Ileus and acute colonic pseudo-obstruction

• Paralytic (adynamic) ileus is the functional slowing or temporary stopping of peristalsis in the absence of a mechanical blockage. Gas and fluid accumulate, the abdomen distends, but there is no transition point.
• Common precipitants are recent abdominal or pelvic surgery, drugs that slow gut motility (opioids, anticholinergics and several centrally acting drugs), depletion of potassium, magnesium or calcium, sepsis, intra-abdominal or retroperitoneal inflammation such as pancreatitis, spinal injury, critical illness, mechanical ventilation and endocrine disease.
• Acute colonic pseudo-obstruction (Ogilvie syndrome) is a functional, acute massive dilation of the colon without mechanical obstruction, usually in a critically ill or recently operated patient. The cecum is the first place to fail, and the risk of perforation becomes high once the cecal diameter is above 12 cm.
• The condition looks like large bowel obstruction: distension, nausea, vomiting, constipation with little or no flatus, reduced or absent bowel sounds. It is often painless or only mildly uncomfortable in paralytic ileus, although Ogilvie syndrome may cause cramping lower abdominal pain.
• Management is stepwise: treat the cause, stop motility-slowing drugs, replace potassium, magnesium and calcium, keep the patient nil by mouth with intravenous fluids, decompress with a nasogastric tube when vomiting occurs, and mobilise early. Postoperative ileus after bowel resection may be accelerated by alvimopan. Ogilvie syndrome is treated conservatively first, then with intravenous neostigmine under cardiac monitoring, then colonoscopic decompression, and with cecostomy or surgery for ischemia or perforation.

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

1. Distinguish paralytic ileus and functional (pseudo-)obstruction from mechanical obstruction, and state what imaging shows in each.
2. List the main surgical, pharmacological, metabolic, infective, inflammatory and systemic causes of ileus.
3. Recognise the presentation of acute colonic pseudo-obstruction (Ogilvie syndrome), including the cecal diameter thresholds at which perforation becomes likely.
4. Plan first-line investigations for suspected ileus, including the roles of plain radiography, CT and water-soluble contrast enema.
5. Outline the conservative, pharmacological, endoscopic and surgical steps in the management of ileus and of Ogilvie syndrome, including neostigmine dosing, monitoring and the role of alvimopan.
6. Explain the practical measures that shorten postoperative ileus, including mobilisation, gum chewing and an accelerated care pathway.
7. Describe the prognosis of paralytic ileus and of Ogilvie syndrome, and adapt investigation and management in low-resource settings.
8. Recognise when an apparently obstructed patient needs emergency laparotomy rather than conservative or endoscopic treatment.

A mechanical obstruction is different: a physical lesion inside, in or around the wall of the bowel blocks the lumen. The distension is confined to bowel proximal to that point, loops often show a transition point on imaging, and surgery is usually definitive. Ileus, by contrast, is a problem of neuromuscular coordination; the bowel is patent, so imaging tends to show gas in both small and large bowel, including the rectum, without a single transition point.

Acute colonic pseudo-obstruction (Ogilvie syndrome, acute colonic pseudo-obstruction, ACPO) is a specific, acute form of functional obstruction in which the colon, and sometimes the distal small bowel, dilates massively without mechanical blockage. It is not a primary colonic disease; it is a systemic disturbance of colonic motility, most often in a patient who is already unwell.^[1] For practical purposes it is treated as a form of ileus confined to, or dominated by, the colon.

Two useful bedside groups are:

• Paralytic ileus proper, usually more diffuse (small and large bowel) and often postoperative.
• Acute colonic pseudo-obstruction, in which the colon is the main dilated organ and the patient is frequently critically ill.

Both share the same first principles of management, but Ogilvie syndrome has its own cecal-diameter thresholds and escalation steps, which is why it is covered separately below.

Ileus is one of the commonest functional problems after abdominal surgery and a frequent complication of serious systemic illness; it prolongs hospital stay and increases cost.^[6]

Acute colonic pseudo-obstruction is uncommon but not rare among hospitalised patients. A large US study estimated an incidence of about 100 cases per 100,000 inpatient admissions.^[1] It most often occurs in the sixth decade of life, with a slight male predominance (about 60% of cases are in men).^[1] Only about 5% of cases are idiopathic; the rest are associated with a recent illness, procedure or surgery.^[1]

Mortality overall is about 15%, and rises to 36 to 44% when intestinal ischemia or perforation complicates the picture.^[1] More recent data suggest mortality as low as 6.4% in 2011, probably reflecting earlier recognition and treatment.^[1]

Ileus is usually an exaggerated intestinal reaction to an insult, most often abdominal or pelvic surgery, that is amplified by other conditions.^[2]

Postoperative ileus is common after intra-abdominal and pelvic operations, and also follows non-abdominal surgery. It affects all segments of the gastrointestinal tract and may last from 5 to 6 days, or longer.^[6] Risk factors include extensive handling of bowel, long operating time, blood loss, opioid analgesia, and poor mobility.

Drugs that inhibit intestinal motility are a leading reversible cause. They include:

• opioids (morphine and other mu-opioid agonists, which are universal in postoperative analgesia);
• anticholinergic and antimuscarinic agents;
• antidepressants and phenothiazines;
• antiparkinsonian agents and other drugs with anticholinergic effects.

In practice, simply reviewing the drug chart and stopping or reducing such agents is one of the most useful interventions.^[1][2]

Depletion of potassium, magnesium or calcium depresses smooth muscle contractility and is a classic precipitant of ileus. Hypokalaemia is the best recognised and is a particular risk after vomiting, nasogastric drainage, diarrhoea or high-output stomas. Hypomagnesaemia and hypocalcaemia act in the same direction and should always be checked, because magnesium deficiency also makes hypokalaemia difficult to correct. Correction of these deficits is a core part of management.^[1][2]

Sepsis, pneumonia, peritonitis, intra-abdominal or retroperitoneal inflammation (pancreatitis, cholecystitis) and pelvic or retroperitoneal infection all precipitate ileus. Inflammatory cytokines and autonomic disturbance reduce gut motility, and the condition may improve only when the infection is controlled.^[1][2]

Trauma (hip, pelvic or other fractures and burns), spinal injury, neurosurgery, stroke, Parkinson disease, multiple sclerosis and other neurological disease can all depress gut motility.^[1] Acute spinal cord injury is a classic cause of paralytic ileus because of interruption of autonomic supply to the bowel.

Critical illness itself, with its increased sympathetic drive, mechanical ventilation, acute respiratory failure, acute renal failure, cardiac dysfunction (myocardial infarction, heart failure, cardiothoracic surgery), malignancy, major vascular events and transplantation surgery, is strongly associated with Ogilvie syndrome.^[1]

Metabolic and endocrine disease can also depress gut motility; hypothyroidism is a recognised systemic cause of ileus, and similar pictures occur in amyloidosis and other infiltrative conditions.^[1][2]

The conditions associated with acute colonic pseudo-obstruction include trauma and burns; infection (pneumonia, herpes zoster, pelvic abscess, sepsis); obstetric and gynaecological events; cardiovascular disease; neurological disease; malignancy (especially retroperitoneal and subdiaphragmatic tumours); gastrointestinal disease including pancreatitis; electrolyte imbalance; pulmonary and renal disease; transplant surgery; and the pharmacological agents listed above.^[1] Only about 5% of cases are idiopathic.^[1]

Normal peristalsis depends on a balance between excitatory (cholinergic, parasympathetic) and inhibitory (adrenergic, sympathetic) inputs, the intramural enteric nervous system and the pacemaker activity of the interstitial cells of Cajal. In ileus, inhibitory influences predominate. Surgery triggers a spinal reflex and local inflammatory response that suppress motility; opioid analgesia adds a potent peripheral mu-opioid receptor effect; electrolyte depletion reduces smooth muscle excitability. Small bowel motility usually returns earlier than colonic motility, which is why the colon is the segment most often left behind; postoperative colonic ileus may last 5 to 6 days, or longer.^[6]

Ogilvie syndrome is an autonomic imbalance in a critically ill patient. The original 1948 description suggested relative parasympathetic overactivity after interruption of sympathetic fibres; more recent work suggests the opposite, relative sympathetic overactivity after parasympathetic (sacral, S2 to S4) interruption. Acute colonic distension also stimulates mechanoreceptors and increases sympathetic discharge through the colocolonic reflex, further halting motility; neostigmine works by augmenting parasympathetic activity.^[1] Whatever the precise mechanism, the clinical danger is the same: progressive dilation of a thin-walled hollow viscus, leading to ischemia and, eventually, perforation.

Postoperative ileus is suspected when a patient expected to be passing flatus and tolerating food by the second or third day after surgery instead has nausea, vomiting, abdominal distension and failure to pass flatus or stool. It is often painless or achy rather than colicky.^[2][6]

Ogilvie syndrome presents in a patient who is already hospitalised, often recently operated or critically ill. Symptoms include lower abdominal cramping, nausea, vomiting and sometimes fever. Constipation is common but not universal: some patients continue to pass flatus and a few have diarrhoea. History should also cover recent medications, new infection, fractures, lines and ventilator status, because the precipitant may be a drug, pneumonia, an electrolyte-losing state or a recent operation.^[1]

• Inspection. Progressive, often massive abdominal distension. In paralytic ileus the whole abdomen may be distended; in Ogilvie syndrome distension can be striking and sometimes asymmetric.
• Auscultation. Bowel sounds are reduced or absent in paralytic ileus; in early mechanical obstruction they are high-pitched and tinkling. This is helpful but not reliable on its own.
• Palpation. The abdomen is tympanitic. In Ogilvie syndrome, tympany is one of the most striking physical findings. Generalised tenderness can occur even with viable bowel; it does not always mean perforation.^[1]
• Rectal examination. Often empty in mechanical large bowel obstruction; in functional ileus the rectum may contain stool.
• Systemic signs. Fever, tachycardia, hypotension, confusion and oliguria warn of ischemia, perforation or sepsis.

The differential diagnosis of a distended, quiet abdomen is broad. The important mimics are mechanical small or large bowel obstruction, mesenteric ischemia, acute colonic pseudo-obstruction, severe constipation and fecal impaction, Clostridioides difficile infection (which can present as pseudo-obstruction without diarrhoea) and pancreatitis. Because the presentations overlap, imaging rather than the bedside makes the diagnosis.^[1]

The aim is to answer three questions: is there an obstruction or ileus, what is causing the distension, and is there ischemia or perforation. Computed tomography answers all three; plain radiography and water-soluble contrast enema are the alternatives when CT is not available.

• Full blood count: anaemia and leukocytosis. In Ogilvie syndrome, leukocytosis is strongly associated with ischemia or perforation: one study reported leukocytosis in 100% of patients with ischemia or perforation against only 26% of those with viable bowel.^[1]
• Urea, creatinine and electrolytes: vomiting, drainage and third spacing cause dehydration, uraemia and depletion of potassium, magnesium and calcium. Replace aggressively and recheck.
• Lactate and arterial blood gas: any elevation in a distended, obstructed abdomen is worrying for ischemia.
• Liver function, coagulation and group-and-save: if surgery is likely.
• C. difficile testing: because C. difficile infection can present very similarly to colonic pseudo-obstruction, patients should be evaluated for C. difficile toxin and treated if positive.^[1]

A three-view series (supine, erect and left lateral decubitus or chest) shows pneumoperitoneum if perforation has occurred. In ileus, gas is seen in both small and large bowel, including the rectum, without a transition point. In Ogilvie syndrome the colon is massively distended, most strikingly the cecum, with gas extending to the rectum. Plain films remain the first and most useful test and are the standard first imaging in Ogilvie syndrome.^[1]

CT with intravenous contrast is the most accurate way to exclude a mechanical obstruction and to assess the bowel wall and mesentery for the danger signs of strangulation (absent mural enhancement, pneumatosis, portal venous gas, free fluid or free air). It measures cecal diameter precisely. Sensitivity and specificity for distinguishing mechanical obstruction from pseudo-obstruction are about 91% for both.^[1]

A water-soluble contrast (for example Gastrografin) enema has a sensitivity of 96% and a specificity of 98% for confirming large bowel obstruction and is well suited to distinguishing mechanical obstruction from pseudo-obstruction, as well as to identifying volvulus. It should not be used when perforation is suspected.^[1]

• Cecal diameter. The cecum is the segment most likely to perforate. Early studies suggested perforation was likely above 9 cm; more recent studies suggest perforation is unlikely below 12 cm, while about 23% of patients with a cecal diameter of 14 cm or more perforate. There is no firm single cutoff. Clinicians should maintain high suspicion between 9 and 12 cm and take serial films every 12 to 24 hours. Above 12 cm, laparotomy is a reasonable option.^[1]
• Leukocytes and lactate as markers of ischemia (above).
• Electrocardiogram and cardiac monitoring before neostigmine.

Ileus and Ogilvie syndrome are clinical diagnoses supported by imaging; there is no single laboratory threshold. Severity is stratified by:

• Hemodynamic status: stable versus hypotensive or septic.
• Presence of ischemia or perforation: fever, peritonism, free air, pneumatosis, portal venous gas, rising lactate, metabolic acidosis and leukocytosis.
• Cecal diameter and trajectory in Ogilvie syndrome (above 12 cm, or rising despite conservative treatment).
• Duration of distension: conservative and pharmacological treatment can be continued up to 5 days if the examination and imaging remain stable; Ogilvie syndrome present for 6 days or longer carries a higher risk of perforation.^[1]
• Underlying cause and fitness: the treatable precipitant (drug, sepsis, electrolyte deficit) and the patient's reserve determine whether non-operative management is safe.
• Passage of contents: a partial ileus may resolve with conservative measures; complete cessation of passage of flatus or stool predicts a slower course.

In the original randomised trial of Ogilvie syndrome, patients were included with abdominal distension, radiographic evidence of colonic dilation and a cecal diameter of at least 10 cm, after at least 24 hours without response to conservative treatment. Ten of 11 patients (91%) who received 2.0 mg of intravenous neostigmine had prompt decompression, against none of 10 who received placebo; the median time to response was 4 minutes (range 3 to 30).^[3]

1. Resuscitate first. Assess airway, breathing and circulation. Give intravenous isotonic crystalloid, replace potassium, magnesium and calcium, and place a urinary catheter in unstable patients.^[1][2]
2. Nil by mouth. No oral intake.
3. Decompression. Place a nasogastric tube if vomiting, distension or aspiration risk is present. In colonic pseudo-obstruction a rectal tube may be tried, but its decompressive effect is limited.^[1]
4. Stop drugs that slow motility. Withdraw or reduce opioids, anticholinergics, antidepressants, phenothiazines and antiparkinsonian agents. Keep opioid analgesia to the lowest effective dose and consider non-opioid analgesia.^[1][2]
5. Treat the cause. Control sepsis, treat pancreatitis, correct endocrine disease, stabilise trauma and manage cardiac or respiratory failure.
6. Replace electrolytes (potassium, magnesium, calcium) and recheck until normal.
7. Mobilise early and advance diet cautiously. Once ileus is resolving, sit the patient up, encourage walking and reintroduce food gradually.
8. Monitor. Serial abdominal examinations and, in Ogilvie syndrome, serial plain films every 12 to 24 hours.

Postoperative ileus is shortened by an accelerated care pathway rather than by any single drug. In the alvimopan registration trials the pathway included early removal of the nasogastric tube (before the first postoperative dose), early ambulation on the day after surgery and early diet advancement (liquids on the first postoperative day after bowel resection, solids from the second).^[6] Applying these measures, together with opioid-sparing analgesia, early feeding as tolerated, glycaemic control and good fluid balance, is the standard of care.

Chewing gum acts as sham feeding: it stimulates vagal and cephalic-vagal reflexes and increases gastrointestinal motility without adding food. A recent systematic review and meta-analysis found that gum chewing significantly reduced time to first flatus by 7.4 hours (p = 0.0003) and time to first defecation by 18.6 hours (p < 0.0001) in general and colorectal surgery, with similar (6.5 and 9.7 hour) reductions in gynaecological surgery.^[5] Chewing sugar-free gum on the first postoperative day is a cheap, safe adjunct; it should not replace a nasogastric tube or surgical review when either is indicated.

Alvimopan is a peripheral mu-opioid receptor antagonist that accelerates recovery of gut motility after surgeries that include partial bowel resection with primary anastomosis. It is for hospital use only:

• Dose. 12 mg orally 30 minutes to 5 hours before surgery, then 12 mg twice daily from the day after surgery until discharge, for a maximum of 7 days; no more than 15 doses in total.^[6]
• Indication. Acceleration of upper and lower gastrointestinal recovery, as part of an opioid-based analgesic regimen.^[6]
• Contraindications and cautions. Do not use in patients who have taken therapeutic doses of opioids for more than 7 consecutive days immediately before starting alvimopan; avoid or use with caution after recent opioid exposure (more than 3 doses in the week before surgery), in severe hepatic impairment, end-stage renal disease, complete gastrointestinal obstruction, and after pancreatic or gastric anastomoses; there is a potential risk of myocardial infarction with long-term use, and the drug is available only through a restricted short-term inpatient programme.^[6]
• Short-term (inpatient) use only. The benefit is on time to gastrointestinal recovery; alvimopan does not treat obstruction and must not be used if complete obstruction is present.

Conservative treatment is the first step and it succeeds in a large proportion of patients:

• nil by mouth;
• nasogastric decompression;
• minimise (or withdraw) opioids and stop other agents that slow motility;
• avoid osmotic laxatives, which increase colonic gas production;
• replace potassium, magnesium and calcium;
• treat the precipitating condition;
• encourage mobilisation;
• place a rectal tube if helpful, although its effect is limited;
• serial abdominal examinations and plain films every 12 to 24 hours.^[1]

Conservative and pharmacological treatment can be continued for up to 5 days provided examination and imaging remain stable. Ogilvie syndrome present for 6 days or more carries a higher risk of perforation, so delay beyond this should be deliberate and documented.^[1]

Neostigmine is an acetylcholinesterase inhibitor (a parasympathomimetic) that produces rapid colonic decompression. In multiple studies a 2.0 mg intravenous dose has initial success rates of 84 to 94%.^[1][3] In the pivotal trial the median time to response was 4 minutes (range 3 to 30).^[3]

Practical points:

• Confirm the diagnosis first (exclude mechanical obstruction) and obtain an electrocardiogram.
• Give 2.0 mg neostigmine intravenously, with the patient on a cardiac monitor, in an area where bradycardia can be treated immediately.
• Watch for abdominal cramping, excess salivation, sweating, nausea, vomiting and bradycardia; treat symptomatic bradycardia with 0.5 to 1.0 mg atropine intravenously.^[1][3]
• Patients with electrolyte abnormalities are less likely to respond, so correct potassium, magnesium and calcium before and during treatment.^[1]
• If decompression occurs but recurrence develops, a second dose of neostigmine may be given or colonoscopic decompression used.

Colonoscopic decompression was the standard treatment before neostigmine and is now reserved for patients who fail neostigmine or for those with contraindications to it. It allows visual exclusion of an obstructing lesion and assessment of mucosal viability. It is technically difficult in an unprepared bowel full of viscous stool, insufflation increases the risk of perforation, and the reported perforation rate is about 2% with a mortality of about 1%.^[1] If ischemia is seen, the procedure should be abandoned in favour of laparotomy.^[1]

Surgery is indicated for failure of conservative and endoscopic measures, or at any time there are signs of peritoneal inflammation or clinical deterioration.^[1] Historically non-operative treatment was limited to 48 to 72 hours; more recent practice allows pharmacological and conservative treatment for up to 5 days if the examination and imaging remain stable.^[1]

• Tube cecostomy provides immediate decompression and is a good option when there are no signs of peritoneal inflammation. It is most often placed through a limited right lower quadrant laparotomy; laparoscopic, CT-guided percutaneous and percutaneous endoscopic approaches are also described.^[1]
• Laparotomy with right hemicolectomy or subtotal colectomy is required for ischemia, perforation, over-distension injury with serosal tears or deterioration. Laparotomy in this setting carries a mortality of 40 to 60%, reflecting both the severity of the disease and the underlying critical illness.^[1]
• Cecopexy and other fixation procedures have higher recurrence and are less favoured than resection.

When laparotomy is performed, a stoma may be safer than an anastomosis in an unstable, under-resuscitated or immunosuppressed patient.

A meta-analysis of the limited comparative evidence found colonoscopic decompression successful in 83% of patients, against 47% for neostigmine, with colonoscopy about five times more likely to succeed (odds ratio 5.45; 95% confidence interval 2.47 to 12.04).^[4] The American Society for Gastrointestinal Endoscopy has recommended neostigmine before colonoscopy, while British emergency colorectal consensus guidelines acknowledge that the evidence comparing the two is weak and that neither is clearly superior.^[4] In practice, neostigmine is usually tried first because it is quick and non-invasive, and colonoscopy is used when neostigmine fails or is contraindicated, when the diagnosis needs confirming, or when there is limited response. The choice should follow local expertise.

• Review drug charts and avoid unnecessary opioids and anticholinergics.
• Correct electrolytes early and monitor them in patients with high-output losses.
• Mobilise patients early after surgery and apply an enhanced recovery pathway.
• Recognise and treat sepsis, pneumonia and pancreatitis promptly.
• In patients with chronic megacolon, pseudo-obstruction or motility disorders, address constipation and avoid constipating drugs.

• Ischemia and perforation, classically in the cecum, with progression to peritonitis and septic shock.
• Aspiration pneumonia from vomiting.
• Dehydration, electrolyte derangement and renal impairment from vomiting, third spacing and poor intake.
• Sepsis from bacterial translocation.
• Prolonged hospital stay and higher cost with postoperative ileus.
• Recurrence of Ogilvie syndrome after successful decompression in some patients, needing a second dose or colonoscopy.
• Postoperative complications after emergency surgery, with mortality of 40 to 60% when laparotomy is required.^[1]

• Paralytic (postoperative) ileus usually resolves within the usual postoperative window (5 to 6 days, or longer in some cases); persistence beyond that suggests an uncorrected precipitant or a developing mechanical obstruction.
• Ogilvie syndrome carries an overall mortality of about 15%, rising to 36 to 44% when ischemia or perforation occurs, and falling to about 6.4% in more recent series with earlier recognition.^[1] Laparotomy carries a mortality of 40 to 60%.^[1]
• Survival and recovery depend heavily on the underlying illness: the distension is often survivable, but the precipitating sepsis, trauma or cardiac failure is what kills.
• Recurrence is uncommon once the precipitant is corrected, but chronic idiopathic intestinal pseudo-obstruction, scleroderma, Parkinson disease and similar disorders predispose to repeated episodes, and those patients may need specialist motility review.

Children. Ogilvie syndrome is rare in children. Paralytic ileus is common after surgery and is managed supportively. Chronic intestinal pseudo-obstruction in childhood belongs to a different, specialist literature and is not covered here.

Pregnancy. Pregnancy and the puerperium are recognised precipitants of Ogilvie syndrome (cesarean section, normal pregnancy), probably through autonomic change and caecal mobility. Management follows the same principles, with early involvement of obstetric and surgical teams and careful attention to the gravid uterus during imaging and surgery.^[1]

Older adults. Older, frail, constipated and institutionalised patients, and those with dementia or chronic megacolon, carry much of the burden of both constipation-related ileus and postoperative decompensation. Resuscitation and definitive treatment should not be delayed because of age, but expectations and reversibility of the precipitant must be considered.

Immunocompromised patients. Steroid-treated, malnourished and immunosuppressed patients develop ileus more readily, have less reliable inflammatory signs and tolerate anastomoses less well. A lower threshold for diversion (stoma rather than anastomosis) at emergency laparotomy is prudent.

• Plain abdominal radiography is widely available and is the first investigation; look for gas in both small and large bowel including the rectum in ileus, and for massive colonic distension in Ogilvie syndrome.
• Water-soluble contrast enema has a sensitivity of 96% and specificity of 98% and is cheap, needing only a radiographer; it both diagnoses and distinguishes mechanical large bowel obstruction from pseudo-obstruction. It should not be used if perforation is suspected.^[1]
• CT should be used when available without delaying treatment. In about one quarter to one third of centres globally, transport for CT may cost more than the information it adds.
• Conservative care costs little and matters most: nil by mouth, nasogastric decompression, intravenous crystalloid, aggressive electrolyte replacement (potassium, magnesium, calcium), withdrawal of motility-slowing drugs, mobilisation and treatment of sepsis or pancreatitis.
• A rectal tube may allow temporary colonic decompression where endoscopic or surgical options are not available, but its effect is limited.
• Neostigmine needs a cardiac monitor and immediate access to atropine; where monitoring is unavailable, transport to a centre with monitoring, or repeated careful assessment, is safer than unsupervised administration.
• Surgery cannot be replaced by endoscopy when there is peritonitis or ischemia: arrange transfer early, before the bowel becomes necrotic. Laparotomy with resection is the treatment for perforation.
• Gum chewing and early mobilisation are free and should be used routinely after abdominal surgery. A rectal tube and a nasogastric tube are the cheapest decompressive tools; keep them patent and record drainage.

Acute abdomen; large bowel obstruction and volvulus; bowel obstruction (small); constipation in adults; pancreatic disease (acute pancreatitis); sepsis recognition and initial management; colorectal cancer; enhanced recovery after surgery; hypokalaemia; C. difficile infection; low-resource abdominal emergencies; peritonitis; postoperative care.

• Ileus is functional, not mechanical: the lumen is patent, but peristalsis is reduced or absent. Imaging shows no transition point and gas in small and large bowel, including the rectum.^[2]
• Postoperative ileus follows abdominal and pelvic surgery and lasts from 5 to 6 days or longer; opioids, electrolyte depletion, excessive handling and immobility prolong it.^[6]
• Paralytic ileus is often painless or achy; mechanical obstruction tends to be colicky with high-pitched bowel sounds. Tenderness alone does not prove perforation.^[2][1]
• Depletion of potassium, magnesium or calcium is a reversible and common cause; check and replace all three, and remember that magnesium deficiency makes hypokalaemia hard to correct.^[1][2]
• Acute colonic pseudo-obstruction (Ogilvie syndrome) is massive colonic dilation without obstruction, usually in a critically ill or recently operated patient; overall mortality is about 15%, and 36 to 44% if ischemia or perforation occurs.^[1]
• About 95% of Ogilvie cases are secondary to an associated condition (surgery, sepsis, cardiac or pulmonary disease, neurology, trauma, malignancy, drugs, electrolyte imbalance); 5% are idiopathic.^[1]
• The cecum is the segment most likely to perforate. Early data suggested 9 cm as dangerous; more recent data suggest perforation is unlikely below 12 cm, about 23% occur with a cecal diameter of 14 cm or more, and laparotomy is reasonable above 12 cm. Serial films every 12 to 24 hours are essential.^[1]
• Conservative treatment (nil by mouth, nasogastric decompression, stop motility-slowing drugs, correct electrolytes, treat the cause, mobilise) is first-line for Ogilvie syndrome and can be continued for up to 5 days if the patient remains stable.^[1]
• Osmotic laxatives increase colonic gas and should be avoided in Ogilvie syndrome.^[1]
• Intravenous neostigmine 2.0 mg produces prompt decompression in 84 to 94% of cases, usually within minutes; monitor the heart and treat bradycardia with atropine 0.5 to 1.0 mg.^[1][3]
• Colonoscopic decompression is reserved for neostigmine failure or contraindication; it has about 2% perforation and 1% mortality rates and confirms the diagnosis.^[1]
• Cecostomy decompresses without resection; laparotomy with right hemicolectomy or subtotal colectomy is needed for ischemia, perforation or deterioration, with mortality 40 to 60%.^[1]
• Alvimopan 12 mg by mouth 30 minutes to 5 hours before surgery, then 12 mg twice daily until discharge (maximum 7 days, no more than 15 doses), accelerates gastrointestinal recovery after bowel resection with primary anastomosis, as part of an opioid-based regimen.^[6]
• Alvimopan is contraindicated after more than 7 consecutive days of therapeutic opioids and is not for use in severe hepatic impairment, end-stage renal disease, complete obstruction, or pancreatic and gastric anastomoses.^[6]
• Early mobilisation, early nasogastric tube removal and early feeding, plus chewing gum, shorten postoperative ileus: gum reduces time to first flatus by 7.4 hours and to first defecation by 18.6 hours in general and colorectal surgery.^[5][6]
• Water-soluble contrast enema (sensitivity 96%, specificity 98%) is the cheap, high-yield test that separates pseudo-obstruction from mechanical obstruction when CT is unavailable.^[1]
• Treatment can be continued for up to 5 days if imaging is stable; 6 days or more of distension carries a higher perforation risk.^[1]
• Prognosis is dominated by the underlying illness; the distension itself is usually survivable if decompressed in time.^[1]