Ischemic colitis is ischemic damage to the colonic mucosa due to inadequate blood flow. Most commonly seen in elderly patients (>60 years). Colon 'watershed' areas with weakest blood flow (splenic flexure — Griffiths point, rectosigmoid junction — Sudeck point) are most commonly affected. Non-occlusive mechanical (low flow — hypotension, heart failure) is the most common cause (95%). Segmental wall thickening, submucosal edema/hemorrhage, and pericolic fat stranding are characteristic on CT. Prognosis is variable — mild cases resolve spontaneously while transmural necrosis mortality reaches 60%.
Age Range
50-90
Peak Age
70
Gender
Female predominant
Prevalence
Uncommon
Ischemic colitis is ischemic damage to colonic mucosa from inadequate blood flow. Colon dual blood supply comes from SMA (right colon) and IMA (left colon) — splenic flexure is the watershed area between these two arteries (Griffiths point). In hypotension, atherosclerosis, cardiac low output, or vasculitis, watershed areas are affected first. Ischemia cascade: hypoxia → mucosal edema → hemorrhagic infiltration → submucosal hemorrhage → ulceration → transmural necrosis. Reperfusion injury also worsens pathology — free oxygen radicals and inflammatory mediators cause additional damage. On CT, this pathophysiology reflects as segmental wall thickening (edema), submucosal hyperdense area (hemorrhage — CT equivalent of 'thumbprinting'), and pericolic fat stranding. Pneumatosis and portal venous gas indicate transmural necrosis.
Segmental concentric wall thickening at splenic flexure or rectosigmoid junction (watershed areas) with submucosal hyperdense hemorrhage (CT equivalent of thumbprinting) is the signature finding of ischemic colitis.
Segmental symmetric/concentric wall thickening (>4 mm, usually 8-15 mm) at splenic flexure or rectosigmoid junction. Watershed area involvement is pathognomonic.
Report Sentence
Segmental concentric wall thickening at the splenic flexure/rectosigmoid junction is seen, consistent with ischemic colitis.
Hyperdense (hemorrhage — 40-60 HU) or hypodense (edema — 10-20 HU) layer in submucosal area. Layered wall structure creates 'target sign'-like appearance (CT equivalent of thumbprinting).
Report Sentence
Submucosal hyperdense area is seen in the thickened bowel wall, consistent with submucosal hemorrhage (thumbprinting).
Pneumatosis intestinalis (intramural air) and portal venous gas — most reliable CT findings of transmural necrosis. Emergency surgical indication.
Report Sentence
Pneumatosis intestinalis in the ischemic colon segment and portal venous gas in the liver are seen, suggesting transmural necrosis; emergency surgical consultation is recommended.
Pericolic fat stranding and free fluid — spread of ischemic inflammation to surrounding tissues.
Report Sentence
Pericolic fat stranding and pelvic free fluid are seen around the ischemic colon segment.
Absent/decreased bowel wall enhancement — reflects loss of arterial supply (transmural ischemia). Normal or increased enhancement indicates mucosal/submucosal ischemia (reperfusion).
Report Sentence
Decreased/absent wall enhancement in the ischemic colon segment is seen, suggesting transmural ischemia/necrosis.
Assessment of SMA/IMA and branches — occlusive (thrombus, embolus) vs non-occlusive (low flow) ischemia distinction. Vascular pathology can be detected by CT angiography.
Report Sentence
No significant occlusion is detected in SMA/IMA and branches, suggesting non-occlusive ischemic colitis.
Criteria
Mucosal/submucosal ischemia. Resolves spontaneously. 50-60% of cases.
Distinct Features
Mild wall thickening, submucosal edema on CT. Conservative treatment (IV fluids, bowel rest, antibiotics) sufficient.
Criteria
Fibrotic stricture after chronic ischemic damage. 10-15% of cases.
Distinct Features
Segmental luminal narrowing, wall thickening (fibrotic) on CT. Endoscopic dilation or segmental resection.
Criteria
Transmural necrosis. Pneumatosis, portal venous gas, absent enhancement. 15-20% of cases.
Distinct Features
Emergency surgery (subtotal/total colectomy). Mortality 60-80%. Peritonitis signs and septic shock accompany.
Distinguishing Feature
Ulcerative colitis shows continuous involvement starting from rectum. Ischemic colitis shows segmental involvement at watershed area, rectum usually spared (dual supply outside IMA).
Distinguishing Feature
Diverticulitis shows focal inflamed diverticulum and diverticula. Ischemic colitis shows segmental wall thickening, submucosal hemorrhage, and absence of diverticula.
Distinguishing Feature
Crohn shows skip lesions, comb sign, fistulae, and young age onset. Ischemic colitis shows watershed area involvement, elderly patient, sudden onset, and vascular risk factors.
Distinguishing Feature
Adenocarcinoma shows focal asymmetric mass, shouldered margins, and lymphadenopathy. Ischemic colitis shows segmental symmetric thickening, submucosal hemorrhage, and absence of mass.
Urgency
emergentManagement
medicalBiopsy
Not NeededFollow-up
3-monthTreatment determined by ischemia severity. Transient/mild ischemic colitis (50-60%): IV fluid resuscitation, bowel rest, broad-spectrum antibiotics, correction of underlying cause (cardiac output optimization, discontinuation of vasoconstrictors). Transmural necrosis/gangrene (15-20%): emergency surgery (subtotal/total colectomy). Surgical indications: pneumatosis + portal venous gas, peritonitis signs, absent enhancement, septic shock, no response to conservative treatment in 24-48 hours. Follow-up: colonoscopy at 2-4 weeks (stricture/chronic change assessment), vascular risk factor management, 3-month clinical follow-up.
Most cases resolve with conservative treatment. Transmural necrosis requires emergency surgery. Pneumatosis and portomesenteric gas are associated with mortality. Stricture may develop in chronic phase.