Ischaemic Bowel disease

  • The three major blood supplies to the intestine are;
    • Coeliac
    • Superior mesenteric
    • Inferior mesenteric

 

  • The severity of injury ranges from;
    • Transmural infarction – involving all visceral layers
    • Mural infarction – of the mucosa and submucosa
    • Mucosal infarction – lesion extends no deeped than the muscularis mucosae
  • Transmural infarction is caused by mechanical compromise of the major mesenteric blood vessels
  • Mucosal or mural infarction is more often caused by hypoperfusion either acute or chronic

 

  • Factors that predispose for ischaemia are;
    • Arterial thrombosis due to atherosclerosis, vasculitis, dissecting aneurism, angiography, surgery, hypercoagulable states
    • Arterial embolism due to cardiac vegetations, angiographic procedures, aortic atheroembolism. Most commonly involves branches of the superior mesenteric artery
    • Venous thrombosis due to hypercoagulable states, cirrhosis, sepsis, surgery and abdominal trauma and neoplasms
    • Nonocclusive injury – cardiac failure, shock, dehydration, vasoconstrictive drugs (digitalis, vasopressin, propranolol)
    • Miscellaneous – radiation, volvulus, stricture, herniation

 

  • Ischaemic injury has two main phases;
    • Initial hypoxic injury
    • Secondary reperfusion – this is when most of the damage is done in ischaemic bowel disease
  • Important factors in the pathogenesis of reperfusion injury are the generation of oxygen free radicals, neutrophilic infiltration, production of inflammatory mediators

 

Morphology

Transmural infarction

  • Sudden and total occlusion of major vasculature with infarction of all bowel layer
  • Any portion of the gut may be affected but the area of large bowel at the splenic flexture is most at risk as it is the watershed between the distribution of the superior and inferior mesenteric arteries
  • Infarct appears haemorrhagic because of blood reflow into the damaged area
  • Bowel appears oedematous, thickened, rubbery and haemorrhagic
  • In arterial occlusion the demarcation from normal bowel is normally sharply defined, in venous occlusions there is no clear cut definition
  • Bacterial overgrowth produces gangrene and perforation can occur within days

 

Mural infarction

  • Complete mucosal necrosis with variable necrosis of the submucosa and muscularis propria
  • Distribution may be patchy but is typically segmental

 

Mucosal infarction

  • Patchy mucosal haemorrhage but with normal serosa
  • Extent of the inflammation depends on the duration of injury

 

Chronic ischaemia

  • With chronic vascular insufficiency mucosal inflammation and ulceration may develop, mimicking both acute enterocolitis and idiopathic IBD
  • Submucosal chronic inflammation and fibrosis may lead to stricture formation

 

Clinical

  • 50-75% mortality rate
  • Typically occurring in severely ill patients, it presents as severe abdo pain, bloody diarrhoea, gross melena, nausea, vomiting, abdominal ridigity

 

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Disclaimer: These notes are my own personal study aid - DO NOT use them for medical advice!