Ischaemic colitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Ischaemic colitis is reduced perfusion of the colon sufficient to cause mucosal injury but not necessarily a major arterial occlusion. Watershed zones around the splenic flexure and rectosigmoid are vulnerable when systemic pressure falls, while isolated right-colon injury can reflect more severe low flow or superior mesenteric artery disease and carries a worse prognosis. Causes include hypotension, dehydration, cardiac failure, sepsis, major surgery, constipation-related intraluminal pressure, thrombosis and vasoconstrictive medicines or drugs. Mucosal haemorrhage produces the familiar sequence of cramping pain and haematochezia. Persistent hypoperfusion extends injury through muscle to gangrene and perforation.

Management depends on severity rather than the label alone. CT identifies distribution, mural oedema, thumbprinting, alternative diagnoses and advanced features, although CT abnormalities are not specific and can underestimate mucosal disease. Limited endoscopy provides direct evidence in stable uncertain left-sided disease and can biopsy carefully, but full colonoscopy, bowel preparation and forceful insufflation add risk. Supportive management treats reversible low flow while the team repeatedly searches for deterioration. Peritonitis is a clinical mandate for surgery even if laboratory values are modest. Right-sided or pain-predominant disease requires explicit consideration of acute mesenteric ischaemia because missing an SMA lesion forfeits an opportunity for revascularisation.

Key points

The typical presentation is sudden cramping, often left-sided abdominal pain followed within hours by urgency and bright red or maroon rectal bleeding, usually after transient hypoperfusion in an older vascular-risk patient.
Generalised peritonitis, shock, perforation or suspected gangrene requires immediate colorectal surgery and no diagnostic endoscopy; resuscitate, give intravenous broad-spectrum antibiotics and proceed to source control.
Contrast-enhanced CT is the initial imaging test in active-treatment candidates; request CT angiography when right-sided disease, severe pain without bleeding or another pattern raises acute mesenteric arterial occlusion.
In a stable patient with uncertain predominantly left-sided disease and no peritonitis or gangrene, limited unprepared flexible sigmoidoscopy within 48 hours is the most accurate confirmation; use minimal insufflation and stop at the distal extent of injury.
Stabilise first: assess shock and peritonism, stop precipitating vasoconstrictors where possible, restore circulating volume and oxygen delivery, rest the bowel and involve colorectal surgery early in moderate or severe disease.
Most non-gangrenous cases improve with bowel rest, intravenous fluids and correction of the trigger; use intravenous broad-spectrum antibiotics in moderate or severe disease because barrier failure can permit bacterial translocation.
Operate for peritonitis, perforation, gangrene, ongoing uncontrolled bleeding or clinical deterioration; the resection boundary depends on viable perfused colon rather than the CT length alone.
After recovery, investigate stricturing symptoms and optimise dehydration, heart failure, arrhythmia, constipation and vascular risks that could provoke recurrence.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Transient low flow

Hypotension, dehydration, heart failure, sepsis or dialysis reduces perfusion first at colonic watershed territories with the weakest collateral supply.

Arterial occlusion

SMA embolism or thrombosis can compromise the right colon and small bowel together, creating a revascularisable acute mesenteric emergency.

Local pressure and small-vessel factors

Raised intraluminal pressure from constipation or obstruction and inflamed or diseased small vessels can reduce mural perfusion despite patent major arteries.

Iatrogenic and drug triggers

Aortic or cardiac surgery can disrupt colonic inflow, while prescribed or illicit vasoconstrictors reduce already marginal microvascular perfusion.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Watershed vulnerability
The splenic flexure and rectosigmoid lie between major arterial territories, so their perfusion falls earliest during systemic hypotension.
2
Mucosal haemorrhage
Early epithelial and capillary injury produces submucosal oedema, superficial ulceration and the characteristic passage of fresh or maroon blood.
3
Transmural extension
If perfusion is not restored, mucosal injury extends through muscle and serosa, causing gangrene, perforation and generalised peritonitis.
4
Fibrotic healing
Deep circumferential inflammation can heal by collagen contraction, leaving a fixed segmental narrowing that presents later with obstructive symptoms.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical transient left-sided disease

Abrupt cramping left lower abdominal pain is followed by urgency and bright red or maroon blood within hours. Tenderness is usually localised without generalised peritonitis.

Low-flow trigger

Recent hypotension, dehydration, sepsis, dialysis, cardiac failure or major aortic/cardiac surgery supports non-occlusive colonic hypoperfusion; ask about vasoconstrictors and constipation.

Right-colon phenotype

Right-sided severe pain, often with little bleeding, is associated with worse outcomes and may be the colonic manifestation of SMA disease rather than isolated watershed injury.

Gangrenous progression

Persistent pain, fever, ileus, peritonism, haemodynamic instability, acidosis and organ dysfunction suggest transmural necrosis; rectal bleeding may disappear as perfusion fails.

Delayed stricture

Weeks after healing, recurrent pain, bloating, altered bowel habit or obstruction can reflect an ischaemic stricture and needs colon assessment once acute perforation risk has passed.

Red flags requiring action

Generalised guarding, rebound, rigidity, haemodynamic instability, rising lactate or organ failure requires emergency surgical assessment; do not perform routine endoscopy through suspected necrotic bowel.
Severe right-sided abdominal pain with little or no rectal bleeding raises concern for isolated right-colon ischaemia and possible SMA compromise; use CT angiography and involve vascular specialists.
Free intraperitoneal gas, pneumatosis with systemic toxicity, portal venous gas, absent bowel-wall enhancement or gangrene indicates advanced ischaemia and likely surgery.
Persistent bleeding, recurrent sepsis, worsening pain or failure to improve after supportive care requires reassessment for infarction, perforation, stricture or an alternative diagnosis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Contrast-enhanced CT abdomen and pelvisFirst step
Why
Initial imaging in suspected colon ischaemia when active treatment is appropriate; define distribution, severity and alternatives.
Interpretation and limitations
Segmental wall thickening, submucosal oedema and pericolic stranding support the diagnosis but are non-specific. Absent enhancement, pneumatosis, portal gas or free air increases concern for infarction.
02
CT angiography
Why
Prioritise when isolated right-colon disease, severe pain without bleeding, recurrent embolic pattern or another feature suggests acute mesenteric arterial occlusion.
Interpretation and limitations
An SMA lesion redirects care toward urgent mesenteric revascularisation plus bowel assessment; normal major vessels can still coexist with low-flow colon ischaemia.
03
Limited unprepared flexible sigmoidoscopy
Why
Most accurate confirmation for a stable patient with uncertain mainly left-sided disease; perform within 48 hours, without bowel preparation, using minimal insufflation.
Interpretation and limitations
Pale or cyanotic mucosa, petechial bleeding, longitudinal ulcers and sharply demarcated injury support ischaemia. Stop at the distal injury margin; avoid in peritonitis, perforation or suspected gangrene.
04
Blood count, renal profile, CRP, coagulation, gas and lactate
Why
Assess bleeding, dehydration, inflammation, renal injury, acidosis and operative risk while serially monitoring physiology.
Interpretation and limitations
No biomarker confirms or excludes the diagnosis. Rising lactate or acidosis supports severe hypoperfusion but a normal value does not make endoscopy or discharge safe by itself.
05
Stool studies when infection remains plausible
Why
Test for bacterial pathogens and C. difficile when diarrhoea, exposures or antimicrobial history suggest infectious colitis.
Interpretation and limitations
A pathogen may establish an alternative or coexist; treatment decisions still follow haemodynamic state, imaging and peritoneal signs.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Infectious colitis

Recent antibiotics, infectious contacts, fever and a positive stool assay support infection, although sepsis and ischaemia may coexist.

Inflammatory bowel disease

Continuous or chronic inflammatory patterns and histology differ, though an acute first presentation can mimic ischaemia.

Diverticulitis

Local left-sided pain and CT inflammation may overlap; luminal blood is more characteristic of mucosal ischaemia.

Acute mesenteric ischaemia

Pain disproportionate to examination, absent rectal bleeding or right-sided disease raises concern for SMA occlusion affecting more than colon.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Worked stable caseLeft-sided pain and bleeding after hypotensionFirst stepAfter dehydration and transient hypotension, a stable older patient develops cramping left-sided pain followed by fresh rectal bleeding, without peritonism.

1Resuscitate, correct the low-flow trigger, stop avoidable vasoconstrictors, rest the bowel and obtain contrast CT to define disease and exclude another emergency.
2If CT and presentation remain uncertain and disease is mainly left sided, arrange limited unprepared flexible sigmoidoscopy within 48 hours using minimal insufflation; do not force passage beyond injured bowel.
3Provide bowel rest and intravenous fluids, add broad-spectrum intravenous antibiotics for moderate or severe disease, and verify improvement through repeated abdominal examination, physiology and laboratory trends.
4Before discharge, restore oral intake cautiously, address the precipitant and provide return advice for recurrent pain, bleeding, fever or obstructive symptoms.

02Preferred severe-disease pathwayPeritonitis or gangrenePreferredThe patient has guarding, rebound, shock, free perforation, absent enhancement or other evidence of transmural injury.

1Resuscitate, provide oxygen and intravenous broad-spectrum antibiotics, cross-match blood and obtain urgent colorectal and critical-care input.
2Do not perform diagnostic colonoscopy; proceed to emergency laparotomy when peritonitis or perforation establishes the need for source control, using CTA only if it will change vascular treatment without harmful delay.
3Assess perfusion and resect non-viable colon, decide diversion or reconstruction according to physiology and contamination, and involve vascular surgery if SMA occlusion or another correctable inflow lesion is present.
4Monitor for ongoing sepsis, further bowel ischaemia, anastomotic failure and need for planned re-look when viability remains uncertain.

03Alternative escalationRight-sided or pain-predominant diseaseAlternativeEscalationSevere right-sided pain, little bleeding or extensive right-colon changes raise concern for AMI.

1Request urgent arterial-and-venous phase CT angiography and state the concern for acute mesenteric ischaemia explicitly.
2Discuss immediately with vascular and gastrointestinal surgical teams; a treatable SMA occlusion may require revascularisation as well as bowel assessment.
3If no occlusion is found, correct low-flow causes and continue close surgical monitoring because non-occlusive mesenteric ischaemia and right-colon infarction remain dangerous.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Gangrene and perforation

Full-thickness colonic death permits bacterial and faecal contamination, causing peritonitis, septic shock and the need for emergency resection.

Major haemorrhage

Extensive ulcerated mucosa can bleed sufficiently to cause anaemia, transfusion dependence or operative haemostasis when supportive care fails.

Ischaemic stricture

Fibrotic remodelling after circumferential injury narrows the lumen, producing delayed pain, bloating, constipation or complete large-bowel obstruction.

Recurrence

Persistent heart failure, episodic hypotension, arrhythmia or renewed vasoconstrictor exposure can reproduce the same colonic perfusion deficit.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat observations and abdominal examination frequently; progression from local tenderness to peritonism is more important than a reassuring initial scan.
Trend haemoglobin, white-cell count, renal function, electrolytes, CRP, pH and lactate according to severity, while recognising none proves mucosal recovery alone.
Record pain, bleeding, urine output, fluid balance and ability to tolerate nutrition; recurrence during feeding can identify unresolved perfusion failure.
After surgery, monitor stoma or anastomosis, sepsis, residual bowel viability and nutritional recovery in a colorectal and critical-care plan.
Arrange follow-up for persistent bleeding or obstructive symptoms because healing can produce segmental stricture; reassess cardiovascular and drug triggers.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Bleeding can be reassuring only in context

Early haematochezia is typical mucosal disease, but absence of bleeding in severe right-sided pain is concerning rather than reassuring because the injury may be deeper or proximal.

Scope is limited by safety

Flexible sigmoidoscopy is valuable in a stable uncertain left-sided presentation. Peritonitis, gangrene and perforation move the patient directly to surgery, and extensive preparation or insufflation adds harm.

CT findings are not the diagnosis alone

Wall thickening and stranding overlap with infection and inflammatory bowel disease. Distribution, low-flow trigger, endoscopic appearance and trajectory establish the clinical diagnosis.

Right colon changes the vascular question

The right colon lies in SMA territory. A pain-dominant right-sided presentation requires CTA for an occlusive mesenteric lesion, not only a colitis work-up.

Recovery does not end surveillance

A healed segment can fibrose and narrow. Later bloating, constipation or obstruction is a reason for planned colonic reassessment, not automatic recurrence treatment.

11Common pitfallsFrequent interpretation and management errors.

01
Sending every patient with rectal bleeding for full colonoscopy and bowel preparation can worsen distension, miss the time window and delay surgery.
02
Using a normal lactate to dismiss ischaemia confuses a late severity marker with a sensitive diagnostic test.
03
Calling right-sided disease routine colitis without arterial-phase imaging can miss superior mesenteric artery occlusion.
04
Continuing dehydration, hypotension or vasoconstrictive treatment while prescribing antibiotics leaves the perfusion mechanism untreated.
05
Waiting for free air before operating ignores peritonitis and haemodynamic deterioration as sufficient evidence of likely transmural disease.

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