary starvation, and underlying diffuse atherosclerotic disease, confirmed by vascular imaging of the mesenteric vessels.