Constipation and faecal incontinence

• Chronic constipation and faecal incontinence (FI) are common, treatable problems of the final common pathway of bowel evacuation; they share machinery and often coexist.
• Most constipation in adults is functional. Rome V (2026) renames "functional constipation" to "chronic constipation" and now requires only one abnormal anorectal test to diagnose dyssynergic defecation. ^[2]
• A handful of alarm features (unexplained iron-deficiency anaemia, unintentional weight loss, overt rectal bleeding, a palpable mass, or a persistent progressive change in bowel habit) should redirect you away from "just constipation" toward investigation. ^[4]
• First-line care is non-pharmacological plus an osmotic laxative (polyethylene glycol 17 g daily). ^[1][4]
• Continence depends on three things that can each fail independently: a tight, reactive anal canal, a compliant rectum with working sensation, and coordinated pelvic-floor relaxation during defecation.
• FI usually has several causes at once. Fixing stool consistency (treating diarrhoea or constipation) is often the single most useful step.

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

1. Explain how normal defecation and continence work, and why each step can fail.
2. List the common and less common causes of chronic constipation and of faecal incontinence.
3. Recognise alarm features and state what investigation they trigger.
4. Apply a practical laxative ladder for chronic idiopathic constipation, with doses and escalation.
5. Distinguish functional defecatory disorder (dyssynergia) from slow-transit constipation, and know when biofeedback is indicated.
6. Outline the assessment and stepped management of faecal incontinence, including when to refer for anorectal physiology testing and surgery.
7. Adapt assessment and treatment to low-resource settings.

Constipation is a symptom, not a disease: the patient's sense that defecation is too infrequent, too difficult, or too incomplete. Faecal incontinence (FI) is the symptom of involuntary or uncontrolled loss of faeces from the anus; "anal incontinence" is the broader term that adds flatus. ^[3] This page covers the adult, with a teaching focus on chronic constipation and on faecal (and anal) incontinence, including the anorectal physiology that links them. It does not cover opioid-induced constipation in depth, paediatric constipation (covered elsewhere), or a detailed surgical atlas.

A useful bedside frame is that the bowel has two jobs to do in series: move content along (transit) and then evacuate it (defecation). Transit problems present as infrequent, hard stools. Evacuation problems present as straining, incomplete evacuation, and a need to use a finger or lean forward. Incontinence presents when the "gate" fails. Many patients have more than one of these at the same time.

Chronic idiopathic constipation affects about 8% to 12% of the United States population. ^[1] In Asia, reported prevalence of chronic constipation ranges from 2.6% to 28.0%, and studies using Rome IV criteria with self-completed online questionnaires in China, Korea and Singapore report 9.5% to 12.5%. ^[4] The typical patient prioritises different symptoms from the clinician: patients focus on straining, bloating, laxative use and dissatisfaction with bowel habit far more than on simple stool frequency. ^[4]

Faecal incontinence is common but variably defined. A systematic review up to 2014 reported a median prevalence of 7.7%, with a wide range of 2.0% to 20.7%; estimates were similar between men (8.1%) and women (8.9%), with lower prevalence in younger people (about 5.7% aged 15 to 34). ^[3] In Japan, prevalence among people aged 65 or over is 8.7% in men and 6.6% in women. ^[3] Nursing-home residents aged 65 or over have a much higher prevalence, 42.8%. ^[3] In a younger Japanese group with a mean age of 35.6 years, anal incontinence (including flatus) was reported by 34.4%, but true faecal incontinence (stool) by only 4.0%; women were affected more than men (42.7% versus 15.5%). ^[3] Prevalence figures in the source literature range from 0.9% to 19.5%, largely because studies differ in definition, survey method, age group and whether flatus is included. ^[3]

Rome V (2026) broadened the FI definition to "at least two episodes of uncontrolled faecal passage in the preceding 12 months" and removed the developmental-age requirement; estimated FI prevalence rose from 1.7% to 4.1%. ^[2] This is the sort of change that explains why older and newer prevalence papers do not match.

It helps to sort constipation by mechanism rather than by a long list.

• Slow transit. The colon moves content slowly; stools are infrequent and hard. This may be primary (idiopathic slow transit, more common in young women) or secondary to drugs, metabolic disease, neurological disease, or rarely colonic inertia after surgery.
• Defecatory (outlet) disorder. Transit is normal but evacuation is impaired: pelvic-floor dyssynergia, rectocele, rectal intussusception, descending perineum syndrome, or Hirschsprung disease. The patient strains, feels incomplete evacuation, and may need digital manoeuvres. ^[4]
• Secondary constipation. Opiates, anticholinergics, calcium-channel blockers, iron and calcium supplements, NSAIDs in some, endocrine disease (hypothyroidism, hypercalcaemia, diabetes), neurological disease (Parkinson disease, multiple sclerosis, spinal cord disease), coeliac disease, and structural lesions. The ANMA/APAGE 2026 consensus also notes that medication review is especially important in Asia where over-the-counter remedies, traditional medicines and supplements are widely used. ^[4]

Irritable bowel syndrome with constipation (IBS-C) and chronic constipation overlap heavily and can switch over time; the defining difference is recurrent abdominal pain or discomfort in IBS-C, versus minimal or none in chronic constipation. ^[4]

Risk factors and modifiers include low fibre intake, low fluid intake (below the lowest quartile), physical inactivity, female sex, older age, depression and anxiety (bidirectional with gut function), and pelvic-floor damage. ^[1][4]

A useful single sentence: FI is rarely single-cause; it is usually several of the following acting together. ^[3]

Seven pathophysiological groups are consistently described. ^[3]

1. Abnormal stool consistency (soft or watery stool). IBS, inflammatory bowel disease, functional diarrhoea, radiation enteritis, malabsorption, and drugs (antibiotics, antineoplastics, peptic-ulcer drugs, immunosuppressants, NSAIDs, antidiabetic drugs, hematopoietic agents) all produce stool that is hard to retain. Microscopic colitis is an under-recognised cause. Dietary triggers (coffee, alcohol, spices) and food allergy are also reported.
2. Decreased anal pressure. Internal anal sphincter weakness lowers resting pressure; external anal sphincter weakness lowers voluntary squeeze pressure. Common causes are obstetric perineal tears and anorectal surgery; neurological causes include spinal cord disease, multiple sclerosis, diabetes mellitus and pudendal neuropathy after vaginal delivery. Cushion (vascular) tissue of the anal canal contributes 10% to 20% of resting pressure and its loss (for example with haemorrhoidectomy damage) can produce incontinence. ^[3]
3. Impaired anorectal sensation. The patient does not feel stool arriving, so the rectum fills and leaks (passive, overflow incontinence). Causes: central or peripheral neuropathy, diabetes, spinal cord injury, multiple sclerosis, dementia, Parkinson disease, and ageing. Rectal hyposensitivity is found in 27% of patients with FI plus constipation. ^[3] The opposite, rectal hypersensitivity, is more typical of IBS and produces urge FI through excessive rectal contractions. ^[3]
4. Defecation disorders. Rectocele, rectal intussusception, impaired coordination and residual stool leak after defecation. ^[3]
5. Abnormal rectal capacity, pressure or compliance. After rectal resection, radiotherapy (radiation proctitis), inflammatory bowel disease, rectal prolapse.
6. Colon dysfunction. IBS with diarrhoea; low anterior resection syndrome, where the sigmoid reservoir is lost and urgency with FI follows.
7. Cognitive or motor dysfunction. Dementia, stroke, frailty, inability to reach the toilet. This "functional" incontinence behaves differently and responds to environmental and behavioural measures rather than sphincter therapy.

Risk factors include older age, female sex (reported variably), obesity, poor general health, physical disability, diabetes mellitus, IBS, inflammatory bowel disease, urinary incontinence, overactive bladder, pelvic organ prolapse, dementia, spinal cord injury, and obstetric factors (number of deliveries, home delivery, first vaginal delivery, forceps or vacuum delivery, fetal weight over 4000 g, prolonged second stage of labour). ^[3]

Continence is not a single sphincter. It is a stack of metres of territory and a reflex arc.

Anal canal resting tone. The internal anal sphincter (smooth muscle, involuntary) generates most of the resting pressure and keeps the canal closed at rest. The external anal sphincter and the puborectalis (striated, voluntary) add squeeze, especially during sudden rises in abdominal pressure such as coughing. ^[3][5]

The anorectal angle. Puborectalis forms a sling around the junction of rectum and anal canal, pulling it forwards and creating an angle of roughly 90 degrees at rest. Straightening this angle by relaxing puborectalis and bearing down is what turns continence into evacuation. ^[3]

Rectoanal inhibitory reflex and sampling. When a stool bolus enters the rectum and stretches its wall, the internal sphincter reflexly relaxes (the rectoanal inhibitory reflex, RAIR). A little content moves to just above the dentate line, where rich sensory epithelium identifies what it is: solid, liquid or gas. This "sampling" lets us decide to pass flatus without losing stool. If this sampling reflex is impaired (for example by scarring, surgery, or neuropathy), even normal pressures may not protect continence. ^[3][5]

Rectal sensation and compliance. The rectum behaves as a compliant reservoir: it holds volume at low pressure and signals fullness. First sensation, urge, urgency and maximal tolerance are measured during balloon distension testing. Normal continence requires you to feel filling in time to reach a toilet. Hyposensitivity removes that warning; hypersensitivity (common in IBS) gives false urgency. ^[5]

Defecation coordination. To defecate, the rectum contracts, intra-abdominal pressure rises, puborectalis relaxes and the anorectal angle straightens, while the external sphincter relaxes. Dyssynergic (paradoxical) contraction of puborectalis or the sphincter blocks this and leaves stool behind; weak propulsion does the same with a different manometric pattern. ^[5]

What failure looks like clinically. Passive incontinence (soiling without urge) maps to internal sphincter or sensory failure. Urge incontinence (unable to hold despite awareness) maps to external sphincter weakness or overwhelming rectal drive. Overflow incontinence (small leaks around a loaded rectum in a constipated patient) is a different problem that resolves when the impaction is cleared. ^[3][5]

This is why the same patient can have "constipation and incontinence" together. Constipation stretches and desensitises the rectum; repeated straining damages pudendal nerves; liquid stool from a proximal problem leaks around hard distal stool. Treating the constipation often improves the incontinence. ^[3]

For chronic constipation, investigate rather than treat on symptoms alone when any of the following are present: unexplained iron-deficiency anaemia, unintentional weight loss, overt rectal bleeding, a palpable abdominal or rectal mass, a persistent and progressive change in bowel habit, or a patient at increased risk of colorectal cancer (age over 50 without up-to-date screening, family history of colorectal cancer or advanced adenoma, hereditary syndromes, inflammatory bowel disease, prior adenoma or cancer). ^[4] Routine metabolic or endocrine blood tests (glucose, calcium, thyroid-stimulating hormone) have low yield in unselected constipation and should be guided by history and examination rather than ordered routinely. ^[4]

For faecal incontinence, the Japan 2024 flowchart makes the same point in a different order: if the patient has alarm signs (blood in stool, recent change in bowel habit, unexpected weight loss, palpable abdominal or rectal tumour), organic disease such as colorectal cancer, inflammatory bowel disease, rectal prolapse or rectovaginal fistula must be excluded and treated first. ^[3]

Ask about stool frequency and form (use the Bristol Stool Form Scale, remembering that some patients consider type III hard), straining, sensation of incomplete evacuation, urge to defecate, bloating and pain, diarrhoea versus constipation, laxative and supplement use, and daily routine. Rome V emphasises that patients and physicians prioritise different symptoms, so record the patient's own priorities as treatment endpoints. ^[4] For incontinence, classify symptoms as urge, passive or mixed, and ask about gas, mucus, solid or liquid leakage, timing (day versus night), ability to distinguish stool from gas, obstetric and surgical history, and diabetes or neurological disease. ^[3]

A bowel diary for several days is useful for both conditions and is specifically recommended in many FI pathways. ^[3]

Digital rectal examination is the cheapest and highest-yield test. It identifies perianal disease, scars, prolapse, fissure, stool impaction, masses, anal tone and voluntary squeeze, and (asked to bear down) impaired relaxation or paradoxical contraction of the sphincter and puborectalis suggestive of dyssynergia. In constipation, the DRE together with the history is recommended as a key component in evaluating pathophysiology. ^[4] An experienced clinician's DRE has acceptable accuracy for detecting dyssynergia. ^[5]

Rome V (2026) renamed "functional constipation" to chronic constipation, broadened FI to 2 or more episodes in 12 months, and redefined dyssynergic defecation to require one difficult-defecation symptom in 25% or more of bowel movements plus only one abnormal test (anorectal manometry, balloon expulsion test, or impaired rectal evacuation on defecography). Structural disorders may coexist. ^[2]

FI under Rome V is recurrent uncontrolled passage of faecal material, with the adult-specific criteria noted above. ^[2]

Severity scores in constipation track outcomes and quality of life rather than diagnose. Severity assessment should include symptom frequency and consistency, straining, incomplete evacuation, overlapping GI symptoms, and psychological factors; in severe or refractory cases, consider descending perineum syndrome and pelvic-floor injury. ^[4] Severity of FI is captured by validated questionnaires (Cleveland Clinic / Jorge-Wexner score, St Mark's / Vaizey score) and by bowel diaries; these are tools for tracking rather than diagnosing.

After the alarm-feature screen, uncomplicated constipation needs no routine labs, imaging, transit or manometry studies. ^[4]

When alarm features are present, investigate for colorectal cancer (colonoscopy) and secondary causes. ^[4] When constipation is refractory, assess pathophysiology before escalating:

• Anorectal manometry plus balloon expulsion test as initial investigations, especially if a pelvic-floor disorder is clinically suspected. ^[4][5]
• Colonic transit study (radiopaque markers, wireless motility capsule, or scintigraphy) to identify slow transit, but note transit can be delayed by a defecatory disorder or outlet obstruction. ^[4]
• Defecography (barium or MRI) for structural abnormalities and impaired rectal evacuation. ^[4]
• Plain abdominal X-ray can locate faecal impaction or obstruction but is not for routine evaluation. ^[4]
• Testing for intestinal methanogen overgrowth may be considered in refractory cases. ^[4]

The AGA recommends anorectal function testing with manometry and balloon expulsion for all patients with chronic constipation not responding to laxatives. ^[5] According to current ACG recommendations cited in the manometry literature, two abnormal anorectal tests plus a clinical history of chronic constipation are required to diagnose a defecatory disorder, and manometry is indicated for all patients with FI who fail conservative measures. ^{[5] [4]}

• Look for organic causes first (colonoscopy/endoscopy if alarm features). ^[3]
• Anorectal manometry with balloon expulsion and rectal sensory testing after failure of conservative measures, to identify sphincter hypotonia/hypocontractility and sensory abnormalities, and to select surgical candidates. ^[5]
• Endoanal ultrasound (or MRI) for sphincter defects; defecography for structural pelvic-floor problems.
• Consider cognitive and motor assessment in suspected "functional" incontinence.

The major differentials are not exotic; they are the categories you can mislabel.

For constipation: colonic cancer or stricture (alarm features), Hirschsprung disease and megacolon (suspect if lifelong, look for absence of RAIR), hypothyroidism and hypercalcaemia, medication effect, IBS-C, pelvic-floor dyssynergia masquerading as "slow transit".

For faecal incontinence: most "diarrhoea" in a constipated patient is overflow soiling, not true diarrhoea. Haemorrhoidal and perianal disease, rectal prolapse, fistula, and post-surgical change are common. In older adults, consider dementia and immobility before launching into sphincter testing.

Lifestyle statements in the 2026 Asia-Pacific consensus are graded and specific: soluble dietary fibre 20 to 30 g per day, fluids 1.5 to 2.0 L per day, and 30 to 60 minutes of regular physical activity such as walking. ^[4] These are adjuncts, not cures. A structured toilet routine (after meals, feet supported, unhurried) helps; polyethylene glycol is usually still needed. ^{[4] [1]}

Response to initial treatment should be assessed within 4 weeks. ^[4]

Osmotic laxatives are recommended as initial pharmacological treatment. ^[4] The AGA/ACG 2023 guideline provides an adult dose framework (initial dose; maximum where stated): ^[1]

Practical rules that follow from the same sources:

• A trial of fibre can be considered before PEG, or combined with it. ^[1]
• PEG has a durable response of at least 6 months and is inexpensive and over-the-counter, so it is sensible to use it early. ^[1]
• Magnesium, lactulose and senna have weaker or very-low-certainty evidence; use them for tolerability, access or preference. ^[1]
• Stimulant laxatives are strongly supported for short-term or rescue use; prolonged or excessive use can cause diarrhoea and electrolyte imbalance. ^[1]
• "Second-line" newer agents (prucalopride, linaclotide, lubiprostone and others such as elobixibat) can be chosen based on symptom profile, safety, access and prior treatment rather than by a rigid sequence. ^[4]
• If monotherapy fails, switch drug class or combine complementary mechanisms after checking adherence. ^[4]

Where sources differ, say so: AGA/ACG strongly recommends PEG and conditionally recommends magnesium, lactulose and senna, while the Asia-Pacific consensus makes osmotic laxatives (as a class) the first-line recommendation with switching or combination if response is inadequate. Both agree that the best drug is the one the patient will take consistently. ^[1][4]

This is the commonest remediable cause of a "constipated" patient who does not respond to laxatives. Suspect it when straining, incomplete evacuation, digitation and a sense of blockage dominate, even if stools are loose. ^[4][5] Orientating physiology: in healthy defecation, rectal pressure rises while the puborectalis and external sphincter relax; in dyssynergia they contract paradoxically or propulsion is inadequate. ^[5]

Diagnosis uses Rome V criteria: one difficult-defecation symptom in 25% or more of bowel movements plus one abnormal test among anorectal manometry, balloon expulsion test, or impaired rectal evacuation on defecography. ^[2] ARM is considered after failure of empirical medical management. ^[5]

Treatment is biofeedback, not more laxative. Randomised trials show clear symptom benefit in 70% to 80% of FDD patients, and biofeedback improves rectal hyposensitivity in up to 92% of patients. ^[5] It is ineffective for functional constipation without FDD. ^[5] The three biofeedback targets are rectal sensitivity training, sphincter strength training, and coordination training to relax the pelvic floor when straining and to counter the RAIR with a voluntary squeeze. ^{[5] [4]}

Before calling constipation refractory, recheck three things: the patient is actually taking the dose, fear or withholding is present, and the bowel was adequately disimpacted. ^[4] Then assess pathophysiology (manometry, transit, defecography). ^[4]

Surgery is a last resort. A multidisciplinary team manages refractory constipation with structurally abnormal outlet obstruction. Colectomy is reserved for highly selected patients after comprehensive evaluation and exclusion of pan-enteric dysmotility. ^[4] Anorectal physiological studies and colonic transit studies should precede any surgery. ^[4]

Management proceeds in three tiers: identify and treat reversible causes, conservative measures for all patients, then specialist interventions for those who do not respond. ^[3]

Treat diarrhoea or constipation: constipation with overflow is managed as constipation; incontinence often improves when stool consistency and transit normalise. ^[3] Adjust medications that cause diarrhoea. Treat inflammatory bowel disease, microscopic colitis, coeliac disease, diabetes control, and pelvic-organ prolapse. For overflow incontinence, a loaded rectum must be cleared. ^[3]

Skin care matters: moisture, enzymes and friction damage the perianal skin. Clean without harsh soaps, dry well, use barrier cream, treat candidiasis.

• Diet and habit advice (fibre titrated, avoidance of personal triggers, regular post-meal toileting).
• Pelvic-floor muscle training and biofeedback (same three modalities as for defecatory disorder).
• Transanal irrigation for carefully selected patients with structured bowel emptying.
• Continence devices (anal plug, vaginal bowel-control insert) where available.
• Behavioural and environmental measures for cognitive or motor incontinence: scheduled toileting, accessible toilets, clothing modifications, timed reminders.

Biofeedback is supported by multiple randomised trials in FI, with 70% to 80% of patients reporting improvement, and it improves rectal hyposensitivity. ^[5] It has benefits in both sensory training and sphincter coordination. ^[5]

Anorectal physiology testing (manometry, balloon expulsion, sensory testing and endoanal ultrasound) guides treatment after conservative measures fail. ^[5] Surgery follows a flowchart. ^[3]

• If incontinence is caused by severe spinal cord impairment, consider antegrade continence enema or stoma. ^[3]
• If not caused by sphincter disruption, sacral neuromodulation is the first-line surgical therapy. ^[3]
• If sphincter disruption is the main cause, either anal sphincteroplasty or sacral neuromodulation should be performed, after informed discussion. ^[3]
• If first-line surgery fails, second-line options are considered; which to try first can depend on patient preference and condition. ^[3]
• Stoma creation is described as a surgical option with implications for postoperative quality of life. ^[3]
• Regenerative therapies (transplantation of autologous cultured myoblasts into the external anal sphincter) are introduced with promising long-term trial outcomes but are not routine. ^[3]

Obstetric incontinence deserves a sentence of its own. A third- or fourth-degree tear occurs in roughly a quarter to a third of primiparas by endoanal ultrasound, yet only about 13% develop anal incontinence; and incontinence occurs after normal vaginal delivery without documented injury, so risk factors (forceps, vacuum, fetal weight over 4000 g, prolonged second stage) matter as much as documented tears. ^[3] The Japan 2024 guidance recommends early referral to a specialised centre when a sphincter injury can be repaired, observation for about a year when no injury is identified, and careful reassessment before mode of delivery in subsequent pregnancies. ^[3]

• Older adults and frailty. Cognitive and motor incontinence dominates; focus on environment, scheduled toileting, diet consistency and skin care. Dementia and immobility increase risk and complicate assessment. ^[3]
• Neurological disease. Combined oral, rectal and often antegrade programmes; specialist multidisciplinary care is essential. ^[3]
• Pregnancy. The AGA/ACG 2023 guideline does not address pregnancy. Lactulose is the only osmotic studied in pregnancy. ^[1]
• IBS overlap. Prioritise constipation control first; reassess overlapping symptoms before adding drugs for bloating or pain. ^[4]

• Faecal impaction and overflow (often mislabelled diarrhoea), with social and school or work consequences.
• Rectal dilatation and hyposensitivity that make recovery slow.
• Anal fissures, bleeding and haemorrhoids from straining.
• Urinary symptoms and urinary tract infections in some constipated patients.
• Pelvic floor damage, which constipation accelerates through straining. ^[4]
• Social, occupational and psychological harm, including anxiety and depression, which feed back on gut function. ^[4]
• Misdiagnosis: treating Hirschsprung disease, cancer or slow-transit constipation as "functional".
• Over-investigation of a healthy constipated person.
• For incontinence: skin breakdown (incontinence-associated dermatitis), social isolation, sexual dysfunction, poor sleep and quality of life. ^[3][4]

Most patients with chronic constipation improve with a consistent regimen once the correct mechanism is addressed (slow transit, evacuation disorder, or secondary cause). Recurrence is common when treatment stops too soon. Defecatory disorders respond best to biofeedback. Faecal incontinence improves substantially when reversible bowel and metabolic contributors are treated and when patients engage with conservative and behavioural programmes; surgical options are effective in selected anatomical situations. Realistic expectations and a bowel diary reduce dropout.

Constipation and incontinence are clinical diagnoses, which is an advantage. ^[4]

• Recognise alarm features early and refer for suspected cancer, inflammatory bowel disease, Hirschsprung disease or significant pelvic-floor injury. ^[3][4]
• Use an affordable osmotic such as lactulose or magnesium (where safe and available) if PEG is unavailable or unaffordable; PEG has the best evidence but is not the only option. ^[1][4]
• Fibre can be supplied cheaply from local fruit, vegetables, pulses and psyllium husk; ensure adequate fluid.
• Behavioural programmes (scheduled toileting, feet supported, rewards, no punishment) are cheap and effective, and are essential in encopresis-type incontinence in children. ^[4]
• Anorectal manometry, transit studies, biofeedback and continence devices are often unavailable; recognise defecatory disorders by history and careful DRE, and refer selected patients to centres that can offer them. ^[5]
• For incontinence, skin protection and continence containment are priorities when specialist therapy is not available; even a scheduled toileting plan helps.

• Constipation and faecal incontinence share mechanisms and frequently coexist; treating constipation improves incontinence in many patients. ^[3]
• Chronic constipation affects about 8% to 12% of the US population; faecal incontinence has a median prevalence of about 7.7% with a wide range, and rises steeply with age. ^[1][3]
• Rome V (2026) renamed functional constipation to chronic constipation, broadened the FI definition, and now allows one abnormal test to diagnose dyssynergic defecation. ^[2]
• Alarm features demand investigation for colorectal cancer and secondary disease before attributing symptoms to constipation. ^[4]
• Non-pharmacological management is soluble fibre 20 to 30 g daily, fluids 1.5 to 2.0 L daily and regular activity; treatment response should be assessed within 4 weeks. ^[4]
• Osmotic laxatives (PEG 17 g daily) are first-line pharmacological treatment for chronic constipation; escalation follows a clear ladder of stimulants, secretagogues and prokinetics with defined doses. ^[1][4]
• Defecatory disorder is the commonest remediable cause of laxative-resistant constipation; it is diagnosed by Rome V criteria and treated with biofeedback, which succeeds in 70% to 80% of patients. ^[2][4][5]
• FI is multi-factorial; stool consistency correction is often the most useful single step. ^[3]
• Anorectal continence rests on resting tone, squeeze, the sampling reflex, rectal sensation and compliance, and coordinated pelvic-floor relaxation. ^[3][5]
• Investigate FI for organic disease first, then use anorectal manometry and ultrasound after conservative measures fail. ^[3][5]
• Surgery for FI follows a flowchart: sacral neuromodulation first if there is no sphincter disruption; sphincteroplasty or neuromodulation if disruption is the main cause; stoma or antegrade procedures reserved for severe spinal impairment. ^[3]
• Biofeedback improves both defecatory disorder and FI but is ineffective for functional constipation without FDD. ^[5]
• Low-resource management rests on clinical diagnosis, affordable osmotics, fibre and fluid, and structured behavioural programmes. ^[4]

Constipation in children and encopresis. Diarrhoea and malabsorption. Colorectal cancer. Inflammatory bowel disease. Coeliac disease. Hypothyroidism. Pelvic floor disorders. Anal fissure, haemorrhoids and pruritus ani. Urinary incontinence. Diabetes mellitus. Multiple sclerosis and spinal cord disease. Dementia. Irritable bowel syndrome. Anorectal disease.

This page relies primarily on the AGA/ACG Clinical Practice Guideline on the pharmacological management of chronic idiopathic constipation (2023), ^[1] the Rome V Criteria for Adults (2026), ^[2] the Japan Society of Coloproctology Practice Guidelines for Fecal Incontinence 2024 (published in English 2026), ^[3] the ANMA/APAGE Chronic Constipation Consensus (2026), ^[4] and a review of the clinical utility of anorectal manometry (2025). ^[5] Where two sources differ (for example in how strongly they recommend magnesium, lactulose or senna for constipation), both positions are stated rather than one being preferred silently.