Ischaemic colitis

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

Ischaemic colitis results when colonic oxygen delivery becomes inadequate for metabolic demand. Most episodes are non-occlusive and transient, arising from systemic hypotension, dehydration or small-vessel vulnerability rather than a single embolus. Segmental watershed areas near the splenic flexure and rectosigmoid are susceptible, although anatomy varies. Mucosal injury produces cramping pain, urgency and blood; deeper injury causes ileus, persistent pain, systemic toxicity and necrosis. Ask about shock, cardiac decompensation, recent aortic or abdominal surgery, dialysis, vigorous exercise, cocaine or vasoconstrictors, constipation and medicines such as diuretics. A younger patient may warrant a different search for drugs, vasculitis or thrombophilia through specialist review.

The main bedside task is to separate a limited colitis from threatened bowel and from acute mesenteric ischaemia. Typical left-sided disease produces pain before modest haematochezia and focal tenderness without generalised rigidity. Right-sided disease, absence of bleeding, atrial fibrillation, very severe pain, metabolic acidosis or small-bowel involvement raises a more proximal arterial event or extensive injury. Infectious colitis often has exposure and fever; IBD has a different history but may first present acutely; diverticulitis usually has focal inflammatory pain with little bleeding. No laboratory result independently confirms or excludes ischaemia. Repeated examination and direct radiology-surgical communication are essential because deterioration can occur after initially modest signs.

Contrast CT is usually the initial stable-patient investigation and may show segmental circumferential thickening, oedema, reduced enhancement or pericolic change, while identifying perforation and alternative disease. CT angiography is appropriate when arterial occlusion or acute mesenteric ischaemia is plausible. In a stable patient without peritonitis or gangrene, early careful flexible sigmoidoscopy or colonoscopy can demonstrate pale oedematous mucosa, petechiae, longitudinal ulcers and sharply demarcated injury; biopsies support but histology is not uniquely diagnostic. Treatment corrects the low-flow cause, stops non-essential precipitating medicines, rests the bowel and monitors closely. Antibiotic practice is severity-dependent and locally governed. Persistent sepsis, peritonism, perforation, gangrene or worsening metabolic state requires urgent resection planning.

Key points

Ischaemic colitis usually presents with sudden cramping abdominal pain followed within hours by rectal blood or bloody diarrhoea after a low-flow or vascular insult.
The left colon and watershed zones are frequently affected, but isolated right-colon involvement carries greater severity and should lower the threshold for urgent surgical review.
Risk factors include older age, atherosclerosis, heart failure, hypotension, dehydration, recent major surgery, dialysis, thrombophilia and vasoconstricting or constipating medicines.
A normal early lactate does not exclude bowel ischaemia; serial physiology, examination and contrast imaging determine urgency.
Contrast CT assesses distribution, wall injury, complications and alternative diagnoses; CT angiography is added when acute mesenteric arterial occlusion or severe right-sided disease is suspected.
In a stable patient without peritonism, limited lower-GI endoscopy with careful insufflation and biopsies can confirm the pattern and exclude IBD, infection or cancer.
Mild transient disease is treated with restoration of perfusion, bowel rest or diet progression and removal of precipitating factors; moderate or severe disease may require antibiotics and closer monitoring.
Surgery is indicated for perforation, peritonitis, gangrene, uncontrolled bleeding or clinical deterioration despite non-operative care, not for every CT segment of thickening.

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

Low-flow hypoperfusion

Hypotension, dehydration, heart failure, dialysis and major surgery reduce colonic perfusion, particularly in vulnerable watershed regions.

Vascular and thrombotic disease

Atherosclerosis, small-vessel disease, embolic events and thrombophilia can limit colonic blood supply, with right-sided disease often more severe.

Medicine and mechanical factors

Vasoconstricting or constipating medicines, severe distension and obstructing lesions can impair mural perfusion without a major arterial occlusion.

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

1
Perfusion-demand mismatch
Transient or sustained reduction in colonic blood flow deprives metabolically active mucosa of oxygen, first affecting watershed areas.
2
Mucosal haemorrhagic injury
Epithelial sloughing, oedema and submucosal bleeding cause cramping pain followed by haematochezia or bloody diarrhoea during reperfusion.
3
Reperfusion or transmural progression
Restored flow may amplify inflammation, while persistent ischaemia extends through muscle to gangrene, perforation and sepsis.

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

Typical transient left-sided disease

Abrupt cramping left abdominal pain followed by urgency and small-to-moderate rectal bleeding after dehydration or hypotension, with local tenderness but stable physiology, fits common non-gangrenous ischaemic colitis.

Severe right-sided patternRed flag

Right abdominal pain, little or no bleeding, kidney failure or shock and CT involvement of the ascending colon predicts a worse course and can overlap acute mesenteric ischaemia.

Transmural infarctionRed flag

Constant worsening pain, involuntary guarding, fever, shock, ileus, acidosis, pneumatosis or portal venous gas suggests necrotic bowel and requires immediate senior surgery rather than diagnostic endoscopy.

Acute mesenteric ischaemiaRed flag

Pain out of proportion, atrial fibrillation, embolic history, severe diffuse pain or small-bowel hypoenhancement indicates a vascular emergency requiring CT angiography and vascular-surgical involvement.

Delayed stricture

Weeks or months after healing, progressive bloating, colicky pain, constipation or obstruction may reflect an ischaemic stricture and needs luminal imaging and colorectal assessment.

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 CT abdomen and pelvisFirst step
Why
Map colonic distribution, grade mural injury and detect perforation, obstruction, malignancy or another cause of acute colitis.
Interpretation and limitations
Segmental thickening and pericolic change support but do not prove ischaemia. Poor enhancement, pneumatosis, portal venous gas, free air or extensive right-sided disease prompts urgent surgical escalation.
02
CT angiography
Why
Evaluate mesenteric arterial occlusion when symptoms, right-sided disease or small-bowel findings suggest acute mesenteric ischaemia rather than isolated transient colitis.
Interpretation and limitations
An arterial filling defect or threatened small bowel redirects to an acute vascular-surgical pathway. Normal major vessels remain compatible with non-occlusive small-vessel ischaemic colitis.
03
Full blood count, renal profile, CRP and clotting
Why
Assess inflammation, haemoconcentration or anaemia, organ injury and procedural or bleeding risk.
Interpretation and limitations
Leucocytosis and CRP reflect severity non-specifically; kidney injury supports hypoperfusion. Normal initial tests cannot exclude early mucosal ischaemia, so trends follow clinical change.
04
Blood gas and lactate
Why
Measure acid-base disturbance and systemic hypoperfusion in moderate or severe illness.
Interpretation and limitations
Rising lactate or metabolic acidosis raises concern for advanced injury but is not colon-specific. A normal early lactate must not defer imaging or surgery when the phenotype is high risk.
05
Limited lower gastrointestinal endoscopy with biopsy
Why
Confirm a compatible mucosal distribution and exclude IBD, infection or malignancy in a stable patient without peritonism.
Interpretation and limitations
Segmental pale oedema, petechiae or longitudinal ulceration with supportive histology strengthens diagnosis. Minimise insufflation and stop if severe injury makes perforation a concern.
06
Stool microbiology
Why
Exclude bacterial and Clostridioides difficile colitis when diarrhoea, antibiotics, exposure or fever creates a plausible infectious alternative.
Interpretation and limitations
A detected pathogen changes isolation and antimicrobial management. A negative result does not establish ischaemia but helps interpret endoscopic and imaging findings.

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

Infectious or inflammatory colitis

Exposure, stool pathogen detection, chronic relapse or continuous endoscopic inflammation supports infection or IBD rather than an abrupt vascular event.

Acute mesenteric ischaemia

Severe pain out of proportion, small-bowel involvement or major vessel occlusion on CT angiography suggests a more extensive arterial emergency.

Diverticulitis

Focal left-lower-quadrant inflammation around diverticula with fever and less prominent bleeding favours diverticulitis over segmental mucosal ischaemia.

Additional chapter-specific clues

Infectious or inflammatory mimic

Prominent diarrhoea, fever, travel, antibiotics or contacts suggests infection, while chronic symptoms, extraintestinal features or continuous rectal disease supports IBD; stool tests and biopsies help discriminate.

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

01Initial assessmentGrade bowel and whole-patient riskFirst stepAcute pain and rectal blood suggest ischaemic colitis.

1Perform ABCDE, establish onset and pain-before-blood sequence, seek shock or vascular triggers and review cardiac, surgical, dialysis and medicine history.
2Examine repeatedly for focal versus generalised tenderness, distension and perfusion, sending bloods, lactate and stool tests without using normal results to dismiss the diagnosis.
3Obtain contrast CT and discuss CT angiography directly with radiology when right-sided, disproportionate or embolic features suggest acute mesenteric ischaemia.
4Involve senior colorectal surgery early for high-risk distribution or physiology, even before peritonism becomes established.

02Non-gangrenous careRestore perfusion and observe closelyImaging and examination support limited disease without peritonism, perforation or organ failure.

1Correct dehydration and hypotension carefully, treat precipitating cardiac or septic illness and stop non-essential vasoconstricting or constipating medicines with appropriate ownership.
2Rest the bowel or progress diet according to symptoms, provide analgesia and venous-thromboembolism assessment, and use local antibiotics when severity warrants them.
3Arrange careful endoscopy with biopsies when it will confirm the diagnosis or exclude a mimic and procedural risk is acceptable.
4Trend pain, observations, abdominal signs, bloods and oral tolerance; any divergence from improvement triggers immediate CT and surgical reassessment.

03Threatened or necrotic bowelMove to definitive surgeryDefinitivePeritonitis, free perforation, gangrene, persistent sepsis, uncontrolled bleeding or worsening acidosis develops.

1Continue resuscitation, broad-spectrum antimicrobial treatment and critical-care support while summoning the consultant colorectal surgeon and anaesthetist.
2Do not delay operation for colonoscopy or repetitive low-yield tests when clinical and imaging evidence indicates transmural injury.
3Plan resection according to viable margins, physiological reserve and contamination, discussing stoma likelihood and uncertainty with the patient or representative when possible.
4After surgery, monitor remaining bowel, nutrition, sepsis and organ support, and investigate the precipitating low-flow or thrombotic cause to reduce recurrence.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Restores circulating volume and colonic perfusion when dehydration or hypotension contributes to non-occlusive injury.

Intravenous crystalloid

Give cautious reassessed boluses under the current resuscitation protocol, then replace ongoing deficits according to perfusion, cardiac reserve, renal function and urine output.

Heart failure and renal disease increase pulmonary oedema risk. Fluid cannot correct an embolic occlusion or necrotic bowel, so definitive imaging and surgical decisions continue in parallel.

Provides enteric bacterial coverage when mucosal barrier failure, systemic toxicity or necrosis creates translocation and sepsis risk.

Broad-spectrum antibiotic

For moderate, severe or surgically threatened disease, use the locally approved intravenous colonic-sepsis regimen and review daily against cultures, source control and recovery.

Evidence and thresholds vary, so mild disease may not require antibiotics. Check allergy, renal function and Clostridioides difficile risk, and never substitute antibiotics for resection of gangrene.

Relieves pain humanely and enables breathing, mobilisation and accurate ongoing clinical assessment during investigation and recovery.

Analgesia

Use titrated paracetamol and, when necessary, carefully monitored opioid analgesia under the acute-care formulary while repeating abdominal examination and perfusion assessment.

NSAIDs may worsen renal perfusion or bleeding, and opioids can aggravate ileus or mask a changing trajectory if observations cease. Rising analgesic requirement is a reassessment trigger.

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

Gangrene and perforation

Full-thickness infarction causes peritonitis, free gas and urgent colectomy, particularly with isolated right-colon disease or systemic deterioration.

Sepsis and multiorgan failure

Barrier loss permits bacterial translocation and contamination, causing shock, kidney injury and respiratory failure if necrotic bowel remains.

Post-ischaemic stricture

Healing after deeper injury can produce fibrotic narrowing, recurrent pain or obstruction weeks later, requiring follow-up investigation.

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

Repeat abdominal examination for spread of tenderness, guarding, rigidity, distension or loss of bowel function, documenting the trajectory rather than a static label.
Trend pulse, blood pressure, temperature, respiratory rate, oxygen need, consciousness, fluid balance and urine output for evolving shock or organ dysfunction.
Repeat haemoglobin, white count, CRP, renal function, acid-base state and lactate according to severity; worsening matters more than an isolated value.
After diet reintroduction, monitor pain, bleeding, stool passage and intake, stepping back and reassessing if symptoms recur.
Arrange follow-up for persistent bowel change or obstructive symptoms and ensure any planned interval endoscopy or stricture imaging has a named reviewer.

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

Pain usually precedes blood

Transient mucosal hypoxia first produces cramp and urgency; bleeding follows sloughing. Blood before pain or painless major loss should broaden the differential.

Right side signals risk

Isolated right-colon disease has poorer outcomes and may indicate superior mesenteric arterial compromise. It deserves early CT angiographic and surgical thought.

Patent arteries do not acquit

Most ischaemic colitis is non-occlusive at a major-vessel level. A CTA without an embolus therefore does not invalidate a compatible segmental mucosal injury.

Lactate is a late witness

Systemic lactate may rise with extensive necrosis or shock but can remain normal during early or limited disease. Clinical probability controls imaging and escalation.

Healing can narrow

Fibrotic stricture is a delayed consequence of deeper injury. New obstructive symptoms after an apparently resolved episode require targeted reassessment rather than laxative escalation.

11Common pitfallsFrequent interpretation and management errors.

01
Excluding bowel ischaemia because the first lactate result is normal.
02
Treating right-sided severe pain as routine left-sided transient colitis without CT angiographic consideration.
03
Performing colonoscopy in a peritonitic patient and delaying definitive surgery.
04
Calling diverticular bleeding when pain clearly preceded bloody diarrhoea and CT shows segmental colitis.
05
Correcting dehydration while failing to address persistent heart failure, sepsis or vasoconstrictor exposure.
06
Discharging without safety-netting for delayed stricture or recurrent pain after eating resumes.