Ischemic colitis

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. It is rare in younger individuals, where it is more likely to be related to vasculitis or hypercoagulable states.

Clinical presentation

Presenting symptoms include abdominal pain and bloody stools. Tenderness may be present particularly on the left side of the abdomen. In cases of isolated right-sided colonic ischaemia patients may present with abdominal pain without haematochezia or melaena. ¹⁴. 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 point) 

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 (ideally with an arterial phase) is the modality of choice. Features include ¹²:

• bowel wall findings
  • bowel wall thickening (common), usually uniform and segmental, rarely localized and mass-like ¹⁰
  • low-density ring of submucosal edema between enhancing mucosa and serosa (target sign)
  • bowel dilatation
  • pneumatosis coli (uncommon) ¹³
• peritoneal/retroperitoneal cavity findings
  • pericolic fluid or fat stranding (common)
  • peritoneal free fluid and mesenteric oedema
  • pneumoperitoneum / pneumoretroperitoneum
• vascular findings
  • vascular occlusion (superior or inferior mesenteric artery or vein)
  • portal and mesenteric venous gas ¹³

Secondary findings supportive of an ischemic etiology include the presence of parenchymal ischemia/infarction in other abdominal organs, such as the liver, kidneys, and spleen.

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 strictures may also require surgery ⁹.

Prognosis is variable ⁶:

• resolution without ongoing complications ~50% 
• persistent colitis ~20%
• ischaemic 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 (particularly in the right colon, where the mass-forming variant of ischaemic colitis has a predelictionpredilection ¹⁰)