Epidemiology
Colonic ischaemia frequently occurs in older people with co-existing morbidities.[4] A systematic review identified 4 studies reporting incidence rates in general populations; three of the studies reported rates between 4.5 and 9 cases per 100,000 person-years and the fourth study reported a rate of 44 cases per 100,000 person-years.[5] These rates are likely to underestimate the true incidence as many patients with mild symptoms do not seek medical care.[5] Irritable bowel syndrome, recent cardiovascular surgery, constipation, chronic obstructive pulmonary disease, and other factors increase the risk of developing colonic ischaemia between two- and fourfold.[5][6][7]
Acute mesenteric ischaemia accounts for less than 0.2% of hospital admissions.[8] It occurs more commonly in those with comorbidities, most notably atrial fibrillation, myocardial infarction, and atherosclerosis. It has been estimated that acute arterial mesenteric ischaemia is responsible for up to 1% of patients presenting with an acute abdomen.[9] One study in Sweden found that between 1970 and 1982, the overall incidence of acute thromboembolic occlusion of the superior mesenteric artery was 8.6 cases per 100,000 person-years, increasing to 216.5 cases per 100,000 person-years in those ages >85 years.[10]
Non-occlusive mesenteric ischaemia (NOMI) accounts for 20% to 30% of acute mesenteric ischaemia.[8][11] The overall incidence of NOMI is 2 cases per 100,000 person-years, increasing to 40 per 100,000 in patients aged >80 years.[12] NOMI may also occur in patients receiving enteral nutrition in intensive care following surgery or trauma; in this context it is associated with a very poor prognosis.[13]
Risk factors
A history of smoking, often in combination with peripheral vascular disease and hypertension, is frequently present.[19]
A strong risk factor for mesenteric venous thrombosis (MVT). Diagnosis of MVT should be particularly suspected in patients who have sudden onset of severe abdominal pain and high risk of thromboembolism; approximately 50% of patients presenting with MVT have had a deep vein thrombosis or pulmonary embolus in the past.[19] Common causes of hypercoagulability include cirrhosis or portal hypertension; inheritable hypercoagulable states such as factor V Leiden, protein C deficiency, or prothrombin G20210A mutation; oral contraceptive use; malignancy; pancreatitis; and a history of recent surgery.[19]
Untreated, atrial fibrillation can result in the formation of thrombi within the atria, which can then embolise to the mesenteric vasculature.[17]
Impaired wall motion secondary to myocardial infarction can act as a nidus for thrombus formation on the ventricular wall, which can then embolise to the mesenteric vessels.
Defects such as right-to-left shunts can increase the risk of emboli to mesenteric vessels.
Rheumatoid arthritis, polyarteritis nodosa, systemic lupus erythematosus, dermatomyositis, Takayasu arteritis, and thrombo-angiitis obliterans can all result in ischaemia of the bowel. The exact clinical picture varies depending upon factors such as the size of the mesenteric vessel involved.
Between 0.6% and 6.7% of patients who have recently undergone cardiac or major vascular procedures develop colonic ischaemia; mortality may be as high as 80% in this population.[2][3] Surgical management of thoracic and abdominal aortic aneurysms (AAAs) is strongly associated with bowel ischaemia; prevalence following repair of ruptured AAA is up to 10% and after elective endovascular repair incidence is up to 2.8%.[3][24] Factors that may underlie these figures include emboli arising from cross-clamping of the aorta, a risk of intestinal hypoperfusion in the postoperative period, and a relatively high incidence of heart failure in these patients. Significant risk factors for mesenteric ischaemia post-cardiac surgery include advanced age (>70 years), prolonged bypass time, emergency surgery, higher volume of blood loss, and other evidence of post-operative organ dysfunction, such as a rise in lactate, transaminases, and creatinine.[25][26]
Hypoperfusion due to shock may exacerbate to a critical level any underlying intestinal low-flow states that may be present due to atherosclerosis. Even in the absence of an existing low-flow state, severe shock can result in ischaemia of the bowel.
Heart failure may exacerbate underlying intestinal low-flow states that may be present due to atherosclerosis. Even in the absence of an existing low-flow state, severe heart failure can lead directly to ischaemia of the bowel.
Atherosclerosis may lead directly to intestinal hypoperfusion and ischaemia due to partial or complete occlusion of vessels supplying the gut. It can also act as a source of emboli.
Severe atherosclerosis in vessels supplying the gut also makes individuals more vulnerable to bowel ischaemia, which are then worsened by congestive heart failure or shock (see above).
Approximately 20% of older patients with colonic ischaemia have a distal obstruction from carcinoma, stricture, faecal impaction, or diverticular disease. The proximal colonic distension leads to intraluminal dilation and increased pressure that may result in decreased mucosal perfusion and ischaemia, typically in the caecum.
Constipation and prolonged straining during defecation result in transient decreased colonic blood flow, which in patients with low-flow states can trigger ischaemia.
Especially in the setting of severe atherosclerosis, use of vasopressors, digoxin, and cocaine have been shown to exacerbate non-occlusive mesenteric ischaemia.[19]
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