Large-bowel obstruction and pseudo-obstruction

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

Large-bowel obstruction prevents onward passage of colonic contents through a mechanical lesion. Colorectal cancer is a major cause, with diverticular stricture, volvulus, hernia, faecal impaction and anastomotic or inflammatory narrowing also important. Symptoms evolve with level, duration and valve competence: distension and constipation usually dominate, pain is initially colicky, and vomiting tends to occur later than in proximal small-bowel obstruction. Complete obstipation supports severity, but early or partial obstruction can produce overflow diarrhoea. A distal rectal examination may reveal tumour or impaction but a normal rectum does not exclude proximal disease. Continuous pain, focal tenderness, fever and tachycardia raise strangulation, perforation or ischaemia.

Acute colonic pseudo-obstruction, or Ogilvie syndrome, is severe dilatation without a mechanical transition. It occurs particularly in older, postoperative, trauma, obstetric or critically ill patients and with electrolyte disturbance, infection, cardiac disease, neurological illness and medicines that inhibit motility. The abdomen may be impressively distended while pain remains mild, but increasing diameter and duration raise ischaemia and perforation risk. Pseudo-obstruction is a diagnosis made after CT excludes a mechanical lesion and volvulus. Ileus often involves both small and large bowel after surgery, whereas pseudo-obstruction predominantly affects colon, especially caecum and ascending colon. Toxic megacolon requires systemic toxicity plus inflammatory or infectious colitis and follows a different pathway.

Treatment follows cause and bowel viability. Both syndromes need resuscitation, electrolyte correction, medication review, venous-thromboembolism assessment and frequent examination. A mechanical cancer obstruction requires a consultant colorectal decision about emergency resection, diversion or a self-expanding metal stent. NICE recommends considering stenting for acute left-sided malignant obstruction in palliative care and offers surgery or stenting as a bridge in selected potentially curative disease, with perforation and oncological trade-offs discussed. Uncomplicated pseudo-obstruction receives conservative decompression and precipitant control. Failure or concerning caecal dilatation prompts specialist neostigmine in a monitored setting or colonoscopic decompression; the sequence varies with contraindications and expertise. Peritonitis, ischaemia or perforation requires surgery, not pharmacological delay.

Key points

Mechanical large-bowel obstruction has a physical transition point, most often colorectal cancer, diverticular stricture or volvulus; pseudo-obstruction has diffuse functional dilatation without that lesion.
Progressive distension, colicky pain, obstipation and later faeculent vomiting are typical, but partial obstruction may still pass liquid stool or flatus.
A competent ileocaecal valve can create a closed loop between an obstructing distal lesion and the valve, rapidly increasing caecal tension and perforation risk.
Contrast CT defines the transition, cause, proximal diameter, metastatic disease and signs of ischaemia or perforation; a plain radiograph alone rarely completes planning.
Initial care is fasting, venous access, fluid and electrolyte correction, analgesia, antiemetic treatment, nasogastric decompression when vomiting and urgent colorectal review.
Malignant left-sided obstruction may be managed with emergency surgery or expert endoscopic stenting as palliation or selected bridge to surgery after multidisciplinary assessment.
Acute colonic pseudo-obstruction often follows surgery, severe illness, trauma, metabolic disturbance or motility-suppressing medicines and commonly dilates caecum and right colon.
Pseudo-obstruction starts with treating the precipitant, stopping anticholinergic and opioid burdens, correcting potassium and magnesium, mobilisation and serial diameter assessment.

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

Malignant mechanical obstruction

Colorectal cancer is a major cause of fixed large-bowel blockage, sometimes presenting before the malignancy has otherwise been recognised.

Benign mechanical obstruction

Diverticular stricture, volvulus, hernia and inflammatory or postoperative narrowing create a structural transition point within the colon.

Acute colonic pseudo-obstruction

Severe illness, surgery, trauma, metabolic disturbance and medicines can disrupt autonomic colonic motility without a physical lesion.

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

1
Proximal accumulation
Gas, stool and secretion build above a transition or functionally inactive segment, causing progressive distension and colicky pain.
2
Wall tension and perfusion loss
Rising caecal and colonic pressure impairs venous then arterial flow, especially in a closed loop with a competent ileocaecal valve.
3
Necrosis and contamination
Persistent pressure or volvulus causes ischaemia, perforation, bacterial translocation and faecal peritonitis if decompression is delayed.

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

Distal mechanical obstructionRed flag

Progressive abdominal distension, colicky pain and obstipation with a CT transition at an annular mass or benign stricture supports mechanical large-bowel obstruction and needs urgent colorectal planning.

Closed-loop dangerRed flag

A distal block with a competent ileocaecal valve produces marked caecal dilatation without small-bowel decompression. Increasing pain, tenderness or reduced enhancement threatens caecal perforation.

Acute colonic pseudo-obstruction

A severely ill or postoperative patient develops predominantly right-colon and caecal dilatation without an occluding lesion, often alongside hypokalaemia and motility-suppressing medicines.

VolvulusRed flag

Abrupt distension and obstruction with a twist, whirl or beak on CT indicates sigmoid or caecal volvulus. Viability and anatomical type determine endoscopic versus operative treatment.

Toxic megacolonRed flag

Systemic toxicity with colonic dilatation during severe ulcerative, Crohn's or infectious colitis is not simple pseudo-obstruction and requires urgent medical-colorectal management with anti-inflammatory or infection-directed care.

Faecal impaction

A loaded rectum, overflow liquid stool and medication or immobility risk may explain obstruction, but proximal cancer must still be considered when symptoms, examination or imaging do not resolve fully.

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
Locate a transition point, identify tumour, stricture or twist, distinguish pseudo-obstruction and assess bowel viability and perforation.
Interpretation and limitations
Abrupt calibre change supports mechanical disease; diffuse dilatation without a lesion supports pseudo-obstruction. Poor enhancement, mesenteric gas, pneumatosis or free air demands immediate surgery.
02
Abdominal radiograph
Why
Rapidly show the distribution and progression of colonic dilatation when CT is pending or serial diameter monitoring is required.
Interpretation and limitations
Peripheral haustrated large-bowel loops and caecal size support obstruction burden, but radiography often cannot define cause or viability and must not delay CT in a stable patient.
03
Full blood count, renal profile, magnesium and CRP
Why
Identify dehydration, kidney injury, infection and reversible electrolyte impairment of motility.
Interpretation and limitations
Hypokalaemia or hypomagnesaemia reinforces pseudo-obstruction and needs correction; leucocytosis and rising CRP can signal ischaemia but remain non-specific.
04
Blood gas and lactate
Why
Assess perfusion and metabolic consequence when pain, sepsis or threatened bowel is suspected.
Interpretation and limitations
Acidosis or rising lactate strengthens concern for advanced compromise. A normal early value does not exclude closed-loop ischaemia and cannot overrule examination or CT.
05
Flexible sigmoidoscopy or colonoscopy
Why
Decompress selected pseudo-obstruction, detorse uncomplicated sigmoid volvulus or inspect a distal malignant lesion under expert care.
Interpretation and limitations
The purpose must be explicit. Suspected perforation or non-viable bowel contraindicates routine endoscopy; a traversed lesion does not by itself determine oncological resectability.
06
Histology and staging imaging
Why
Confirm malignancy and establish extent once immediate obstruction is controlled or when biopsy can be obtained safely.
Interpretation and limitations
Pathology and staging support multidisciplinary curative or palliative planning. Emergency relief of obstruction should not wait for every staging detail when bowel viability is threatened.

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

Small-bowel obstruction

Earlier vomiting, central dilated small-bowel loops and a small-bowel transition point favour SBO, though distal obstruction can dilate both compartments.

Generalised ileus

Diffuse small- and large-bowel dilatation without a transition after surgery, sepsis or electrolyte disturbance suggests ileus rather than focal colonic blockage.

Toxic megacolon

Systemic toxicity with severe colitis and non-obstructive dilatation requires inflammatory or infectious colitis management rather than routine decompression.

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

01Mechanical obstructionResuscitate and define a transitionFirst stepDistension, colic and obstipation suggest an occluding colonic lesion.

1Keep fasting, obtain venous access, correct fluid and electrolyte deficits, provide analgesia and antiemetic treatment, and insert a nasogastric tube when vomiting or proximal dilatation warrants it.
2Perform rectal and hernia examination, send urgent bloods and obtain contrast CT with direct radiology discussion about transition, caecal risk, metastases and viability.
3Call senior colorectal surgery early and involve anaesthesia or critical care for physiological compromise; give local antibiotics when perforation, ischaemia or sepsis is suspected.
4Choose resection, diversion or expert stenting according to cause, site, viability, curative intent, comorbidity and available service, documenting stoma and perforation trade-offs.

02Pseudo-obstructionReverse drivers and decompressCT shows colonic dilatation without a mechanical lesion and there is no peritonitis or ischaemia.

1Treat infection, cardiac or respiratory failure and other precipitating illness, correct potassium, magnesium and hydration, and stop or reduce opioids and anticholinergic medicines where safe.
2Use fasting or cautious intake, nasogastric and rectal decompression where appropriate, regular repositioning and mobilisation, with serial examination and radiographic caecal measurements.
3If conservative management fails or risk rises, obtain specialist agreement for monitored neostigmine or endoscopic decompression based on cardiac, respiratory and procedural contraindications.
4EscalationEscalate immediately to surgery for tenderness, peritonism, perforation, ischaemia or continuing expansion despite appropriate decompression.

03Malignant decisionMatch relief to treatment intentCT identifies a likely obstructing colorectal cancer without free perforation.

1Define left- versus right-sided site, metastatic burden, physiological fitness, bowel viability and whether treatment is potentially curative or palliative.
2Discuss emergency surgery, diversion and self-expanding metal stent with colorectal, endoscopy, radiology and oncology expertise, using NICE guidance and local capability.
3For a stent, explain perforation, migration, re-obstruction and how a complication could change oncological options; ensure an experienced operator and rescue plan.
4After decompression, complete histology and staging promptly, optimise nutrition and comorbidity, and return the case to colorectal multidisciplinary planning.

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

Corrects dehydration and reversible neuromuscular impairment while definitive decompression or surgery is planned.

Intravenous crystalloid and electrolytes

Give reassessed isotonic fluid and replace potassium or magnesium through the current hospital protocol, accounting for kidney function, cardiac reserve and measured deficits.

Avoid blind large-volume administration in heart or renal failure and monitored potassium over-replacement. Biochemical correction does not resolve a mechanical transition or threatened bowel.

Increases colonic parasympathetic activity and can rapidly decompress acute colonic pseudo-obstruction that persists despite conservative treatment.

Neostigmine

Use only the specialist-approved intravenous regimen in a monitored area after CT excludes mechanical obstruction and the team confirms viable bowel and appropriate resuscitation support.

Mechanical obstruction, peritonitis and doubtful viability are contraindications. Bradycardia, asystole and bronchospasm can occur; continuous monitoring, immediate resuscitation capability and atropine availability are required.

Treats enteric contamination or bacterial translocation while urgent operative source control is arranged.

Broad-spectrum antibiotic

Use the locally recommended IV colonic-sepsis regimen when perforation, ischaemia or septic obstruction is suspected, adjusting promptly to renal function and microbiology.

Do not give routinely for uncomplicated pseudo-obstruction. Allergy, Clostridioides difficile risk and kidney injury matter, and antibiotics cannot relieve pressure behind an obstructing lesion.

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

Ischaemia and perforation

Threatened caecum or twisted bowel can progress to necrosis, free perforation and urgent colectomy if decompression or surgery is delayed.

Volume and respiratory compromise

Vomiting and third spacing cause kidney injury and electrolyte loss, while massive distension splints the diaphragm and increases aspiration risk.

Sepsis and multiorgan failure

Mucosal breakdown and perforation cause bacteraemia, shock, acidosis and organ dysfunction, sometimes before dramatic peritoneal signs appear.

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

Record pain character, distension, flatus and stool, vomiting, abdominal tenderness and girth or radiographic caecal diameter at defined intervals.
Trend pulse, blood pressure, temperature, respiratory rate, urine output and fluid balance for sepsis, dehydration or compression-related respiratory compromise.
Repeat potassium, magnesium, renal function, CRP, white count and lactate according to severity and after active electrolyte replacement.
During neostigmine, use continuous cardiac observation with staff and atropine immediately available, documenting response and cholinergic adverse effects.
After stenting or endoscopic decompression, monitor recurrent distension, pain, fever and peritonism and ensure definitive oncological or surgical follow-up is not lost.

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

Diarrhoea does not exclude

Liquid stool can pass around a partial obstruction or an impaction. Progressive distension and colic still require mechanical assessment despite apparent diarrhoea.

Valve competence creates danger

When the ileocaecal valve does not vent pressure into small bowel, the caecum becomes the vulnerable end of a closed loop and may perforate remotely from the distal tumour.

Pseudo still perforates

Absence of a physical lesion does not make acute colonic pseudo-obstruction benign. Diameter, duration and wall perfusion determine escalating risk.

Neostigmine needs an ecosystem

The medicine is a monitored intervention, not a ward trial. Diagnostic exclusion, ECG surveillance, atropine, airway support and immediate response to bradycardia are inseparable from prescribing.

A stent is a strategy

Self-expanding metal stenting is not merely a technical success. Its benefit depends on intent, lesion site, operator expertise, perforation risk and the next oncological or surgical step.

11Common pitfallsFrequent interpretation and management errors.

01
Assuming passage of a small amount of liquid stool excludes mechanical obstruction.
02
Treating pseudo-obstruction before CT has excluded a distal cancer or volvulus.
03
Giving neostigmine on an unmonitored ward without atropine and resuscitation capability.
04
Waiting for lactate elevation before escalating a closed-loop caecum with worsening tenderness.
05
Inserting a malignant colonic stent without defining curative versus palliative intent and rescue surgery.
06
Correcting potassium repeatedly while leaving opioids, anticholinergics and immobility unaddressed.