Ischemic colitis
Updates to Article Attributes
Ischaemic colitis refers to inflammation of the colon secondary to vascular insufficiency and ischaemia. It is sometimes considered under the same spectrum as intestinal ischaemia. The severity and consequences of the disease are highly variable.
Epidemiology
Ischaemic bowel is typically a disease of the elderly (age >60 years) where atherosclerotic disease or low flow states are usually the cause 2. InIt is rare in younger individuals, the diseasewhere it is more likely to be related to vasculitis or hyper coagulablehypercoagulable states.
The causes can be categorised as follows:
-
arterial occlusion:arteriosclerosisvasculitidesarterial emboli
-
venous thrombosis:hyper coagulative states including malignancy and OCP useprimary mesenteric venous thrombosis
-
low flow states:hypotensioncongestive heart failurecardiac arrhythmias
-
others:sickle cell diseaseradiation therapy
Clinical presentation
Presenting symptoms include abdominal pain and bloody stools. Tenderness may be present particularly in the left side of the abdomen. In severe cases where necrosis and perforation have occurred the signs and symptoms are those of peritonitis.
Distribution
Location of the ischaemia relates to the anatomy of the mesenteric vessels:
- superior mesenteric artery (SMA): supplies the right colon from the caecum to the splenic flexure
- inferior mesenteric artery (IMA): supplies the left colon from the splenic flexure to the rectum
-
watershed areas 9 :
- splenic flexure (Griffiths
'point) - rectosigmoid junction (Sudeck
'spoint)
- splenic flexure (Griffiths
Low flow states and non-occlusive vessel disease are most common and typically lead to ischaemic colitis in watershed areas while complete vessel occlusion can produce an involvement of the entire vascular territory, e.g. acute SMA occlusion.
Pathology
Diminished or absent blood flow leads to bowel wall ischaemia and secondary inflammation. Bacterial contamination may produce superimposed pseudomembranous inflammation. If necrosis develops then ulcerations or perforation can occur. Following the acute event, fibrosis may lead to stricture of the bowel lumen. Different pathological outcomes include 9 :
- gangrenous (15-20%)
- non-gangrenous (80-85%):
- reversible
- non-reversible (chronic colitis, stricture formation)
Aetiology
The causes can be categorised as follows:
-
arterial occlusion:
- arteriosclerosis
- vasculitides
- arterial emboli
-
venous thrombosis:
- hypercoagulative states including malignancy and oral contraceptive pill use
- primary mesenteric venous thrombosis
-
low flow states:
- hypotension
- congestive heart failure
- cardiac arrhythmias
-
others:
- sickle cell disease
- radiation therapy
Radiographic features
Plain radiograph
Abdominal radiographs are often normal, but signs include:
- dilatation due to ileus
- 'thumbprinting' due to mucosal oedema/haemorrhage
- localised intramural gas (pneumatosis coli) if necrotic
- free intraperitoneal gas if perforated
Fluoroscopy
Contrast enema is abnormal in 90% 7 but is rarely used for diagnostic purposes:
- segmental region of abnormality
- 'thumbprinting' which is classically obliterated by air insufflation 8
- spasm
- ulcerations 'serrated mucosa' 7
- stricture from fibrosis as a late complication of ischaemia
Ultrasound
Ultrasound is of limited use due to bowel gas but may show:
- luminal thickening of the affected segment with or without stratification 3
- hypoechoic wall due to oedema
- areas of increased echogenicity if haemorrhage
- echogenic foci with shadowing if intramural gas
- reduced peristalsis may be observed
- Doppler imaging of the SMA origin can be useful in assessing for stenoses
CT
Contrast enhanced imaging is the modality of choice. Features include:
- segmental region of abnormality
- symmetrical or lobulated thickening of the bowel wall
- irregularly narrowed lumen
- submucosal oedema may produce low-density ring bordering lumen (target sign)
- intramural or portal venous gas
- mesenteric oedema
- superior mesenteric artery or vein thrombus/occlusion may be demonstrated
Angiography (DSA)
Can show mesenteric artery occlusion if present. Otherwise, angiography may show increased arterial calibre, accelerated arteriovenous transit time and dilated draining veins due to the inflammatory response.In mesenteric venous thrombosis, the veins may not be visualised, and collateral venous filling may be seen 7.
Nuclear medicine
Increased uptake of Tc99m (V) DMSA tracer in the ischaemic bowel may be present but is unreliable 4.
Treatment and prognosis
Mesenteric arterial or venous occlusion can be treated with anticoagulation or thrombolysis, either systemically or locally. Percutaneous vascular intervention in acute mesenteric artery occlusion is often successful and may involve a combination of thrombus aspiration, thrombolysis and arterial stenting 5. Surgical resection is indicated in cases of peritonitis, perforation, severe sepsis and massive haemorrhage. Symptomatic Symptomatic strictures may also require surgery 9 .
Prognosis is variable 6:
- resolution without ongoing complications ~50%
- persistent colitis ~20%
- ischemic stricture ~10%
- gangrene or perforation ~20%
Occlusive mesenteric infarction (embolus or thrombosis) has a high mortality rate (~90%) compared to non-occlusive ischaemia (~10%).
Differential diagnosis
Imaging differential considerations include:
- other colitides
- ulcerative colitis
- Crohn colitis
- infective colitis: pseudomembranous, amebiasis, schistosomiasis
- radiation colitis
- intramural haemorrhage
- diverticulitis
- lymphoma or carcinoma
-<p><strong>Ischaemic colitis </strong>refers to inflammation of the colon secondary to vascular insufficiency and ischaemia. It is sometimes considered under the same spectrum as <a href="/articles/intestinal-ischaemia">intestinal ischaemia</a>. The severity and consequences of the disease are highly variable.</p><h4>Epidemiology</h4><p>Ischaemic bowel is typically a disease of the elderly (age >60 years) where atherosclerotic disease or low flow states are usually the cause <sup>2</sup>. In younger individuals, the disease is more likely to be related to vasculitis or hyper coagulable states.</p><p>The causes can be categorised as follows:</p><ul>- +<p><strong>Ischaemic colitis </strong>refers to inflammation of the colon secondary to vascular insufficiency and ischaemia. It is sometimes considered under the same spectrum as <a href="/articles/intestinal-ischaemia">intestinal ischaemia</a>. The severity and consequences of the disease are highly variable.</p><h4>Epidemiology</h4><p>Ischaemic bowel is typically a disease of the elderly (age >60 years) where atherosclerotic disease or low flow states are usually the cause <sup>2</sup>. It is rare in younger individuals, where it is more likely to be related to vasculitis or hypercoagulable states.</p><h4>Clinical presentation</h4><p>Presenting symptoms include abdominal pain and bloody stools. Tenderness may be present particularly in the left side of the abdomen. In severe cases where necrosis and perforation have occurred the signs and symptoms are those of peritonitis.</p><h5>Distribution</h5><p>Location of the ischaemia relates to the anatomy of the mesenteric vessels:</p><ul>
- +<li>
- +<a href="/articles/superior-mesenteric-artery">superior mesenteric artery (SMA)</a>: supplies the right colon from the caecum to the splenic flexure</li>
- +<li>
- +<a href="/articles/inferior-mesenteric-artery">inferior mesenteric artery (IMA)</a>: supplies the left colon from the splenic flexure to the rectum</li>
- +<li>
- +<a href="/articles/watershed-area">watershed areas</a> <sup>9</sup> :<ul>
- +<li>splenic flexure (<a href="/articles/griffiths-point-2">Griffiths point</a>)</li>
- +<li>rectosigmoid junction (<a href="/articles/sudeck-point">Sudeck point</a>) </li>
- +</ul>
- +</li>
- +</ul><p>Low flow states and non-occlusive vessel disease are most common and typically lead to ischaemic colitis in watershed areas while complete vessel occlusion can produce an involvement of the entire vascular territory, e.g. <a href="/articles/acute-superior-mesenteric-artery-occlusion">acute SMA occlusion</a>. </p><h4>Pathology</h4><p>Diminished or absent blood flow leads to bowel wall ischaemia and secondary inflammation. Bacterial contamination may produce superimposed pseudomembranous inflammation. If necrosis develops then ulcerations or perforation can occur. Following the acute event, fibrosis may lead to stricture of the bowel lumen. Different pathological outcomes include <sup>9</sup> :</p><ul>
- +<li>gangrenous (15-20%)</li>
- +<li>non-gangrenous (80-85%):<ul>
- +<li>reversible</li>
- +<li>non-reversible (chronic colitis, stricture formation)</li>
- +</ul>
- +</li>
- +</ul><h5>Aetiology</h5><p>The causes can be categorised as follows:</p><ul>
-<li>hyper coagulative states including malignancy and OCP use</li>- +<li>hypercoagulative states including malignancy and oral contraceptive pill use</li>
-<li>congestive heart failure</li>- +<li><a title="Congestive heart failure" href="/articles/congestive-cardiac-failure">congestive heart failure</a></li>
-</ul><h4>Clinical presentation</h4><p>Presenting symptoms include abdominal pain and bloody stools. Tenderness may be present particularly in the left side of the abdomen. In severe cases where necrosis and perforation have occurred the signs and symptoms are those of peritonitis.</p><h5>Distribution</h5><p>Location of the ischaemia relates to the anatomy of the mesenteric vessels:</p><ul>-<li>-<a href="/articles/superior-mesenteric-artery">superior mesenteric artery (SMA)</a>: supplies the right colon from the caecum to the splenic flexure</li>-<li>-<a href="/articles/inferior-mesenteric-artery">inferior mesenteric artery (IMA)</a>: supplies the left colon from the splenic flexure to the rectum</li>-<li>-<a href="/articles/watershed-area">watershed areas</a> <sup>9</sup> :<ul>-<li>splenic flexure (<a href="/articles/griffiths-point-2">Griffiths' point</a>)</li>-<li>rectosigmoid junction (<a href="/articles/sudeck-point">Sudeck's point</a>) </li>-</ul>-</li>-</ul><p>Low flow states and non-occlusive vessel disease are most common and typically lead to ischaemic colitis in watershed areas while complete vessel occlusion can produce an involvement of the entire vascular territory, e.g. <a href="/articles/acute-superior-mesenteric-artery-occlusion">acute SMA occlusion</a>. </p><h4>Pathology</h4><p>Diminished or absent blood flow leads to bowel wall ischaemia and secondary inflammation. Bacterial contamination may produce superimposed pseudomembranous inflammation. If necrosis develops then ulcerations or perforation can occur. Following the acute event, fibrosis may lead to stricture of the bowel lumen. Different pathological outcomes include <sup>9</sup> :</p><ul>-<li>gangrenous (15-20%)</li>-<li>non-gangrenous (80-85%):<ul>-<li>reversible</li>-<li>non-reversible (chronic colitis, stricture formation)</li>-</ul>-</li>-</ul><h5>Angiography (DSA)</h5><p>Can show mesenteric artery occlusion if present. Otherwise, angiography may show increased arterial calibre, accelerated arteriovenous transit time and dilated draining veins due to the inflammatory response.In mesenteric venous thrombosis, the veins may not be visualised, and collateral venous filling may be seen <sup>7</sup>.</p><h5>Nuclear medicine</h5><p>Increased uptake of Tc<sup>99</sup>m (V) DMSA tracer in the ischaemic bowel may be present but is unreliable <sup>4</sup>.</p><h4>Treatment and prognosis</h4><p>Mesenteric arterial or venous occlusion can be treated with anticoagulation or thrombolysis, either systemically or locally. Percutaneous vascular intervention in acute mesenteric artery occlusion is often successful and may involve a combination of thrombus aspiration, thrombolysis and arterial stenting <sup>5</sup>. Surgical resection is indicated in cases of peritonitis, perforation, severe sepsis and massive haemorrhage. Symptomatic strictures may also require surgery <sup>9</sup> .</p><p>Prognosis is variable <sup>6</sup>:</p><ul>- +</ul><h5>Angiography (DSA)</h5><p>Can show mesenteric artery occlusion if present. Otherwise, angiography may show increased arterial calibre, accelerated arteriovenous transit time and dilated draining veins due to the inflammatory response.In mesenteric venous thrombosis, the veins may not be visualised, and collateral venous filling may be seen <sup>7</sup>.</p><h5>Nuclear medicine</h5><p>Increased uptake of Tc<sup>99</sup>m (V) DMSA tracer in the ischaemic bowel may be present but is unreliable <sup>4</sup>.</p><h4>Treatment and prognosis</h4><p>Mesenteric arterial or venous occlusion can be treated with anticoagulation or thrombolysis, either systemically or locally. Percutaneous vascular intervention in acute mesenteric artery occlusion is often successful and may involve a combination of thrombus aspiration, thrombolysis and arterial stenting <sup>5</sup>. Surgical resection is indicated in cases of peritonitis, perforation, severe sepsis and massive haemorrhage. Symptomatic strictures may also require surgery <sup>9</sup> .</p><p>Prognosis is variable <sup>6</sup>:</p><ul>