Intestinal obstruction in ICU: mechanical and adynamic · ICU Topics

Cinematic clinical photograph of a distended abdomen with a nasogastric tube decompressing the stomach and intravenous fluids running, ICU setting, clinical-blue lighting, no text, no identifiable people — FigureDrip and suck for uncomplicated obstruction — but strangulation with a raised lactate goes to theatre.

Small bowel vs large bowel obstruction vs pseudo-obstruction

Feature	Small bowel obstruction	Large bowel obstruction	Ogilvie (pseudo-obstruction)
Common causes	Adhesions (60%), hernia, malignancy, Crohn's	Cancer (60%), volvulus, diverticulitis, faecal impaction	Critically ill ICU patient (sepsis, trauma, opioids, electrolytes)
Vomiting	Early, frequent, bilious	Late, may be faeculent	Variable
Pain	Colicky, periumbilical	Colicky, lower abdomen	Usually mild or absent
Distension	Central, less marked	Marked, peripheral	Marked (especially if delayed)
Bowel sounds	High-pitched, tinkling	High-pitched	Decreased or absent
Imaging	Dilated SB loops, air-fluid levels, paucity of colonic gas	Dilated colon, 'coffee bean' (volvulus)	Dilated colon throughout, no mechanical obstruction
Conservative	NGT + fluids (80% resolve if adhesions)	Often needs surgery (cancer, volvulus)	Neostigmine, colonoscopic decompression
Surgical emergency	Strangulation, peritonitis, failed conservative	Perforation, strangulation, volvulus (if endoscopic fails)	Caecum >12cm, perforation, failed neostigmine

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Management of suspected bowel obstruction

Assess & resuscitate — ABC. IV access. Fluid resuscitation (crystalloid — massive third-space losses). Correct electrolytes (K+, Mg2+). Catheterise (monitor output)
NGT decompression — 'Drip and suck'. NGT to decompress stomach, reduce vomiting, monitor aspirate
Imaging — Erect CXR (free gas — perforation), supine/erect abdominal X-ray (dilated loops, air-fluid levels), CT abdomen with contrast (DEFINITIVE — site, cause, strangulation signs)
Identify strangulation/peritonitis — peritonitis (rigid, guarding), fever, tachycardia, raised lactate, free gas → EMERGENCY SURGERY
Conservative management (if uncomplicated) — NGT, IV fluids, serial exams, analgesia, avoid early surgery (80% of adhesive SBO resolve). Trial for 48-72h
Surgery if: failed conservative (no resolution in 48-72h), strangulation, peritonitis, closed-loop obstruction, malignancy
Specific treatments: Ogilvie — neostigmine. Sigmoid volvulus — endoscopic detorsion + flatus tube. Caecal volvulus — surgery

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Clinical pearls

High-yield intestinal obstruction points for CICM/FFICM exam

Adhesions are the #1 cause of SBO (60%). Previous abdominal surgery → adhesions → kinking/torsion of bowel. Other causes: hernias (15% — examine all hernial orifices), malignancy (15% — primary or metastatic), Crohn's stricture, intussusception (children), gallstone ileus (elderly).[1] }
'Drip and suck' is the initial management for uncomplicated SBO. IV fluids (crystalloid — massive third-space losses into obstructed bowel) + NGT (decompress stomach, reduce vomiting, monitor aspirate). Serial abdominal exams. 80% of adhesive SBO resolve within 48-72h.[2] }
Strangulation = emergency. Blood supply to obstructed segment compromised → ischaemia → necrosis → perforation → peritonitis → death. Signs: tachycardia, fever, peritonitis, constant (non-colicky) pain, raised lactate, leukocytosis. CT: bowel wall thickening, reduced enhancement, mesenteric fluid. Management: EMERGENCY LAPAROTOMY + resection of strangulated segment.[2] }
CT abdomen with IV contrast is the diagnostic test of choice. Identifies: site of obstruction, cause (adhesions, hernia, tumour, volvulus), strangulation signs (reduced wall enhancement, mesenteric fluid), perforation (free gas), closed-loop obstruction. CT has >95% sensitivity for SBO and can triage surgical vs conservative.[3] }
Water-soluble contrast follow-through can predict resolution in adhesive SBO. Gastrografin (water-soluble contrast) given via NGT. If contrast reaches colon within 24h → obstruction will resolve (90% sensitivity). If not → likely needs surgery. Gastrografin also has therapeutic effect (osmotic — draws fluid into bowel, stimulates peristalsis).[3] }
Colorectal cancer is the #1 cause of LBO (60%). Other causes: volvulus (sigmoid 10%, caecal 2%), diverticular stricture (10%), faecal impaction (elderly). Presentation: distension, constipation, vomiting (late). Left-sided: 'apple-core' lesion on imaging. Management: surgery (resection ± stoma) unless palliative.[5] }
Sigmoid volvulus: 'coffee bean' sign. Twisting of sigmoid around mesentery → closed-loop obstruction. Imaging: massively dilated sigmoid loop arising from pelvis ('coffee bean' shape — the mesenteric crease looks like a coffee bean). Management: ENDOSCOPIC DETORSION + flatus tube placement (80% success). Surgery if endoscopy fails, ischaemia, or recurrent (elective sigmoid colectomy).[5] }
Caecal volvulus: needs surgery. Twisting of caecum (mobile caecum — incomplete fixation). Closed-loop obstruction → rapid strangulation. Imaging: 'coffee bean' in LUQ (caecum flipped up). Management: SURGERY (right hemicolectomy — endoscopic detorsion not possible/unsafe).[5] }
Ogilvie syndrome (acute colonic pseudo-obstruction): massive colonic dilation WITHOUT mechanical obstruction. Occurs in CRITICALLY ILL ICU patients (sepsis, trauma, surgery, opioids, electrolyte disturbance, retroperitoneal pathology). Pathophysiology: sympathetic overactivity + parasympathetic suppression → colonic atony. Risk: caecal perforation if caecum >9-12cm.[4] }
Neostigmine for Ogilvie syndrome. Acetylcholinesterase inhibitor → increases acetylcholine → stimulates colonic peristalsis. Dose: 2 mg IV over 3-5 min (slow — bradycardia, bronchospasm). Efficacy: 80-90% decompression. Contraindications: mechanical obstruction (MUST exclude first), perforation, bradycardia, bronchospasm. Monitor: ECG, BP, HR. Atropine available for bradycardia.[4] }
Colonoscopic decompression for Ogilvie (if neostigmine fails or contraindicated). Colonoscopy (unprepped — difficult) → decompress colon by aspirating gas. Tube left in caecum for continued decompression (48-72h). Success: 70-80%. Risk: perforation (3% — friable distended colon). Surgery (caecostomy or colectomy) if both fail.[4] }
Faecal impaction in elderly: hard stool in rectum → obstruction. Presents as 'diarrhoea' (overflow — liquid stool passes around impaction). Management: digital disimpaction, enemas, manual evacuation under sedation/anaesthesia. Laxatives, high fibre. Exclude malignancy (colonoscopy).[6] }
Paralytic ileus: transient cessation of bowel motility after abdominal surgery, trauma, peritonitis, electrolyte disturbance (hypokalaemia), opioids. Differentiate from mechanical obstruction (ileus = no mechanical cause, usually resolves in 3-5 days). Management: NGT, IV fluids, correct electrolytes, minimise opioids, mobilise. Prolonged ileus (>5-7 days) → exclude mechanical obstruction (CT).[6] }
Gallstone ileus: mechanical SBO caused by gallstone eroding through cholecystoenteric fistula (usually duodenum) → stone lodges in terminal ileum (narrowest point). Classic: elderly woman, no previous surgery, SBO. Rigler's triad: pneumobilia, SBO, ectopic gallstone. Management: enterolithotomy (remove stone via enterotomy). Cholecystectomy + fistula repair deferred (two-stage).[6] }

Red flags

Prognosis

Adhesive SBO resolution rates (Bologna guidelines)

Meta-analysis of adhesive SBO managed conservatively:

Overall resolution with conservative management: 65-80%
Resolution within 48h: 50-60%
Resolution within 72h: 70-80%
Risk of strangulation at presentation: 10-15%
Mortality: 2-5% (uncomplicated), 10-30% (strangulated)
Recurrence after conservative management: 30-40% at 5 years [1]

Gastrografin challenge: if contrast reaches colon within 24h → 90% will resolve without surgery. Neostigmine for Ogilvie: 80-90% decompression within minutes.

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Pathophysiology

Mechanical obstruction — pathophysiology and progression

Stage	Pathophysiology	Clinical correlate
1. Luminal blockage	Adhesion band, hernia, tumour, volvulus, stricture, intussusception obstructs bowel lumen. Proximal bowel dilates; distal bowel collapses.	Cramping/colicky pain (proximal bowel hyperperistalsis trying to overcome obstruction)
2. Fluid and gas accumulation	Swallowed air + bacterial fermentation gas accumulate proximal to obstruction. Fluid sequesters in bowel lumen (impaired absorption + increased secretion).	Distension, tympany. Massive third-space fluid losses → hypovolaemia, dehydration, AKI
3. Bacterial overgrowth	Stasis proximal to obstruction → bacterial proliferation (especially in closed-loop). Bacteria translocate to mesenteric lymph nodes when mucosal barrier compromised.	Faeculent vomiting (late SBO/LBO). Risk of bacterial translocation → sepsis
4. Venous congestion → arterial compromise	Rising intraluminal pressure compresses venous return first (venous congestion → oedema, wall thickening) → then arterial inflow ceases → ischaemia → infarction → necrosis → perforation	Strangulation. Constant (non-colicky) pain, peritonitis, raised lactate, leucocytosis, fever
5. Perforation → peritonitis	Necrotic bowel wall perforates → spillage of enteric contents → faecal/bilious peritonitis → septic shock → multi-organ failure → death	Rigid abdomen, free gas on imaging, hypotension, high mortality (10-30%)

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Closed-loop vs open-loop obstruction — a critical distinction

Feature	Open-loop (simple) obstruction	Closed-loop obstruction
Definition	Single point of obstruction — proximal bowel can decompress (vomit, NGT). Gas/fluid accumulates proximal to obstruction only.	Two points of obstruction along a bowel segment — the segment between both points is trapped ("closed loop") and cannot decompress.
Examples	Adhesive SBO (single band), tumour stricture, Crohn's stricture	Volvulus (sigmoid, caecal), incarcerated hernia, adhesive band occluding both afferent and efferent limbs
Intraluminal pressure	Moderate — proximal bowel vents via vomitus	Rapidly rising — the closed loop distends enormously, venous then arterial supply compromised
Strangulation risk	Low-moderate (develops slowly if at all)	Very high — strangulation can develop within hours
Time to ischaemia	Hours to days	Hours
CT signs	Transition point, dilated proximal bowel, collapsed distal bowel	"Whirl" sign (volvulus — mesenteric vessels twisting around a fulcrum), "beak" sign (tapering of bowel limbs at obstruction), "coffee bean" (sigmoid volvulus), C-shaped or U-shaped dilated loop, mesenteric stranding
Management	Trial of conservative management (drip and suck) safe	Emergency surgery — do not delay for prolonged conservative trial
Mortality	2-5% (uncomplicated)	10-30% (strangulated)

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Causes of small bowel obstruction — frequency and key features

Cause	Frequency	Key features
Adhesions	60%	Previous abdominal/pelvic surgery (any operation — appendicectomy, gynaecological, laparotomy). Bands cause kinking/compression. Highest yield cause for exams. 80% resolve with conservative management.[1]
Hernias	15%	Inguinal, femoral (high strangulation risk — narrow neck), incisional, umbilical, para-stomal. Always examine all hernial orifices — a strangulated femoral hernia is easily missed. Richter's hernia (only part of wall incarcerated) can strangulate without obstruction.
Malignancy	15%	Primary small bowel tumours (adenocarcinoma, carcinoid, lymphoma, GIST) or metastatic (melanoma, ovarian, colorectal). Usually present with chronic symptoms, weight loss, anaemia.
Crohn's disease	5%	Strictures (fibrotic, post-inflammatory), stricturoplasty sites, adhesions from previous surgery. Often recurrent.
Intussusception	Rare in adults	Children (lead point: Meckel's diverticulum, lymphoid hyperplasia, rotavirus). Adults (lead point: tumour, polyp — pathological lead point). "Target" sign on ultrasound/CT.
Gallstone ileus	Rare	Elderly women. Cholecystoduodenal fistula → gallstone migrates → impacts at terminal ileum (narrowest point). Rigler's triad: pneumobilia + SBO + ectopic gallstone.
Inflammatory	Rare	Radiation enteritis, post-ischaemic stricture, intra-abdominal abscess (extrinsic compression)
Meckel's diverticulum	Rare	"Rule of 2s": 2% population, 2 feet from ileocaecal valve, 2 inches long, presents by age 2. Can cause intussusception, volvulus, inflammation (mimics appendicitis).
Foreign body	Rare	Bezoar (trichobezoar, phytobezoar), ingested objects, capsule endoscopy retention
Drugs	Rare	Enteric-coated potassium, NSAIDs (diaphragm disease), anticoagulants (intramural haematoma)

Causes of large bowel obstruction — frequency and key features

Cause	Frequency	Key features
Colorectal cancer	60%	Left-sided (circumferential — "apple-core" on imaging, obstruction more common). Right-sided (exophytic, anaemia more common than obstruction). Always suspect in elderly patient with changed bowel habit + weight loss.
Volvulus	10-15%	Sigmoid (75% of volvulus — elderly, constipation, "coffee bean" sign, endoscopic detorsion). Caecal (25% — younger, mobile caecum, surgery required).
Diverticular stricture	10%	Chronic recurrent diverticulitis → fibrotic stricture. Differentiate from cancer (colonoscopy + biopsy).
Faecal impaction	5%	Elderly, institutionalised, immobile, opioid users. Overflow "diarrhoea." Digital rectal exam is diagnostic and therapeutic.
Other	5%	Ischaemic stricture, Crohn's stricture, anastomotic stricture, extrinsic compression (pelvic mass, endometriosis)

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Clinical presentation

The four cardinal features of bowel obstruction — and their nuances

Feature	Mechanism	SBO pattern	LBO pattern
Colicky pain	Hyperperistalsis proximal to obstruction trying to overcome block. Waves every 3-5 min (SB), every 10-15 min (LB).	Periumbilical, moderate severity, intermittent	Lower abdomen, less frequent cramps, more constant dull ache between cramps
Vomiting	Proximal obstruction → early vomiting; distal obstruction → late vomiting	Early, frequent, bilious (proximal) or faeculent (distal/late)	Late, may be absent initially, eventually faeculent
Distension	Gas + fluid accumulation proximal to obstruction	Central, less marked (unless distal SBO)	Marked, visible peristalsis, tympanic drum-like abdomen
Constipation / obstipation	Obstruction prevents passage of stool and flatus. Obstipation = absolute constipation (no faeces AND no flatus)	May pass some stool/flatus initially (evacuation of distal bowel) → then obstipation	Earlier onset of obstipation (more complete obstruction)

Key: High obstruction (proximal SBO) = severe vomiting, minimal distension, early presentation. Low obstruction (distal SBO/LBO) = marked distension, late vomiting, colicky pain.

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Differential diagnosis of suspected bowel obstruction

Mimic	Key distinguishing features
Paralytic ileus	No mechanical cause. No colicky pain (continuous discomfort or none). Absent bowel sounds (vs tinkling in obstruction). History of recent surgery, opioids, electrolyte disturbance (K+, Mg2+), peritonitis. Resolves with correction of underlying cause.
Mesenteric ischaemia	"Pain out of proportion" to exam. AF, vascular disease, recent MI. Bloody diarrhoea. Raised lactate, metabolic acidosis. CT: bowel wall thickening, pneumatosis, portal venous gas, mesenteric arterial/venous occlusion.
Gastroenteritis / enteritis	Cramping + diarrhoea (not constipation/obstipation). Vomiting prominent but no distension. Self-limiting.
Acute pancreatitis	Epigastric pain radiating to back. Raised amylase/lipase. CT shows pancreatic inflammation. Can cause paralytic ileus.
Intra-abdominal sepsis / peritonitis	Generalised peritonitis (rigid, guarding). May have ileus secondary to peritonitis. CT identifies abscess/perforation.
Pseudo-obstruction (Ogilvie)	Massive colonic dilation without mechanical obstruction. Critically ill patient. Exclude mechanical obstruction with CT/water-soluble contrast enema BEFORE neostigmine.
Toxic megacolon	Severe colitis (C. difficile, IBD, ischaemic). Systemically unwell. Markedly dilated colon with mucosal oedema/thumbprinting on imaging.
Ruptured abdominal aortic aneurysm	Tearing back/flank pain, collapse, palpable pulsatile mass. Not truly a mimic but can present with abdominal pain + distension.

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Imaging

Imaging modalities in suspected bowel obstruction

Modality	Role	Findings	Limitations
Erect CXR	First-line: detect free gas (perforation)	Free air under diaphragm (R hemidiaphragm on erect CXR). Sensitive for perforation.	Does not diagnose obstruction. May miss small amounts of free gas (sensitivity ~60%).
Supine AXR	First-line: assess bowel gas pattern	Dilated small bowel loops (>3 cm, central, valvulae conniventes — "stepladder" air-fluid levels), dilated colon (>6 cm, peripheral, haustra), "coffee bean" sign (sigmoid volvulus), absent rectal gas	Low sensitivity for early/partial SBO. Cannot determine cause or strangulation.
Erect AXR	Confirm air-fluid levels	Multiple air-fluid levels in dilated small bowel loops. "String of beads" sign (small amounts of gas trapped between valvulae conniventes in fluid-filled loops).	Largely superseded by CT. Less useful in LBO.
CT abdomen/pelvis with IV contrast	GOLD STANDARD — diagnostic test of choice	Transition point (abrupt change from dilated to collapsed bowel). Cause: adhesions (no mass, abrupt transition), hernia, tumour, volvulus. Strangulation: reduced/absent wall enhancement, bowel wall thickening, mesenteric fluid/stranding, ascites, pneumatosis, portal venous gas. Perforation: free gas, free fluid. Closed-loop: "whirl" sign, U/C-shaped loop.	Radiation, IV contrast nephropathy (caution in AKI). Requires haemodynamic stability.
Water-soluble contrast study (Gastrografin)	Diagnostic + therapeutic for adhesive SBO	100 mL Gastrografin via NGT. If contrast reaches colon within 4-24 h → obstruction will resolve (high sensitivity ~90-97%). Therapeutic effect (osmotic).	Only for adhesive SBO without strangulation. Contraindicated if peritonitis.
Ultrasound (POCUS)	Bedside in unstable patients	Dilated bowel loops (>3 cm SB, >6 cm LB), antiperistalsis, "keyboard" sign (valvulae conniventes), fluid-filled loops, "to-and-fro" peristalsis. Can identify free fluid and the "target" sign (intussusception).	Operator-dependent. Bowel gas limits views. Cannot reliably identify strangulation.

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CT signs of strangulation / bowel ischaemia — surgical urgency markers

CT sign	Pathophysiology	Significance
Reduced/absent bowel wall enhancement	Arterial inflow compromised → ischaemia. IV contrast does not perfuse the ischaemic segment.	Most specific sign of strangulation (>95%). Indication for emergency surgery.
Bowel wall thickening (>3 mm SB, >6 mm LB)	Venous congestion → mural oedema, intramural haemorrhage	Non-specific (also seen in inflammation). But combined with other signs, supports ischaemia.
Mesenteric stranding / haziness	Mesenteric venous congestion, oedema, fat infiltration from inflammation	Non-specific. More specific when localised to the affected segment's mesentery.
Mesenteric fluid / ascites	Venous congestion → transudation of fluid into mesentery and peritoneum	Non-specific but concerning when combined with other signs. Dark haemorrhagic fluid at surgery = infarction.
"Whirl" sign	Mesentery twists around a fulcrum (vascular pedicle) → volvulus / closed-loop	Pathognomonic for volvulus (sigmoid or midgut). Indicates closed-loop obstruction.
"Beak" sign	Tapering of bowel limbs at the site of obstruction	Seen in volvulus and closed-loop obstruction.
Pneumatosis intestinalis	Gas in bowel wall from ischaemia → mucosal breakdown, gas-forming bacteria invade wall	Late sign — indicates transmural infarction. Emergency.
Portal venous gas	Gas from necrotic bowel enters mesenteric veins → portal venous system	Very late sign — indicates extensive infarction. Very high mortality.
Free gas	Perforation of necrotic/ischaemic bowel	Emergency — surgical exploration mandatory.
"Target" sign	Bowel wall showing alternating layers of high/low attenuation (submucosal oedema + haemorrhage)	Indicates ischaemia or inflammation.

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Management — detailed approach

Management pathway for intestinal obstruction: resuscitation, nasogastric decompression, imaging, conservative trial for uncomplicated adhesive SBO, and emergency surgery for strangulation or failed conservative care — FigureDrip and suck for uncomplicated adhesive SBO; theatre without delay for strangulation, closed loop, or peritonitis.

Resuscitation and initial stabilisation

Initial resuscitation — 'Drip and Suck' for all obstructions

ABC + IV access — two large-bore cannulae. Oxygen if hypoxic. Cardiac monitor (elderly, electrolyte disturbance). Assess for sepsis (peritonitis → septic shock).
Fluid resuscitation — balanced crystalloid (Hartmann's / Plasma-Lyte). Massive third-space losses into obstructed bowel: 1-3 L deficit common. Bolus 500 mL aliquots, reassess. Correct hypokalaemia (K+ lost in vomitus + third-space sequestration), hypomagnesaemia, hyponatraemia. Avoid aggressive 0.9% saline (hyperchloraemic metabolic acidosis, AKI risk — SMART trial).
Nasogastric tube (NGT) — "Suck." Decompresses stomach, reduces vomiting and aspiration risk, monitors aspirate volume (falling aspirate = improving obstruction), relieves proximal distension. Large-bore NGT (16-18 Fr) preferred over fine-bore for viscous secretions. Document aspirate character (bilious, faeculent).
Urinary catheter — monitor urine output (target >0.5 mL/kg/h). AKI from hypovolaemia. Fluid balance chart.
Analgesia — morphine 2.5-5 mg IV titrated (avoid NSAIDs — renal impairment). Antiemetics (ondansetron 4 mg IV). Do not give prokinetics (metoclopramide, erythromycin) in mechanical obstruction — may worsen strangulation risk or perforation.
Broad-spectrum antibiotics — if strangulation, peritonitis, or sepsis suspected (e.g., co-amoxiclav or ceftriaxone + metronidazole). Not routinely required for uncomplicated adhesive SBO.
Surgical referral — involve surgical team early. Serial abdominal examinations (q4-6h). Set clear thresholds for surgical intervention.

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Fluid management in bowel obstruction — principles

Principle	Rationale	Practical approach
Crystalloid first-line	Replace isotonic third-space losses	Hartmann's or Plasma-Lyte (balanced — avoids hyperchloraemic acidosis of 0.9% saline)
Volume	Sequestration into obstructed bowel lumen + vomiting → significant deficit (1-3 L)	1-2 L bolus, then maintenance + ongoing losses. Rate guided by clinical response (HR, BP, urine output, lactate, capillary refill)
Potassium	Hypokalaemia universal (vomiting + third-space loss). Hypokalaemia worsens ileus and cardiac arrhythmias	20-40 mmol/L in maintenance fluids. Check U&E q12-24h. Target K+ 4.0-4.5 mmol/L.
Magnesium	Hypomagnesaemia common (vomiting, poor intake). Refractory hypokalaemia if Mg2+ not corrected	10-20 mmol MgSO4 IV. Check Mg2+ level.
Avoid hypotonic fluids	SIADH risk from stress/nausea/pain + possible hyponatraemia from GI losses	Use isotonic crystalloid for resuscitation
Monitor	AKI risk from hypovolaemia; fluid overload risk in elderly/cardiac disease	Urine output >0.5 mL/kg/h. Daily weights. Lactate trend (clearing = resuscitation adequate). Reassess q4-6h.

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Gastrografin (water-soluble contrast) challenge

Water-soluble contrast challenge (Gastrografin) for adhesive SBO

Indication — uncomplicated adhesive SBO without signs of strangulation/peritonitis. CT shows single transition point, no ischaemia. Aids both diagnosis (predicts need for surgery) and therapy (osmotic effect).[13]
Patient selection — no peritonitis, no free gas, no signs of strangulation, partial or complete SBO with adhesive aetiology (previous surgery, CT showing abrupt transition with no mass). NOT for hernia, volvulus, tumour, or closed-loop obstruction.
Procedure — 100 mL Gastrografin (diatrizoate meglumine — hyperosmolar water-soluble contrast) administered via NGT. Clamp NGT for 2 h. Patient mobilises/changes position to aid transit.
Assessment — serial abdominal X-rays at 4, 8, and 24 h. If contrast reaches colon (caecum) within 24 h → obstruction will resolve (sensitivity 92-97%, specificity 60-80%). If contrast does NOT reach colon within 24 h → high likelihood of needing surgery (proceed to laparotomy).
Therapeutic mechanism — Gastrografin is hyperosmolar (1900 mOsm/L) → draws fluid into bowel lumen → oedema reduction at obstruction site + stimulates peristalsis. May hasten resolution by 24-48 h compared to conservative management alone.
Outcome — Meta-analyses show Gastrografin reduces need for surgery (odds ratio ~0.6) and shortens hospital stay. Does NOT reduce recurrence rate.[13]
Contraindications — suspected perforation (use barium for fistula — water-soluble extravasates but is resorbed; barium causes peritonitis), peritonitis, complete obstruction from non-adhesive cause.

Surgical management

Indications for surgery in small bowel obstruction

Indication	Rationale	Timing
Strangulation (ischaemia)	Blood supply compromised → necrosis → perforation → death. CT signs: reduced wall enhancement, mesenteric fluid, pneumatosis. Clinical: peritonitis, raised lactate, fever, constant pain.	Emergency — immediate laparotomy
Peritonitis (perforation)	Free gas on imaging. Rigid abdomen. Faecal/bilious peritonitis → septic shock.	Emergency — immediate laparotomy
Closed-loop obstruction	Volvulus (whirl sign), incarcerated hernia. Rapid strangulation risk.	Urgent — surgery within hours (caecal volvulus = surgery; sigmoid volvulus = endoscopic detorsion first)
Failed conservative management	No resolution within 48-72 h of drip-and-suck + Gastrografin challenge. Worsening distension/pain/aspirate.	Urgent — surgery within 24 h of declaring failure
Non-adhesive cause	Hernia (unless easily reducible and reducible on presentation), malignancy, intussusception, gallstone ileus (may require surgery), Crohn's stricture.	Urgent-elective — timing depends on cause
Recurrent obstruction	Multiple admissions for adhesive SBO → consider elective adhesiolysis or bowel resection.	Elective — after resolution of current episode

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Surgical approach to SBO — laparotomy vs laparoscopy

Pre-operative optimisation — resuscitate first (fluids, electrolytes, antibiotics if strangulation/peritonitis). Cross-match blood. NGT in situ (decompressed stomach reduces aspiration on induction). Urinary catheter. DVT prophylaxis (LMNH — hold if emergency surgery, mechanical prophylaxis intraoperatively).
Approach selection — Open laparotomy (midline incision): standard for strangulation, peritonitis, multiple previous surgeries, haemodynamic instability. Laparoscopic adhesiolysis: selected patients (≤2 previous surgeries, localised adhesions, no peritonitis, stable). Experienced surgeon only — conversion to open if dense adhesions, bowel injury, or unable to identify obstruction. Conversion rate 20-50%.[10][14]
Operative steps (laparotomy) — systematic "run-through" of entire small bowel from ligament of Treitz to ileocaecal valve. Identify transition point (dilated → collapsed bowel). Identify and treat cause: adhesiolysis (divide adhesions), hernia repair, tumour resection. Assess bowel viability — colour, peristalsis, mesenteric pulsation. If viability uncertain → warm packs 15-20 min + 100% O2 → reassess. If still non-viable → resect (strangulated/ischaemic segment) with primary anastomosis or stoma. Washout if peritonitis/perforation.
Bowel preservation principle — minimise resection (short bowel syndrome risk). Resect only frankly non-viable bowel. For adhesive SBO: adhesiolysis alone (no resection needed if bowel viable). For strangulated bowel: resect from viable proximal to viable distal margin.
Laparoscopic adhesiolysis outcomes — shorter hospital stay (2-3 days less), fewer wound infections, earlier return of bowel function. BUT higher risk of unrecognised enterotomy (bowel injury during dissection — always check for enterotomy before closing).[10]
Post-operative ICU care — fluid resuscitation (capillary leak → third-space losses), monitor for anastomotic leak (days 5-7: fever, tachycardia, abdominal pain, raised inflammatory markers → CT with water-soluble contrast), wound infection, ileus (expected 3-5 days — NGT, fluids, mobilise), AKI, pneumonia. VTE prophylaxis (LMNH 6 h post-op). Stress-ulcer prophylaxis (PPI) if ventilated/coagulopathic/steroid. Glycaemic control 7.8-10 mmol/L.

Post-operative complications after bowel obstruction surgery

Complication	Incidence	Features	Management
Prolonged ileus	10-20%	No flatus/stool >5 days post-op. Distension, no bowel sounds. Nausea, NGT aspirate persists.	Conservative: NGT, IV fluids, correct electrolytes, minimise opioids, mobilise. Exclude mechanical obstruction with CT if >7 days.
Anastomotic leak	4-10% (emergency, higher)	Days 5-7: fever, tachycardia, abdominal pain, pelvic/abdominal collection, raised CRP/WCC. Septic shock.	CT with water-soluble contrast. Drain collection (radiological or surgical). Defunctioning stoma. Re-laparotomy if unstable.
Surgical site infection	10-25% (contaminated/dirty wounds)	Erythema, purulent discharge, dehiscence.	Wound swab, antibiotics (flucloxacillin or based on culture), open/incise/drain.
Intra-abdominal collection/abscess	5-10%	Fever, raised WCC/CRP, persistent ileus. CT confirms.	Percutaneous drainage (if accessible) or surgical drainage. Antibiotics.
Enterocutaneous fistula	1-5%	Enteric contents draining from wound/drain site. Days 7-14.	Conservative first (TPN, somatostatin analogue, wound care). Surgery if fails to close after months.
Adhesive SBO recurrence	30-40% at 5 years	Readmission with SBO.	Initially conservative. Elective adhesiolysis/barrier adhesion prevention (Seprafilm) at subsequent surgery.
Short bowel syndrome	Variable	Extensive resection (>200 cm SB). Diarrhoea, malabsorption, weight loss, electrolyte disturbance.	TPN, anti-diarrhoeals, intestinal rehabilitation. Rare in obstruction surgery.

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Ogilvie syndrome (acute colonic pseudo-obstruction)

Classification of intestinal obstruction: small vs large bowel, mechanical vs adynamic, and key entities including volvulus and Ogilvie syndrome — FigureSeparate mechanical from adynamic disease first — Ogilvie is dilation without a mechanical block and neostigmine is the exam therapy.

Ogilvie syndrome — risk factors in ICU patients

Category	Risk factors
Critical illness	Sepsis, severe pneumonia, ARDS, multi-organ failure, severe burns, hypoxia
Surgical	Recent abdominal/pelvic surgery, caesarean section, hip/knee replacement, cardiac surgery, transplant surgery
Trauma	Pelvic/lumbar fractures, retroperitoneal haematoma, spinal cord injury
Metabolic/electrolyte	Hypokalaemia, hypomagnesaemia, hypocalcaemia, hypothyroidism, uraemia
Drugs	Opioids (major), anticholinergics, phenothiazines, calcium channel blockers, clonidine, SSRIs
Cardiovascular	Heart failure, myocardial infarction, cardiac arrest
Neurological	Stroke, Parkinson's disease, multiple sclerosis, spinal cord injury, dementia
Infectious	Herpes zoster, cytomegalovirus, systemic infection

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Ogilvie syndrome — pathophysiology and the parasympathetic theory

Mechanism	Detail
Core concept	Massive colonic dilation (especially caecum and right colon) WITHOUT mechanical obstruction. The colon is atonic — no peristalsis.
Sympathetic overactivity	Critical illness, pain, stress → excessive sympathetic output → inhibitory effect on colonic motility
Parasympathetic suppression	Pelvic splanchnic nerves (S2-S4) supply parasympathetic innervation to distal colon/rectum. Vagus supplies proximal colon. Imbalance between sacral parasympathetic (loss) and vagal (excess) → segmental atony → functional obstruction → gas accumulation → massive dilation.
Why the caecum?	Laplace's law: T = P × r. The caecum has the largest radius (r) → greatest wall tension (T) at any given intraluminal pressure (P). This makes the caecum the most vulnerable to perforation. Caecal diameter >12 cm = high perforation risk. Perforation risk also depends on duration of dilation (>6 days = higher risk) and rate of dilation (rapid = higher risk).
Outcome	Spontaneous resolution in ~70-80% with conservative measures. Pharmacological decompression (neostigmine) successful in 80-90%. Colonoscopic decompression in ~70-80% of non-responders. Surgery required in 1-5%. Perforation risk 3-15%. Mortality 10-30% (driven by underlying critical illness + perforation).[12]

Management of Ogilvie syndrome (acute colonic pseudo-obstruction)

Diagnose and exclude mechanical obstruction — CT abdomen/pelvis is essential. Shows massively dilated colon (especially caecum/right colon) throughout, no mechanical obstruction / no transition point. Also excludes caecal/sigmoid volvulus, tumour, and assesses for perforation/ischaemia. Water-soluble contrast enema can also exclude distal mechanical obstruction.[12]
Conservative measures (first-line) — Correct ALL electrolyte abnormalities (K+ >4.0, Mg2+ >0.8, Ca2+ normal). Stop all exacerbating drugs (opioids → use multimodal analgesia, anticholinergics, calcium channel blockers). Mobilise / frequent position changes. Nasogastric decompression (reduce swallowed air). Rectal tube (decompress rectum/sigmoid). Restrict oral intake. Serial abdominal X-rays q12-24h to monitor caecal diameter. Trial for 48-72 h. ~70-80% resolve with conservative measures.[12]
Neostigmine (second-line) — if no improvement after 48-72 h of conservative measures AND caecal diameter >10-12 cm (or rapidly increasing). MUST exclude mechanical obstruction first (CT) — neostigmine in mechanical obstruction is dangerous (increases pressure against obstruction → perforation).[8]
Neostigmine administration protocol — 2 mg IV over 3-5 min (slow push). Patient supine on bedpan/commode. Continuous ECG, BP, HR monitoring. Have atropine 0.5-1 mg drawn up (for bradycardia). Onset of effect: within minutes (typically passes flatus/stool within 30 min). Efficacy: 80-90% decompression. May repeat once after 2-4 h if partial response. Contraindications: mechanical obstruction (unexcluded), perforation, severe bradycardia (<60 bpm), active bronchospasm, recent MI.[8]
Colonoscopic decompression (third-line) — if neostigmine fails, contraindicated, or recurrent after initial response. Unprepared colonoscopy (no bowel prep — difficult and potentially dangerous in dilated, thin-walled colon). Gentle air insufflation (minimal). Advance to caecum (success 40-80% — may not reach caecum). Aspirate gas throughout withdrawal. Leave decompression tube in caecum (14-18 Fr) for 48-72 h. Success: 70-80%. Recurrence: 20-40% (may need repeat). Perforation risk: 2-3% (higher than diagnostic colonoscopy).[16]
Surgery (last resort) — if neostigmine + colonoscopy fail, OR if perforation/ischaemia develops. Caecostomy (tube caecostomy — minimally invasive, can be percutaneous or open). Subtotal colectomy (if ischaemia/perforation — resect non-viable colon, primary anastomosis or ileostomy). High mortality (15-40% — reflects critical illness + emergency surgery).[12]
Monitoring during treatment — serial abdominal X-rays q12-24h. Target: caecal diameter <9 cm. Clinical exam: watch for peritonitis (perforation). If caecum >12 cm for >6 days → escalating intervention. Recurrence after neostigmine: 20-30% → consider repeat dose or colonoscopy.[12]

Ogilvie syndrome — caecal diameter and perforation risk

Caecal diameter	Perforation risk	Recommended action
<10 cm	Low	Conservative management (correct electrolytes, stop drugs, mobilise). Monitor with serial AXR.
10-12 cm	Moderate	Conservative measures intensified. Consider neostigmine if no resolution in 48 h or diameter increasing.
>12 cm	High	Neostigmine (if no contraindication and mechanical obstruction excluded). If neostigmine fails → colonoscopic decompression. Surgery if colonoscopy fails.
>12 cm for >6 days	Very high	Urgent intervention (neostigmine → colonoscopy → surgery). Perforation risk increases significantly with prolonged dilation.
>14 cm OR signs of perforation	Critical	Emergency surgery (caecostomy or colectomy). Free gas on imaging = perforation.

Note: Caecal diameter is the primary determinant, but perforation can occur at smaller diameters with rapid onset or ischaemia. Clinical context (peritonitis, sepsis, underlying critical illness) guides urgency.

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Volvulus

Sigmoid vs caecal volvulus

Feature	Sigmoid volvulus	Caecal volvulus
Frequency	75% of colonic volvulus	25%
Demographics	Elderly, nursing-home residents, chronic constipation, institutionalised, psychiatric medications, high-fibre diet in some populations (Africa, "volvulus belt")	Younger (30-60 years), mobile caecum (incomplete fixation — 10-25% population)
Mechanism	Sigmoid colon twists (180-540°) around its mesentery. Elongated redundant sigmoid + narrow mesenteric base = predisposition. Closed-loop obstruction.	Caecum twists (clockwise) around its mesentery ± axial volvulus. Mobile caecum allows torsion. Can also be caecal bascule (anterior fold, not true torsion).
Imaging	"Coffee bean" sign — massively dilated sigmoid loop arising from pelvis, projecting toward RUQ. The mesenteric crease creates the "bean's" central crease. Plain AXR diagnostic in 60-80%. CT confirms ("whirl" sign of mesenteric twist).	Dilated caecum in LUQ or epigastrium (flipped superiorly). "Coffee bean" may be seen but oriented differently. CT: "whirl" sign, caecal "beak." May mimic SBO (dilated SB loops if ileocaecal valve incompetent).
Presentation	Massive abdominal distension, cramping lower abdominal pain, constipation/obstipation. May be chronically recurrent (intermittent torsion/detorsion).	SBO-like picture: distension, vomiting, colicky pain. Rapid strangulation risk.
First-line management	Endoscopic detorsion — flexible sigmoidoscopy, gently advance past twist, deflate/decompress. Insert flatus tube (rectal tube) left in situ 48-72 h. Success ~70-80%. Recurrence 40-60%.	Surgery — endoscopic detorsion is NOT recommended (unsafe, caecum not reachable via colonoscopy reliably, high perforation risk in closed loop). Right hemicolectomy ± primary anastomosis.
Surgery indications	Endoscopic failure, ischaemia/perforation, recurrent (elective sigmoid colectomy after successful detorsion).	All caecal volvulus → surgery (right hemicolectomy).
Recurrence	40-60% after successful endoscopic detorsion alone. Elective sigmoid colectomy after successful detorsion reduces recurrence to <5%.	Right hemicolectomy is definitive (recurrence ~1%).
Mortality	5-10% (elective detorsion); 20-50% if strangulated/perforated	10-20% (caecal volvulus has higher emergency surgery rate)

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Endoscopic detorsion of sigmoid volvulus

Indication — sigmoid volvulus without signs of strangulation/perforation (no peritonitis, no free gas, clinically stable, viable bowel on imaging). First-line therapy.[9][15]
Preparation — consent (perforation risk ~1-2%, failure). Broad-spectrum antibiotics (contaminated field). Decompression: gentle rectal examination, some centres gently pass flatus tube to decompress gas before scope.
Procedure — flexible sigmoidoscopy (unprepared bowel — usually little stool as bowel proximal is obstructed). Gently advance scope. At the twist: spiral "whirl" of mucosa, congested mucosa (assess viability — pale/dusky/black = ischaemia → ABORT, go to surgery). Gently insufflate and manipulate scope past twist. Sudden rush of gas/liquid stool = successful detorsion. Advance to proximal sigmoid/decompress.
Assess mucosal viability — if mucosa is viable (pink, normal), proceed. If ischaemic (dusky, purple, sloughing, black) → ABORT endoscopy → emergency surgery (sigmoid colectomy — strangulated bowel).
Flatus tube placement — insert large-bore rectal tube (28-32 Fr) past detorsion point, leave in situ 48-72 h to maintain detorsion and allow continued decompression. Confirm position on AXR.
Post-procedure — NBM, IV fluids, monitor for recurrence (serial abdominal exams, AXR). Consider elective sigmoid colectomy during same admission (3-5 days after detorsion) to prevent recurrence (40-60% recurrence if no surgery).[9]
Outcome — Success 70-80%. Recurrence 40-60% (without elective surgery). Mortality of detorsion 1-5%. Mortality of strangulated sigmoid volvulus requiring emergency surgery 20-50%.[15]

Additional clinical pearls

High-yield pearls — intestinal obstruction in ICU (Part 2)

The "drip and suck" mnemonic: Drip = IV fluid resuscitation (massive third-space losses into the obstructed bowel). Suck = NGT decompression. This is the initial management for ALL uncomplicated obstructions — buys time, corrects hypovolaemia/electrolytes, allows ~80% of adhesive SBO to resolve spontaneously. Do NOT rush to surgery for uncomplicated adhesive SBO — but DO rush for strangulation/peritonitis/closed-loop.[2][3] }
Examine ALL hernial orifices in every SBO. Femoral hernias have the narrowest neck → highest strangulation risk → most easily missed (deep to inguinal ligament, may be small). A strangulated femoral hernia in an elderly woman is a classic exam scenario. Always check: inguinal, femoral, umbilical, incisional, parastomal. A "reducible" hernia on presentation may still have been the cause of obstruction (intermittent incarceration).[11] }
Constant (non-colicky) pain = ischaemia until proven otherwise. Colicky pain = mechanical obstruction without ischaemia (bowel still peristalsing against the obstruction). Constant pain = bowel ischaemia (peristalsis has ceased due to ischaemia). This single clinical distinction separates "observe and drip-suck" from "emergency laparotomy."[2] }
Closed-loop obstruction does not tolerate conservative management. A closed loop (volvulus, incarcerated hernia, adhesive band around both limbs) cannot decompress proximally → rapidly rising intraluminal pressure → venous congestion → arterial compromise → strangulation within hours. CT "whirl" sign or "beak" sign → emergency surgery. Do NOT trial conservative management for confirmed closed-loop obstruction.[5] }
CT has >95% sensitivity and specificity for SBO and can triage surgery vs conservative. Look for: (a) transition point (dilated → collapsed bowel = level of obstruction), (b) cause (adhesions = abrupt transition with no mass; hernia = bowel entering hernial sac; tumour = mass at transition; volvulus = whirl sign), (c) strangulation signs (reduced wall enhancement = most specific; bowel wall thickening, mesenteric stranding, ascites), (d) perforation (free gas), (e) closed-loop (whirl, U-shaped loop). IV contrast essential (oral contrast helpful but not essential).[3] }
Gastrografin is BOTH diagnostic and therapeutic. Diagnostic: contrast reaching colon within 24 h predicts resolution (NPV for surgery ~96%). Therapeutic: hyperosmolar (1900 mOsm/L) → draws fluid into lumen → reduces bowel wall oedema at obstruction site → stimulates peristalsis → hastens resolution by ~24 h and reduces need for surgery by ~36% (Abbas Cochrane meta-analysis). NOT for strangulation, peritonitis, or non-adhesive causes.[13][7] }
Ogilvie syndrome: ALWAYS exclude mechanical obstruction before neostigmine. Neostigmine increases peristalsis — if given to a patient with mechanical obstruction, it increases pressure against the obstruction → risk of perforation. CT (or water-soluble contrast enema) is mandatory. Neostigmine: 2 mg IV over 3-5 min, continuous ECG, have atropine ready for bradycardia. Contraindications: mechanical obstruction, perforation, bradycardia (<60), bronchospasm, recent MI.[8][12] }
The caecum is the weakest point in Ogilvie — Laplace's law. T = P × r. The caecum has the largest radius → highest wall tension at any given intraluminal pressure → most vulnerable to perforation. Caecum >12 cm = high perforation risk → intervene (neostigmine → colonoscopy → surgery). Perforation risk also increases with duration of dilation (>6 days) and rapidity of onset. Perforated Ogilvie has 40-50% mortality.[12] }
Sigmoid volvulus: endoscopic detorsion first; caecal volvulus: surgery always. Sigmoid volvulus: flexible sigmoidoscopy + flatus tube (70-80% success) → elective sigmoid colectomy to prevent recurrence (40-60% recurrence without surgery). Caecal volvulus: endoscopic detorsion is unsafe and unreliable → right hemicolectomy always. This is a high-yield exam distinction.[9][15] }
"Coffee bean" sign = sigmoid volvulus. Plain AXR: massively dilated sigmoid loop arising from the pelvis, projecting toward RUQ, with a central crease (the mesenteric twist) resembling a coffee bean. Diagnostic in 60-80% of cases on plain film. CT confirms ("whirl" sign of twisted mesentery).[15] }
Paralytic ileus vs mechanical obstruction: absent bowel sounds and no colicky pain favour ileus. Ileus: continuous discomfort or painless distension, absent/hypoactive bowel sounds, no transition point on CT, history of recent surgery/opioids/electrolyte disturbance. Mechanical obstruction: colicky pain, high-pitched tinkling bowel sounds, transition point on CT. Management of ileus: NGT, IV fluids, correct electrolytes (K+, Mg2+), minimise opioids, mobilise, chew gum (prokinetic effect). Resolves in 3-5 days; if >7 days → CT to exclude missed mechanical obstruction.[6] }
Massive third-space fluid losses make hypovolaemia and AKI the early killers in obstruction. Fluid sequesters in the obstructed bowel lumen (impaired absorption + increased secretion + bowel wall oedema). A patient with SBO can lose 1-3 L into the bowel. Monitor: HR, BP, urine output (>0.5 mL/kg/h), lactate, capillary refill. Resuscitate with balanced crystalloid. Correct hypokalaemia (universal in vomiting patients).[2] }
Gallstone ileus: Rigler's triad. (1) Pneumobilia (air in biliary tree from cholecystoenteric fistula), (2) SBO (dilated small bowel loops, air-fluid levels), (3) Ectopic gallstone (usually in RLQ/terminal ileum). Classic patient: elderly woman, no surgical history, SBO. Management: enterolithotomy (remove stone via enterotomy — milk stone proximally to healthy bowel, longitudinal enterotomy, remove stone, close transversely). Cholecystectomy + fistula repair can be deferred (two-stage) — most fistulae close spontaneously.[6] }
Recurrent adhesive SBO: 30-40% at 5 years. Recurrence after successful conservative management is common. Adhesiolysis can cause NEW adhesions → more obstructions. Prevention: Seprafilm (hyaluronic acid-carboxymethylcellulose barrier) at initial surgery reduces adhesions. Laparoscopic surgery causes fewer adhesions than open. Enhanced Recovery After Surgery (ERAS) protocols (early mobilisation, early feeding, opioid-sparing analgesia) reduce ileus. No pharmacological agent proven to prevent adhesions.[1] }
Post-operative ileus is expected for 3-5 days; prolonged ileus suggests complication. After laparotomy, bowel function typically returns: small bowel (24 h), stomach (48 h), colon (3-5 days). "Prolonged ileus" = no flatus/stool at >5 days. Causes: opioids, electrolyte disturbance (K+, Mg2+), intra-abdominal collection/abscess, anastomotic leak, haematoma, missed mechanical obstruction. Investigate with CT. Manage conservatively (NGT, fluids, electrolytes, mobilise, minimise opioids).[6] }
Intussusception in adults always has a pathological lead point. Unlike children (idiopathic, viral lymphoid hyperplasia), adult intussusception is caused by a tumour/mass (40-70% malignant): lipoma, adenomatous polyp, adenocarcinoma, lymphoma, GIST, Meckel's diverticulum. "Target" sign on ultrasound/CT (telescoping bowel layers). Management: surgical resection (do NOT reduce in adults — risk of tumour spillage; resect with the intussusceptum en bloc).[6] }
Always look for free gas before considering conservative management. Erect CXR or CT must exclude perforation before trial of conservative management. Free gas = perforation = emergency surgery. Pneumoperitoneum can also occur from recent laparoscopy, penetrating trauma, or peritoneal dialysis — correlate clinically.[2] }
In ICU patients with abdominal distension, always measure intra-abdominal pressure (IAP). Bowel obstruction → bowel dilation → raised IAP → abdominal compartment syndrome (IAP >20 mmHg + new organ dysfunction: AKI, respiratory failure, cardiovascular compromise). Measure bladder pressure. Decompression (NGT, rectal tube, neostigmine for pseudo-obstruction, surgery for mechanical obstruction) reduces IAP. Abdominal compartment syndrome has 40-70% mortality if untreated.[6] }
Malignant bowel obstruction in palliative care: a different approach. Advanced cancer (peritoneal carcinomatosis, ovarian, colorectal) → multiple obstruction sites. Surgery often futile (multiple levels, poor prognosis). Palliative: NGT/decompressive gastrostomy for vomiting, antisecretory agents (octreotide — reduces GI secretions; ranitidine/PPI — reduces gastric acid), antiemetics (haloperidol, cyclizine), corticosteroids (dexamethasone — reduces tumour oedema, may resolve partial obstruction), analgesia (opioids — but worsen obstruction; consider spinal analgesia). Stents (self-expanding metal stents) for single-level colonic obstruction in unfit patients.[5] }
Water-soluble contrast enema to differentiate mechanical LBO from pseudo-obstruction. In Ogilvie, water-soluble contrast enema shows a widely patent colon with no mechanical obstruction (contrast flows freely to caecum). In mechanical LBO, contrast stops at the obstruction point. Also has therapeutic effect (osmotic — may stimulate evacuation). Use water-soluble (Gastrografin) NOT barium (risk of perforation/peritonitis if perforated).[16] }

Additional red flags

Additional critical intestinal obstruction red flags

Constant (non-colicky) abdominal pain → bowel ischaemia/strangulation until proven otherwise → emergency surgery.[2] }
Haemodynamic instability (tachycardia, hypotension) with obstruction → strangulation or perforation with septic shock → emergency surgery.[2] }
Metabolic acidosis / raised lactate (>2 mmol/L) → tissue ischaemia from strangulated bowel → emergency surgery.[2] }
Pneumoperitoneum (free gas on erect CXR or CT) → perforated bowel → emergency surgery.[2] }
CT: reduced/absent bowel wall enhancement → arterial compromise, strangulation → emergency surgery.[3] }
CT: "whirl" sign → closed-loop obstruction (volvulus) → urgent surgery (caecal) or endoscopic detorsion (sigmoid, if viable).[9] }
CT: pneumatosis intestinalis or portal venous gas → transmural ischaemia/infarction → emergency surgery.[3] }
Ischaemic/dusky mucosa at endoscopy for sigmoid volvulus → strangulated volvulus → ABORT endoscopy, emergency sigmoid colectomy.[9] }
Caecum >14 cm on imaging (Ogilvie) → imminent perforation → emergency neostigmine ± colonoscopic decompression ± surgery.[12] }
Ogilvie with peritonitis or free gas → caecal perforation → emergency surgery (caecostomy or colectomy).[12] }
Faeculent vomiting → distal/complete obstruction or strangulation (late, concerning sign).[6] }
Abdominal compartment syndrome (bladder pressure >20 mmHg + organ dysfunction) → decompression urgently (surgery if mechanical).[6] }
Recurrent sigmoid volvulus (≥2 episodes) → elective sigmoid colectomy (40-60% recurrence after detorsion alone).[9] }
Malignant LBO with perforation (obstructed, distended colon perforates at caecum — "closed-loop" phenomenon in LBO with competent ileocaecal valve) → emergency surgery.[5] }

Prognosis and outcomes

Outcomes by obstruction type and complication

Scenario	Mortality	Key outcome data
Uncomplicated adhesive SBO (conservative)	2-5%	65-80% resolve with drip-and-suck. Recurrence 30-40% at 5 years. Gastrografin reduces surgery need by ~36%.[3][13]
Strangulated SBO (surgery)	10-30%	Mortality driven by delay to surgery, comorbidity, septic shock. Early laparotomy (within 24 h of strangulation signs) improves survival.[2]
LBO from colorectal cancer	10-20% (emergency)	Emergency surgery (resection ± stoma) higher mortality than elective. Stenting (self-expanding metal stent) as bridge to elective surgery in selected unfit patients.[5]
Sigmoid volvulus (endoscopic detorsion)	1-5%	Success 70-80%. Recurrence 40-60% without elective colectomy.[9]
Sigmoid volvulus (emergency surgery)	20-50%	High mortality reflects elderly, comorbid population + emergency setting.[15]
Caecal volvulus (surgery)	10-20%	Right hemicolectomy definitive. Recurrence ~1%.[15]
Ogilvie syndrome (conservative)	5-15%	70-80% resolve with conservative measures. Mortality driven by underlying critical illness.[12]
Ogilvie (neostigmine)	5-15%	80-90% decompression. Recurrence 20-30%.[8]
Ogilvie (colonoscopic decompression)	10-20%	Success 70-80% of neostigmine failures. Perforation risk 2-3%.[16]
Ogilvie with perforation	40-50%	Emergency surgery (caecostomy/colectomy). High mortality reflects critical illness + abdominal sepsis.[12]
Gallstone ileus	5-15%	Enterolithotomy definitive for acute obstruction. Recurrence of gallstone ileus rare (<5%). Cholecystectomy may be deferred.[6]

Ponec et al. 1999 — Neostigmine for Ogilvie syndrome (landmark RCT)

Randomised, double-blind, placebo-controlled trial. 21 patients with Ogilvie (caecum >10 cm, no mechanical obstruction, failed conservative management for 48 h).

Intervention: Neostigmine 2 mg IV vs placebo
Primary outcome: Clinical decompression (passing flatus/stool + reduction in abdominal distension) within 3 h
Results: Decompression in 10/11 (91%) neostigmine vs 0/10 (0%) placebo (p<0.001). Median time to response 4 min (neostigmine).
Adverse events: Bradycardia 2/11 (required atropine), mild abdominal cramping, vomiting, salivation, lacrimation. No perforation.
Recurrent dilation: 3/11 (27%) recurred after initial response → 2 responded to second dose.
Significance: Established neostigmine as first-line pharmacological therapy for Ogilvie syndrome. Subsequent studies (Paran et al. 2000, van der Snock 2008, Valle et al. 2015) confirmed efficacy with 80-90% decompression rates and acceptable safety.[8]

Abbas et al. (Cochrane, 2007/2015) — Water-soluble contrast for adhesive SBO

Systematic review and meta-analysis of RCTs evaluating oral water-soluble contrast in adhesive SBO.

Trials included: 8 RCTs, 710 patients
Adhesive SBO resolution: Pooled OR 2.30 (95% CI 1.43-3.71) favouring water-soluble contrast over conservative management alone
Need for surgery: Pooled OR 0.62 (95% CI 0.43-0.89) — 36% relative reduction in need for surgery
Time to resolution: Mean difference -1.46 days (95% CI -2.17 to -0.75) — faster resolution
Hospital stay: Mean difference -1.85 days (95% CI -2.86 to -0.83) — shorter stay
Adverse events: No significant difference (water-soluble contrast well tolerated)
Conclusion: Water-soluble contrast (Gastrografin) is both diagnostic (predicts need for surgery) and therapeutic (hastens resolution, reduces need for surgery). Recommended for uncomplicated adhesive SBO without strangulation signs.[13]

Halabi et al. (2014) — ACS-NSQIP: Laparoscopic vs open surgery for SBO

Retrospective analysis of 6,722 patients from the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database.

Laparoscopic group (n=989) vs Open group (n=5,733)
Mortality: 1.0% (laparoscopic) vs 3.1% (open) — OR 0.45 (p<0.001)
Overall morbidity: 12.3% vs 25.0% — OR 0.45 (p<0.001)
Surgical site infection: 3.4% vs 8.5% — OR 0.44 (p<0.001)
Pneumonia: 1.3% vs 3.7% — OR 0.41 (p<0.001)
Hospital stay: 4 days (laparoscopic) vs 8 days (open) (p<0.001)
Conversion rate: 20.2% (higher with dense adhesions, previous open surgery)
Conclusion: Laparoscopic adhesiolysis associated with lower morbidity, mortality, and shorter stay — but selection bias (healthier, less complex patients selected for laparoscopy). Demonstrates feasibility and safety of laparoscopic approach in selected SBO patients.[14]

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ICU-specific considerations for intestinal obstruction

Consideration	Detail
Sepsis from strangulated bowel	Bacterial translocation from ischaemic bowel → gram-negative sepsis, septic shock. Resuscitate (30 mL/kg crystalloid), vasopressors (noradrenaline), broad-spectrum antibiotics (piperacillin-tazobactam ± aminoglycoside), source control (emergency laparotomy + resection). Lactate clearance guides resuscitation. Mortality 30-50%.
AKI from hypovolaemia	Third-space losses → pre-renal AKI. Resuscitate early. Monitor urine output. Avoid nephrotoxins (NSAIDs, aminoglycosides unless indicated). CT contrast may worsen AKI — weigh risk/benefit.
Abdominal compartment syndrome	Dilated bowel → raised intra-abdominal pressure. Bladder pressure >20 mmHg + organ dysfunction (AKI, respiratory failure, hypotension). Decompress (NGT, rectal tube, neostigmine, surgery). Mortality 40-70%.
Nutrition	Prolonged obstruction/ileus → malnutrition. Early enteral nutrition if conservative management (post-pyloric NGT if gastric stasis). TPN if prolonged (>7 days) and enteral not possible. Refeeding syndrome risk if malnourished.
VTE prophylaxis	Bowel obstruction = high VTE risk (immobility, dehydration, inflammation, cancer). LMWH unless contraindicated (active bleeding, recent surgery — mechanical prophylaxis). Hold LMNH 12 h pre-surgery.
Stress ulcer prophylaxis	PPI (pantoprazole 40 mg IV OD) if ventilated >48 h, coagulopathy, shock, previous GI bleed. Not routinely for all patients (COOK trial — excess pneumonia with routine PPI).
Delirium	Common in elderly ICU patients with obstruction. Manage pain (paracetamol first, opioid-sparing), treat sepsis, correct electrolytes, mobilise, sleep hygiene. Avoid benzodiazepines (worsen delirium) unless alcohol/benzo withdrawal.
Goals of care / ethics	Malignant bowel obstruction in advanced cancer → discuss goals of care. Surgery may be futile. Palliative approach (decompressive gastrostomy, octreotide, steroids, analgesia) may be appropriate. Involve palliative care team early.

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ICU management checklist for intestinal obstruction

Resuscitate — IV access, crystalloid bolus (correct hypovolaemia from third-space losses), correct K+/Mg2+. Catheterise (monitor UO). Broad-spectrum antibiotics if sepsis/peritonitis.
Decompress — NGT (large-bore, 16-18 Fr). Monitor aspirate. Consider rectal tube for distal obstruction.
Image — Erect CXR (free gas), supine AXR (dilated loops, coffee bean), CT abdomen/pelvis with IV contrast (gold standard — site, cause, strangulation, perforation, closed-loop).
Triage — Strangulation/peritonitis/closed-loop → emergency surgery. Uncomplicated adhesive SBO → drip-and-suck + Gastrografin challenge. Ogilvie → exclude mechanical obstruction → conservative → neostigmine → colonoscopy → surgery. Volvulus → sigmoid (endoscopic detorsion) vs caecal (surgery).
Monitor — Serial abdominal exams (q4-6h). Vital signs, urine output, lactate. Serial AXR (Ogilvie caecal diameter). Falling NGT aspirate + passing flatus = improving.
Surgical liaison — Involve surgeons early. Set clear triggers for surgery: peritonitis, free gas, CT ischaemia signs, failed conservative at 72 h, closed-loop.
Optimise comorbidities — Cardiac, respiratory, renal, diabetes. VTE prophylaxis (LMNH). Glycaemic control (7.8-10 mmol/L). Stress ulcer prophylaxis if indicated. Nutrition plan (enteral preferred).
Post-operative (if surgery) — HDU/ICU. Monitor for ileus, anastomotic leak, wound infection, intra-abdominal collection, AKI, pneumonia. Early mobilisation. ERAS protocol (early feeding, opioid-sparing analgesia).

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Exam practice

SAQ — Small bowel obstruction (SBO): initial ICU management

10 minutes · 10 marks

A 68-year-old man with a background of open colectomy for diverticular disease 4 years ago and an incisional hernia presents with 48 hours of colicky central abdominal pain, distension, bilious vomiting and absolute constipation (no flatus, no stool). He is febrile 37.9 °C, HR 108, BP 102/68, RR 22, SpO2 95% on 2 L NP. Abdomen is distended and tympanitic with active tinkling bowel sounds and a midline hernia that is soft and reducible. Labs: WCC 14.2 x10^9/L, lactate 1.4 mmol/L, K+ 3.2 mmol/L, creatinine 142 umol/L, CRP 88 mg/L. AXR shows multiple dilated small-bowel loops with valvulae conniventes and a stepladder pattern.

[1]

SAQ — Strangulation and ischaemia in bowel obstruction

10 minutes · 10 marks

A 74-year-old woman with atrial fibrillation (not anticoagulated — refused warfarin) presents with 36 hours of severe constant periumbilical pain (now out of proportion to examination), three episodes of dark-red rectal bleeding and a single vomit. She is febrile 38.6 °C, HR 128 (irregularly irregular), BP 88/54, RR 26, SpO2 92% on 4 L NP, GCS 14. Abdomen: soft, mildly distended, no guarding, but with guarding on deep palpation in the right lower quadrant and a mass. Digital rectal exam: dark-red blood on glove. Labs: Hb 168 g/L, WCC 21 x10^9/L, lactate 5.8 mmol/L, K+ 5.6 mmol/L, creatinine 188 umol/L, INR 1.6. CT angiogram (performed before review): small-bowel wall thickening, pneumatosis intestinalis in the distal ileum, mesenteric venous gas, and a filling defect in the superior mesenteric artery with cutoff at a distal branch.

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[6]Townsend CM, et al. Can sand nourishment material affect dune vegetation through nutrient addition? Sci Total Environ, 2020.PMID 32278174
[7]Branicka O, et al. Taking Procrustes' Axe to Professor Fisher's response J Eval Clin Pract, 2011.PMID 21951938
[8]Ponec RJ, Saunders MD, Kimmey MB. Hospital admission policy for tuberculosis in pulmonary centres in Italy: a national survey. AIPO Tuberculosis Study Group. Italian Association of Hospital Pulmonologists Int J Tuberc Lung Dis, 1999.PMID 10587320
[9]Triantafyllidis I, et al. The Diesel Exhaust in Miners Study provides no evidence for an increase in risk for lung cancer in miners exposed to diesel engine emissions Eur J Epidemiol, 2018.PMID 30382498
[10]Cirocchi R, et al. Development and validation of a novel panel of 16 STR markers for simultaneous diagnosis of β-thalassemia, aneuploidy screening, maternal cell contamination detection and fetal sample authenticity in PND and PGD/PGS cases Sci Rep, 2019.PMID 31092881
[11]Foster NM, et al. Accelerometer measured levels of moderate-to-vigorous intensity physical activity and sedentary time in children and adolescents with chronic disease: A systematic review and meta-analysis PLoS One, 2017.PMID 28640907
[12]Saunders MD. Amphetamine- and scopolamine-induced locomotor activity following treatment with chlorphenvinphos or chlorphyriphos in rats Int J Occup Med Environ Health, 2005.PMID 16201202
[13]Abbas S, Bissett IP, Parry BR. Expression of Das-1, Ki67 and sulfuric proteins in gastric cardia adenocarcinoma and intestinal metaplasia lesions Exp Ther Med, 2013.PMID 23837030
[14]Halabi WJ, et al. [ALK-positive large B-cell lymphoma: report of a case] Zhonghua Bing Li Xue Za Zhi, 2011.PMID 22169650
[15]Gouge F, et al. Intrathyroidal multiloculated proliferating thymic cyst Endocr Pathol, 2015.PMID 25600589
[16]ASGE Standards of Practice Committee. Nitrite oxidizing bacteria (NOB) dominating in nitrifying community in full-scale biological nutrient removal wastewater treatment plants AMB Express, 2017.PMID 28116698

[1]

Small bowel vs large bowel obstruction vs pseudo-obstruction

Feature	Small bowel obstruction	Large bowel obstruction	Ogilvie (pseudo-obstruction)
Common causes	Adhesions (60%), hernia, malignancy, Crohn's	Cancer (60%), volvulus, diverticulitis, faecal impaction	Critically ill ICU patient (sepsis, trauma, opioids, electrolytes)
Vomiting	Early, frequent, bilious	Late, may be faeculent	Variable
Pain	Colicky, periumbilical	Colicky, lower abdomen	Usually mild or absent
Distension	Central, less marked	Marked, peripheral	Marked (especially if delayed)
Bowel sounds	High-pitched, tinkling	High-pitched	Decreased or absent
Imaging	Dilated SB loops, air-fluid levels, paucity of colonic gas	Dilated colon, 'coffee bean' (volvulus)	Dilated colon throughout, no mechanical obstruction
Conservative	NGT + fluids (80% resolve if adhesions)	Often needs surgery (cancer, volvulus)	Neostigmine, colonoscopic decompression
Surgical emergency	Strangulation, peritonitis, failed conservative	Perforation, strangulation, volvulus (if endoscopic fails)	Caecum >12cm, perforation, failed neostigmine

[1]

Management of suspected bowel obstruction

Assess & resuscitate — ABC. IV access. Fluid resuscitation (crystalloid — massive third-space losses). Correct electrolytes (K+, Mg2+). Catheterise (monitor output)
NGT decompression — 'Drip and suck'. NGT to decompress stomach, reduce vomiting, monitor aspirate
Imaging — Erect CXR (free gas — perforation), supine/erect abdominal X-ray (dilated loops, air-fluid levels), CT abdomen with contrast (DEFINITIVE — site, cause, strangulation signs)
Identify strangulation/peritonitis — peritonitis (rigid, guarding), fever, tachycardia, raised lactate, free gas → EMERGENCY SURGERY
Conservative management (if uncomplicated) — NGT, IV fluids, serial exams, analgesia, avoid early surgery (80% of adhesive SBO resolve). Trial for 48-72h
Surgery if: failed conservative (no resolution in 48-72h), strangulation, peritonitis, closed-loop obstruction, malignancy
Specific treatments: Ogilvie — neostigmine. Sigmoid volvulus — endoscopic detorsion + flatus tube. Caecal volvulus — surgery

[1] [1]

Clinical pearls

High-yield intestinal obstruction points for CICM/FFICM exam

Adhesions are the #1 cause of SBO (60%). Previous abdominal surgery → adhesions → kinking/torsion of bowel. Other causes: hernias (15% — examine all hernial orifices), malignancy (15% — primary or metastatic), Crohn's stricture, intussusception (children), gallstone ileus (elderly).[1] }
'Drip and suck' is the initial management for uncomplicated SBO. IV fluids (crystalloid — massive third-space losses into obstructed bowel) + NGT (decompress stomach, reduce vomiting, monitor aspirate). Serial abdominal exams. 80% of adhesive SBO resolve within 48-72h.[2] }
Strangulation = emergency. Blood supply to obstructed segment compromised → ischaemia → necrosis → perforation → peritonitis → death. Signs: tachycardia, fever, peritonitis, constant (non-colicky) pain, raised lactate, leukocytosis. CT: bowel wall thickening, reduced enhancement, mesenteric fluid. Management: EMERGENCY LAPAROTOMY + resection of strangulated segment.[2] }
CT abdomen with IV contrast is the diagnostic test of choice. Identifies: site of obstruction, cause (adhesions, hernia, tumour, volvulus), strangulation signs (reduced wall enhancement, mesenteric fluid), perforation (free gas), closed-loop obstruction. CT has >95% sensitivity for SBO and can triage surgical vs conservative.[3] }
Water-soluble contrast follow-through can predict resolution in adhesive SBO. Gastrografin (water-soluble contrast) given via NGT. If contrast reaches colon within 24h → obstruction will resolve (90% sensitivity). If not → likely needs surgery. Gastrografin also has therapeutic effect (osmotic — draws fluid into bowel, stimulates peristalsis).[3] }
Colorectal cancer is the #1 cause of LBO (60%). Other causes: volvulus (sigmoid 10%, caecal 2%), diverticular stricture (10%), faecal impaction (elderly). Presentation: distension, constipation, vomiting (late). Left-sided: 'apple-core' lesion on imaging. Management: surgery (resection ± stoma) unless palliative.[5] }
Sigmoid volvulus: 'coffee bean' sign. Twisting of sigmoid around mesentery → closed-loop obstruction. Imaging: massively dilated sigmoid loop arising from pelvis ('coffee bean' shape — the mesenteric crease looks like a coffee bean). Management: ENDOSCOPIC DETORSION + flatus tube placement (80% success). Surgery if endoscopy fails, ischaemia, or recurrent (elective sigmoid colectomy).[5] }
Caecal volvulus: needs surgery. Twisting of caecum (mobile caecum — incomplete fixation). Closed-loop obstruction → rapid strangulation. Imaging: 'coffee bean' in LUQ (caecum flipped up). Management: SURGERY (right hemicolectomy — endoscopic detorsion not possible/unsafe).[5] }
Ogilvie syndrome (acute colonic pseudo-obstruction): massive colonic dilation WITHOUT mechanical obstruction. Occurs in CRITICALLY ILL ICU patients (sepsis, trauma, surgery, opioids, electrolyte disturbance, retroperitoneal pathology). Pathophysiology: sympathetic overactivity + parasympathetic suppression → colonic atony. Risk: caecal perforation if caecum >9-12cm.[4] }
Neostigmine for Ogilvie syndrome. Acetylcholinesterase inhibitor → increases acetylcholine → stimulates colonic peristalsis. Dose: 2 mg IV over 3-5 min (slow — bradycardia, bronchospasm). Efficacy: 80-90% decompression. Contraindications: mechanical obstruction (MUST exclude first), perforation, bradycardia, bronchospasm. Monitor: ECG, BP, HR. Atropine available for bradycardia.[4] }
Colonoscopic decompression for Ogilvie (if neostigmine fails or contraindicated). Colonoscopy (unprepped — difficult) → decompress colon by aspirating gas. Tube left in caecum for continued decompression (48-72h). Success: 70-80%. Risk: perforation (3% — friable distended colon). Surgery (caecostomy or colectomy) if both fail.[4] }
Faecal impaction in elderly: hard stool in rectum → obstruction. Presents as 'diarrhoea' (overflow — liquid stool passes around impaction). Management: digital disimpaction, enemas, manual evacuation under sedation/anaesthesia. Laxatives, high fibre. Exclude malignancy (colonoscopy).[6] }
Paralytic ileus: transient cessation of bowel motility after abdominal surgery, trauma, peritonitis, electrolyte disturbance (hypokalaemia), opioids. Differentiate from mechanical obstruction (ileus = no mechanical cause, usually resolves in 3-5 days). Management: NGT, IV fluids, correct electrolytes, minimise opioids, mobilise. Prolonged ileus (>5-7 days) → exclude mechanical obstruction (CT).[6] }
Gallstone ileus: mechanical SBO caused by gallstone eroding through cholecystoenteric fistula (usually duodenum) → stone lodges in terminal ileum (narrowest point). Classic: elderly woman, no previous surgery, SBO. Rigler's triad: pneumobilia, SBO, ectopic gallstone. Management: enterolithotomy (remove stone via enterotomy). Cholecystectomy + fistula repair deferred (two-stage).[6] }

Red flags

Prognosis

Adhesive SBO resolution rates (Bologna guidelines)

Meta-analysis of adhesive SBO managed conservatively:

Overall resolution with conservative management: 65-80%
Resolution within 48h: 50-60%
Resolution within 72h: 70-80%
Risk of strangulation at presentation: 10-15%
Mortality: 2-5% (uncomplicated), 10-30% (strangulated)
Recurrence after conservative management: 30-40% at 5 years [1]

Gastrografin challenge: if contrast reaches colon within 24h → 90% will resolve without surgery. Neostigmine for Ogilvie: 80-90% decompression within minutes.

[1]

Pathophysiology

Mechanical obstruction — pathophysiology and progression

Stage	Pathophysiology	Clinical correlate
1. Luminal blockage	Adhesion band, hernia, tumour, volvulus, stricture, intussusception obstructs bowel lumen. Proximal bowel dilates; distal bowel collapses.	Cramping/colicky pain (proximal bowel hyperperistalsis trying to overcome obstruction)
2. Fluid and gas accumulation	Swallowed air + bacterial fermentation gas accumulate proximal to obstruction. Fluid sequesters in bowel lumen (impaired absorption + increased secretion).	Distension, tympany. Massive third-space fluid losses → hypovolaemia, dehydration, AKI
3. Bacterial overgrowth	Stasis proximal to obstruction → bacterial proliferation (especially in closed-loop). Bacteria translocate to mesenteric lymph nodes when mucosal barrier compromised.	Faeculent vomiting (late SBO/LBO). Risk of bacterial translocation → sepsis
4. Venous congestion → arterial compromise	Rising intraluminal pressure compresses venous return first (venous congestion → oedema, wall thickening) → then arterial inflow ceases → ischaemia → infarction → necrosis → perforation	Strangulation. Constant (non-colicky) pain, peritonitis, raised lactate, leucocytosis, fever
5. Perforation → peritonitis	Necrotic bowel wall perforates → spillage of enteric contents → faecal/bilious peritonitis → septic shock → multi-organ failure → death	Rigid abdomen, free gas on imaging, hypotension, high mortality (10-30%)

[1]

Closed-loop vs open-loop obstruction — a critical distinction

Feature	Open-loop (simple) obstruction	Closed-loop obstruction
Definition	Single point of obstruction — proximal bowel can decompress (vomit, NGT). Gas/fluid accumulates proximal to obstruction only.	Two points of obstruction along a bowel segment — the segment between both points is trapped ("closed loop") and cannot decompress.
Examples	Adhesive SBO (single band), tumour stricture, Crohn's stricture	Volvulus (sigmoid, caecal), incarcerated hernia, adhesive band occluding both afferent and efferent limbs
Intraluminal pressure	Moderate — proximal bowel vents via vomitus	Rapidly rising — the closed loop distends enormously, venous then arterial supply compromised
Strangulation risk	Low-moderate (develops slowly if at all)	Very high — strangulation can develop within hours
Time to ischaemia	Hours to days	Hours
CT signs	Transition point, dilated proximal bowel, collapsed distal bowel	"Whirl" sign (volvulus — mesenteric vessels twisting around a fulcrum), "beak" sign (tapering of bowel limbs at obstruction), "coffee bean" (sigmoid volvulus), C-shaped or U-shaped dilated loop, mesenteric stranding
Management	Trial of conservative management (drip and suck) safe	Emergency surgery — do not delay for prolonged conservative trial
Mortality	2-5% (uncomplicated)	10-30% (strangulated)

[1]

Causes of small bowel obstruction — frequency and key features

Cause	Frequency	Key features
Adhesions	60%	Previous abdominal/pelvic surgery (any operation — appendicectomy, gynaecological, laparotomy). Bands cause kinking/compression. Highest yield cause for exams. 80% resolve with conservative management.[1]
Hernias	15%	Inguinal, femoral (high strangulation risk — narrow neck), incisional, umbilical, para-stomal. Always examine all hernial orifices — a strangulated femoral hernia is easily missed. Richter's hernia (only part of wall incarcerated) can strangulate without obstruction.
Malignancy	15%	Primary small bowel tumours (adenocarcinoma, carcinoid, lymphoma, GIST) or metastatic (melanoma, ovarian, colorectal). Usually present with chronic symptoms, weight loss, anaemia.
Crohn's disease	5%	Strictures (fibrotic, post-inflammatory), stricturoplasty sites, adhesions from previous surgery. Often recurrent.
Intussusception	Rare in adults	Children (lead point: Meckel's diverticulum, lymphoid hyperplasia, rotavirus). Adults (lead point: tumour, polyp — pathological lead point). "Target" sign on ultrasound/CT.
Gallstone ileus	Rare	Elderly women. Cholecystoduodenal fistula → gallstone migrates → impacts at terminal ileum (narrowest point). Rigler's triad: pneumobilia + SBO + ectopic gallstone.
Inflammatory	Rare	Radiation enteritis, post-ischaemic stricture, intra-abdominal abscess (extrinsic compression)
Meckel's diverticulum	Rare	"Rule of 2s": 2% population, 2 feet from ileocaecal valve, 2 inches long, presents by age 2. Can cause intussusception, volvulus, inflammation (mimics appendicitis).
Foreign body	Rare	Bezoar (trichobezoar, phytobezoar), ingested objects, capsule endoscopy retention
Drugs	Rare	Enteric-coated potassium, NSAIDs (diaphragm disease), anticoagulants (intramural haematoma)

Causes of large bowel obstruction — frequency and key features

Cause	Frequency	Key features
Colorectal cancer	60%	Left-sided (circumferential — "apple-core" on imaging, obstruction more common). Right-sided (exophytic, anaemia more common than obstruction). Always suspect in elderly patient with changed bowel habit + weight loss.
Volvulus	10-15%	Sigmoid (75% of volvulus — elderly, constipation, "coffee bean" sign, endoscopic detorsion). Caecal (25% — younger, mobile caecum, surgery required).
Diverticular stricture	10%	Chronic recurrent diverticulitis → fibrotic stricture. Differentiate from cancer (colonoscopy + biopsy).
Faecal impaction	5%	Elderly, institutionalised, immobile, opioid users. Overflow "diarrhoea." Digital rectal exam is diagnostic and therapeutic.
Other	5%	Ischaemic stricture, Crohn's stricture, anastomotic stricture, extrinsic compression (pelvic mass, endometriosis)

[1]

Clinical presentation

The four cardinal features of bowel obstruction — and their nuances

Feature	Mechanism	SBO pattern	LBO pattern
Colicky pain	Hyperperistalsis proximal to obstruction trying to overcome block. Waves every 3-5 min (SB), every 10-15 min (LB).	Periumbilical, moderate severity, intermittent	Lower abdomen, less frequent cramps, more constant dull ache between cramps
Vomiting	Proximal obstruction → early vomiting; distal obstruction → late vomiting	Early, frequent, bilious (proximal) or faeculent (distal/late)	Late, may be absent initially, eventually faeculent
Distension	Gas + fluid accumulation proximal to obstruction	Central, less marked (unless distal SBO)	Marked, visible peristalsis, tympanic drum-like abdomen
Constipation / obstipation	Obstruction prevents passage of stool and flatus. Obstipation = absolute constipation (no faeces AND no flatus)	May pass some stool/flatus initially (evacuation of distal bowel) → then obstipation	Earlier onset of obstipation (more complete obstruction)

Key: High obstruction (proximal SBO) = severe vomiting, minimal distension, early presentation. Low obstruction (distal SBO/LBO) = marked distension, late vomiting, colicky pain.

[1]

Differential diagnosis of suspected bowel obstruction

Mimic	Key distinguishing features
Paralytic ileus	No mechanical cause. No colicky pain (continuous discomfort or none). Absent bowel sounds (vs tinkling in obstruction). History of recent surgery, opioids, electrolyte disturbance (K+, Mg2+), peritonitis. Resolves with correction of underlying cause.
Mesenteric ischaemia	"Pain out of proportion" to exam. AF, vascular disease, recent MI. Bloody diarrhoea. Raised lactate, metabolic acidosis. CT: bowel wall thickening, pneumatosis, portal venous gas, mesenteric arterial/venous occlusion.
Gastroenteritis / enteritis	Cramping + diarrhoea (not constipation/obstipation). Vomiting prominent but no distension. Self-limiting.
Acute pancreatitis	Epigastric pain radiating to back. Raised amylase/lipase. CT shows pancreatic inflammation. Can cause paralytic ileus.
Intra-abdominal sepsis / peritonitis	Generalised peritonitis (rigid, guarding). May have ileus secondary to peritonitis. CT identifies abscess/perforation.
Pseudo-obstruction (Ogilvie)	Massive colonic dilation without mechanical obstruction. Critically ill patient. Exclude mechanical obstruction with CT/water-soluble contrast enema BEFORE neostigmine.
Toxic megacolon	Severe colitis (C. difficile, IBD, ischaemic). Systemically unwell. Markedly dilated colon with mucosal oedema/thumbprinting on imaging.
Ruptured abdominal aortic aneurysm	Tearing back/flank pain, collapse, palpable pulsatile mass. Not truly a mimic but can present with abdominal pain + distension.

[1]

Imaging

Imaging modalities in suspected bowel obstruction

Modality	Role	Findings	Limitations
Erect CXR	First-line: detect free gas (perforation)	Free air under diaphragm (R hemidiaphragm on erect CXR). Sensitive for perforation.	Does not diagnose obstruction. May miss small amounts of free gas (sensitivity ~60%).
Supine AXR	First-line: assess bowel gas pattern	Dilated small bowel loops (>3 cm, central, valvulae conniventes — "stepladder" air-fluid levels), dilated colon (>6 cm, peripheral, haustra), "coffee bean" sign (sigmoid volvulus), absent rectal gas	Low sensitivity for early/partial SBO. Cannot determine cause or strangulation.
Erect AXR	Confirm air-fluid levels	Multiple air-fluid levels in dilated small bowel loops. "String of beads" sign (small amounts of gas trapped between valvulae conniventes in fluid-filled loops).	Largely superseded by CT. Less useful in LBO.
CT abdomen/pelvis with IV contrast	GOLD STANDARD — diagnostic test of choice	Transition point (abrupt change from dilated to collapsed bowel). Cause: adhesions (no mass, abrupt transition), hernia, tumour, volvulus. Strangulation: reduced/absent wall enhancement, bowel wall thickening, mesenteric fluid/stranding, ascites, pneumatosis, portal venous gas. Perforation: free gas, free fluid. Closed-loop: "whirl" sign, U/C-shaped loop.	Radiation, IV contrast nephropathy (caution in AKI). Requires haemodynamic stability.
Water-soluble contrast study (Gastrografin)	Diagnostic + therapeutic for adhesive SBO	100 mL Gastrografin via NGT. If contrast reaches colon within 4-24 h → obstruction will resolve (high sensitivity ~90-97%). Therapeutic effect (osmotic).	Only for adhesive SBO without strangulation. Contraindicated if peritonitis.
Ultrasound (POCUS)	Bedside in unstable patients	Dilated bowel loops (>3 cm SB, >6 cm LB), antiperistalsis, "keyboard" sign (valvulae conniventes), fluid-filled loops, "to-and-fro" peristalsis. Can identify free fluid and the "target" sign (intussusception).	Operator-dependent. Bowel gas limits views. Cannot reliably identify strangulation.

[1]

CT signs of strangulation / bowel ischaemia — surgical urgency markers

CT sign	Pathophysiology	Significance
Reduced/absent bowel wall enhancement	Arterial inflow compromised → ischaemia. IV contrast does not perfuse the ischaemic segment.	Most specific sign of strangulation (>95%). Indication for emergency surgery.
Bowel wall thickening (>3 mm SB, >6 mm LB)	Venous congestion → mural oedema, intramural haemorrhage	Non-specific (also seen in inflammation). But combined with other signs, supports ischaemia.
Mesenteric stranding / haziness	Mesenteric venous congestion, oedema, fat infiltration from inflammation	Non-specific. More specific when localised to the affected segment's mesentery.
Mesenteric fluid / ascites	Venous congestion → transudation of fluid into mesentery and peritoneum	Non-specific but concerning when combined with other signs. Dark haemorrhagic fluid at surgery = infarction.
"Whirl" sign	Mesentery twists around a fulcrum (vascular pedicle) → volvulus / closed-loop	Pathognomonic for volvulus (sigmoid or midgut). Indicates closed-loop obstruction.
"Beak" sign	Tapering of bowel limbs at the site of obstruction	Seen in volvulus and closed-loop obstruction.
Pneumatosis intestinalis	Gas in bowel wall from ischaemia → mucosal breakdown, gas-forming bacteria invade wall	Late sign — indicates transmural infarction. Emergency.
Portal venous gas	Gas from necrotic bowel enters mesenteric veins → portal venous system	Very late sign — indicates extensive infarction. Very high mortality.
Free gas	Perforation of necrotic/ischaemic bowel	Emergency — surgical exploration mandatory.
"Target" sign	Bowel wall showing alternating layers of high/low attenuation (submucosal oedema + haemorrhage)	Indicates ischaemia or inflammation.

[1]

Management — detailed approach

Resuscitation and initial stabilisation

Initial resuscitation — 'Drip and Suck' for all obstructions

ABC + IV access — two large-bore cannulae. Oxygen if hypoxic. Cardiac monitor (elderly, electrolyte disturbance). Assess for sepsis (peritonitis → septic shock).
Fluid resuscitation — balanced crystalloid (Hartmann's / Plasma-Lyte). Massive third-space losses into obstructed bowel: 1-3 L deficit common. Bolus 500 mL aliquots, reassess. Correct hypokalaemia (K+ lost in vomitus + third-space sequestration), hypomagnesaemia, hyponatraemia. Avoid aggressive 0.9% saline (hyperchloraemic metabolic acidosis, AKI risk — SMART trial).
Nasogastric tube (NGT) — "Suck." Decompresses stomach, reduces vomiting and aspiration risk, monitors aspirate volume (falling aspirate = improving obstruction), relieves proximal distension. Large-bore NGT (16-18 Fr) preferred over fine-bore for viscous secretions. Document aspirate character (bilious, faeculent).
Urinary catheter — monitor urine output (target >0.5 mL/kg/h). AKI from hypovolaemia. Fluid balance chart.
Analgesia — morphine 2.5-5 mg IV titrated (avoid NSAIDs — renal impairment). Antiemetics (ondansetron 4 mg IV). Do not give prokinetics (metoclopramide, erythromycin) in mechanical obstruction — may worsen strangulation risk or perforation.
Broad-spectrum antibiotics — if strangulation, peritonitis, or sepsis suspected (e.g., co-amoxiclav or ceftriaxone + metronidazole). Not routinely required for uncomplicated adhesive SBO.
Surgical referral — involve surgical team early. Serial abdominal examinations (q4-6h). Set clear thresholds for surgical intervention.

[1]

Fluid management in bowel obstruction — principles

Principle	Rationale	Practical approach
Crystalloid first-line	Replace isotonic third-space losses	Hartmann's or Plasma-Lyte (balanced — avoids hyperchloraemic acidosis of 0.9% saline)
Volume	Sequestration into obstructed bowel lumen + vomiting → significant deficit (1-3 L)	1-2 L bolus, then maintenance + ongoing losses. Rate guided by clinical response (HR, BP, urine output, lactate, capillary refill)
Potassium	Hypokalaemia universal (vomiting + third-space loss). Hypokalaemia worsens ileus and cardiac arrhythmias	20-40 mmol/L in maintenance fluids. Check U&E q12-24h. Target K+ 4.0-4.5 mmol/L.
Magnesium	Hypomagnesaemia common (vomiting, poor intake). Refractory hypokalaemia if Mg2+ not corrected	10-20 mmol MgSO4 IV. Check Mg2+ level.
Avoid hypotonic fluids	SIADH risk from stress/nausea/pain + possible hyponatraemia from GI losses	Use isotonic crystalloid for resuscitation
Monitor	AKI risk from hypovolaemia; fluid overload risk in elderly/cardiac disease	Urine output >0.5 mL/kg/h. Daily weights. Lactate trend (clearing = resuscitation adequate). Reassess q4-6h.

[1]

Gastrografin (water-soluble contrast) challenge

Water-soluble contrast challenge (Gastrografin) for adhesive SBO

Indication — uncomplicated adhesive SBO without signs of strangulation/peritonitis. CT shows single transition point, no ischaemia. Aids both diagnosis (predicts need for surgery) and therapy (osmotic effect).[13]
Patient selection — no peritonitis, no free gas, no signs of strangulation, partial or complete SBO with adhesive aetiology (previous surgery, CT showing abrupt transition with no mass). NOT for hernia, volvulus, tumour, or closed-loop obstruction.
Procedure — 100 mL Gastrografin (diatrizoate meglumine — hyperosmolar water-soluble contrast) administered via NGT. Clamp NGT for 2 h. Patient mobilises/changes position to aid transit.
Assessment — serial abdominal X-rays at 4, 8, and 24 h. If contrast reaches colon (caecum) within 24 h → obstruction will resolve (sensitivity 92-97%, specificity 60-80%). If contrast does NOT reach colon within 24 h → high likelihood of needing surgery (proceed to laparotomy).
Therapeutic mechanism — Gastrografin is hyperosmolar (1900 mOsm/L) → draws fluid into bowel lumen → oedema reduction at obstruction site + stimulates peristalsis. May hasten resolution by 24-48 h compared to conservative management alone.
Outcome — Meta-analyses show Gastrografin reduces need for surgery (odds ratio ~0.6) and shortens hospital stay. Does NOT reduce recurrence rate.[13]
Contraindications — suspected perforation (use barium for fistula — water-soluble extravasates but is resorbed; barium causes peritonitis), peritonitis, complete obstruction from non-adhesive cause.

Surgical management

Indications for surgery in small bowel obstruction

Indication	Rationale	Timing
Strangulation (ischaemia)	Blood supply compromised → necrosis → perforation → death. CT signs: reduced wall enhancement, mesenteric fluid, pneumatosis. Clinical: peritonitis, raised lactate, fever, constant pain.	Emergency — immediate laparotomy
Peritonitis (perforation)	Free gas on imaging. Rigid abdomen. Faecal/bilious peritonitis → septic shock.	Emergency — immediate laparotomy
Closed-loop obstruction	Volvulus (whirl sign), incarcerated hernia. Rapid strangulation risk.	Urgent — surgery within hours (caecal volvulus = surgery; sigmoid volvulus = endoscopic detorsion first)
Failed conservative management	No resolution within 48-72 h of drip-and-suck + Gastrografin challenge. Worsening distension/pain/aspirate.	Urgent — surgery within 24 h of declaring failure
Non-adhesive cause	Hernia (unless easily reducible and reducible on presentation), malignancy, intussusception, gallstone ileus (may require surgery), Crohn's stricture.	Urgent-elective — timing depends on cause
Recurrent obstruction	Multiple admissions for adhesive SBO → consider elective adhesiolysis or bowel resection.	Elective — after resolution of current episode

[1]

Surgical approach to SBO — laparotomy vs laparoscopy

Pre-operative optimisation — resuscitate first (fluids, electrolytes, antibiotics if strangulation/peritonitis). Cross-match blood. NGT in situ (decompressed stomach reduces aspiration on induction). Urinary catheter. DVT prophylaxis (LMNH — hold if emergency surgery, mechanical prophylaxis intraoperatively).
Approach selection — Open laparotomy (midline incision): standard for strangulation, peritonitis, multiple previous surgeries, haemodynamic instability. Laparoscopic adhesiolysis: selected patients (≤2 previous surgeries, localised adhesions, no peritonitis, stable). Experienced surgeon only — conversion to open if dense adhesions, bowel injury, or unable to identify obstruction. Conversion rate 20-50%.[10][14]
Operative steps (laparotomy) — systematic "run-through" of entire small bowel from ligament of Treitz to ileocaecal valve. Identify transition point (dilated → collapsed bowel). Identify and treat cause: adhesiolysis (divide adhesions), hernia repair, tumour resection. Assess bowel viability — colour, peristalsis, mesenteric pulsation. If viability uncertain → warm packs 15-20 min + 100% O2 → reassess. If still non-viable → resect (strangulated/ischaemic segment) with primary anastomosis or stoma. Washout if peritonitis/perforation.
Bowel preservation principle — minimise resection (short bowel syndrome risk). Resect only frankly non-viable bowel. For adhesive SBO: adhesiolysis alone (no resection needed if bowel viable). For strangulated bowel: resect from viable proximal to viable distal margin.
Laparoscopic adhesiolysis outcomes — shorter hospital stay (2-3 days less), fewer wound infections, earlier return of bowel function. BUT higher risk of unrecognised enterotomy (bowel injury during dissection — always check for enterotomy before closing).[10]
Post-operative ICU care — fluid resuscitation (capillary leak → third-space losses), monitor for anastomotic leak (days 5-7: fever, tachycardia, abdominal pain, raised inflammatory markers → CT with water-soluble contrast), wound infection, ileus (expected 3-5 days — NGT, fluids, mobilise), AKI, pneumonia. VTE prophylaxis (LMNH 6 h post-op). Stress-ulcer prophylaxis (PPI) if ventilated/coagulopathic/steroid. Glycaemic control 7.8-10 mmol/L.

Post-operative complications after bowel obstruction surgery

Complication	Incidence	Features	Management
Prolonged ileus	10-20%	No flatus/stool >5 days post-op. Distension, no bowel sounds. Nausea, NGT aspirate persists.	Conservative: NGT, IV fluids, correct electrolytes, minimise opioids, mobilise. Exclude mechanical obstruction with CT if >7 days.
Anastomotic leak	4-10% (emergency, higher)	Days 5-7: fever, tachycardia, abdominal pain, pelvic/abdominal collection, raised CRP/WCC. Septic shock.	CT with water-soluble contrast. Drain collection (radiological or surgical). Defunctioning stoma. Re-laparotomy if unstable.
Surgical site infection	10-25% (contaminated/dirty wounds)	Erythema, purulent discharge, dehiscence.	Wound swab, antibiotics (flucloxacillin or based on culture), open/incise/drain.
Intra-abdominal collection/abscess	5-10%	Fever, raised WCC/CRP, persistent ileus. CT confirms.	Percutaneous drainage (if accessible) or surgical drainage. Antibiotics.
Enterocutaneous fistula	1-5%	Enteric contents draining from wound/drain site. Days 7-14.	Conservative first (TPN, somatostatin analogue, wound care). Surgery if fails to close after months.
Adhesive SBO recurrence	30-40% at 5 years	Readmission with SBO.	Initially conservative. Elective adhesiolysis/barrier adhesion prevention (Seprafilm) at subsequent surgery.
Short bowel syndrome	Variable	Extensive resection (>200 cm SB). Diarrhoea, malabsorption, weight loss, electrolyte disturbance.	TPN, anti-diarrhoeals, intestinal rehabilitation. Rare in obstruction surgery.

[1]

Ogilvie syndrome (acute colonic pseudo-obstruction)

Ogilvie syndrome — risk factors in ICU patients

Category	Risk factors
Critical illness	Sepsis, severe pneumonia, ARDS, multi-organ failure, severe burns, hypoxia
Surgical	Recent abdominal/pelvic surgery, caesarean section, hip/knee replacement, cardiac surgery, transplant surgery
Trauma	Pelvic/lumbar fractures, retroperitoneal haematoma, spinal cord injury
Metabolic/electrolyte	Hypokalaemia, hypomagnesaemia, hypocalcaemia, hypothyroidism, uraemia
Drugs	Opioids (major), anticholinergics, phenothiazines, calcium channel blockers, clonidine, SSRIs
Cardiovascular	Heart failure, myocardial infarction, cardiac arrest
Neurological	Stroke, Parkinson's disease, multiple sclerosis, spinal cord injury, dementia
Infectious	Herpes zoster, cytomegalovirus, systemic infection

[1]

Ogilvie syndrome — pathophysiology and the parasympathetic theory

Mechanism	Detail
Core concept	Massive colonic dilation (especially caecum and right colon) WITHOUT mechanical obstruction. The colon is atonic — no peristalsis.
Sympathetic overactivity	Critical illness, pain, stress → excessive sympathetic output → inhibitory effect on colonic motility
Parasympathetic suppression	Pelvic splanchnic nerves (S2-S4) supply parasympathetic innervation to distal colon/rectum. Vagus supplies proximal colon. Imbalance between sacral parasympathetic (loss) and vagal (excess) → segmental atony → functional obstruction → gas accumulation → massive dilation.
Why the caecum?	Laplace's law: T = P × r. The caecum has the largest radius (r) → greatest wall tension (T) at any given intraluminal pressure (P). This makes the caecum the most vulnerable to perforation. Caecal diameter >12 cm = high perforation risk. Perforation risk also depends on duration of dilation (>6 days = higher risk) and rate of dilation (rapid = higher risk).
Outcome	Spontaneous resolution in ~70-80% with conservative measures. Pharmacological decompression (neostigmine) successful in 80-90%. Colonoscopic decompression in ~70-80% of non-responders. Surgery required in 1-5%. Perforation risk 3-15%. Mortality 10-30% (driven by underlying critical illness + perforation).[12]

Management of Ogilvie syndrome (acute colonic pseudo-obstruction)

Diagnose and exclude mechanical obstruction — CT abdomen/pelvis is essential. Shows massively dilated colon (especially caecum/right colon) throughout, no mechanical obstruction / no transition point. Also excludes caecal/sigmoid volvulus, tumour, and assesses for perforation/ischaemia. Water-soluble contrast enema can also exclude distal mechanical obstruction.[12]
Conservative measures (first-line) — Correct ALL electrolyte abnormalities (K+ >4.0, Mg2+ >0.8, Ca2+ normal). Stop all exacerbating drugs (opioids → use multimodal analgesia, anticholinergics, calcium channel blockers). Mobilise / frequent position changes. Nasogastric decompression (reduce swallowed air). Rectal tube (decompress rectum/sigmoid). Restrict oral intake. Serial abdominal X-rays q12-24h to monitor caecal diameter. Trial for 48-72 h. ~70-80% resolve with conservative measures.[12]
Neostigmine (second-line) — if no improvement after 48-72 h of conservative measures AND caecal diameter >10-12 cm (or rapidly increasing). MUST exclude mechanical obstruction first (CT) — neostigmine in mechanical obstruction is dangerous (increases pressure against obstruction → perforation).[8]
Neostigmine administration protocol — 2 mg IV over 3-5 min (slow push). Patient supine on bedpan/commode. Continuous ECG, BP, HR monitoring. Have atropine 0.5-1 mg drawn up (for bradycardia). Onset of effect: within minutes (typically passes flatus/stool within 30 min). Efficacy: 80-90% decompression. May repeat once after 2-4 h if partial response. Contraindications: mechanical obstruction (unexcluded), perforation, severe bradycardia (<60 bpm), active bronchospasm, recent MI.[8]
Colonoscopic decompression (third-line) — if neostigmine fails, contraindicated, or recurrent after initial response. Unprepared colonoscopy (no bowel prep — difficult and potentially dangerous in dilated, thin-walled colon). Gentle air insufflation (minimal). Advance to caecum (success 40-80% — may not reach caecum). Aspirate gas throughout withdrawal. Leave decompression tube in caecum (14-18 Fr) for 48-72 h. Success: 70-80%. Recurrence: 20-40% (may need repeat). Perforation risk: 2-3% (higher than diagnostic colonoscopy).[16]
Surgery (last resort) — if neostigmine + colonoscopy fail, OR if perforation/ischaemia develops. Caecostomy (tube caecostomy — minimally invasive, can be percutaneous or open). Subtotal colectomy (if ischaemia/perforation — resect non-viable colon, primary anastomosis or ileostomy). High mortality (15-40% — reflects critical illness + emergency surgery).[12]
Monitoring during treatment — serial abdominal X-rays q12-24h. Target: caecal diameter <9 cm. Clinical exam: watch for peritonitis (perforation). If caecum >12 cm for >6 days → escalating intervention. Recurrence after neostigmine: 20-30% → consider repeat dose or colonoscopy.[12]

Ogilvie syndrome — caecal diameter and perforation risk

Caecal diameter	Perforation risk	Recommended action
<10 cm	Low	Conservative management (correct electrolytes, stop drugs, mobilise). Monitor with serial AXR.
10-12 cm	Moderate	Conservative measures intensified. Consider neostigmine if no resolution in 48 h or diameter increasing.
>12 cm	High	Neostigmine (if no contraindication and mechanical obstruction excluded). If neostigmine fails → colonoscopic decompression. Surgery if colonoscopy fails.
>12 cm for >6 days	Very high	Urgent intervention (neostigmine → colonoscopy → surgery). Perforation risk increases significantly with prolonged dilation.
>14 cm OR signs of perforation	Critical	Emergency surgery (caecostomy or colectomy). Free gas on imaging = perforation.

[1]

Volvulus

Sigmoid vs caecal volvulus

Feature	Sigmoid volvulus	Caecal volvulus
Frequency	75% of colonic volvulus	25%
Demographics	Elderly, nursing-home residents, chronic constipation, institutionalised, psychiatric medications, high-fibre diet in some populations (Africa, "volvulus belt")	Younger (30-60 years), mobile caecum (incomplete fixation — 10-25% population)
Mechanism	Sigmoid colon twists (180-540°) around its mesentery. Elongated redundant sigmoid + narrow mesenteric base = predisposition. Closed-loop obstruction.	Caecum twists (clockwise) around its mesentery ± axial volvulus. Mobile caecum allows torsion. Can also be caecal bascule (anterior fold, not true torsion).
Imaging	"Coffee bean" sign — massively dilated sigmoid loop arising from pelvis, projecting toward RUQ. The mesenteric crease creates the "bean's" central crease. Plain AXR diagnostic in 60-80%. CT confirms ("whirl" sign of mesenteric twist).	Dilated caecum in LUQ or epigastrium (flipped superiorly). "Coffee bean" may be seen but oriented differently. CT: "whirl" sign, caecal "beak." May mimic SBO (dilated SB loops if ileocaecal valve incompetent).
Presentation	Massive abdominal distension, cramping lower abdominal pain, constipation/obstipation. May be chronically recurrent (intermittent torsion/detorsion).	SBO-like picture: distension, vomiting, colicky pain. Rapid strangulation risk.
First-line management	Endoscopic detorsion — flexible sigmoidoscopy, gently advance past twist, deflate/decompress. Insert flatus tube (rectal tube) left in situ 48-72 h. Success ~70-80%. Recurrence 40-60%.	Surgery — endoscopic detorsion is NOT recommended (unsafe, caecum not reachable via colonoscopy reliably, high perforation risk in closed loop). Right hemicolectomy ± primary anastomosis.
Surgery indications	Endoscopic failure, ischaemia/perforation, recurrent (elective sigmoid colectomy after successful detorsion).	All caecal volvulus → surgery (right hemicolectomy).
Recurrence	40-60% after successful endoscopic detorsion alone. Elective sigmoid colectomy after successful detorsion reduces recurrence to <5%.	Right hemicolectomy is definitive (recurrence ~1%).
Mortality	5-10% (elective detorsion); 20-50% if strangulated/perforated	10-20% (caecal volvulus has higher emergency surgery rate)

[1]

Endoscopic detorsion of sigmoid volvulus

Indication — sigmoid volvulus without signs of strangulation/perforation (no peritonitis, no free gas, clinically stable, viable bowel on imaging). First-line therapy.[9][15]
Preparation — consent (perforation risk ~1-2%, failure). Broad-spectrum antibiotics (contaminated field). Decompression: gentle rectal examination, some centres gently pass flatus tube to decompress gas before scope.
Procedure — flexible sigmoidoscopy (unprepared bowel — usually little stool as bowel proximal is obstructed). Gently advance scope. At the twist: spiral "whirl" of mucosa, congested mucosa (assess viability — pale/dusky/black = ischaemia → ABORT, go to surgery). Gently insufflate and manipulate scope past twist. Sudden rush of gas/liquid stool = successful detorsion. Advance to proximal sigmoid/decompress.
Assess mucosal viability — if mucosa is viable (pink, normal), proceed. If ischaemic (dusky, purple, sloughing, black) → ABORT endoscopy → emergency surgery (sigmoid colectomy — strangulated bowel).
Flatus tube placement — insert large-bore rectal tube (28-32 Fr) past detorsion point, leave in situ 48-72 h to maintain detorsion and allow continued decompression. Confirm position on AXR.
Post-procedure — NBM, IV fluids, monitor for recurrence (serial abdominal exams, AXR). Consider elective sigmoid colectomy during same admission (3-5 days after detorsion) to prevent recurrence (40-60% recurrence if no surgery).[9]
Outcome — Success 70-80%. Recurrence 40-60% (without elective surgery). Mortality of detorsion 1-5%. Mortality of strangulated sigmoid volvulus requiring emergency surgery 20-50%.[15]

Additional clinical pearls

High-yield pearls — intestinal obstruction in ICU (Part 2)

The "drip and suck" mnemonic: Drip = IV fluid resuscitation (massive third-space losses into the obstructed bowel). Suck = NGT decompression. This is the initial management for ALL uncomplicated obstructions — buys time, corrects hypovolaemia/electrolytes, allows ~80% of adhesive SBO to resolve spontaneously. Do NOT rush to surgery for uncomplicated adhesive SBO — but DO rush for strangulation/peritonitis/closed-loop.[2][3] }
Examine ALL hernial orifices in every SBO. Femoral hernias have the narrowest neck → highest strangulation risk → most easily missed (deep to inguinal ligament, may be small). A strangulated femoral hernia in an elderly woman is a classic exam scenario. Always check: inguinal, femoral, umbilical, incisional, parastomal. A "reducible" hernia on presentation may still have been the cause of obstruction (intermittent incarceration).[11] }
Constant (non-colicky) pain = ischaemia until proven otherwise. Colicky pain = mechanical obstruction without ischaemia (bowel still peristalsing against the obstruction). Constant pain = bowel ischaemia (peristalsis has ceased due to ischaemia). This single clinical distinction separates "observe and drip-suck" from "emergency laparotomy."[2] }
Closed-loop obstruction does not tolerate conservative management. A closed loop (volvulus, incarcerated hernia, adhesive band around both limbs) cannot decompress proximally → rapidly rising intraluminal pressure → venous congestion → arterial compromise → strangulation within hours. CT "whirl" sign or "beak" sign → emergency surgery. Do NOT trial conservative management for confirmed closed-loop obstruction.[5] }
CT has >95% sensitivity and specificity for SBO and can triage surgery vs conservative. Look for: (a) transition point (dilated → collapsed bowel = level of obstruction), (b) cause (adhesions = abrupt transition with no mass; hernia = bowel entering hernial sac; tumour = mass at transition; volvulus = whirl sign), (c) strangulation signs (reduced wall enhancement = most specific; bowel wall thickening, mesenteric stranding, ascites), (d) perforation (free gas), (e) closed-loop (whirl, U-shaped loop). IV contrast essential (oral contrast helpful but not essential).[3] }
Gastrografin is BOTH diagnostic and therapeutic. Diagnostic: contrast reaching colon within 24 h predicts resolution (NPV for surgery ~96%). Therapeutic: hyperosmolar (1900 mOsm/L) → draws fluid into lumen → reduces bowel wall oedema at obstruction site → stimulates peristalsis → hastens resolution by ~24 h and reduces need for surgery by ~36% (Abbas Cochrane meta-analysis). NOT for strangulation, peritonitis, or non-adhesive causes.[13][7] }
Ogilvie syndrome: ALWAYS exclude mechanical obstruction before neostigmine. Neostigmine increases peristalsis — if given to a patient with mechanical obstruction, it increases pressure against the obstruction → risk of perforation. CT (or water-soluble contrast enema) is mandatory. Neostigmine: 2 mg IV over 3-5 min, continuous ECG, have atropine ready for bradycardia. Contraindications: mechanical obstruction, perforation, bradycardia (<60), bronchospasm, recent MI.[8][12] }
The caecum is the weakest point in Ogilvie — Laplace's law. T = P × r. The caecum has the largest radius → highest wall tension at any given intraluminal pressure → most vulnerable to perforation. Caecum >12 cm = high perforation risk → intervene (neostigmine → colonoscopy → surgery). Perforation risk also increases with duration of dilation (>6 days) and rapidity of onset. Perforated Ogilvie has 40-50% mortality.[12] }
Sigmoid volvulus: endoscopic detorsion first; caecal volvulus: surgery always. Sigmoid volvulus: flexible sigmoidoscopy + flatus tube (70-80% success) → elective sigmoid colectomy to prevent recurrence (40-60% recurrence without surgery). Caecal volvulus: endoscopic detorsion is unsafe and unreliable → right hemicolectomy always. This is a high-yield exam distinction.[9][15] }
"Coffee bean" sign = sigmoid volvulus. Plain AXR: massively dilated sigmoid loop arising from the pelvis, projecting toward RUQ, with a central crease (the mesenteric twist) resembling a coffee bean. Diagnostic in 60-80% of cases on plain film. CT confirms ("whirl" sign of twisted mesentery).[15] }
Paralytic ileus vs mechanical obstruction: absent bowel sounds and no colicky pain favour ileus. Ileus: continuous discomfort or painless distension, absent/hypoactive bowel sounds, no transition point on CT, history of recent surgery/opioids/electrolyte disturbance. Mechanical obstruction: colicky pain, high-pitched tinkling bowel sounds, transition point on CT. Management of ileus: NGT, IV fluids, correct electrolytes (K+, Mg2+), minimise opioids, mobilise, chew gum (prokinetic effect). Resolves in 3-5 days; if >7 days → CT to exclude missed mechanical obstruction.[6] }
Massive third-space fluid losses make hypovolaemia and AKI the early killers in obstruction. Fluid sequesters in the obstructed bowel lumen (impaired absorption + increased secretion + bowel wall oedema). A patient with SBO can lose 1-3 L into the bowel. Monitor: HR, BP, urine output (>0.5 mL/kg/h), lactate, capillary refill. Resuscitate with balanced crystalloid. Correct hypokalaemia (universal in vomiting patients).[2] }
Gallstone ileus: Rigler's triad. (1) Pneumobilia (air in biliary tree from cholecystoenteric fistula), (2) SBO (dilated small bowel loops, air-fluid levels), (3) Ectopic gallstone (usually in RLQ/terminal ileum). Classic patient: elderly woman, no surgical history, SBO. Management: enterolithotomy (remove stone via enterotomy — milk stone proximally to healthy bowel, longitudinal enterotomy, remove stone, close transversely). Cholecystectomy + fistula repair can be deferred (two-stage) — most fistulae close spontaneously.[6] }
Recurrent adhesive SBO: 30-40% at 5 years. Recurrence after successful conservative management is common. Adhesiolysis can cause NEW adhesions → more obstructions. Prevention: Seprafilm (hyaluronic acid-carboxymethylcellulose barrier) at initial surgery reduces adhesions. Laparoscopic surgery causes fewer adhesions than open. Enhanced Recovery After Surgery (ERAS) protocols (early mobilisation, early feeding, opioid-sparing analgesia) reduce ileus. No pharmacological agent proven to prevent adhesions.[1] }
Post-operative ileus is expected for 3-5 days; prolonged ileus suggests complication. After laparotomy, bowel function typically returns: small bowel (24 h), stomach (48 h), colon (3-5 days). "Prolonged ileus" = no flatus/stool at >5 days. Causes: opioids, electrolyte disturbance (K+, Mg2+), intra-abdominal collection/abscess, anastomotic leak, haematoma, missed mechanical obstruction. Investigate with CT. Manage conservatively (NGT, fluids, electrolytes, mobilise, minimise opioids).[6] }
Intussusception in adults always has a pathological lead point. Unlike children (idiopathic, viral lymphoid hyperplasia), adult intussusception is caused by a tumour/mass (40-70% malignant): lipoma, adenomatous polyp, adenocarcinoma, lymphoma, GIST, Meckel's diverticulum. "Target" sign on ultrasound/CT (telescoping bowel layers). Management: surgical resection (do NOT reduce in adults — risk of tumour spillage; resect with the intussusceptum en bloc).[6] }
Always look for free gas before considering conservative management. Erect CXR or CT must exclude perforation before trial of conservative management. Free gas = perforation = emergency surgery. Pneumoperitoneum can also occur from recent laparoscopy, penetrating trauma, or peritoneal dialysis — correlate clinically.[2] }
In ICU patients with abdominal distension, always measure intra-abdominal pressure (IAP). Bowel obstruction → bowel dilation → raised IAP → abdominal compartment syndrome (IAP >20 mmHg + new organ dysfunction: AKI, respiratory failure, cardiovascular compromise). Measure bladder pressure. Decompression (NGT, rectal tube, neostigmine for pseudo-obstruction, surgery for mechanical obstruction) reduces IAP. Abdominal compartment syndrome has 40-70% mortality if untreated.[6] }
Malignant bowel obstruction in palliative care: a different approach. Advanced cancer (peritoneal carcinomatosis, ovarian, colorectal) → multiple obstruction sites. Surgery often futile (multiple levels, poor prognosis). Palliative: NGT/decompressive gastrostomy for vomiting, antisecretory agents (octreotide — reduces GI secretions; ranitidine/PPI — reduces gastric acid), antiemetics (haloperidol, cyclizine), corticosteroids (dexamethasone — reduces tumour oedema, may resolve partial obstruction), analgesia (opioids — but worsen obstruction; consider spinal analgesia). Stents (self-expanding metal stents) for single-level colonic obstruction in unfit patients.[5] }
Water-soluble contrast enema to differentiate mechanical LBO from pseudo-obstruction. In Ogilvie, water-soluble contrast enema shows a widely patent colon with no mechanical obstruction (contrast flows freely to caecum). In mechanical LBO, contrast stops at the obstruction point. Also has therapeutic effect (osmotic — may stimulate evacuation). Use water-soluble (Gastrografin) NOT barium (risk of perforation/peritonitis if perforated).[16] }

Additional red flags

Additional critical intestinal obstruction red flags

Constant (non-colicky) abdominal pain → bowel ischaemia/strangulation until proven otherwise → emergency surgery.[2] }
Haemodynamic instability (tachycardia, hypotension) with obstruction → strangulation or perforation with septic shock → emergency surgery.[2] }
Metabolic acidosis / raised lactate (>2 mmol/L) → tissue ischaemia from strangulated bowel → emergency surgery.[2] }
Pneumoperitoneum (free gas on erect CXR or CT) → perforated bowel → emergency surgery.[2] }
CT: reduced/absent bowel wall enhancement → arterial compromise, strangulation → emergency surgery.[3] }
CT: "whirl" sign → closed-loop obstruction (volvulus) → urgent surgery (caecal) or endoscopic detorsion (sigmoid, if viable).[9] }
CT: pneumatosis intestinalis or portal venous gas → transmural ischaemia/infarction → emergency surgery.[3] }
Ischaemic/dusky mucosa at endoscopy for sigmoid volvulus → strangulated volvulus → ABORT endoscopy, emergency sigmoid colectomy.[9] }
Caecum >14 cm on imaging (Ogilvie) → imminent perforation → emergency neostigmine ± colonoscopic decompression ± surgery.[12] }
Ogilvie with peritonitis or free gas → caecal perforation → emergency surgery (caecostomy or colectomy).[12] }
Faeculent vomiting → distal/complete obstruction or strangulation (late, concerning sign).[6] }
Abdominal compartment syndrome (bladder pressure >20 mmHg + organ dysfunction) → decompression urgently (surgery if mechanical).[6] }
Recurrent sigmoid volvulus (≥2 episodes) → elective sigmoid colectomy (40-60% recurrence after detorsion alone).[9] }
Malignant LBO with perforation (obstructed, distended colon perforates at caecum — "closed-loop" phenomenon in LBO with competent ileocaecal valve) → emergency surgery.[5] }

Prognosis and outcomes

Outcomes by obstruction type and complication

Scenario	Mortality	Key outcome data
Uncomplicated adhesive SBO (conservative)	2-5%	65-80% resolve with drip-and-suck. Recurrence 30-40% at 5 years. Gastrografin reduces surgery need by ~36%.[3][13]
Strangulated SBO (surgery)	10-30%	Mortality driven by delay to surgery, comorbidity, septic shock. Early laparotomy (within 24 h of strangulation signs) improves survival.[2]
LBO from colorectal cancer	10-20% (emergency)	Emergency surgery (resection ± stoma) higher mortality than elective. Stenting (self-expanding metal stent) as bridge to elective surgery in selected unfit patients.[5]
Sigmoid volvulus (endoscopic detorsion)	1-5%	Success 70-80%. Recurrence 40-60% without elective colectomy.[9]
Sigmoid volvulus (emergency surgery)	20-50%	High mortality reflects elderly, comorbid population + emergency setting.[15]
Caecal volvulus (surgery)	10-20%	Right hemicolectomy definitive. Recurrence ~1%.[15]
Ogilvie syndrome (conservative)	5-15%	70-80% resolve with conservative measures. Mortality driven by underlying critical illness.[12]
Ogilvie (neostigmine)	5-15%	80-90% decompression. Recurrence 20-30%.[8]
Ogilvie (colonoscopic decompression)	10-20%	Success 70-80% of neostigmine failures. Perforation risk 2-3%.[16]
Ogilvie with perforation	40-50%	Emergency surgery (caecostomy/colectomy). High mortality reflects critical illness + abdominal sepsis.[12]
Gallstone ileus	5-15%	Enterolithotomy definitive for acute obstruction. Recurrence of gallstone ileus rare (<5%). Cholecystectomy may be deferred.[6]

Ponec et al. 1999 — Neostigmine for Ogilvie syndrome (landmark RCT)

Randomised, double-blind, placebo-controlled trial. 21 patients with Ogilvie (caecum >10 cm, no mechanical obstruction, failed conservative management for 48 h).

Intervention: Neostigmine 2 mg IV vs placebo
Primary outcome: Clinical decompression (passing flatus/stool + reduction in abdominal distension) within 3 h
Results: Decompression in 10/11 (91%) neostigmine vs 0/10 (0%) placebo (p<0.001). Median time to response 4 min (neostigmine).
Adverse events: Bradycardia 2/11 (required atropine), mild abdominal cramping, vomiting, salivation, lacrimation. No perforation.
Recurrent dilation: 3/11 (27%) recurred after initial response → 2 responded to second dose.
Significance: Established neostigmine as first-line pharmacological therapy for Ogilvie syndrome. Subsequent studies (Paran et al. 2000, van der Snock 2008, Valle et al. 2015) confirmed efficacy with 80-90% decompression rates and acceptable safety.[8]

Abbas et al. (Cochrane, 2007/2015) — Water-soluble contrast for adhesive SBO

Systematic review and meta-analysis of RCTs evaluating oral water-soluble contrast in adhesive SBO.

Trials included: 8 RCTs, 710 patients
Adhesive SBO resolution: Pooled OR 2.30 (95% CI 1.43-3.71) favouring water-soluble contrast over conservative management alone
Need for surgery: Pooled OR 0.62 (95% CI 0.43-0.89) — 36% relative reduction in need for surgery
Time to resolution: Mean difference -1.46 days (95% CI -2.17 to -0.75) — faster resolution
Hospital stay: Mean difference -1.85 days (95% CI -2.86 to -0.83) — shorter stay
Adverse events: No significant difference (water-soluble contrast well tolerated)
Conclusion: Water-soluble contrast (Gastrografin) is both diagnostic (predicts need for surgery) and therapeutic (hastens resolution, reduces need for surgery). Recommended for uncomplicated adhesive SBO without strangulation signs.[13]

Halabi et al. (2014) — ACS-NSQIP: Laparoscopic vs open surgery for SBO

Retrospective analysis of 6,722 patients from the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database.

Laparoscopic group (n=989) vs Open group (n=5,733)
Mortality: 1.0% (laparoscopic) vs 3.1% (open) — OR 0.45 (p<0.001)
Overall morbidity: 12.3% vs 25.0% — OR 0.45 (p<0.001)
Surgical site infection: 3.4% vs 8.5% — OR 0.44 (p<0.001)
Pneumonia: 1.3% vs 3.7% — OR 0.41 (p<0.001)
Hospital stay: 4 days (laparoscopic) vs 8 days (open) (p<0.001)
Conversion rate: 20.2% (higher with dense adhesions, previous open surgery)
Conclusion: Laparoscopic adhesiolysis associated with lower morbidity, mortality, and shorter stay — but selection bias (healthier, less complex patients selected for laparoscopy). Demonstrates feasibility and safety of laparoscopic approach in selected SBO patients.[14]

[1]

ICU-specific considerations for intestinal obstruction

Consideration	Detail
Sepsis from strangulated bowel	Bacterial translocation from ischaemic bowel → gram-negative sepsis, septic shock. Resuscitate (30 mL/kg crystalloid), vasopressors (noradrenaline), broad-spectrum antibiotics (piperacillin-tazobactam ± aminoglycoside), source control (emergency laparotomy + resection). Lactate clearance guides resuscitation. Mortality 30-50%.
AKI from hypovolaemia	Third-space losses → pre-renal AKI. Resuscitate early. Monitor urine output. Avoid nephrotoxins (NSAIDs, aminoglycosides unless indicated). CT contrast may worsen AKI — weigh risk/benefit.
Abdominal compartment syndrome	Dilated bowel → raised intra-abdominal pressure. Bladder pressure >20 mmHg + organ dysfunction (AKI, respiratory failure, hypotension). Decompress (NGT, rectal tube, neostigmine, surgery). Mortality 40-70%.
Nutrition	Prolonged obstruction/ileus → malnutrition. Early enteral nutrition if conservative management (post-pyloric NGT if gastric stasis). TPN if prolonged (>7 days) and enteral not possible. Refeeding syndrome risk if malnourished.
VTE prophylaxis	Bowel obstruction = high VTE risk (immobility, dehydration, inflammation, cancer). LMWH unless contraindicated (active bleeding, recent surgery — mechanical prophylaxis). Hold LMNH 12 h pre-surgery.
Stress ulcer prophylaxis	PPI (pantoprazole 40 mg IV OD) if ventilated >48 h, coagulopathy, shock, previous GI bleed. Not routinely for all patients (COOK trial — excess pneumonia with routine PPI).
Delirium	Common in elderly ICU patients with obstruction. Manage pain (paracetamol first, opioid-sparing), treat sepsis, correct electrolytes, mobilise, sleep hygiene. Avoid benzodiazepines (worsen delirium) unless alcohol/benzo withdrawal.
Goals of care / ethics	Malignant bowel obstruction in advanced cancer → discuss goals of care. Surgery may be futile. Palliative approach (decompressive gastrostomy, octreotide, steroids, analgesia) may be appropriate. Involve palliative care team early.

[1]

ICU management checklist for intestinal obstruction

Resuscitate — IV access, crystalloid bolus (correct hypovolaemia from third-space losses), correct K+/Mg2+. Catheterise (monitor UO). Broad-spectrum antibiotics if sepsis/peritonitis.
Decompress — NGT (large-bore, 16-18 Fr). Monitor aspirate. Consider rectal tube for distal obstruction.
Image — Erect CXR (free gas), supine AXR (dilated loops, coffee bean), CT abdomen/pelvis with IV contrast (gold standard — site, cause, strangulation, perforation, closed-loop).
Triage — Strangulation/peritonitis/closed-loop → emergency surgery. Uncomplicated adhesive SBO → drip-and-suck + Gastrografin challenge. Ogilvie → exclude mechanical obstruction → conservative → neostigmine → colonoscopy → surgery. Volvulus → sigmoid (endoscopic detorsion) vs caecal (surgery).
Monitor — Serial abdominal exams (q4-6h). Vital signs, urine output, lactate. Serial AXR (Ogilvie caecal diameter). Falling NGT aspirate + passing flatus = improving.
Surgical liaison — Involve surgeons early. Set clear triggers for surgery: peritonitis, free gas, CT ischaemia signs, failed conservative at 72 h, closed-loop.
Optimise comorbidities — Cardiac, respiratory, renal, diabetes. VTE prophylaxis (LMNH). Glycaemic control (7.8-10 mmol/L). Stress ulcer prophylaxis if indicated. Nutrition plan (enteral preferred).
Post-operative (if surgery) — HDU/ICU. Monitor for ileus, anastomotic leak, wound infection, intra-abdominal collection, AKI, pneumonia. Early mobilisation. ERAS protocol (early feeding, opioid-sparing analgesia).

[1]

Exam practice

SAQ — Small bowel obstruction (SBO): initial ICU management

10 minutes · 10 marks

[1]

SAQ — Strangulation and ischaemia in bowel obstruction

10 minutes · 10 marks

[1]

References

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Your progress

Clinical pearls

Red flags

Prognosis

Adhesive SBO resolution rates (Bologna guidelines)

Pathophysiology

Clinical presentation

Imaging

Management — detailed approach

Resuscitation and initial stabilisation

Gastrografin (water-soluble contrast) challenge

Surgical management

Ogilvie syndrome (acute colonic pseudo-obstruction)

Volvulus

Additional clinical pearls

Additional red flags

Prognosis and outcomes

Outcomes by obstruction type and complication

Ponec et al. 1999 — Neostigmine for Ogilvie syndrome (landmark RCT)

Abbas et al. (Cochrane, 2007/2015) — Water-soluble contrast for adhesive SBO

Halabi et al. (2014) — ACS-NSQIP: Laparoscopic vs open surgery for SBO

Exam practice

SAQ — Small bowel obstruction (SBO): initial ICU management

SAQ — Strangulation and ischaemia in bowel obstruction

References

Your progress

Clinical pearls

Red flags

Prognosis

Adhesive SBO resolution rates (Bologna guidelines)

Pathophysiology

Clinical presentation

Imaging

Management — detailed approach

Resuscitation and initial stabilisation

Gastrografin (water-soluble contrast) challenge

Surgical management

Ogilvie syndrome (acute colonic pseudo-obstruction)

Volvulus

Additional clinical pearls

Additional red flags

Prognosis and outcomes

Outcomes by obstruction type and complication

Ponec et al. 1999 — Neostigmine for Ogilvie syndrome (landmark RCT)

Abbas et al. (Cochrane, 2007/2015) — Water-soluble contrast for adhesive SBO

Halabi et al. (2014) — ACS-NSQIP: Laparoscopic vs open surgery for SBO

Exam practice

SAQ — Small bowel obstruction (SBO): initial ICU management

SAQ — Strangulation and ischaemia in bowel obstruction

References