Ischaemic colitis

• Ischaemic colitis (IC) is the most common form of bowel ischaemia: a sudden, usually non-occlusive drop in colonic blood flow that is inadequate for the metabolic needs of a segment of colon. It is not the same as acute mesenteric ischaemia of the small bowel, which is far more immediately life-threatening.
• The watershed areas are the splenic flexure (Griffith's point) and the sigmoid or rectosigmoid junction (Sudeck's point), where the marginal arterial supply between the superior and inferior mesenteric arteries is weakest. The rectum is almost always spared.
• It presents with sudden, crampy, often mild left lower abdominal pain, an urgent desire to defecate, and bright red or maroon blood, or bloody diarrhoea, within 24 hours. Fever, peritonism or shock suggest transmural infarction rather than reversible mucosal injury.
• Most cases are benign and self-limited; symptoms usually ease within 2 to 3 days and the mucosa heals within 1 to 2 weeks. About 10 to 25 per cent of patients develop chronic or recurrent patterns, and gangrene occurs in roughly 15 per cent.
• Diagnosis is usually made by CT, which shows segmental wall thickening and thumbprinting, followed by colonoscopy within 48 hours showing segmental pale, cyanotic or haemorrhagic mucosa with a sharp cut-off. Air (carbon dioxide) insufflation must be gentle. Management is supportive, with broad-spectrum antibiotics for moderate or severe disease and surgery for gangrene, perforation, fulminant colitis, or persistent symptomatic disease.

By the end of this page you should be able to:

1. Explain why the colon is vulnerable to ischaemia, and name the two principal watershed areas and the two major arteries involved.
2. Describe the typical clinical presentation of non-isolated right-colon ischaemia and contrast it with isolated right-colon ischaemia.
3. List the major risk factors and drugs that predispose to ischaemic colitis.
4. Plan the investigation of suspected ischaemic colitis, interpret CT and colonoscopic findings, and know when to add CT angiography.
5. Apply a severity classification to decide on hospitalisation, antibiotics, CT angiography and surgical referral.
6. Explain the supportive medical management, the antibiotic strategy, and the indications for surgery, and state the prognosis and long-term complications.

The word "ischaemia" derives from a Greek root meaning a stopping of blood, but flow need only diminish markedly; complete cessation is not required. Ischaemia may be compounded by reperfusion injury, and the threshold for damage depends on how suddenly the flow drops, how much collateral circulation already exists, and how long the low-flow state persists.^[1]

Some authors separate reversible disease, in which subepithelial haemorrhage and oedema are resorbed "rather promptly, usually within 3 days", from colitis, in which ulceration may persist for months even though the patient is usually asymptomatic by then.^[1] A widely used classification divides the clinical course into reversible colopathy, transient ischaemic colitis, chronic ulcerating colitis, stricture, gangrene and fulminant universal (pancolonic) disease.^[2]

Ischaemic colitis is the most common form of bowel ischaemia and probably the most common cause of bloody diarrhoea in hospitalised older patients.^[1] It accounts for 1 in 1000 hospitalisations, although its incidence is underestimated because many episodes are mild and transient.^[2]

The absence of a specific ICD code makes case-finding difficult; most series rely on careful record review.^[1] Depending on the method used, ischaemic colitis accounts for 9 to 24 per cent of hospitalisations for acute lower gastrointestinal bleeding, and ranks first, second or third behind colorectal cancer in large epidemiological surveys.^[1]

Incidence figures cluster around 15 to 18 per 100,000 per year. A US insurance claims-based survey found 17.7 cases per 100,000 per year, while a population-based record review in Kaiser San Diego gave 15.6 per 100,000 per year, with women at 22.6 and men at 8.0.^[1] That study estimated a nearly fourfold increase in incidence over 34 years, and reported that 6 per cent of episodes developed after hospitalisation for another illness or for surgery.^[1]

The disease is predominantly one of adults, especially older adults: roughly 90 per cent of cases occur in people over 60 years of age, although younger patients are affected (see "Special groups").^[2] One series of over 400 patients found mortality ranging from 4 to 12 per cent in large series, with the spread explained by differences in case mix, ascertainment and rates of comorbidity and surgery.^[1] Women outnumber men; 57 to 76 per cent of patients in large series have been women, and in one survey women were especially predominant after 69 years and all patients under 40 years were women.^[1]

Recurrences are uncommon but accumulate over time: cumulative recurrence in one study was 3 per cent at 1 year, 5 per cent at 2 to 3 years, 6 per cent at 4 years and 10 per cent at 5 to 6 years; another gave 3.3 per cent at 2 years and 7.5 per cent at 5 years.^[1]

No single cause is identified in most patients; most episodes are attributed to localised non-occlusive ischaemia, probably small-vessel disease (sometimes called Type I disease), whereas Type II disease has a recognisable precipitant such as hypotension, decreased cardiac output or aortic surgery.^[1] Commonly the patient is elderly with diffuse small-vessel disease and many comorbidities.^[2]

The ACG 2015 guideline suggests that the most robust independent associations fall into following groups (the association does not prove causation, and many patients have several factors):^[1]

• Cardiovascular and metabolic disease. Hypertension, diabetes mellitus, coronary artery disease, dyslipidaemia, congestive heart failure, atrial fibrillation, peripheral vascular disease, chronic kidney disease and chronic obstructive pulmonary disease are all frequent comorbidities.^[1] A first presentation with ischaemic colitis may even herald or accompany acute myocardial infarction (within 3 days in 0.13 per cent of patients after infarction).^[1] Renal failure appears particularly strongly linked to ischaemia of the right colon.^[1][2]
• Hypoperfusion and shock. Any state that reduces mesenteric perfusion, including dehydration, hypovolaemic or septic shock, heart failure, trauma and severe immune reactions, can produce non-occlusive ischaemia.^[2]
• Aortic and vascular surgery. Abdominal aortic aneurysm repair carries an overall postoperative ischaemic colitis rate of 2.2 per cent: 8.9 per cent after repair of a ruptured aneurysm, 1.9 per cent after open elective repair and 0.5 per cent after endovascular repair, largely through sacrifice of the inferior mesenteric artery.^[1] It has also followed coronary artery bypass and, rarely, colonoscopy.^[1][2]
• Constipation and irritable bowel syndrome. History of constipation and of irritable bowel syndrome are repeatedly associated with ischaemic colitis; possible mechanisms include raised intracolonic pressure and reduced blood flow from impacted stool.^[1] Constipation may immediately precede the illness and is a useful diagnostic clue.^[1]
• Vasculitis, coagulopathy and sickle cell disease. Rheumatic autoimmune disease, inherited and acquired thrombophilia (protein C or S deficiency, antithrombin deficiency, factor V Leiden, antiphospholipid syndrome) and sickle cell crises have all been described.^[1][2]
• Strenuous exercise and drugs. Long-distance running has produced ischaemic colitis, mainly in women aged 26 to 42, with right-sided predominance; and sickle cell crises, trauma, pheochromocytoma and other rare associations are listed.^[1][2]

Drugs deserve a separate memory list because they are modifiable and commonly missed.^[1][2] Constipation-inducing agents, immunomodulators and illicit drugs are the best-supported causes, but many classes have been implicated: vasopressors, cardiac glycosides, diuretics, ergot alkaloids, decongestants (pseudoephedrine, phenylephrine), cocaine and amphetamines, hormonal therapy including oral contraceptives, chemotherapeutic agents (vinca alkaloids, taxanes), antibiotics, NSAIDs, psychotropic agents, serotonin (5-HT3) antagonists (including alosetron, withdrawn from some markets after reports in women with diarrhoea-predominant irritable bowel syndrome), vasoconstrictor drugs generally, statins, and laxative or digitalis overuse.^[1][2]

Two arteries supply most of the colon: the superior mesenteric artery (ascending and transverse colon) and the inferior mesenteric artery (descending and sigmoid colon), with the rectum receiving dual supply from the inferior mesenteric artery and the internal iliac arteries. Between the two arterial territories, collateral flow through the arcades and the marginal artery of Drummond is abundant in many people but highly variable, and weak points exist.^[1][2]

Watershed areas at the borders of these territories are most vulnerable during systemic hypoperfusion, because they have the fewest collaterals:

• Splenic flexure (Griffith's point): between the territory of the middle colic artery (superior mesenteric) and the left colic artery (inferior mesenteric), where arcades may be limited. The marginal artery of Drummond, which helps supply the flexure, is diminished or absent in about 5 per cent of the population.^[3]
• Sigmoid and rectosigmoid junction (Sudeck's point): at the last sigmoid branch from the inferior mesenteric artery.^[1]
• Right colon can also be vulnerable: the marginal artery of Drummond is poorly developed in about 50 per cent of the population there, and the vasa recta are smaller.^[3]

The arterial supply of the colon is very sensitive to vasoconstrictors, an evolutionary adaptation that shunts blood toward the heart and brain in stress. Drug-induced vasoconstriction (vasopressors, cocaine, ergot alkaloids) can therefore produce non-occlusive ischaemic colitis directly.^[2] Reperfusion injury contributes to the final damage once flow returns.^[1][2]

The rectum is rarely involved because of its rich dual blood supply.^[1][2]

The lesion mirrors severity. Mild cases show mucosal and submucosal haemorrhage and oedema, sometimes with mild necrosis or ulceration. With more severe ischaemia the picture can resemble inflammatory bowel disease (chronic ulcerations, crypt abscesses, pseudopolyps). The most severe cases show transmural infarction, gangrene and perforation; after healing, the muscularis propria may be replaced by fibrous tissue forming a stricture.^[1][2]

The colon about which the patient complains is usually the left colon; about 25 to 26 per cent of cases are isolated right-colon ischaemia (IRCI), which behaves differently. The classic triad of sudden crampy left lower abdominal pain, an urgent desire to defecate and bloody diarrhoea or rectal bleeding within 24 hours is present in nearly half of cases, although pain may be the only early symptom in IRCI.^[1][2]

Symptoms of presentation (non-IRCI). Abdominal pain occurs in about 87 per cent, rectal bleeding in 84 per cent and diarrhoea in 56 per cent in one large series, with nausea in 30 per cent, vomiting in 30 per cent, dizziness in 10 per cent and syncope in 6 per cent.^[1] A Canadian biopsy-proven series reported abdominal pain in 77.8 per cent, haematochezia in 58.3 per cent, bloody diarrhoea in 34.7 per cent and non-bloody diarrhoea in 19.4 per cent.^[1] The pain is usually mild to moderate and precedes the bleeding; it is located over the affected segment, often the left lower abdomen or hypogastrium. Abdominal tenderness is usual over the involved segment.^[1] An associated ileus may cause anorexia, nausea and vomiting.^[2]

Notably, patients with IRCI are more likely to present with pain than with rectal bleeding: only 25 to 46 per cent have rectal bleeding. Suspect IRCI in a patient with acute, severe abdominal pain and no haematochezia or diarrhoea if there are risk factors such as dialysis, sepsis, hypotension or shock.^[1]

Clinical phases of worsening ischaemia have been described:^[2]

• Hyperactive phase: severe pain and passage of bloody stools; many patients recover here.
• Paralytic phase: pain becomes more diffuse, tenderness generalised, motility falls, the abdomen distends, bowel sounds disappear and bleeding stops.
• Shock phase: fluid leaks through the damaged mucosa, producing systemic hypovolaemia, tachycardia, hypotension, confusion and metabolic acidosis; these patients are critically ill.

In severe (gangrenous) colitis, pain is present in about 86 per cent but bleeding in only 31 per cent; peritoneal signs, fever, leukocytosis, rising temperature, paralytic ileus and signs of sepsis dominate.^[1][2] Universal fulminant colitis is a rare, rapid, toxic form with signs of peritonitis and, typically, does not show the classic triad.^[1]

Physical examination also demonstrates mild to moderate tenderness over the affected segment and haem-positive stool on rectal examination; rectal bleeding is usually mild. Fever is unusual in mild disease, but white cell counts are generally raised. Severe haematochezia with haemodynamic instability or need for transfusion (required in under 5 per cent of patients) suggests an alternative or a gangrenous course.^[1][2] A haemoglobin below 12 g per dl is found in 36 to 42 per cent of patients, and severe bleeding is more frequent in women, in those with severe lung disease, and when creatinine and glucose are raised.^[1]

Long-distance running and other exertional events deserve specific questioning, because young women presenting with left-sided pain and bloody diarrhoea after a marathon or similar endurance event may have ischaemic colitis; two cases found after the Brighton marathon made headlines.^[1][2]

The diagnosis of ischaemic colitis is clinical and often uncertain at first; only 9 per cent of patients presenting with abdominal pain and bloody diarrhoea were correctly identified at the time of presentation in one emergency-department study.^[1] The differential diagnosis is broad.

Segmental distribution of ischaemia with sparing of the rectum, and rapid resolution of both symptoms and endoscopic appearances, are the findings that most reliably separate ischaemic colitis from chronic inflammatory bowel disease.^[2] Where two conditions overlap, for example ischaemic colitis and inflammatory bowel disease, the history of acute onset and subsequent spontaneous recovery is decisive.

The evaluation aims both to confirm ischaemia and to exclude the alternatives above.

No blood test diagnoses ischaemic colitis, but testing helps with the differential diagnosis and with prognosis.^[1][2] ACG 2015 recommends initial complete blood count, comprehensive metabolic panel, stool culture, ova and parasite examination, Clostridioides difficile toxin assay and serum lactate, LDH, creatine kinase and amylase, plus E. coli O157:H7 testing because that organism has been implicated in causing ischaemic injury.^[1]

The following are markers of severity rather than of diagnosis: white cell count above 15 x 10^9 per litre (or 15,000 per mm3), haemoglobin under 12 g per dl, albumin under 2.8 g per litre, hyponatraemia (sodium under 136 mmol per litre) and lactate dehydrogenase above 350 to 450 units per litre. No single laboratory test is sensitive or specific.^[1][2]

Plain abdominal films are often normal and may show only thumbprinting or distended loops; their main role is to detect perforation or gangrene (pneumoperitoneum, pneumatosis, portal venous gas).^[1][2]

CT with intravenous and oral contrast is the imaging modality of choice for suspected ischaemic colitis: it assesses distribution and phase, excludes other causes and identifies complications.^[1] Segmental bowel-wall thickening, thumbprinting (subepithelial oedema or haemorrhage), pericolic fat stranding and ascites are the supportive findings. CT also identifies pneumatosis or portomesenteric gas, which suggest transmural infarction, and can distinguish ischaemic from malignant segments (tumoral wall is usually thicker and shorter).^[1]

Multiphasic CT angiography (CTA) should be performed in any patient with suspected IRCI, and in any patient in whom acute mesenteric ischaemia cannot be excluded, for example because of severe pain with little or no bleeding or atrial fibrillation.^[1] Early reports of IRCI as a heralding presentation for superior mesenteric artery disease are emerging but not based on published comparative data. In IRCI where CTA is negative but suspicion of vascular occlusion remains, traditional splanchnic angiography may still be considered.^[1]

Imaging by ultrasound or MRI is sometimes used but is less standard and lacks firm diagnostic criteria in this setting.^[1][2]

Colonoscopy is the most accurate diagnostic test and the usual confirmatory step after CT has suggested a segment of colitis.^[1][2] The ACG 2015 guideline recommends early colonoscopy within 48 hours of presentation, with minimal insufflation, and biopsies except when gangrene is obvious.^[1] Colonoscopy should be avoided in peritonitis or established gangrene.^[1]

Typical (usually left-sided) findings are segmental mucosal oedema, erythema and fragility, longitudinal ulcers, petechial haemorrhages interspersed with pale areas, purple haemorrhagic nodules (which are commonest when scoping occurs within 48 hours), blue-black nodules suggestive of gangrene, and a sharp transition between abnormal and normal mucosa. The single-stripe sign, a single longitudinal band of erythema with erosion, is highly specific and carries a better prognosis.^[1][2] The rectum is usually spared, helping to separate the condition from inflammatory bowel disease.^[1][2]

Timing matters: haemorrhagic nodules were seen in 47 per cent of patients scoped within 48 hours, 33 per cent at 2 to 5 days and only 10 per cent after day 5. Scoping late can therefore miss the most characteristic signs even when the clinical diagnosis is unchanged.^[1]

Insufflation pressure matters too. Animal and cadaver data show that colonoscopic insufflation can reduce colonic blood flow; carbon dioxide is absorbed about ten times faster than room air, causes less prolonged distension and has been shown in a model to increase colonic blood flow rather than decrease it. Carbon dioxide is therefore preferred, but it has not been formally studied in humans with ischaemic colitis.^[1] In practice, gentle technique with CO2 if available is the recommendation.^[1][2]

Histology is rarely conclusive: ghost cells and mucosal infarction each occur in only a minority of biopsies (7.7 per cent in one series, 20 to 63 per cent in resected specimens). More often biopsy shows mucosal and submucosal haemorrhage and oedema, capillary fibrin thrombi and neutrophils, all supporting, not proving, the diagnosis.^[1]

Endoscopic findings favouring ischaemic rather than inflammatory bowel disease are segmental distribution, rectal sparing and rapid resolution on repeat examination.^[2]

There are no formal diagnostic criteria for ischaemic colitis; the diagnosis rests on a high index of suspicion, the clinical setting, and subsequent CT and colonoscopic confirmation. The ACG 2015 guideline proposes a severity classification based on the risk factors that predict need for surgery or death:^[1]

• Mild: typical segmental colitis (not isolated to the right colon) without any of the following:
• Moderate: up to three of male sex; hypotension (systolic blood pressure under 90 mmHg); tachycardia (heart rate over 100 per minute); abdominal pain without rectal bleeding; blood urea nitrogen above 20 mg per dl; haemoglobin under 12 g per dl; lactate dehydrogenase above 350 units per litre; serum sodium under 136 mmol per litre; white cell count above 15 x 10^9 per litre; or colonoscopically visible ulceration.
• Severe: more than three of the above, or any peritoneal signs, pneumatosis on CT, gangrene at colonoscopy, pancolonic distribution, or isolated right-colon ischaemia.

This proposed scheme is not yet validated but gathers the strongest available predictors. Retrospective work has further produced an Ischaemic Colitis Mortality Risk (ICMR) score from factors such as low cardiac output, acute kidney injury, lactate above 2.5 mmol per litre, subtotal colectomy and catecholamine use; mortality in one series rose from about 10.5 per cent with zero points to 100 per cent with five points.^[1]

Management follows severity.

• Bowel rest (nothing by mouth), intravenous fluids and electrolyte repletion to resuscitate extracellular volume and reduce intestinal oxygen demand.^[1][2]
• Parenteral nutrition if prolonged rest or major contraindications to surgery are anticipated.^[1][2]
• Optimise cardiac function and oxygenation; Swan-Ganz catheterisation may help in haemodynamic instability.^[2]
• Treat the precipitating condition (heart failure, hypovolaemia, sepsis).^[1][2]
• Stop vasoconstrictors and any drug thought responsible.^[1][2]
• No oral cathartics or bowel preparations, which may precipitate perforation or toxic dilatation.^[2]
• NG tube if ileus is present; rectal tube decompression can help a distended colon.^[2]
• Surgery and intensive care liaison early for moderate or severe disease.^[1]

There has never been a rigorous human trial of antibiotics in ischaemic colitis. ACG 2015 nevertheless recommends antimicrobial therapy for patients with moderate or severe disease, extrapolating from animal work showing reduced mucosal damage, inflammation, complement and immunoglobulin deposition and bacterial translocation across ischaemic mucosa.^[1] Antibiotics covering both aerobes and anaerobes are therefore justified, particularly because severity is hard to predict at presentation and bacterial translocation is well demonstrated after even 30 minutes of ischaemia.^[1][2]

The ACG recommendation is an anti-anaerobic agent plus a fluoroquinolone, an aminoglycoside or a third-generation cephalosporin, continued at least 72 hours and, if the patient improves, followed by a 7-day course.^[1] The 2008 review similarly recommends empiric broad-spectrum coverage.^[2] Glucocorticoids are not recommended, unless the colitis complicates a vasculitis (when they treat the vasculitis), and there is no evidence for aminosalicylates, sulfasalazine or local steroid enemas.^[1] NSAIDs appear to be a cause of colonic ulceration, although one large study associated lack of NSAID use with more severe disease, and fatty-acid enemas have only anecdotal support.^[1]

Surgical intervention should be considered for ischaemic colitis accompanied by hypotension, tachycardia or abdominal pain without rectal bleeding; for isolated right-colon or pancolonic ischaemia; and in the presence of gangrene.^[1] Table 9 in the source gives further indications.^[1]

Indications for surgery in a practical list:

• peritoneal signs, rising fever, refractory leukocytosis or tachycardia despite conservative therapy;
• gangrene, pneumatosis or portal venous gas;
• persistent symptoms beyond 2 to 3 weeks, or a continuing protein-losing colopathy beyond 14 days;
• recurrent sepsis thought to arise from an unhealed segment;
• a symptomatic ischaemic stricture.

Operations depend on distribution and include right hemicolectomy, segmental colectomy, subtotal or total colectomy, usually with a diverting stoma or Hartmann's pouch rather than primary anastomosis. Mortality after surgery remains high, 37 to 47 per cent in published series.^[1] Prognostic factors include ASA class above 3 or 4, elevated peak lactate, renal failure requiring dialysis, intraoperative vasopressor use and major blood loss.^[1]

Surgery is also the treatment for symptomatic strictures and for chronic segmental colitis once medical therapy has failed.

There is no proved benefit in repeating colonoscopy to document healing in patients who become asymptomatic after their index episode. Colonoscopic or virtual-colonographic screening for cancer should be arranged some weeks after recovery in anyone who has not been screened recently, because an adenocarcinoma can be hidden distal to the ischaemic segment.^[1]

Complications arise mainly in severe disease: transmural infarction, gangrene, perforation with peritonitis, sepsis and septic shock. Anal passage of an infarcted colonic cast (mucosa, submucosa or full thickness) 2 to 4 weeks after the acute event, 25 to 120 cm in length, has been described in about 21 reported patients, mostly after aortic surgery.^[1]

Long-term complications develop in a minority:

• Chronic ischaemic (segmental) colitis in about 20 to 25 per cent of patients, depending on the definition and diagnostic rigour used, with recurrent abdominal pain, bloody diarrhoea, weight loss and sepsis. It is often treated by resection of the affected segment.^[1][2]
• Colonic stricture, fibrous narrowing from replacement of the muscularis propria by scar, in 3 to 14 per cent (up to 14 per cent after moderate disease); many are asymptomatic and resolve over 12 to 24 months. Surgery is reserved for obstruction.^[1][2]
• Rare late complications include recurrent sepsis from an unhealed segment and, rarely, toxic megacolon.

Outcome depends almost entirely on the severity and anatomic distribution of the ischaemia. Most ischaemic colitis is benign and self-limited: symptoms resolve within 2 to 3 days (and often within 24 to 48 hours), the colon heals in 1 to 2 weeks, and with severe but reversible injury the segmental colitic phase may take 1 to 6 months to heal, during which the patient is usually asymptomatic.^[1][2]

Large series report mortality of 4 to 12 per cent overall, reflecting case mix and surgical practice. Non-gangrenous ischaemic colitis has a far better prognosis, whereas gangrene worsens outcomes dramatically and surgical mortality after laparotomy is 37 to 47 per cent in published series. Pancolonic ischaemia carried a 21.7 per cent mortality in one large series. Isolated right-colon ischaemia (IRCI) is consistently worse than other patterns: 30-day mortality 20.3 versus 9.0 per cent, surgery in 54.9 versus 10.9 per cent, and an overall unfavourable outcome in 59.2 versus 17.3 per cent.^[1] A meta-analysis-free retrospective synthesis reported 19.6 per cent of patients requiring surgery with a surgical mortality of 39.3 per cent, versus 80.3 per cent managed medically with a 6.2 per cent mortality.^[1]

As many as 8 to 19.8 per cent of hospitalised, biopsy-proven patients require surgery, and much higher proportions (up to 45.2 per cent) among patients on a surgical service, numbers that reflect selection bias rather than true population risk.^[1] Isolated cecal necrosis occurs mainly in older patients with cardiovascular disease or diabetes and peritoneal signs, and usually needs urgent laparotomy.^[1][2]

There is no screening test for ischaemic colitis. Sensible prevention targets the provoking factors: avoid unnecessary prolonged constipation, review vasoconstrictive medications, maintain hydration during exertion and promptly treat hypotension and heart failure. Patients with abdominal aortic aneurysm or who have undergone colonic or vascular surgery may need careful postoperative bowel inspection. Follow-up colonoscopy is aimed at cancer screening rather than documenting mucosal healing.^[1][2]

Older adults. Ischaemic colitis is a disease of older adults and comorbidities dominate outcome (chronic kidney disease and COPD increase mortality; coronary disease, atrial fibrillation and renal failure especially predispose to IRCI).^[1]

Younger adults. When a young patient, particularly a woman, presents with segmental left-sided colitis, consider ischaemic triggers such as long-distance running, cocaine or methamphetamine, oral contraceptives or hormonal therapy, vasculitis, hypercoagulability and sickle cell disease. Young women with diarrhoea-predominant irritable bowel syndrome who have received alosetron are a special risk group.^[1][2]

Pregnancy. No evidence-based specific guidance; hormonal therapy is one of the recognised associations, so pregnancy-related cases should be managed case by case with obstetric input.^[2]

Children. Rare, reported in association with conditions that precipitate hypoperfusion.^[1]

Renal impairment and dialysis. These patients have a high rate of right-sided ischaemia and poor outcomes.^[1][2]

Where CT, angiography and urgent surgery are limited, the following practical points matter:

• Diagnosis can be made clinically in a sick older patient with sudden left-sided pain and bloody diarrhoea; colonoscopy (or even gentle flexible sigmoidoscopy) within 48 hours is the most informative test, with biopsies.
• Plain films (and, if available, ultrasound) can exclude perforation or show thumbprinting; do not perform barium enema if gangrene or perforation is suspected.^[1][2]
• Careful serial clinical assessment (peritoneal signs, temperature, haemodynamics) is the main monitor of progression to gangrene.
• Supportive care (bowel rest, intravenous fluids, stop vasoconstrictors, optimise oxygenation, correct hypovolaemia) and broad-spectrum antibiotics covering aerobes and anaerobes are the affordable mainstays.^[1][2]
• Angiography has little routine role because colonic flow has usually returned to normal by presentation; CTA is reserved for suspected right-sided (mesenteric) ischaemia or when acute mesenteric ischaemia cannot be excluded.^[1][2]
• Patients with peritonitis, gangrene or progressive sepsis need laparotomy as soon as possible; many low-resource services will need to refer to a surgical centre, and delaying operation in gangrene approaches 100 per cent mortality.^[1][2]
• Asymptomatic strictures should be observed for 12 to 24 months; endoscopic dilation is an alternative to surgery but is unproven.^[1][2]

• Ischaemic colitis is the most common bowel ischaemia, usually a non-occlusive, segmental, left-sided mucosal injury from temporary hypoperfusion.
• Watershed areas are the splenic flexure (Griffith's point) and the rectosigmoid (Sudeck's point); the rectum is usually spared.
• Typical presentation: sudden crampy left lower abdominal pain, urgency, and bloody diarrhoea within 24 hours. Fever, peritoneal signs or shock point to gangrene.
• Isolated right-colon ischaemia presents with severe pain without bleeding, affects sicker (often dialysis or cardiac) patients, and carries worse outcomes.
• Over 90 per cent of patients are over 60, with cardiovascular and renal comorbidities, constipation, and various drugs (vasopressors, estrogens, pseudoephedrine, cocaine, alosetron, taxanes, decongestants) among risk factors.
• Non-gangrenous disease is 80 to 85 per cent of cases and is reversible in about half; gangrene about 15 per cent; fulminant pancolitis about 1 per cent; chronic colitis about 20 to 25 per cent; strictures about 10 to 15 per cent.
• CT shows segmental wall thickening, thumbprinting and pericolic fat stranding; pneumatosis or portal venous gas suggest transmural infarction. Colonoscopy within 48 hours is the best diagnostic test, with CO2 insufflation and biopsies, but avoid it in peritonitis or gangrene.
• CTA is reserved for right-sided (isolated) ischaemia or when acute mesenteric ischaemia cannot be excluded. Angiography has little role because flow has usually returned.
• Management is supportive; antibiotics (at least 72 hours, then a 7-day course) for moderate to severe disease, usually surgical consultation and surgery for gangrene, perforation, fulminant colitis, or persistent disease.
• Most patients recover within days, although mortality overall is 4 to 12 per cent and postoperative mortality 37 to 47 per cent.

Read next: acute mesenteric ischaemia; infectious colitis and gastroenteritis; inflammatory bowel disease (ulcerative colitis and Crohn disease); lower gastrointestinal bleeding; abdominal aortic aneurysm.