Constipation
Constipation is a functional bowel disorder characterized by infrequent, difficult, or incomplete evacuation of hard stools.
Constipation
Constipation is not a disease but a symptom — a subjective complaint about unsatisfactory defecation. It is critically important to define what exactly the patient means by constipation [1], because the word means different things to different people:
- Infrequent stools (typically < 3 spontaneous bowel movements per week)
- Hard or lumpy stool consistency (Bristol Stool Form Scale types 1–2)
- Straining or excessive effort to evacuate
- Sense of incomplete evacuation
- Sensation of anorectal obstruction/blockage
- Need for manual manoeuvres (digital evacuation, splinting of perineum/vagina) to facilitate defecation
The word itself comes from Latin: con- (together) + stipare (to press/pack) — literally "packed together," which is a perfect description of the hard, compacted stool these patients experience.
Rome IV Criteria (2016, still the international standard in 2025–2026) define functional constipation as the presence of ≥2 of the following for ≥3 months (onset ≥6 months prior), with insufficient criteria for IBS-C:
- Straining in > 25% of defecations
- Lumpy or hard stools (BSFS 1–2) in > 25% of defecations
- Sensation of incomplete evacuation in > 25% of defecations
- Sensation of anorectal obstruction/blockage in > 25% of defecations
- Manual manoeuvres to facilitate defecation in > 25% of defecations
- Fewer than 3 spontaneous bowel movements per week
Clinical Pearl
"Define what exactly the patient means by constipation" [1] — this is the first step. Many patients who complain of "constipation" actually have normal stool frequency but are bothered by straining or hard stools. Others may be worried about not going daily (a common lay misconception). Always clarify.
2. Epidemiology
- Functional constipation affects approximately 10–15% of adults worldwide (varies by diagnostic criteria used)
- Up to 25% of the population in some East Asian surveys report constipation symptoms [3]
- A community-based study in Hong Kong found self-reported constipation prevalence of approximately 14% using Rome III criteria
- More common in older adults — prevalence rises steeply after age 65 (up to 20–30% in elderly populations)
- Alarm symptom threshold is particularly important in Hong Kong, where colorectal cancer (CRC) is the most common cancer overall (males #1, females #2) — so new-onset constipation in anyone > 40 must trigger a high index of suspicion [1]
- Female predominance: women are ~2–3× more likely to report constipation than men (related to hormonal effects on gut motility, pelvic floor anatomy, and psychosocial factors)
- Elderly: age-related decline in gut motility, polypharmacy, reduced mobility, reduced fluid and fibre intake
- Institutionalised patients: prevalence up to 50–75% in nursing homes
- Pregnancy: up to 40% of pregnant women experience constipation (progesterone-mediated smooth muscle relaxation + mechanical compression by gravid uterus)
| Category | Risk Factors | Mechanism |
|---|---|---|
| Demographics | Female sex, elderly age | Hormonal effects (progesterone relaxes smooth muscle); age-related enteric neuronal loss |
| Dietary | Low fibre diet, inadequate fluid intake | Fibre adds bulk to stool and retains water → stimulates peristalsis; dehydration → harder stools |
| Lifestyle | Physical inactivity/immobility, ignoring urge to defecate | Physical activity stimulates colonic motility; habitual suppression → rectal hyposensitivity |
| Drugs | Opiates (esp. codeine), iron, TCAs, anticholinergics, calcium channel blockers (CCBs), SSRIs, aluminium-containing antacids, benzodiazepines, cough mixtures [1] | See detailed drug mechanisms below |
| Metabolic/Endocrine | Hypothyroidism, hypercalcaemia, hypokalaemia, diabetes mellitus [1][2] | Thyroid hormone is needed for GI smooth muscle contractility; Ca²⁺ reduces smooth muscle excitability; K⁺ depletion impairs smooth muscle contraction; DM autonomic neuropathy |
| Neurological | Spinal dysfunction (severe only), Parkinson's disease, multiple sclerosis, spinal cord injury [1] | Disruption of extrinsic innervation to colon and/or pelvic floor dyssynergia |
| Structural/Anorectal | Rectocele, rectal prolapse, anal stricture, obstructing CRC | Physical obstruction to stool passage |
| Psychosocial | Depression, anxiety, eating disorders (anorexia nervosa), somatisation [1] | Central-enteric nervous system cross-talk; reduced food intake; behavioural patterns |
| Other | Pregnancy, chronic constipation itself (vicious cycle), post-surgical, ICU patients | Progesterone effect; colonic dilatation from chronic faecal loading leads to further dysmotility |
High Yield – Drug-Induced Constipation
"Drugs selected associated with constipation: analgesics, opioids esp. codeine, TCAs, antacids esp. aluminium hydroxide, Ca channel blockers, SSRIs, cough mixtures, anticholinergics, benzodiazepines" [1]. Always take a thorough drug history — drug-induced constipation is extremely common and is one of the most easily reversible causes.
Beware Hypokalaemia in the Elderly on Diuretics
"Beware of hypokalaemia causing constipation in the elderly patient on diuretic treatment" [1]. This is a classic exam pitfall. An elderly patient on thiazides or loop diuretics develops constipation → check K⁺! Hypokalaemia impairs smooth muscle contraction throughout the gut, and the fix is electrolyte correction, not laxatives.
3. Anatomy and Physiology of Normal Defecation
Understanding constipation requires understanding the anatomy and physiology of the colon, rectum, and pelvic floor — because constipation is essentially a failure of one or more parts of this coordinated system.
The colon is approximately 1.5 m long and is divided into:
- Caecum (with appendix)
- Ascending colon (right colon)
- Transverse colon
- Descending colon (left colon)
- Sigmoid colon — this is the narrowest segment → by Laplace's law (wall tension = pressure × radius / wall thickness), the narrowest lumen generates the highest intraluminal pressure [4]. This is why the sigmoid is the most common site of diverticulosis in Western populations and is particularly prone to the effects of chronic constipation.
- Rectum — approximately 12–15 cm long; the last reservoir before evacuation
- Anal canal — approximately 4 cm long; divided by the dentate (pectinate) line into upper 2/3 (autonomic innervation, columnar epithelium) and lower 1/3 (somatic innervation, stratified squamous epithelium) [5]
The colon has an outer longitudinal muscle layer condensed into three taeniae coli (taenia libera, omentalis, mesocolica) and an inner circular muscle layer. The rectum, by contrast, has a complete outer longitudinal muscle coat — which is why diverticula essentially never occur in the rectum [4].
The primary functions relevant to constipation are:
-
Water and electrolyte absorption: The colon absorbs approximately 1–1.5 L of water per day from the ~1.5 L of chyme entering from the ileum. The longer stool stays in the colon, the more water is absorbed → harder, drier stool. This is the fundamental mechanism of slow-transit constipation.
-
Propulsion: Three types of colonic motility:
- Segmental contractions (haustral churning): non-propulsive; mix contents and increase mucosal contact for absorption
- Peristaltic contractions: propel content distally
- High-amplitude propagating contractions (HAPCs): mass movements that occur 1–3 times per day (often post-prandially due to the gastro-colic reflex); these are the main mechanism that moves stool from the transverse colon into the sigmoid/rectum, triggering the urge to defecate
-
Storage: The sigmoid colon and rectum serve as reservoirs. The rectum is normally empty or near-empty; stool entry into the rectum triggers the defecation reflex.
Key points:
- The internal anal sphincter (IAS) is smooth muscle under autonomic (involuntary) control — it provides ~70–80% of resting anal tone
- The external anal sphincter (EAS) is striated muscle under somatic (voluntary) control via the pudendal nerve (S2–S4)
- The puborectalis muscle (part of levator ani) forms a sling around the anorectal junction creating the anorectal angle (~90° at rest). When it relaxes, the angle opens to ~130°, straightening the path for stool evacuation. Failure of puborectalis relaxation (paradoxical contraction) = dyssynergic defecation (a key cause of functional outlet obstruction)
| Level | Structure | Function |
|---|---|---|
| Enteric Nervous System (Auerbach's/myenteric plexus, Meissner's/submucosal plexus) | Intrinsic pacemaker of gut | Generates peristalsis independently; coordinates segmental and propulsive contractions |
| Parasympathetic (vagus for proximal colon up to splenic flexure; pelvic splanchnic nerves S2–S4 for distal colon/rectum) | Stimulatory | Increases motility and secretion; promotes defecation |
| Sympathetic (T10–L2 via inferior mesenteric ganglion, superior and inferior hypogastric plexuses) | Inhibitory | Decreases motility; contracts IAS (maintains continence) |
| Somatic (pudendal nerve S2–S4) | Voluntary control of EAS and puborectalis | Allows voluntary continence and voluntary defecation |
| Supraspinal (pontine defecation centre, cerebral cortex) | Coordination and voluntary override | Pontine centre coordinates detrusor-like reflex; cortex allows voluntary initiation/suppression |
Why does this matter for constipation? Because disruption at ANY level — from the enteric neurons (e.g. Hirschsprung disease, where ganglia are absent), to the parasympathetic outflow (e.g. spinal cord injury), to the voluntary pelvic floor control (e.g. dyssynergia), to the supraspinal centres (e.g. Parkinson's disease) — can cause constipation.
4. Aetiology and Pathophysiology
The causes of constipation can be broadly divided into primary (functional/idiopathic) and secondary causes. In clinical practice, most constipation is primary/functional, but the job of the clinician is to exclude secondary causes, especially dangerous ones like colorectal malignancy.
4.1 Primary (Functional) Constipation
Three pathophysiological subtypes — these are not mutually exclusive and often overlap:
- The most common subtype (~60% of functional constipation)
- Objective colonic transit time is actually normal on testing
- Patients perceive difficulty with defecation — likely due to visceral hypersensitivity, altered perception, or psychosocial factors
- Often overlaps with IBS-C (IBS with constipation) [3] — the distinction is that IBS-C has prominent abdominal pain associated with defecation, whereas NTC may not
- Reduced frequency of high-amplitude propagating contractions (HAPCs)
- Pathophysiology: may involve:
- Reduced interstitial cells of Cajal (the "pacemaker" cells of the gut) in the colonic wall
- Reduced enteric neurons in the myenteric plexus
- Altered neurotransmitter balance (e.g. ↓serotonin, ↓substance P, ↑nitric oxide)
- Result: stool moves very slowly through the colon → excessive water absorption → very hard, infrequent stools
- More common in young women
- Diagnosed by radio-opaque marker transit study (Sitz markers) or wireless motility capsule
- Also called pelvic floor dyssynergia, anismus, or obstructed defecation
- Pathophysiology: failure of coordinated relaxation of the pelvic floor muscles during attempted defecation:
- Paradoxical contraction of puborectalis (the muscle contracts instead of relaxing → the anorectal angle does not open)
- Inadequate relaxation of EAS
- Inadequate rectal propulsive force
- Structural causes of outlet obstruction include:
- Rectocele (herniation of rectum into vagina — stool gets trapped in the pouch)
- Rectal intussusception / rectal prolapse [6]
- Enterocele / sigmoidocele
- Descending perineum syndrome
- Megarectum (chronic rectal distension → ↓rectal sensation → ever-larger volumes needed to trigger urge)
- Diagnosed by anorectal manometry, balloon expulsion test, defecography (conventional or MR)
IBS-C vs Functional Constipation
Both are functional (no structural cause), but:
- IBS-C: constipation + predominant abdominal pain related to defecation, ≥1 day/week for 3 months [3]
- Functional constipation: constipation criteria met but insufficient criteria for IBS
In practice, these exist on a spectrum and patients may shift between categories over time. IBS w/ constipation (IBS-C): hard stools ≥25% with loose/watery stools < 25% of bowel movements [3].
4.2 Secondary Causes of Constipation
This is the critical list to work through systematically. The mnemonic from the lecture slides is essentially a checklist:
Key secondary causes from lecture slides [1]:
- Depression
- Diabetes (rarely)
- Drugs (opiates, iron, others) — see list
- Thyroid disorder (hypothyroidism)
- Spinal dysfunction (severe only)
- May be functional (e.g. depression, anorexia nervosa)
Let's expand each systematically:
This is the most common secondary cause and the most reversible. Understanding mechanisms is key:
| Drug Class | Examples | Mechanism of Constipation |
|---|---|---|
| Opioids | Codeine, morphine, tramadol, oxycodone, fentanyl | Bind μ-opioid receptors on myenteric and submucosal neurons → ↓ACh release → ↓peristalsis + ↑segmental contractions (non-propulsive) + ↑water absorption + ↑anal sphincter tone. Codeine is particularly constipating because it is a pro-drug of morphine with incomplete metabolism. |
| Anticholinergics | Atropine, anti-histamines, anti-spasmodics, anti-psychotics, anti-depressants (TCAs) [7] | Block muscarinic M₃ receptors on colonic smooth muscle → ↓contractility → ↓propulsion |
| Calcium channel blockers | CCBs (verapamil worst, nifedipine, diltiazem) [2] | Block L-type Ca²⁺ channels in GI smooth muscle → ↓intracellular Ca²⁺ → ↓smooth muscle contraction |
| Iron supplements | Ferrous sulphate, ferrous fumarate | Unabsorbed iron in the gut lumen is directly toxic to intestinal mucosa + alters gut microbiota → ↓motility |
| Aluminium-containing antacids | Aluminium hydroxide [1] | Aluminium ions directly inhibit smooth muscle contraction |
| SSRIs | Fluoxetine, sertraline, paroxetine [1] | Paradoxically — while 5-HT usually promotes motility, SSRIs can desensitise 5-HT receptors over time in some patients, or cause anticholinergic-like effects |
| Benzodiazepines | Diazepam, lorazepam [1] | Central and peripheral GABA-mediated muscle relaxation → ↓colonic motility |
| Cough mixtures | Often contain codeine or dextromethorphan [1] | Opioid component as above |
| Diuretics | Thiazides, loop diuretics | Not directly constipating but cause hypokalaemia → impaired smooth muscle contraction [1] |
| Others | Clonidine, 5-HT₃ antagonists (ondansetron), bile acid sequestrants (cholestyramine) | Various mechanisms: ↓sympatholytic effect, ↓serotonin-mediated secretion, bile acid binding ↓colonic secretion |
| Condition | Mechanism |
|---|---|
| Hypothyroidism [1] | Thyroid hormone (T₃) is required for normal GI smooth muscle contractility and metabolic rate. Deficiency → ↓basal metabolic rate → ↓gut motility → slow transit. Also may have myxoedematous infiltration of bowel wall. |
| Hypercalcaemia [1][2] | Ca²⁺ excess → ↓smooth muscle excitability (Ca²⁺ stabilises cell membranes, making them less likely to depolarise) → ↓colonic contraction. Causes: primary hyperparathyroidism, malignancy, sarcoidosis. Classic exam question! |
| Hypokalaemia [1][2] | K⁺ is essential for smooth muscle cell repolarisation. Depletion → smooth muscle cells remain relatively hyperpolarised → ↓contractility. Think of the elderly on diuretics. |
| Diabetes mellitus [1] | Autonomic neuropathy (particularly affecting vagal and sacral parasympathetic fibres) → ↓colonic propulsion. Also may have associated enteric neuropathy. |
| Uraemia | Uraemic toxins affect enteric neural function; also associated with reduced fluid intake and polypharmacy |
| Hypomagnasaemia | Mg²⁺ depletion → similar mechanism to hypokalaemia (both affect smooth muscle excitability) |
| Phaeochromocytoma (rare) | Catecholamine excess → sympathetic overdrive → ↓GI motility |
| Condition | Mechanism |
|---|---|
| Spinal cord injury/dysfunction [1] | Disrupts the descending control from pontine defecation centre and voluntary cortical control → loss of coordinated defecation reflex + pelvic floor dyssynergia [8] |
| Parkinson's disease | Lewy body pathology affects the enteric nervous system (even before motor symptoms appear) → ↓colonic motility. Also: ↓physical activity, anticholinergic medications |
| Multiple sclerosis | Demyelination of spinal cord pathways → neurogenic bowel (similar to SCI) |
| Stroke | Immobility, altered consciousness, medications, and direct disruption of cortical defecation control |
| Hirschsprung disease | Congenital absence of ganglion cells (Auerbach's and Meissner's plexuses) in a segment of colon → aganglionic segment cannot relax or propagate peristalsis → functional obstruction [6]. Almost always presents in neonates/infants but rare cases present in adults. |
| Autonomic neuropathy (DM, amyloidosis) | Loss of parasympathetic drive to the colon |
| Chagas disease (not in HK but worth knowing) | Trypanosoma cruzi destroys myenteric plexus neurons → megacolon |
| Condition | Mechanism |
|---|---|
| Colorectal cancer | Physical obstruction of the lumen. Alarm symptom: recent constipation in those > 40 years [1] |
| Diverticular stricture | Chronic inflammation from diverticulitis → fibrosis → luminal narrowing [4] |
| Anal stricture/fissure | Pain on defecation → voluntary withholding → worsening constipation (vicious cycle). Fissure also causes IAS spasm (reflex) → further obstruction |
| Rectocele | Herniation of anterior rectal wall into vagina → stool pockets into the rectocele instead of being evacuated [6] |
| Rectal prolapse | Associated with constipation both as a cause (obstructed defecation) and a consequence (chronic straining) [6] |
| Post-surgical adhesions | Can cause partial obstruction → slow transit |
| Extrinsic compression | Pelvic masses (ovarian cyst, fibroid, pregnancy) compress the rectosigmoid |
| Condition | Mechanism |
|---|---|
| Depression [1] | ↓physical activity, ↓appetite/food intake, psychomotor retardation, medications (TCAs, SSRIs) all contribute. Also direct CNS-enteric nervous system interaction via the brain-gut axis |
| Anorexia nervosa [1] | Markedly ↓food intake → ↓faecal bulk → ↓stimulus for colonic motility. Also: electrolyte disturbances (hypokalaemia), laxative abuse paradoxically worsens constipation over time |
| Anxiety/somatisation | Sympathetic overdrive → ↓GI motility (fight-or-flight response diverts blood away from GI tract) |
| Behavioural | Habitual suppression of defecation urge (busy professionals, school children, patients in unfamiliar environments) → rectal hyposensitivity over time |
Is the patient trying to tell me something?
"May be functional (e.g. depression, anorexia nervosa)" [1]. Constipation may be the presenting complaint of a psychiatric disorder. Always screen for mood and eating habits, especially in young women with chronic constipation and no obvious secondary cause.
Constipation is not just a standalone problem — it contributes to other pathology throughout the body:
| Condition | How constipation contributes |
|---|---|
| GERD | Constipation → straining → ↑intra-abdominal pressure → ↑gastro-oesophageal reflux [9] |
| Haemorrhoids | Constipation → straining → ↑intra-abdominal pressure → engorgement of anal vascular cushions + shearing of supporting connective tissue [5][10] |
| Anal fissure | Hard, large stools → mechanical tearing of anoderm |
| Rectal prolapse | Chronic straining → pelvic floor weakening → all layers of rectum protrude through anus [6] |
| Sigmoid volvulus | Chronic faecal overloading from constipation → elongation and dilatation of sigmoid colon → predisposes to twisting around narrow mesenteric attachment [6][11] |
| Diverticular disease | Increased intraluminal pressure (from straining with constipation) at weakest points of colonic wall (where vasa recta penetrate circular muscle) → mucosal herniation [4] |
| Acute retention of urine (AROU) | Constipation is a common precipitating factor for AROU (particularly in males with background BPH) — faecal loading compresses the bladder neck/prostatic urethra [7][8] |
| Faecal impaction → overflow incontinence | Paradoxical diarrhoea: liquid stool leaks around impacted mass |
| Hernia | Chronic straining → ↑intra-abdominal pressure → abdominal wall weakening [12] |
| Varicose veins | Increased abdominal pressure such as chronic cough and constipation [13] → ↑venous pressure transmitted to lower limb veins |
5. Classification
- Acute constipation: recent onset (days to weeks) — always consider obstruction (mechanical or functional), new medication, or acute illness
- Chronic constipation: ≥3 months duration (Rome IV) — more likely primary/functional
| Subtype | Mechanism | Key Features |
|---|---|---|
| Normal-transit constipation (NTC) | Normal colonic transit; altered perception | Most common; often a/w IBS-C overlap |
| Slow-transit constipation (STC) | ↓colonic propulsive activity | Infrequent stools, ↓urge, often young women |
| Defecatory disorder (outlet obstruction) | Impaired rectal evacuation (functional or structural) | Straining, incomplete evacuation, need for digital manoeuvres |
| Mixed | Combination of STC + defecatory disorder | Common in practice |
- Primary (functional/idiopathic): NTC, STC, defecatory disorder
- Secondary: drugs, metabolic/endocrine, neurological, structural, psychosocial (as detailed in Section 4.2)
A practical clinical tool for categorising stool consistency:
| Type | Description | Clinical Significance |
|---|---|---|
| 1 | Separate hard lumps (like nuts) | Severe constipation |
| 2 | Sausage-shaped but lumpy | Mild constipation |
| 3 | Sausage-shaped with cracks on surface | Normal |
| 4 | Smooth, soft sausage or snake | Normal (ideal) |
| 5 | Soft blobs with clear-cut edges | Lacking fibre |
| 6 | Fluffy pieces with ragged edges | Mild diarrhoea |
| 7 | Watery, no solid pieces | Severe diarrhoea |
Constipation = predominantly Type 1–2.
6. Clinical Features
Every symptom should be understood in terms of why it occurs:
| Symptom | Pathophysiological Basis |
|---|---|
| Infrequent defecation (< 3/week) | Slow colonic transit → prolonged colonic water absorption → insufficient faecal mass to trigger defecation reflex |
| Hard, lumpy stools (BSFS 1–2) | Prolonged colonic transit → excessive water absorption from stool → dry, hard faecal pellets |
| Straining | Either: (a) hard stool requires more expulsive force, or (b) pelvic floor dyssynergia → paradoxical contraction of puborectalis/EAS → patient must generate very high intra-abdominal pressure to overcome outlet obstruction |
| Sensation of incomplete evacuation | Residual stool in rectum after defecation → persistent rectal distension → ongoing stretch receptor stimulation. Also seen in rectocele (stool pocketed in rectocele) |
| Sensation of anorectal blockage | Functional: dyssynergic defecation (puborectalis fails to relax). Structural: rectocele, rectal intussusception, large haemorrhoids |
| Need for digital manoeuvres | Patient may digitally evacuate stool or splint vaginal wall posteriorly (to support rectocele and redirect stool). This strongly suggests defecatory disorder |
| Abdominal pain/discomfort/bloating | Faecal distension of the colon → visceral afferent stimulation → crampy/colicky pain. Gas accumulation (bacterial fermentation of retained stool) → bloating. If pain is prominent and related to defecation, consider IBS-C [3] |
| Nausea/anorexia | Severe constipation with faecal loading → retrograde distension → reflex nausea via vagal afferents |
| Rectal bleeding | Hard stools cause mechanical trauma to anal mucosa → anal fissure (sharp pain on defecation + bright red blood on paper) or exacerbation of haemorrhoids (painless bright red blood coating stool) [5] |
| Overflow incontinence (paradoxical diarrhoea) | Severe faecal impaction in the rectum → liquid stool from above seeps around the impacted mass → patient reports "diarrhoea" when they are actually severely constipated. Classic in elderly/demented patients. |
| Abdominal distension | Gas and stool accumulation → visible and palpable distension, tympanitic on percussion |
| Tenesmus | Persistent urge to defecate despite incomplete or no evacuation → rectal mucosal irritation or residual stool. If persistent, consider rectal pathology (malignancy, proctitis) |
Red Flag — Overflow Incontinence in the Elderly
A common exam scenario: an elderly nursing home resident presents with "diarrhoea." The inexperienced student prescribes anti-diarrhoeals. Always do a rectal examination first — this may be overflow incontinence from faecal impaction, and anti-diarrhoeals would be disastrous. The treatment is disimpaction, not loperamide.
| Sign | How to Elicit | Pathophysiological Basis |
|---|---|---|
| Abdominal distension | Inspection | Faecal and gas accumulation in the colon |
| Palpable faecal masses | Palpation — typically in left iliac fossa and along the course of the descending/sigmoid colon | Firm, indentable masses that follow the course of the colon. Can be indented (unlike tumour, which is hard and non-indentable). The sigmoid colon is the most common site because it is the narrowest segment and the last "holding area" before the rectum. |
| Tympanitic percussion | Percussion over distended colon | Gas accumulation proximal to faecal loading |
| Reduced or altered bowel sounds | Auscultation | May be normal, or tinkling (if partial obstruction), or reduced (if adynamic ileus) |
| Rectal examination findings [1] | Key examination | Must be performed in every patient with constipation: |
| — Empty rectum | DRE | May suggest slow-transit constipation (stool hasn't reached the rectum), or proximal obstruction |
| — Loaded rectum with hard stool | DRE | Faecal impaction — the most common finding in chronic constipation |
| — Rectal mass | DRE | Suspect colorectal cancer — firm, irregular, fixed mass |
| — Anal stricture | DRE — finger cannot pass easily | Scarring from previous surgery, Crohn's disease, radiation, or chronic fissure |
| — Reduced anal tone | DRE | May indicate neurological cause (cauda equina, S2–S4 lesion) |
| — Paradoxical puborectalis contraction | DRE — ask patient to "bear down" / simulate defecation; the puborectalis should relax (examiner feels posterior pull releasing); if it contracts instead, this is paradoxical contraction | Suggests dyssynergic defecation |
| Perianal sensation and anal reflex [1] | Light touch perianally; pin-prick at anal margin should cause reflex EAS contraction ("anal wink") | Tests integrity of S2–S4 arc. Absent anal reflex suggests cauda equina syndrome or sacral nerve lesion — a neurological emergency if acute |
| Signs of hypothyroidism | General examination: dry skin, periorbital oedema, bradycardia, delayed relaxation of ankle jerks, goitre | Hypothyroidism is a secondary cause [1] |
| Signs of hypercalcaemia | Confusion, polyuria, polydipsia, muscle weakness, short QT on ECG | Hypercalcaemia → ↓smooth muscle excitability [2] |
| Signs of Parkinson's disease | Resting tremor, rigidity, bradykinesia, postural instability | Enteric Lewy body pathology → ↓colonic motility |
| Abdominal scars | Inspection | Previous surgery → adhesions → possible partial obstruction |
Key Examination Steps
"The important aspects are abdominal palpation and rectal examination. Test perianal sensation and the anal reflex. Perform sigmoidoscopy." [1]
The rectal examination is the single most important physical examination in constipation. It can identify:
- Faecal impaction
- Rectal mass (cancer)
- Rectocele
- Anal fissure/stricture
- Anal tone (neurological cause)
- Pelvic floor dyssynergia (paradoxical contraction on bearing down)
These are the features that should prompt urgent investigation (primarily to exclude colorectal cancer):
"Alarm symptoms are rectal bleeding, recent constipation in those > 40 years and family history of cancer." [1]
"Bleeding suggests cancer, haemorrhoids, diverticular disorder and inflammatory bowel disease." [1]
| Alarm Feature | Why It's Alarming |
|---|---|
| Rectal bleeding | May indicate CRC, IBD, or advanced diverticular disease [1] |
| Recent onset constipation in age > 40 | New-onset change in bowel habit in this age group has a significant risk of CRC [1] |
| Family history of colorectal cancer | Hereditary CRC syndromes (Lynch syndrome, FAP) significantly increase risk [1] |
| Unintentional weight loss | Suggests malignancy or systemic disease |
| Iron-deficiency anaemia | Occult GI blood loss — right-sided colon cancers classically present with anaemia rather than overt bleeding |
| Palpable abdominal or rectal mass | Direct evidence of tumour |
| Progressive worsening | Constipation that is steadily getting worse despite treatment suggests a progressive organic cause |
| Narrow-calibre ("pencil-thin") stools | Suggests distal colorectal/rectal lesion narrowing the lumen |
Hong Kong Context — CRC Screening
Colorectal cancer is the #1 cancer in Hong Kong by incidence (both sexes combined). The HK government provides a Colorectal Cancer Screening Programme for those aged 50–75. Any new-onset constipation in this age group must have CRC excluded. "If appropriate refer for sigmoidoscopy or colonoscopy and radiological studies (e.g. CT colonography, bowel transit studies)" [1].
Based on the lecture slides and clinical approach:
"The history should include stool consistency, frequency, ease of evacuation, pain on defecation and the presence of blood or mucus. A dietary and drug history is important." [1]
Structured History:
-
Characterise the constipation:
- Frequency of bowel movements per week
- Stool consistency (use Bristol Stool Form Scale)
- Straining? Sense of incomplete evacuation? Sensation of blockage?
- Need for digital manoeuvres?
- Duration: acute vs chronic
- Progression: stable, improving, or worsening
-
Associated symptoms:
- Bleeding (bright red per rectum? On paper? Mixed with stool? Dark/melaena?)
- Mucus (may suggest IBS, villous adenoma, rectal prolapse)
- Pain on defecation (anal fissure, thrombosed haemorrhoids)
- Abdominal pain (location, character, relationship to defecation — colicky pain relieved by defecation → IBS-C)
- Weight loss, appetite change, fatigue (alarm features)
- Nausea/vomiting (suggests severe impaction or obstruction)
-
Dietary history:
- Daily fibre intake (recommended 25–30 g/day)
- Daily fluid intake (recommended ≥1.5–2 L/day)
- Types of food (processed vs whole grain, fruits, vegetables)
-
Drug history [1]:
- Go through the drug list systematically (opioids, anticholinergics, CCBs, iron, antacids, TCAs, SSRIs, benzodiazepines, diuretics)
- Including OTC medications and supplements
-
Medical history:
- Hypothyroidism, DM, hypercalcaemia, neurological disease, psychiatric history
- Previous abdominal/pelvic surgery (adhesions)
- Previous colonoscopy results
-
Family history:
- CRC, IBD, polyposis syndromes
-
Psychosocial history:
- Depression screen, eating disorder screen
- Physical activity level
- Impact on quality of life
-
Obstetric/gynaecological history (in women):
- Multiparity, vaginal delivery (pelvic floor damage)
- Pelvic organ prolapse symptoms
"Basic tests are FBE/ESR, occult blood in stool. Consider serum calcium, potassium, CEA and TFTs. If appropriate refer for sigmoidoscopy or colonoscopy and radiological studies (e.g. CT colonography, bowel transit studies)." [1]
| Investigation | What You're Looking For |
|---|---|
| FBE (full blood examination) | Iron-deficiency anaemia (microcytic, ↓ferritin) → occult GI blood loss → CRC |
| ESR / CRP | Elevated in IBD, malignancy, infection |
| Occult blood in stool (FIT/FOBT) | Occult GI bleeding → CRC screening |
| Serum calcium | Hypercalcaemia → constipation [1] |
| Serum potassium | Hypokalaemia → constipation [1] |
| TFTs | Hypothyroidism → constipation [1] |
| CEA | Tumour marker for CRC (not diagnostic alone, but useful in monitoring) |
| Fasting glucose / HbA1c | Diabetes (autonomic neuropathy) |
| Renal function (Cr, BUN) | Uraemia, also needed for medication dosing |
| Sigmoidoscopy [1] | Visualise rectosigmoid — common site of CRC, can identify mucosal disease |
| Colonoscopy | Gold standard for excluding CRC in patients with alarm features |
| CT colonography | Alternative to colonoscopy in those who cannot tolerate or have incomplete colonoscopy |
| Bowel transit studies (radio-opaque markers) | Differentiate slow-transit from normal-transit constipation |
| Anorectal manometry + balloon expulsion test | Diagnose defecatory disorders / dyssynergia |
| Defecography (MRI or barium) | Identify structural outlet obstruction (rectocele, intussusception, perineal descent) |
High Yield Summary
Key Points for Constipation (Pre-DDx/Dx/Mx):
-
Definition: Always clarify what the patient means — constipation is subjective. Rome IV criteria define functional constipation (≥2 of 6 symptoms for ≥3 months).
-
Epidemiology: ~10–15% global prevalence; more common in females, elderly, institutionalised. In HK, CRC is the #1 cancer — always exclude malignancy in new-onset constipation > 40 years.
-
Three functional subtypes: Normal-transit (most common), slow-transit, and defecatory disorder (outlet obstruction). Often overlap.
-
Secondary causes (must exclude): Drugs (most common reversible cause: opioids, anticholinergics, CCBs, iron, TCAs, SSRIs, benzodiazepines, aluminium antacids), hypothyroidism, hypercalcaemia, hypokalaemia, diabetes, spinal dysfunction, depression, anorexia nervosa, CRC.
-
Drug-induced constipation is extremely common and reversible — always take a thorough drug history.
-
Alarm features: Rectal bleeding, new constipation > 40 years, family history of CRC, weight loss, anaemia, palpable mass, progressive worsening.
-
Key examination: Abdominal palpation + rectal examination (loaded rectum? mass? tone? dyssynergia?) + perianal sensation + anal reflex + sigmoidoscopy.
-
Key basic investigations: FBE, ESR, occult blood in stool, serum Ca²⁺, K⁺, TFTs, CEA. Colonoscopy if alarm features present.
-
Constipation causes other problems: ↑IAP → GERD, haemorrhoids, hernia, varicose veins, rectal prolapse; faecal loading → sigmoid volvulus, diverticular disease; precipitates AROU (especially in males with BPH).
Active Recall - Constipation: Definition, Epidemiology, Aetiology, Pathophysiology and Clinical Features
[1] Lecture slides: murtagh merge.pdf (Chronic constipation section, p31) [2] Senior notes: maxim.md (Section 4.6 – Constipation DDx: IBS, drugs e.g. CCB, hypothyroidism, hyperCa, hypoK, cord compression, IO) [3] Senior notes: Ryan Ho GI.pdf (Section 3.2.1 – Irritable Bowel Syndrome, p118) [4] Senior notes: maxim.md (Diverticular disease section – pathophysiology, risk factors) [5] Senior notes: felixlai.md (Hemorrhoids – anatomy of anal canal, risk factors including constipation) [6] Senior notes: felixlai.md (Rectal prolapse, sigmoid volvulus – constipation as risk factor) [7] Senior notes: felixlai.md (Acute retention of urine – constipation as outflow obstruction cause/precipitant) [8] Senior notes: Ryan Ho Fundamentals.pdf (p349–350: AROU – constipation as precipitating factor) [9] Senior notes: Ryan Ho GI.pdf (p57: GERD – constipation as cause of increased IAP) [10] Senior notes: maxim.md (Haemorrhoids – risk factors including constipation) [11] Senior notes: maxim.md (Volvulus – risk factors including chronic constipation) [12] Senior notes: felixlai.md (Hernia – risk factors including chronic constipation) [13] Senior notes: felixlai.md (Varicose veins – risk factors including constipation)
Differential Diagnosis of Constipation
The approach to differential diagnosis of constipation is fundamentally about sorting the common from the dangerous and the reversible from the irreversible. The lecture slides provide a superb clinical reasoning framework using Murtagh's Diagnostic Strategy [1], which organises differentials by clinical probability rather than by organ system. Let's work through this systematically.
This is a structured clinical reasoning tool that every HKU medical student should know. It forces you to think in layers of probability:
1. Probability Diagnosis (Most Common)
These are the diagnoses you will encounter most frequently in clinical practice. They account for the vast majority of constipation presentations.
- Why it's most common: Modern diets (particularly in urban Hong Kong) are low in fibre. The average HK adult consumes approximately 10–15 g fibre/day vs the recommended 25–30 g/day. Combined with sedentary lifestyle and habitual suppression of the urge to defecate (e.g. busy office workers, school children), this is by far the most frequent cause.
- Mechanism: ↓fibre → ↓faecal bulk → ↓stimulation of colonic stretch receptors → ↓peristalsis → ↑colonic transit time → ↑water absorption → hard, dry stools. Poor fluid intake compounds this by reducing the water available for stool softening.
- "Bad habit" refers to ignoring the call to stool — when you repeatedly suppress the defecation reflex, rectal stretch receptors undergo accommodation (desensitisation), so over time the rectum tolerates larger volumes before signalling urgency. This leads to progressively harder, larger stools and a vicious cycle.
- Also called colonic inertia
- Mechanism: ↓high-amplitude propagating contractions (HAPCs) → stool moves slowly through the colon → excessive water absorption → very infrequent, hard stools
- Pathology may involve reduced interstitial cells of Cajal (gut pacemaker cells) and reduced enteric neuronal density
- More common in young women
- Patients often report ↓urge to defecate (because stool rarely reaches the rectum)
- Diagnosed by radio-opaque marker (Sitz marker) transit study or wireless motility capsule
- i.e. IBS-C (IBS with constipation) [3]
- Objective colonic transit is actually normal, but patients perceive difficulty
- Key distinguishing feature: IBS-C has prominent abdominal pain (≥1 day/week for 3 months) that is characteristically associated with defecation — either improved or worsened by it [3]
- Pathophysiology involves visceral hypersensitivity, altered brain-gut axis, psychosocial factors, and possibly ↓5-HT release (serotoninergic imbalance — ↓serotonin in IBS-C vs ↑serotonin in IBS-D) [3]
- Rome IV criteria for IBS: recurrent abdominal pain ≥1 day/week for 3 months, associated with ≥2 of: related to defecation, change in stool frequency, change in stool form [3]
DDx of constipation from maxim.md: IBS, drugs (e.g. CCB), hypothyroidism, hyperCa, hypoK, cord compression, IO [2]
2. Serious Disorders Not to Be Missed
These are the diagnoses that, if missed, could lead to significant morbidity or mortality. They must be actively excluded in every patient.
- Colorectal cancer (CRC) is the #1 cancer in Hong Kong by incidence. This cannot be overemphasised.
- Why CRC causes constipation: a growing tumour progressively narrows the colonic lumen → mechanical obstruction to stool passage. Left-sided/sigmoid/rectal cancers are more likely to cause constipation (because the lumen is narrower and stool is more formed at this point). Right-sided cancers more often present with iron-deficiency anaemia (occult bleeding) rather than obstruction.
- Key red flags: recent onset constipation in those > 40 years, rectal bleeding, family history of cancer [1 — from prior section], alternating constipation and diarrhoea, pencil-thin stools, tenesmus, weight loss, iron-deficiency anaemia [4]
- Pencil-thin stools → the tumour creates a narrow stricture, so stool must squeeze through a constricted lumen, producing thin, ribbon-like stools
- Alternating constipation and diarrhoea → the partial obstruction causes build-up of stool proximally (constipation), then when liquid stool eventually passes the obstruction, the patient has a burst of loose stool (diarrhoea)
- Mechanism: extrinsic compression of the colon/rectum by a pelvic or abdominal mass
- Ovarian cancer: often presents late with vague abdominal symptoms — bloating, pelvic pressure, constipation. The mass compresses the rectosigmoid externally.
- Lymphoma: mesenteric or retroperitoneal lymphadenopathy can compress the bowel. Also consider lymphomatous infiltration of the bowel wall.
- "Hirschsprung" → named after Harald Hirschsprung, but the name can be broken down conceptually: it is a disease of absent ganglion cells (aganglionosis)
- Pathophysiology: congenital absence of ganglion cells in both Auerbach's (myenteric) and Meissner's (submucosal) plexuses in a segment of colon → the aganglionic segment cannot relax and cannot propagate peristalsis → functional obstruction [5]
- The aganglionic segment is always distal (starts at the internal anal sphincter and extends proximally for a variable distance — most commonly rectosigmoid ~75%)
- Classic presentation: neonate who fails to pass meconium within 48 hours of birth, bilious vomiting, abdominal distension [5]
- Can rarely present in older children/adults with chronic constipation (ultra-short segment or short-segment Hirschsprung)
- Gold standard diagnosis: full-thickness rectal suction biopsy showing absent ganglion cells + hypertrophied nerve trunks [5]
- Anorectal manometry: absence of the rectoanal inhibitory reflex (RAIR) — normally, rectal distension causes IAS relaxation; in Hirschsprung, this reflex is absent because the aganglionic segment cannot relay the inhibitory signal [5]
Why does the aganglionic segment not relax?
Normal IAS relaxation during defecation depends on inhibitory neurons in the myenteric plexus that release nitric oxide (NO) and vasoactive intestinal peptide (VIP). In Hirschsprung disease, these neurons are absent → the IAS and affected bowel segment remain tonically contracted → functional obstruction despite a structurally patent lumen. The bowel proximal to the aganglionic segment dilates massively (megacolon) because it has normal ganglion cells and is trying to overcome the downstream obstruction.
3. Pitfalls (Often Missed)
These are diagnoses that clinicians frequently overlook. They are the "gotcha" conditions on exams and in real clinical practice.
- Why it's a pitfall: patients (especially elderly, demented, or bedbound) may present with paradoxical "overflow diarrhoea" — liquid stool leaks around a hard faecal mass in the rectum, and the inexperienced clinician treats it as diarrhoea instead of recognising the underlying impaction
- Mechanism: chronic constipation → large, hard faecal mass accumulates in the rectum → stretches the rectum beyond the point where normal defecation reflexes can expel it → liquid stool from above seeps around the mass
- Diagnosis: simple — digital rectal examination reveals a rock-hard mass in the rectum
- Treatment: manual disimpaction ± enemas, NOT anti-diarrhoeals
- Why it's a pitfall: the patient may not volunteer information about anal symptoms due to embarrassment; the clinician who doesn't examine the anus will miss this
- Mechanism of constipation: anal fissure causes intense pain on defecation → the patient consciously avoids defecation (fear-avoidance) → stool accumulates and hardens → even more painful to pass → vicious cycle. Additionally, the fissure causes reflex spasm of the IAS, creating a functional outlet obstruction [6]
- Typical anal fissure: single, posterior midline, with sentinel skin tag and hypertrophied anal papilla if chronic [6]
- Two aspects:
- Drug-induced constipation: as detailed in the prior section — opioids, anticholinergics, CCBs, iron, etc. [2]
- Purgative (laxative) abuse: paradoxically, chronic stimulant laxative use causes constipation. Mechanism: chronic stimulation of myenteric neurons by stimulant laxatives (e.g. senna, bisacodyl) → enteric neuronal damage and melanosis coli (brown-black pigmentation of colonic mucosa from lipofuscin-laden macrophages) → the colon becomes dependent on laxatives and loses intrinsic motility → cathartic colon (dilated, atonic colon)
Laxative Abuse — A Paradoxical Cause of Constipation
This is a classic exam trap. A young woman with an eating disorder takes stimulant laxatives (senna/bisacodyl) daily for years → develops chronic constipation that is worse than before she started laxatives. On colonoscopy, you see melanosis coli (dark brown mucosa). The treatment is gradual laxative withdrawal and switch to osmotic agents (e.g. PEG/macrogol), NOT more stimulant laxatives.
- A classic pitfall, especially in the elderly on diuretic therapy [1 — from prior section]
- Mechanism: K⁺ depletion → smooth muscle cells remain relatively hyperpolarised (because the resting membrane potential becomes more negative when extracellular K⁺ is low) → ↓contractility of GI smooth muscle → ↓colonic motility → constipation
- Other causes of hypokalaemia to consider: vomiting, diarrhoea, hyperaldosteronism, renal tubular acidosis
- ECG findings: ↓T wave flattening, ↑U wave amplitude, prolonged QT interval [8]
- Mechanism: multifactorial — psychomotor retardation → ↓physical activity → ↓colonic motility; ↓appetite → ↓food intake → ↓faecal bulk; medications (TCAs, SSRIs) directly constipating; altered brain-gut axis via autonomic dysfunction
- A pitfall because patients may present with somatic complaints (constipation, fatigue, pain) without volunteering psychological symptoms
- Always screen for depression in chronic constipation, especially if no obvious secondary cause identified
- Distinguished from congenital megacolon (Hirschsprung)
- Acquired megacolon refers to chronic dilatation of the colon from long-standing constipation or other causes
- Mechanism: chronic faecal retention → progressive rectal/colonic dilatation → rectal hyposensitivity (stretch receptors accommodate to the chronically distended wall) → ever-larger volumes needed to trigger defecation urge → further distension → vicious cycle
- Causes include: chronic idiopathic constipation, psychiatric illness, neurological disease (Parkinson's, MS), Chagas disease
- Risk: sigmoid volvulus (elongated, dilated sigmoid with narrow mesenteric base can twist) [9], faecal impaction, stercoral ulceration, perforation
- Why it causes constipation: symptomatic uncomplicated diverticular disease (SUDD) can cause altered bowel habits including constipation and/or diarrhoea. Complicated diverticulitis with fibrotic stricture can cause mechanical large bowel obstruction [10].
- Mechanism of diverticula formation: bowel weakening with aging + increased intraluminal pressure (from constipation) → outpouching at weakest points where vasa recta penetrate circular muscle [10]
- Constipation is both a cause of diverticular disease (chronic straining → ↑intraluminal pressure) and a consequence (stricture formation from chronic diverticulitis)
- Most common site: right-sided in Asia, sigmoid in Western countries [10]
| Rare Differential | Mechanism of Constipation |
|---|---|
| Lead poisoning | Lead inhibits smooth muscle contraction and damages the enteric nervous system → colicky abdominal pain ("lead colic") + constipation. Also causes basophilic stippling of RBCs, wrist/foot drop, and blue gum line (Burton's line). |
| Hypercalcaemia | Ca²⁺ stabilises cell membranes → ↓smooth muscle excitability → ↓colonic contraction. "Bones, stones, abdominal moans (constipation), and psychic groans." |
| Hyperparathyroidism | The most common cause of hypercalcaemia → constipation via the mechanism above |
| Dolichocolon / megarectum | "Dolicho-" from Greek dolikhos = long; an abnormally long colon → ↑transit time → ↑water absorption → constipation. Megarectum = abnormally dilated rectum → rectal hyposensitivity |
| Chagas disease | Trypanosoma cruzi infection destroys myenteric plexus neurons → acquired aganglionosis → megacolon/megaoesophagus. Endemic in South America, essentially absent in HK but important for differential diagnosis knowledge. |
| Systemic sclerosis (scleroderma) | Fibrosis and atrophy of GI smooth muscle (particularly the inner circular layer) + vascular damage → ↓colonic motility. Can affect the entire GI tract — oesophageal dysmotility is the most common GI manifestation, but colonic involvement causes severe constipation. |
The "Masquerades Checklist" [1] is Murtagh's systematic screen for common conditions that masquerade as many different presentations. For constipation, the relevant masquerades are:
| Masquerade | Relevance to Constipation |
|---|---|
| Depression [1] | As above — psychomotor retardation, ↓appetite, medications |
| Diabetes (rarely) [1] | Autonomic neuropathy → ↓colonic motility. "Rarely" because it is an uncommon presentation of DM; most diabetic patients with constipation have other contributing factors. |
| Drugs (opiates, iron, others) [1] | The most important masquerade — always check the medication list |
| Thyroid disorder (hypothyroidism) [1] | ↓T₃ → ↓basal metabolic rate → ↓GI smooth muscle contractility → slow transit |
| Spinal dysfunction (severe only) [1] | Disrupts extrinsic neural control of defecation; must be severe (e.g. cord compression, cauda equina) to cause constipation as a presenting complaint |
Masquerades — Don't Forget the Basics
When you're stuck with a patient whose constipation doesn't make sense, run through the masquerades: Depression, Diabetes, Drugs, Thyroid, Spine. These are conditions that "dress up" as other things and are easily missed if you don't actively look for them.
"May be functional (e.g. depression, anorexia nervosa)" [1]
This is Murtagh's reminder to consider the psychosocial dimension. Some patients use somatic complaints as a way to seek help for underlying psychological distress:
- Depression: constipation may be the "ticket of entry" to medical care for someone who is actually severely depressed but reluctant to discuss mood
- Anorexia nervosa: severe caloric restriction → ↓faecal bulk → constipation; also associated with laxative abuse (see above) [7]
- Somatisation disorder: multiple unexplained physical symptoms including constipation, in the context of psychological distress
- Sexual abuse / trauma: some patients (especially children, adolescents) with constipation/encopresis may have underlying abuse — always consider in the appropriate context
6. Additional Important Differentials Not Explicitly in Murtagh's
These deserve mention for completeness and exam preparation:
- IO is listed in maxim.md's DDx of constipation [2]
- Absolute constipation (inability to pass both faeces AND flatus = obstipation) is a cardinal feature of complete bowel obstruction [11]
- Causes of large bowel obstruction: CRC (most common), diverticular stricture, volvulus (sigmoid > caecal)
- Causes of small bowel obstruction: adhesions (most common, 60%), hernia (10%), tumour (20%) [11]
- Key distinguishing feature: obstipation + colicky abdominal pain + abdominal distension + vomiting. The pattern differs between SBO and LBO (SBO: early vomiting, less distension; LBO: late vomiting, more distension) [11]
- Cord compression is listed in maxim.md's DDx [2]
- Conus medullaris syndrome: mixed UMN + LMN signs, saddle anaesthesia, early sphincter failure → painless AROU + constipation + incontinence [12]
- Cauda equina syndrome: pure LMN signs, saddle anaesthesia, sphincter failure → constipation + AROU + incontinence [12]
- Why constipation occurs: disruption of sacral parasympathetic outflow (S2–S4) → loss of the defecation reflex → inability to initiate coordinated colonic propulsion and rectal evacuation
- This is a neurosurgical emergency if acute — irreversible if not decompressed early
- Ogilvie's syndrome (acute colonic pseudo-obstruction): S/S of mechanical obstruction in the absence of a mechanical cause
- Mechanism: autonomic imbalance (↓parasympathetic / ↑sympathetic) → aperistalsis [13]
- Causes: metabolic disturbance (DM, hypoK, hypothyroidism, uraemia), drugs (opioids, CCB), post-operative, neurological disease (Parkinson's, MS) [13]
- Key differentiating signs from mechanical obstruction: normal bowel sounds, dilated rectum on PR exam (cf. collapsed rectum in mechanical obstruction) [13]
- Constipation is one of the most common non-motor symptoms of PD and may precede motor symptoms by years
- Mechanism: Lewy body pathology directly affects the enteric nervous system (alpha-synuclein deposits in myenteric plexus neurons) → ↓colonic motility. Also: ↓physical activity, anticholinergic medications
- Constipation: common, consider high-fibre diet, bulk/osmotic laxative, ↑fluid intake/exercise [14]
| Category | Differential | Key Distinguishing Feature(s) |
|---|---|---|
| Probability | Simple constipation (low fibre, poor fluid, lifestyle) [1] | No alarm features; dietary history reveals inadequate fibre/fluid; improves with lifestyle modification |
| Slow-transit constipation [1] | Young women; ↓urge; prolonged transit on Sitz marker study | |
| IBS-C [1][3] | Prominent abdominal pain associated with defecation; Rome IV criteria; no alarm features | |
| Serious | Colorectal cancer [1] | Age > 40; rectal bleeding; weight loss; anaemia; pencil-thin stools; alternating constipation/diarrhoea; palpable mass |
| Extrinsic malignancy (lymphoma, ovarian CA) [1] | Pelvic mass; constitutional symptoms; lymphadenopathy | |
| Hirschsprung disease (children) [1][5] | Neonatal: failure to pass meconium; abdominal distension; absent RAIR on manometry; absent ganglion cells on biopsy | |
| Pitfalls | Impacted faeces [1] | Overflow diarrhoea in elderly; hard mass on DRE |
| Anal fissure [1][6] | Severe pain on defecation; bright red blood on paper; posterior midline tear on inspection | |
| Drug/purgative abuse [1][7] | Thorough drug Hx; melanosis coli on colonoscopy (stimulant laxative abuse); eating disorder Hx | |
| Hypokalaemia [1][8] | Elderly on diuretics; K⁺ < 3.5 mmol/L; ECG changes (flat T, prominent U wave) | |
| Depressive illness [1] | Low mood; anhedonia; sleep disturbance; psychomotor retardation; ↓appetite | |
| Acquired megacolon [1] | Chronic constipation Hx; massively dilated colon on AXR; rectal hyposensitivity | |
| Diverticular disease [1][10] | Colicky LLQ pain (or RLQ in Asia) relieved by defecation; stricture causing obstruction; history of diverticulitis | |
| Rare | Lead poisoning, hypercalcaemia, hyperparathyroidism, dolichocolon, Chagas disease, systemic sclerosis [1] | Specific features of each condition (see table above) |
| Masquerades | Depression, Diabetes, Drugs, Thyroid disorder, Spinal dysfunction [1] | Systematic screening: mood, HbA1c, drug review, TFTs, neurological exam |
| Psychosocial | Depression, anorexia nervosa [1][7] | "Is the patient trying to tell me something?" — screen for psychiatric/eating disorders |
| Mechanical IO | Adhesions, hernia, volvulus, tumour [2][11] | Obstipation (no flatus); colicky pain; distension; vomiting; radiological evidence of obstruction |
| Neurological | Cord compression, cauda equina, Parkinson's [2][12][14] | Saddle anaesthesia, sphincter disturbance; TRAP signs in PD |
| Functional IO | Pseudo-obstruction (Ogilvie's) [13] | Features of obstruction but normal bowel sounds + dilated rectum on DRE; diagnosis of exclusion |
The key clinical question when evaluating constipation is: Is this functional/primary, or is there a secondary cause I must identify and treat?
The Two Critical Questions in Constipation DDx
- Is there a dangerous cause I must not miss? → CRC, cord compression, extrinsic malignancy → Look for alarm features
- Is there a reversible secondary cause? → Drugs, hypothyroidism, hypercalcaemia, hypokalaemia, depression → Systematic screen
If the answer to both is "no," you are dealing with primary/functional constipation and can proceed with lifestyle modification and, if refractory, physiological testing to subclassify.
| Feature | IBS-C | Slow-Transit | Defecatory Disorder | CRC | Mechanical IO |
|---|---|---|---|---|---|
| Pain | Prominent, related to defecation | Minimal | Straining-related | Progressive, may be colicky | Colicky, severe |
| Stool frequency | Variable | Very infrequent | Variable (often normal frequency but incomplete evacuation) | Progressive ↓ | Absent (obstipation) |
| Bloating | Prominent | Variable | Less prominent | Late | Prominent |
| Rectal bleeding | Absent | Absent | Possible (haemorrhoids from straining) | Common | Late (if ischaemia) |
| DRE | Normal | Empty rectum | Stool present, paradoxical contraction | Mass may be palpable | Empty rectum (distal collapse) |
| Weight loss | Absent | Absent | Absent | Common | Possible (late) |
| Vomiting | Absent | Absent | Absent | Late | Early (SBO) or late (LBO) |
| Flatus | Present (often excessive) | Present | Present | Present (early) | Absent (complete IO) |
| Rome IV criteria | Met | Not met for IBS | Not met for IBS | N/A | N/A |
| Transit study | Normal | Prolonged | Normal or prolonged | N/A | N/A |
| Anorectal manometry | Normal | Normal | Abnormal (↓rectal pressure, paradoxical contraction) | N/A | N/A |
| Balloon expulsion | Normal | Normal | Failed (cannot expel balloon) | N/A | N/A |
High Yield Summary — Differential Diagnosis of Constipation
Murtagh's Framework [1]:
- Probability diagnosis: Simple constipation (low fibre/fluid/lifestyle), slow-transit constipation, IBS-C
- Serious not to miss: CRC (intrinsic neoplasia), extrinsic malignancy (lymphoma, ovarian CA), Hirschsprung (children)
- Pitfalls: Impacted faeces (overflow diarrhoea!), anal fissure, drug/purgative abuse, hypokalaemia (elderly on diuretics!), depressive illness, acquired megacolon, diverticular disease
- Masquerades: Depression, Diabetes, Drugs, Thyroid (hypothyroidism), Spinal dysfunction
- Psychosocial: "Is the patient trying to tell me something?" — depression, anorexia nervosa
Additional important DDx [2]: IO (mechanical), cord compression/cauda equina, pseudo-obstruction (Ogilvie's), Parkinson's disease
First priorities: Exclude alarm features → investigate for CRC. Exclude reversible secondary causes (drugs, metabolic, neurological). Only then classify as primary/functional.
Active Recall - Differential Diagnosis of Constipation
References
[1] Lecture slides: murtagh merge.pdf (Chronic constipation — Murtagh's Diagnostic Strategies, p30–31) [2] Senior notes: maxim.md (Section 4.6 — Constipation DDx: IBS, drugs e.g. CCB, hypothyroidism, hyperCa, hypoK, cord compression, IO) [3] Senior notes: Ryan Ho GI.pdf (Section 3.2.1 — Irritable Bowel Syndrome, p118–119) [4] Senior notes: Ryan Ho Fundamentals.pdf (p283 — Worrying signs of colorectal CA) [5] Senior notes: felixlai.md (Hirschsprung disease — pathophysiology, clinical manifestation, diagnosis) [6] Senior notes: felixlai.md (Anal fissure — clinical manifestation, differential diagnosis) [7] Senior notes: Ryan Ho Psychiatry.pdf (p216 — Bulimia nervosa: stimulant laxative causing chronic constipation, melanosis coli) [8] Senior notes: Ryan Ho Urogenital.pdf (p25 — Hypokalaemia clinical features: GI dysfunction, constipation, ECG changes) [9] Senior notes: felixlai.md (Sigmoid volvulus — chronic faecal overloading predisposing to volvulus) [10] Senior notes: maxim.md (Diverticular disease — pathophysiology, risk factors, complications) [11] Senior notes: felixlai.md (Intestinal obstruction — cardinal features, aetiology) [12] Senior notes: Ryan Ho Neurology.pdf (p53 — Conus medullaris and cauda equina syndrome: constipation, sphincter failure) [13] Senior notes: maxim.md (Pseudo-obstruction — Ogilvie's syndrome, clinical features, differentiating signs) [14] Senior notes: Ryan Ho Neurology.pdf (p121 — Parkinson's disease non-motor symptoms: constipation)
Diagnostic Criteria, Algorithm and Investigations for Constipation
1. Diagnostic Criteria
The diagnosis of constipation operates on two levels: (1) establishing that the patient has constipation (which is primarily clinical, using standardised criteria), and (2) identifying the underlying cause (primary vs secondary). Let me walk through both.
These are the internationally accepted criteria. "Rome" refers to the Rome Foundation, which periodically convenes to define functional GI disorders. The criteria exist because constipation is subjective — you need a standardised definition for clinical practice and research.
Rome IV Diagnostic Criteria for Functional Constipation:
Must include ≥2 of the following (for the last 3 months, with symptom onset ≥6 months before diagnosis):
- Straining during > 25% of defecations
- Lumpy or hard stools (Bristol Stool Form Scale 1–2) in > 25% of defecations
- Sensation of incomplete evacuation in > 25% of defecations
- Sensation of anorectal obstruction/blockage in > 25% of defecations
- Manual manoeuvres to facilitate defecation (e.g. digital evacuation, perineal/vaginal splinting) in > 25% of defecations
- Fewer than 3 spontaneous bowel movements per week
AND:
- Loose stools are rarely present without the use of laxatives
- Insufficient criteria for IBS (i.e. abdominal pain is NOT the predominant symptom)
Why these specific criteria? Each criterion maps onto a specific pathophysiological mechanism:
- Criteria 1, 4, 5 → suggest defecatory disorder (outlet obstruction/dyssynergia)
- Criterion 2 → suggests slow transit (excessive water absorption) or inadequate fibre
- Criterion 3 → suggests either defecatory disorder (residual stool) or rectal hyposensitivity
- Criterion 6 → suggests slow transit or severe outlet obstruction
Rome IV: Functional Constipation vs IBS-C
The key distinction is abdominal pain. If the patient meets Rome IV criteria for IBS (recurrent abdominal pain ≥1 day/week for 3 months, associated with ≥2 of: related to defecation, change in stool frequency, change in stool form) [3], they have IBS-C, not functional constipation. In practice, patients often straddle the boundary, and the distinction matters mainly for treatment selection (IBS-C-specific therapies like linaclotide target both pain and constipation) [3].
The BSFS is incorporated into Rome IV as an objective measure of stool consistency. Constipation corresponds to Type 1 (separate hard lumps) and Type 2 (lumpy sausage-shaped). The scale is used because verbal descriptions of "hard" or "soft" vary enormously between patients — the visual scale standardises this.
Rome IV criteria are designed for primary/functional constipation in the absence of alarm features. The criteria should only be applied after excluding secondary causes and red flags:
"Alarm symptoms are rectal bleeding, recent constipation in those > 40 years and family history of cancer" [1]
If alarm features are present, you do not apply Rome IV — you investigate immediately to exclude organic pathology (especially colorectal cancer).
The algorithm below integrates the lecture slides' approach [1] with current guidelines (AGA 2024, BSG 2023). The principle is: exclude dangerous → exclude reversible → classify and treat.
Let me elaborate on each step:
3. Investigation Modalities — Detailed
Before ordering any test, the history and examination will direct your entire workup.
History — as stated in the lecture slides [1]:
"Define what exactly the patient means by constipation. The history should include stool consistency, frequency, ease of evacuation, pain on defecation and the presence of blood or mucus. A dietary and drug history is important." [1]
| History Component | What to Ask | Why |
|---|---|---|
| Stool consistency | Use BSFS chart — show the patient | Determines if truly constipated (Type 1–2) vs just infrequent |
| Frequency | How many spontaneous BMs per week? | < 3/week = one of the Rome IV criteria |
| Ease of evacuation | Straining? How long on the toilet? | Suggests defecatory disorder if excessive straining |
| Pain on defecation | Sharp/tearing pain? Where exactly? | Suggests anal fissure [6] → fear-avoidance → worsening constipation |
| Blood | On paper? Mixed with stool? Dark? | "Bleeding suggests cancer, haemorrhoids, diverticular disorder and inflammatory bowel disease" [1] |
| Mucus | Mucus per rectum? | Suggests IBS, villous adenoma, rectal prolapse |
| Digital manoeuvres | Do you need to use fingers to help evacuate? Splint vagina/perineum? | Strongly suggests defecatory disorder or rectocele |
| Dietary history | Fibre intake? Fluid intake? | Low fibre/fluid = most common cause |
| Drug history [1] | Systematic review of all medications | "Drugs selected associated with constipation: analgesics, opioids esp. codeine, TCAs, antacids esp. aluminium hydroxide, Ca channel blockers, SSRIs, cough mixtures, anti-cholinergics, benzodiazepines" [1] |
| Laxative use | What type? How often? How long? | Chronic stimulant laxative abuse → cathartic colon |
| Psychiatric screen | Mood? Appetite? Sleep? Body image? | Depression, anorexia nervosa [1] |
Physical Examination — lecture slides emphasise three key components [1]:
"The important aspects are abdominal palpation and rectal examination. Test perianal sensation and the anal reflex. Perform sigmoidoscopy." [1]
| Examination | Technique | Key Findings and Interpretation |
|---|---|---|
| Abdominal palpation | Systematic palpation of all 9 regions | Palpable faecal masses (firm, indentable, follow colonic course — especially LIF along sigmoid); abdominal distension; tenderness (suggests complication — diverticulitis, obstruction); palpable mass (suspect malignancy if hard, irregular, fixed) |
| Digital rectal examination (DRE) [1] | Inspect perianal area first (fissure, skin tags, external haemorrhoids, prolapse); then digital examination assessing tone, squeeze, masses, stool | See detailed DRE interpretation table below |
| Perianal sensation [1] | Light touch with cotton wool in the perianal region (dermatomes S2–S4) | Absent/reduced sensation → sacral nerve lesion, cauda equina syndrome |
| Anal reflex [1] | Stroke perianal skin with orange stick → observe for reflex contraction of EAS ("anal wink") | Absent anal wink → disruption of S2–S4 reflex arc → neurosurgical emergency if acute (cauda equina) |
| Sigmoidoscopy [1] | Rigid or flexible sigmoidoscopy in the office | Visualise rectosigmoid mucosa for tumour, polyps, proctitis, melanosis coli (laxative abuse), solitary rectal ulcer |
DRE — Detailed Interpretation:
| DRE Finding | Interpretation | Significance |
|---|---|---|
| Hard impacted stool | Faecal impaction | Most common finding in chronic constipation; may cause overflow incontinence in elderly |
| Empty rectum | Stool has not reached rectum | Suggests slow-transit constipation (stool still in proximal colon) or recent evacuation |
| Rectal mass — hard, irregular, fixed | Suspect rectal carcinoma | Urgent colonoscopy + biopsy required |
| Reduced resting tone | IAS dysfunction or neurological cause | Consider neurogenic bowel (S2–S4 lesion) |
| Reduced squeeze pressure | EAS weakness | Pudendal neuropathy, obstetric injury |
| Paradoxical contraction on bearing down | Ask patient to "push" as if defecating; puborectalis should relax (felt as posterior release). If it contracts instead → dyssynergia | Strongly suggests defecatory disorder — the single most useful bedside test for this |
| Rectocele | Anterior bulge of rectal wall palpable through posterior vaginal wall | Stool can pocket into rectocele during evacuation |
| Tenderness, fluctuance | Abscess (perianal or ischiorectal) | May be causing reflex constipation from pain avoidance |
| Smooth, symmetrically enlarged prostate | BPH | Not directly causing constipation, but constipation can precipitate AROU in men with BPH [15] |
The DRE is Non-Negotiable
A common mistake is to skip the DRE. In constipation, DRE provides critical information that no blood test or scan can give you: faecal impaction, rectal mass, anal tone, and dyssynergia. "Key examination: The important aspects are abdominal palpation and rectal examination" [1]. If you do nothing else, do a DRE.
These are the "key investigations" from the lecture slides [1]:
"Basic tests are FBE/ESR, occult blood in stool. Consider serum calcium, potassium, CEA and TFTs." [1]
| Investigation | What It Tests | Key Findings | Why / What It Excludes |
|---|---|---|---|
| FBE (Full Blood Examination / CBC) [1] | Complete blood count with differential | Microcytic hypochromic anaemia (↓MCV, ↓MCH, ↓ferritin, ↑TIBC) = iron-deficiency anaemia | Occult GI blood loss from colorectal cancer (especially right-sided tumours that bleed insidiously). Also check for leukocytosis (infection, obstruction) and eosinophilia (parasitic, allergic) |
| ESR [1] | Erythrocyte sedimentation rate (acute phase reactant) | ↑ESR | Non-specific but elevated in malignancy, IBD, infection, inflammation. Helps identify if there's an underlying organic process vs purely functional |
| Occult blood in stool [1] | Faecal immunochemical test (FIT) or guaiac-based FOBT | Positive = occult GI bleeding | Screens for CRC and other mucosal lesions. FIT is preferred over guaiac FOBT because it is specific for human haemoglobin and does not require dietary restriction. A positive FIT mandates colonoscopy. |
| Serum calcium [1] | Total Ca²⁺ (always correct for albumin: corrected Ca = measured Ca + 0.02 × (40 − albumin in g/L)) | Hypercalcaemia ( > 2.6 mmol/L or corrected Ca > 10.5 mg/dL) | Ca²⁺ excess stabilises cell membranes → ↓smooth muscle excitability → constipation. "Stones, bones, groans, moans, thrones, psychiatric overtones" [16]. Causes: primary hyperPTH, malignancy (esp breast, lung, myeloma), granulomatous disease (TB, sarcoidosis) [16] |
| Serum potassium [1] | Serum K⁺ | Hypokalaemia ( < 3.5 mmol/L) | K⁺ depletion → smooth muscle hyperpolarisation → ↓contractility → constipation + ileus. "Beware of hypokalaemia causing constipation in the elderly patient on diuretic treatment" [1]. ECG: ↓T wave flattening and ↑U wave amplitude [17] |
| TFTs (Thyroid Function Tests) [1] | TSH (± free T₄) | ↑TSH + ↓fT₄ = primary hypothyroidism | Hypothyroidism → ↓metabolic rate → ↓GI smooth muscle contractility → slow transit constipation. One of the classic "masquerades" [1] |
| CEA (Carcinoembryonic Antigen) [1] | Tumour marker | ↑CEA ( > 4.7 ng/mL) | Low sensitivity (~50%) and low specificity for CRC — can be elevated in smoking, pregnancy, TB, IBD, other carcinomas [18]. NOT diagnostic alone, but useful for: (a) raising suspicion when elevated in context of alarm features, (b) baseline pre-treatment level for monitoring, (c) detection of recurrence post-operatively. False negatives common because CEA may be first-pass metabolised by the liver [18] |
| Fasting glucose / HbA1c | Screen for diabetes | ↑glucose or HbA1c ≥ 6.5% | Diabetic autonomic neuropathy → ↓colonic motility [1] |
| RFT (Renal Function Tests) | Creatinine, BUN, electrolytes | ↑Cr/BUN = uraemia | Uraemic toxins affect enteric neural function; also important for medication dosing |
| CRP / Fecal calprotectin | Inflammatory markers | ↑CRP or ↑fecal calprotectin | Fecal calprotectin is a 24kDa calcium-binding protein released by neutrophils; elevated in IBD, infection, and CRC [19]. A negative fecal calprotectin makes serious organic colonic pathology unlikely — excellent triage test |
Fecal Calprotectin — The Triage Workhorse
Fecal calprotectin is increasingly used as a first-line triage test in patients with altered bowel habits. It is stable at room temperature, cheap, and has a high negative predictive value for organic disease [19]. A normal fecal calprotectin ( < 50 μg/g) strongly argues against IBD or CRC and supports a functional diagnosis (IBS-C or functional constipation). However, it does NOT replace colonoscopy when alarm features are present.
"If appropriate refer for sigmoidoscopy or colonoscopy and radiological studies (e.g. CT colonography, bowel transit studies)" [1]
| Investigation | Indications | Procedure | Key Findings | Limitations |
|---|---|---|---|---|
| Sigmoidoscopy [1] | Initial office evaluation in all constipation patients (rigid); screening in those with lower GI symptoms | Rigid: 25 cm reach; Flexible: 60 cm reach (to splenic flexure) | Rectal/sigmoid tumour, polyps, proctitis, melanosis coli (brown-black pigmentation = chronic stimulant laxative abuse), solitary rectal ulcer, internal haemorrhoids, fissure | Cannot visualise proximal colon — insufficient for excluding right-sided CRC |
| Colonoscopy [1] | Gold standard when alarm features present or when CRC needs to be excluded; age > 40–50 with new-onset constipation; positive FIT/FOBT; FHx CRC | Full colonoscopy to caecum with biopsy capability | Tumour (exophytic, ulcerated, circumferential → "apple core" on barium), polyps (synchronous polyps in 30–50% of CRC), IBD (mucosal inflammation, ulceration), diverticulosis, melanosis coli, stricture. Biopsy provides histological diagnosis [18][20] | Requires bowel preparation; procedural risk (perforation < 1/10,000, bleeding 3/10,000) [20]; contraindicated in suspected perforation, acute diverticulitis, toxic megacolon [20] |
| Flexible sigmoidoscopy + colonoscopy for CRC workup | Suspicious lower GI symptoms: PRB, abdominal pain, altered bowel habit, constipation, etc. [20] | See above | See above | If colonoscopy cannot reach caecum (11–12% incomplete), supplement with CT colonography [18] |
Colonoscopy — Key Points for Constipation:
- When CRC is suspected: colonoscopy is the gold standard investigation — it is both diagnostic (direct visualisation + biopsy) and therapeutic (polypectomy, stenting for malignant obstruction, decompression in volvulus) [18][20]
- Important to scope the entire colon: synchronous tumours occur in 3–5% of CRC patients, and synchronous polyps in 30–50% [18]
- If the tumour is small, tattooing (injection of ink/carbon) is used to mark the location for the surgeon during subsequent resection [18]
- Melanosis coli: if you see diffuse brown-black pigmentation of the colonic mucosa, this indicates chronic stimulant laxative use (senna, bisacodyl) — the pigment is lipofuscin deposited in macrophages within the lamina propria
- After treatment of acute diverticulitis: colonoscopy should be performed after resolution of the acute episode (usually 6–8 weeks) to exclude CRC (which can mimic diverticulitis on CT) [10]
| Investigation | Indications | Key Findings and Interpretation | When to Use |
|---|---|---|---|
| CT colonography [1] | Alternative to colonoscopy when colonoscopy is incomplete, contraindicated, or unavailable; patient preference | Virtual fly-through of colon; detects masses > 1 cm with similar sensitivity to colonoscopy [18]; also provides extra-luminal information (liver mets, lymphadenopathy, pelvic masses). Requires mechanical bowel preparation. | When colonoscopy cannot be completed; in patients with significant comorbidities precluding sedation; CRC screening in some settings |
| Abdominal X-ray (AXR) | Suspected faecal impaction or bowel obstruction; baseline assessment | Faecal loading: multiple faecal densities throughout colon/rectum [15]. Bowel obstruction: dilated loops ( > 6 cm for LB, > 3 cm for SB, > 9 cm for caecum = "3-6-9 rule"), air-fluid levels on erect film [15][21]. Volvulus: coffee bean sign (sigmoid), absent rectal gas. Megacolon: colonic dilatation > 6 cm. | First-line imaging if suspecting obstruction or impaction; NOT routine for simple chronic constipation |
| CT abdomen/pelvis with contrast | Suspected mechanical obstruction, complication (perforation, abscess), or when aetiology unclear on AXR | Identifies transition point (site of obstruction), cause (tumour, stricture, volvulus — "whirl sign"), complications (pneumatosis intestinalis, portal venous gas = ischaemia; free air = perforation) [21]. For diverticulitis: bowel wall thickening, pericolic fat stranding, abscess [10] | When AXR is inconclusive; when complications suspected; staging of malignancy |
| Bowel transit studies (radio-opaque markers) [1] | Refractory chronic constipation not responding to empirical treatment; to differentiate slow-transit from normal-transit | Sitz marker study: patient swallows a capsule containing 24 radio-opaque markers (Sitz markers) on Day 0. AXR on Day 5. Normal: ≤5 markers retained ( < 20%). Slow transit: > 5 markers (≥20%) diffusely distributed throughout colon. Outlet obstruction: markers clustered in rectosigmoid. | After failure of 4–8 weeks empirical treatment; to guide subtype-specific treatment |
| Wireless motility capsule (SmartPill) | Alternative to Sitz markers; also assesses gastric emptying and small bowel transit | Ingestible capsule measures pH, pressure, and temperature throughout GI tract → calculates regional transit times. Colonic transit time > 59 hours = slow transit. | Specialist investigation; not widely available in HK |
The 3-6-9 Rule on AXR
On a supine AXR, bowel dilatation is defined as [15][21]:
- Small bowel > 3 cm
- Large bowel > 6 cm
- Caecum > 9 cm (at risk of perforation if > 12 cm)
This rule is essential for identifying bowel obstruction on plain film. In constipation, you may see faecal loading (multiple faecal densities) without significant dilatation — this is faecal impaction, not obstruction. If you see both faecal loading AND dilatation, think about pseudo-obstruction or mechanical obstruction.
These are specialist investigations performed when chronic constipation is refractory to empirical treatment and you need to subclassify the functional type to guide targeted therapy.
| Investigation | What It Measures | Technique | Key Findings | Interpretation |
|---|---|---|---|---|
| Anorectal manometry (ARM) | Anal sphincter pressures, rectal sensation, rectoanal reflexes, defecation dynamics | High-resolution catheter with pressure sensors inserted into anal canal and rectum; measures pressures at rest, during squeeze, and during simulated defecation (bearing down) | (1) Resting anal pressure (predominantly IAS tone): normal ~40–70 mmHg. (2) Squeeze pressure (EAS function): should ↑ above resting. (3) Rectoanal inhibitory reflex (RAIR): rectal balloon inflation should cause IAS relaxation. (4) Defecation dynamics: rectal pressure should ↑ (push effort) while anal pressure ↓ (sphincter relaxation) | Absent RAIR: suggestive of Hirschsprung disease [5] (absent inhibitory neurons → IAS cannot relax). Paradoxical ↑anal pressure during defecation: diagnostic of dyssynergic defecation (Types I–IV — see below). ↓Rectal sensation thresholds: rectal hyposensitivity (megarectum). |
| Balloon expulsion test (BET) | Ability to expel a simulated stool | Water-filled balloon (50 mL) placed in rectum; patient asked to expel it while sitting on a commode. Normal: expulsion within 1–3 minutes. | Failed expulsion ( > 3 minutes or unable to expel) | Highly suggestive of defecatory disorder. Simple, cheap, and has good sensitivity. Often used as a screening test before formal defecography. |
| Defecography (conventional or MR) | Structural and dynamic anatomy of the rectum, pelvic floor, and anal canal during defecation | Conventional: barium paste inserted into rectum; fluoroscopic imaging during rest and simulated defecation. MR defecography: preferred where available — no radiation, better soft tissue contrast, can visualise all pelvic compartments simultaneously. | Rectocele: anterior bulge of rectum > 2 cm with contrast retention. Rectal intussusception: infolding of rectal wall. Rectal prolapse: full-thickness protrusion beyond anal canal. Descending perineum syndrome: perineum descends > 3 cm below pubococcygeal line. Enterocele/sigmoidocele: small bowel or sigmoid herniating into rectovaginal septum. Non-relaxing puborectalis: puborectalis impression persists during defecation (anorectal angle doesn't open). | Identifies structural causes of outlet obstruction that can be surgically corrected. Also confirms dyssynergia seen on manometry. MR defecography is increasingly the investigation of choice for pelvic floor disorders. |
| Colonic transit study (Sitz markers) | Colonic transit time and pattern | As described above (Section 3.4) | See above | Differentiates normal-transit from slow-transit constipation; also identifies outlet-pattern delay (markers clustered in rectosigmoid) |
Dyssynergic Defecation — Manometric Subtypes (Rao Classification):
| Type | Rectal Pressure (Push Effort) | Anal Pressure (Sphincter) | Interpretation |
|---|---|---|---|
| Type I | Adequate ↑ | Paradoxical ↑ (contraction) | Good push but sphincter contracts instead of relaxing |
| Type II | Inadequate ↑ | Paradoxical ↑ (contraction) | Poor push AND sphincter contracts — worst pattern |
| Type III | Adequate ↑ | Absent or incomplete ↓ (no relaxation) | Good push but sphincter fails to relax adequately |
| Type IV | Inadequate ↑ | Absent or incomplete ↓ (no relaxation) | Poor push and no relaxation |
All four types are amenable to biofeedback therapy — the most effective treatment for dyssynergic defecation (response rates 70–80%).
The RAIR and Hirschsprung Disease
The recto-anal inhibitory reflex (RAIR) is the reflex relaxation of the internal anal sphincter when the rectum is distended (balloon inflation). This is mediated by inhibitory neurons in the myenteric plexus releasing NO and VIP. In Hirschsprung disease, these neurons are absent → the RAIR is absent. This makes anorectal manometry a useful screening test for Hirschsprung — if RAIR is present, Hirschsprung is excluded [5]. However, absence of RAIR requires confirmation by rectal suction biopsy (gold standard showing absent ganglion cells + hypertrophied nerve trunks) [5].
| Investigation | Indication | What It Shows |
|---|---|---|
| Colonic manometry | Refractory slow-transit constipation being considered for surgery (subtotal colectomy) | Measures colonic motor activity; helps distinguish true colonic inertia (absent HAPCs even with bisacodyl provocation) from generalised GI dysmotility. Important because surgery will fail if the problem is pan-GI dysmotility rather than isolated colonic inertia. |
| Electromyography (EMG) of pelvic floor | Suspected pelvic floor dyssynergia or pudendal neuropathy | Confirms paradoxical puborectalis contraction; assesses pudendal nerve function |
| Pudendal nerve terminal motor latency (PNTML) | Suspected pudendal neuropathy (e.g. from obstetric injury, chronic straining) [6] | Prolonged latency = pudendal neuropathy → EAS weakness → may not benefit from standard biofeedback |
| Full-thickness rectal biopsy | Suspected Hirschsprung disease (children or rare adult cases) | Gold standard for HD: absent ganglion cells + hypertrophied nerve trunks + increased acetylcholinesterase staining [5]. Must be taken ≥2 cm above dentate line to avoid the 1–2 cm zone of physiological hypoganglionosis [5] |
| Barium or water-soluble contrast enema | Suspected Hirschsprung disease (to delineate transition zone) | Transition zone: change from narrow distal aganglionic segment to dilated proximal ganglionic colon. Rectosigmoid index: normally > 1 (rectum wider than sigmoid); reversal ( < 1) suggests HD [5]. Perform unprepped (without bowel cleanout) and obtain 24-hour delayed film to look for retained contrast [5]. Limitation: lower sensitivity than biopsy — absence of transition zone does NOT entirely exclude HD [5] |
| Phase | Who | Investigations | Purpose |
|---|---|---|---|
| Phase 1: All patients | Every patient with constipation | History (stool characteristics, diet, drugs, psych) + Examination (abdo palpation, DRE, perianal sensation, anal reflex) + Sigmoidoscopy [1] | Characterise the constipation; identify alarm features; detect obvious secondary causes; identify anal pathology |
| Phase 2: Basic bloods | All patients, especially those without obvious simple cause | FBE/ESR, occult blood in stool, serum Ca²⁺, K⁺, TFTs ± CEA, glucose, RFT [1] | Exclude secondary metabolic/endocrine causes; screen for occult GI blood loss |
| Phase 3: Endoscopy/imaging | Patients with alarm features OR age > 40–50 with new-onset constipation | Colonoscopy with biopsy (gold standard) or CT colonography [1] | Exclude CRC, IBD, stricture, and other structural causes |
| Phase 4: Empirical treatment trial | Patients without alarm features after secondary causes excluded | 4–8 week trial of lifestyle modification + fibre + osmotic laxative | Most patients will respond; non-responders proceed to Phase 5 |
| Phase 5: Physiological testing | Refractory chronic constipation not responding to empirical treatment | Colonic transit study (Sitz markers), anorectal manometry, balloon expulsion test, ± defecography | Subclassify into NTC vs STC vs defecatory disorder → guide targeted treatment |
| Phase 6: Specialist | Highly refractory or surgical candidates | Colonic manometry, EMG, PNTML, rectal biopsy (Hirschsprung) | Pre-surgical assessment; exclude pan-GI dysmotility; confirm rare diagnoses |
High Yield Summary — Diagnosis of Constipation
-
Rome IV criteria define functional constipation: ≥2 of 6 symptoms for ≥3 months. Key exclusion: if prominent abdominal pain → consider IBS-C instead.
-
History and examination are paramount: "stool consistency, frequency, ease of evacuation, pain on defecation, blood or mucus, dietary and drug history" [1]. DRE is non-negotiable — it identifies impaction, mass, tone, and dyssynergia.
-
Basic investigations: FBE/ESR, occult blood in stool, serum Ca²⁺, K⁺, TFTs, ± CEA [1]. These exclude the common reversible secondary causes (hypothyroidism, hypercalcaemia, hypokalaemia, CRC).
-
Colonoscopy is the gold standard for excluding CRC — indicated when alarm features present, age > 40 with new-onset constipation, positive FIT, or FHx CRC.
-
Physiological testing (transit study + anorectal manometry + balloon expulsion test ± defecography) is reserved for refractory cases to subclassify into NTC, STC, or defecatory disorder.
-
Anorectal manometry: absent RAIR = Hirschsprung; paradoxical anal contraction during defecation = dyssynergia. Balloon expulsion test: failed expulsion > 3 min = defecatory disorder.
-
Sitz marker transit study: > 5/24 markers retained at Day 5 = slow transit. Markers clustered in rectosigmoid = outlet obstruction pattern.
Active Recall - Diagnostic Criteria, Algorithm and Investigations for Constipation
References
[1] Lecture slides: murtagh merge.pdf (Chronic constipation, p30–31) [3] Senior notes: Ryan Ho GI.pdf (Section 3.2.1 — Irritable Bowel Syndrome, p118–119) [5] Senior notes: felixlai.md (Hirschsprung disease — diagnosis: rectal biopsy, barium enema, anorectal manometry) [6] Senior notes: felixlai.md (Anal fissure — clinical manifestation; Rectal prolapse — pelvic physiology studies) [10] Senior notes: maxim.md (Diverticular disease — investigations, CT abdomen, colonoscopy after resolution) [15] Senior notes: Ryan Ho GI.pdf (p136 — Diagnostic evaluation of intestinal obstruction: AXR, 3-6-9 rule) [16] Senior notes: Ryan Ho Chemical Path.pdf (p22 — Hypercalcaemia: stones, bones, groans, moans, thrones) [17] Senior notes: Ryan Ho Urogenital.pdf (p25 — Hypokalaemia: ECG changes, GI dysfunction including constipation) [18] Senior notes: maxim.md (CRC investigations — colonoscopy with biopsy gold standard, CEA, CT colonoscopy) [19] Senior notes: Ryan Ho Fundamentals.pdf (p291 — Stool calprotectin: elevated in IBD, infection, CRC; stable at room temperature) [20] Senior notes: maxim.md (Colonoscopy — indications including suspicious lower GI symptoms, contraindications) [21] Senior notes: felixlai.md (Intestinal obstruction — CT findings, AXR findings)
Management of Constipation
The overarching principle is: treat the cause first, then treat the symptom. This sounds simple, but it structures every decision. A patient whose constipation is caused by codeine doesn't need laxatives — they need a different analgesic. A patient with dyssynergic defecation doesn't need stronger laxatives — they need biofeedback. Getting the management right depends entirely on getting the diagnosis right.
2. Step 0: Treat Secondary Causes First
Before reaching for any laxative, ask: is there an identifiable and correctable cause?
"Drugs selected associated with constipation: analgesics, opioids esp. codeine, TCAs, antacids esp. aluminium hydroxide, Ca channel blockers, SSRIs, cough mixtures, anti-cholinergics, benzodiazepines" [1]
| Drug | Management Approach |
|---|---|
| Opioids | Reduce dose if possible; rotate to less constipating opioid (e.g. fentanyl patch, tapentadol); add peripherally-acting μ-opioid receptor antagonists (PAMORAs) — naloxegol, methylnaltrexone (see below); co-prescribe laxatives prophylactically whenever starting opioids |
| Anticholinergics | Review necessity; switch to agents with less anticholinergic burden (e.g. switch amitriptyline to nortriptyline or SNRI; switch chlorpheniramine to cetirizine) |
| CCBs | Switch verapamil (worst) to dihydropyridine (amlodipine) or different antihypertensive class |
| Iron | Take with vitamin C (improves absorption → can ↓dose); switch to ferrous gluconate (less constipating) or IV iron if oral not tolerated |
| Aluminium antacids | Switch to magnesium-based antacid or PPI |
| Cause | Treatment |
|---|---|
| Hypothyroidism [1] | Levothyroxine replacement — constipation resolves as euthyroid state is achieved |
| Hypercalcaemia [1] | IV normal saline hydration → loop diuretic (furosemide) → treat underlying cause (parathyroidectomy for primary hyperPTH, bisphosphonates for malignancy) |
| Hypokalaemia [1] | K⁺ replacement (oral KCl slow-release or IV if severe); treat underlying cause (adjust diuretic, treat hyperaldosteronism) |
| Diabetes | Optimise glycaemic control; prokinetics may help autonomic gastroparesis/colonic dysmotility |
Impacted faeces [1] is a common pitfall that requires active disimpaction before any maintenance laxative regimen can work:
| Step | Intervention | Rationale |
|---|---|---|
| 1. Soften the mass | Glycerine suppositories or mineral oil (liquid paraffin) enema | Lubricate and soften the hard faecal mass to facilitate passage |
| 2. Stimulate evacuation | Phosphate enema (Fleet enema) or sodium citrate micro-enema | Osmotically draws water into the rectum → softens stool + distends rectum → triggers defecation reflex |
| 3. Manual disimpaction | Digital manual disimpaction under sedation/analgesia if enemas fail | For rock-hard impaction that cannot be broken up by enemas alone — common in elderly/bedbound patients |
| 4. High-volume washout | Oral PEG-based bowel preparation (e.g. GoLYTELY, Klean-Prep) at bowel-prep doses | Flushes out residual impacted stool from proximal colon after rectal disimpaction |
| 5. Maintenance | Once clear, start maintenance regimen (osmotic laxative ± stimulant) to prevent re-impaction | Impaction is a recurrent problem if the underlying cause is not addressed |
Treat the Cause of AROU
Constipation is a common precipitating factor for acute retention of urine in men with BPH [22][23]. Management includes: "Treat reversible causes: stop offending drugs, treat constipation (e.g. fleet enema) and UTI" [22]. Relieving the faecal loading removes mechanical compression of the prostatic urethra and may allow the patient to void spontaneously.
This is the foundation of management for all patients, whether primary or secondary constipation.
| Intervention | Target | Mechanism | Evidence/Notes |
|---|---|---|---|
| ↑Dietary fibre | 25–30 g/day | Fibre is either soluble (absorbs water → gel → softens stool) or insoluble (adds bulk → stimulates colonic stretch receptors → ↑peristalsis). Both ↑faecal mass and ↓transit time. | Effective for mild-moderate constipation. Must be increased gradually to avoid bloating and flatulence. Ineffective in severe slow-transit constipation (may actually worsen bloating). |
| ↑Fluid intake | ≥1.5–2 L/day | Water hydrates stool and is required for fibre to exert its bulking effect. Dehydration → harder stools. | Important adjunct to fibre supplementation — fibre without adequate fluid can worsen constipation. |
| Regular physical exercise | ≥30 min moderate activity most days | Exercise stimulates colonic motility via mechanical stimulation of the colon, ↑parasympathetic tone, and ↑blood flow to the GI tract. | Constipation: common, consider high-fibre diet, bulk/osmotic laxative, ↑fluid intake/exercise [14] |
| Establish bowel routine | Regular toilet time, ideally after meals (utilise gastro-colic reflex) | The gastro-colic reflex is a physiological ↑in colonic motility triggered by gastric distension after eating. Sitting on the toilet at this time takes advantage of the natural propulsive wave. | Particularly important for patients who have habitual suppression of defecation urge |
| Proper defecation posture | Knees above hips (squatting position or use of footstool) | Straightens the anorectal angle by relaxing the puborectalis sling → facilitates stool passage. The Western sitting toilet creates a ~90° anorectal angle; a squatting-type posture opens it to ~130°. | Simple, free, and effective — especially for patients with mild outlet obstruction |
| Don't ignore the urge | Respond to defecation urge promptly | Repeated suppression → rectal hyposensitivity → accommodative relaxation → larger harder stools needed to trigger urge → vicious cycle | Behavioural retraining component |
4. Step 2: Pharmacological Treatment — Laxatives
When lifestyle modification alone is insufficient (typically after 2–4 weeks), pharmacological agents are added. The choice of laxative should be rational, based on understanding how each class works.
4.2 Detailed Pharmacology of Each Class
| Agent | Mechanism | Dose | Onset | Key Points |
|---|---|---|---|---|
| Psyllium (ispaghula husk) — e.g. Fybogel, Metamucil | Soluble fibre that absorbs water in the colonic lumen → forms a viscous gel → ↑faecal bulk → stretches colonic wall → stimulates peristalsis via mechanoreceptors | 3.5 g 1–3 times daily, dissolved in ≥200 mL water | 12–72 hours | First-line supplement when dietary fibre alone insufficient. Must take with adequate water — otherwise can cause oesophageal/intestinal obstruction. Dietary fibre (Psyllium) is recommended for IBS-C [3]. Soluble fibre (psyllium) is better tolerated than insoluble (wheat bran) because it causes less bloating. |
| Methylcellulose | Synthetic cellulose derivative; similar bulk-forming mechanism | 2 tablets TDS with water | 12–72 hours | Less gas production than psyllium; useful in patients with excessive flatulence on psyllium |
| Sterculia (Normacol) | Natural gum; similar bulk-forming mechanism | 1–2 sachets daily | 12–72 hours | Available in HK |
Contraindications: intestinal obstruction, faecal impaction, dysphagia (risk of oesophageal obstruction), colonic atony.
Why bulk-forming agents fail in severe slow-transit constipation: in STC, the colon's propulsive activity is intrinsically reduced. Adding more bulk to a colon that cannot push it forward simply causes more distension and bloating without improving evacuation.
These work by creating an osmotic gradient that draws water into the intestinal lumen.
| Agent | Mechanism | Dose | Onset | Key Points |
|---|---|---|---|---|
| Polyethylene glycol (PEG) / Macrogol — e.g. MiraLAX, Movicol, Klean-Prep | Large, inert polymer (MW ~3350) that is NOT absorbed. It is osmotically active → retains water in the colonic lumen → softens stool and ↑volume → stimulates peristalsis | Regular use: 1–2 sachets daily in 125–250 mL water. Faecal impaction: 8 sachets in 1L water over 6 hours (bowel-prep regimen) | 24–48 hours | Laxative (PEG) is recommended for IBS-C [3]. Best-evidence osmotic laxative — predictable, dose-titratable, well-tolerated. Does not cause electrolyte disturbance at regular doses. Drug of choice for chronic constipation in most guidelines (AGA, BSG, ACG). |
| Lactulose | Synthetic disaccharide (galactose + fructose) NOT digested by human enzymes → reaches colon intact → fermented by colonic bacteria → produces short-chain fatty acids (SCFAs) + lactic acid + CO₂ + H₂ → ↓colonic pH + osmotic effect → draws water in | 15–30 mL (10–20 g) 1–2 times daily | 24–48 hours | Cheaper than PEG but causes more bloating and flatulence (from bacterial fermentation). Taste disliked by many patients. Also used in hepatic encephalopathy (different dose: 30–45 mL TDS–QDS; mechanism: ↓colonic pH → converts NH₃ to NH₄⁺ which is trapped in lumen and excreted) |
| Magnesium salts (Mg hydroxide = Milk of Magnesia; Mg citrate; Mg sulphate = Epsom salt) | Poorly absorbed Mg²⁺ salts create osmotic gradient in the lumen; also stimulate cholecystokinin (CCK) release → ↑colonic motility + ↑fluid secretion | Mg hydroxide: 30–60 mL at bedtime | 0.5–6 hours | Fast-acting. Caution in renal impairment — Mg²⁺ is renally excreted; accumulation can cause hypermagnesaemia (↓reflexes, respiratory depression, cardiac arrest). Avoid in CKD. |
| Sorbitol | Sugar alcohol; similar osmotic mechanism to lactulose | 30–150 mL of 70% solution | 24–48 hours | Cheaper alternative to lactulose; similar efficacy and side-effect profile |
Contraindications for osmotic laxatives: intestinal obstruction or perforation; Mg salts specifically contraindicated in renal impairment.
PEG vs Lactulose — Which to Choose?
PEG (macrogol) is preferred over lactulose in most guidelines because:
- It is NOT fermented by colonic bacteria → less bloating and flatulence
- More predictable dose-response relationship
- Better evidence from RCTs (higher stool frequency and softer stools vs lactulose)
- Better tolerated long-term
Lactulose remains widely used in HK due to cost and familiarity, but PEG is the first-line osmotic agent in current international guidelines.
These directly stimulate the enteric nervous system and colonic smooth muscle.
| Agent | Mechanism | Dose | Onset | Key Points |
|---|---|---|---|---|
| Senna (sennosides) | Pro-drug: colonic bacteria convert sennosides → active rhein anthrone → (1) stimulates Auerbach's (myenteric) plexus → ↑peristalsis; (2) inhibits water and electrolyte absorption → ↑fluid in lumen; (3) stimulates Cl⁻ secretion | 2–4 tablets (15–30 mg) at bedtime | 6–12 hours | Best taken at bedtime → effect in the morning. Chronic daily use should be avoided — can cause enteric neuronal damage → cathartic colon (acquired megacolon) and melanosis coli (brown pigmentation from lipofuscin in macrophages). However, intermittent or short-term use is safe. |
| Bisacodyl | Diphenylmethane derivative; hydrolysed in the gut → active metabolite → stimulates myenteric plexus + ↑PGE₂ production → ↑peristalsis + ↑fluid secretion | Oral: 5–10 mg at bedtime. Suppository: 10 mg | Oral: 6–12 hours. Suppository: 15–60 min | Available as oral tablet and suppository. Suppository form useful when rapid rectal evacuation needed. Enteric-coated → do NOT crush or chew (causes gastric irritation). |
| Sodium picosulfate | Pro-drug; converted by colonic bacteria → active diphenol metabolite (same as bisacodyl) → same mechanism | 5–10 mg at bedtime | 6–12 hours | Liquid formulation useful in patients who cannot swallow tablets |
Contraindications: intestinal obstruction, acute inflammatory bowel disease (risk of toxic megacolon), acute abdominal conditions (appendicitis, peritonitis), severe dehydration.
Are Stimulant Laxatives Harmful Long-Term?
There is a persistent myth that stimulant laxatives always cause "lazy bowel." The evidence actually shows that intermittent or moderate chronic use of stimulant laxatives is relatively safe and does not inevitably lead to colonic inertia. The concern about melanosis coli and cathartic colon applies primarily to prolonged high-dose abuse (e.g. eating-disorder-associated laxative misuse). Current guidelines (ACG 2021, AGA 2024) state that stimulant laxatives can be used as rescue therapy (PRN, up to 2–3 times per week) or as a regular supplement to osmotic agents in refractory cases.
| Agent | Mechanism | Dose | Key Points |
|---|---|---|---|
| Docusate sodium (Colace) | Surfactant (detergent) → ↓surface tension of stool → allows water and lipid to penetrate the faecal mass → softens stool | 100–300 mg daily in divided doses | Weak evidence for efficacy as monotherapy; mainly used as adjunct. Less effective than PEG or stimulants alone. Its main use is in patients who must avoid straining (e.g. post-anorectal surgery, post-MI). |
| Liquid paraffin (mineral oil) | Lubricates the stool and intestinal mucosa → ↓friction → ↓water absorption from stool | 15–30 mL at bedtime | Avoid in elderly/neurologically impaired (risk of lipoid aspiration pneumonia if aspirated). Avoid long-term use (↓fat-soluble vitamin absorption: A, D, E, K). Useful short-term for faecal impaction as an enema. |
These represent the most significant pharmacological advance in constipation management in the last 15 years. They increase intestinal fluid secretion by specific mechanisms.
| Agent | Mechanism (from first principles) | Dose | Onset | Indications | Key Points |
|---|---|---|---|---|---|
| Linaclotide | "Lina-" = linear peptide; "-clotide" = guanylate cyclase. It is a guanylate cyclase-C (GC-C) agonist. GC-C is expressed on the luminal surface of intestinal epithelial cells. Binding → ↑intracellular cGMP → activates CFTR (cystic fibrosis transmembrane conductance regulator) Cl⁻ channel → Cl⁻ secretion into lumen → Na⁺ and water follow paracellularly → ↑intestinal fluid secretion. Also: ↑cGMP → ↓visceral afferent pain signalling → analgesic effect. | 72 μg daily (constipation) or 290 μg daily (IBS-C) on empty stomach | 1–2 weeks for full effect | Chronic idiopathic constipation (CIC) and IBS-C — guanylate cyclase C agonist (linaclotide) [3] | Taken ≥30 min before breakfast. Main side effect: diarrhoea (dose-dependent — the mechanism that helps constipation can overshoot). The analgesic effect on visceral pain makes it particularly suitable for IBS-C. Minimally absorbed → very low systemic side effects. |
| Lubiprostone | "Lubi-" from lubricant; "-prostone" from prostaglandin. It is a chloride channel (ClC-2) activator — a bicyclic fatty acid derived from prostaglandin E₁. Activates ClC-2 channels on apical surface of intestinal epithelial cells → Cl⁻ secretion → Na⁺ and water follow → ↑intestinal fluid secretion | 24 μg BD with food | Days to weeks | CIC, IBS-C, opioid-induced constipation (OIC). Chloride channel activator (lubiprostone) [3]. Causes diarrhoea, only for IBS-C [3] | Must take with food to ↓nausea (most common side effect). Contraindicated in mechanical bowel obstruction. Pregnancy category C — avoid in women of childbearing potential without contraception. |
| Plecanatide | Another GC-C agonist (like linaclotide); structurally similar to uroguanylin (endogenous intestinal peptide) | 3 mg daily | Days to weeks | CIC, IBS-C | Similar mechanism to linaclotide but may cause less diarrhoea (pH-dependent activation — more active in slightly acidic proximal small intestine than in colon). |
| Agent | Mechanism | Dose | Indications | Key Points |
|---|---|---|---|---|
| Prucalopride | "Pruca-" + "-pride" (serotonin). It is a highly selective 5-HT₄ receptor agonist. 5-HT₄ receptors are expressed on enteric neurons in the myenteric plexus. Activation → ↑ACh release → ↑high-amplitude propagating contractions (HAPCs) → ↑colonic propulsion. Unlike older 5-HT₄ agonists (cisapride, tegaserod), prucalopride has minimal affinity for hERG K⁺ channels and 5-HT₂B receptors → no cardiac arrhythmia risk. | 2 mg daily (1 mg in elderly > 65y or CKD/hepatic impairment) | Chronic constipation in adults who have failed ≥2 classes of laxatives at optimal dose for ≥6 months | First prokinetic specifically licensed for chronic constipation. NNT ≈ 6. Most common side effects: headache, nausea, diarrhoea, abdominal pain (usually transient, resolve within first week). Safe for long-term use. |
Why Not Use Metoclopramide or Erythromycin for Constipation?
Metoclopramide and erythromycin are prokinetics but predominantly act on the upper GI tract (stomach, duodenum). They have minimal effect on colonic motility and are not effective for constipation. Prucalopride is the only prokinetic with strong evidence for colonic-specific prokinesis via the 5-HT₄ pathway.
Opioid-induced constipation (OIC) is mechanistically distinct from other forms of constipation because opioids directly inhibit GI motility via peripheral μ-receptors. Standard laxatives are often insufficient. PAMORAs block opioid receptors in the gut without crossing the blood-brain barrier, so they reverse GI dysmotility without affecting central analgesia.
| Agent | Mechanism | Dose | Key Points |
|---|---|---|---|
| Naloxegol (Movantik) | "Nal-" = naloxone derivative; "-egol" = PEGylated (PEG chain attached to prevent CNS penetration). Peripherally-acting μ-opioid receptor antagonist. Blocks μ-receptors on enteric neurons → reverses opioid-induced ↓peristalsis, ↑water absorption, and ↑sphincter tone. | 25 mg daily on empty stomach | Oral, first-line PAMORA. Must take on empty stomach (high-fat meal ↑absorption → risk of CNS penetration → opioid withdrawal). Contraindicated with strong CYP3A4 inhibitors (e.g. ketoconazole). |
| Methylnaltrexone (Relistor) | Quaternary amine derivative of naltrexone → positively charged → cannot cross BBB → peripheral-only action | 8–12 mg SC every other day | Subcutaneous injection. Used in palliative care patients on chronic opioids who cannot tolerate oral medications. Onset within 30–60 min. |
| Naldemedine (Symproic) | Similar to naloxegol; peripheral μ-opioid receptor antagonist | 0.2 mg daily | Oral. Does not require empty stomach administration. |
Contraindications for all PAMORAs: known or suspected GI obstruction (blocking opioid receptors in the setting of obstruction can precipitate perforation).
| Agent | Mechanism | Onset | Key Points |
|---|---|---|---|
| Glycerine suppository | Osmotic + lubricant + mild rectal irritant → softens stool + stimulates rectal contraction | 15–30 min | Gentle; first-line for mild rectal loading. Safe in pregnancy and children. |
| Bisacodyl suppository (10 mg) | Direct contact with rectal mucosa → stimulates myenteric plexus → ↑rectal peristalsis | 15–60 min | More potent than glycerine; useful for acute evacuation before procedures |
| Phosphate enema (Fleet enema) | Hypertonic sodium phosphate solution → osmotically draws water into rectum → softens stool + rectal distension → triggers defecation reflex | 2–15 min | Fleet enema used to treat constipation contributing to AROU [22]. Caution in renal impairment — can cause dangerous hyperphosphataemia, hypocalcaemia, and hypernatraemia. Avoid in CKD/elderly with renal impairment. |
| Sodium citrate micro-enema (Microlax) | Osmotic + surfactant → softens stool + draws water in | 5–15 min | Safer than phosphate enemas in elderly/renal impairment; smaller volume (5 mL). |
| Arachis oil retention enema | Lubricant → softens hard impacted stool | Retained overnight | Useful for faecal impaction — softens the mass overnight before manual disimpaction next morning. Contraindicated in peanut allergy (arachis = peanut). |
5. Step 3: Subtype-Specific Treatment (After Physiological Testing)
This step is reached only in refractory chronic constipation that has not responded to Steps 1–2 after 4–8 weeks. Physiological testing (colonic transit study, anorectal manometry, balloon expulsion test ± defecography) classifies the constipation subtype and directs targeted treatment.
- Often overlaps with IBS-C [3]
- Management:
- Continue/optimise osmotic laxatives (PEG)
- Add secretory agent (linaclotide is particularly good if there is co-existing abdominal pain → IBS-C overlap) [3]
- Reassurance — explain that transit is objectively normal and that the symptom is real but not due to a structural or motility problem
- Psychotherapy if refractory to medications [3] — cognitive behavioural therapy (CBT), hypnotherapy
- Antispasmodics (otilonium, mebeverine) for abdominal pain component [3]
- Tricyclic antidepressant (amitriptyline, desipramine) or SSRI (citalopram, paroxetine, sertraline) if pain-predominant and refractory — work via central modulation of visceral pain [3]
IBS-C Management Summary from Ryan Ho GI
Management of IBS-C [3]:
- Education and reassurance — may already be sufficient
- Diet: High dietary fibre diet
- Drugs: Dietary fibre (Psyllium), Laxative (PEG), Chloride channel activator (lubiprostone), Guanylate cyclase C agonist (linaclotide)
- For abdominal pain: Peppermint oil, Antispasmodics (otilonium, mebeverine), Tricyclic antidepressant (amitriptyline, desipramine), SSRI (citalopram, paroxetine, sertraline)
- Psychological treatment if refractory
-
Medical management:
- Osmotic laxatives (PEG) remain first-line
- Prucalopride (5-HT₄ agonist) — specifically indicated for STC; ↑HAPCs
- Secretory agents (linaclotide, lubiprostone) — ↑intestinal fluid secretion to counteract excessive water absorption
- Combination therapy often needed
- Avoid bulk-forming agents in severe STC (↑bloating without ↑propulsion)
-
Surgical management (last resort for truly refractory STC):
| Procedure | Description | Indications | Key Points |
|---|---|---|---|
| Subtotal colectomy with ileorectal anastomosis (IRA) | Removal of entire colon with primary anastomosis of ileum to rectum | Proven colonic inertia on transit study AND colonic manometry showing absent HAPCs even with bisacodyl provocation; must exclude defecatory disorder (will persist post-operatively); must exclude generalised GI dysmotility (gastroparesis, small bowel dysmotility — surgery will fail if pan-GI) | Significant improvement in ~90% of carefully selected patients. Main complications: diarrhoea (now too little absorption — the opposite problem), SBO from adhesions, recurrent constipation if defecatory disorder was missed. Patient must understand irreversibility and functional consequences. |
| Segmental colectomy | Partial resection if transit study shows isolated segmental delay (rare) | Very rarely indicated; most STC involves the whole colon | Less morbidity than subtotal colectomy but higher recurrence rate |
| Ileostomy / colostomy | Diversion without colonic resection | Patients too frail for major resection; palliative in severe cases | Avoids colectomy but permanent stoma required |
Pre-Surgical Checklist for STC
Before offering subtotal colectomy, you MUST confirm:
- Slow transit proven on Sitz marker study or wireless motility capsule
- Defecatory disorder excluded (normal balloon expulsion test + anorectal manometry) — if dyssynergia is present, biofeedback must be tried first
- Generalised GI dysmotility excluded (gastric emptying study + small bowel transit normal) — if pan-GI, colectomy will not help
- Colonic manometry ideally showing absent HAPCs — confirms true colonic inertia
- Psychological assessment — patients with significant psychiatric comorbidity have poorer surgical outcomes
5.3 Defecatory Disorder (Dyssynergic Defecation / Outlet Obstruction)
This is where management differs most dramatically from the standard "give more laxatives" approach. Laxatives do not fix the fundamental problem — the pelvic floor is not coordinating properly.
| Treatment | Description | Evidence |
|---|---|---|
| Biofeedback therapy (FIRST-LINE) | Patient is taught to coordinate pelvic floor relaxation with abdominal push effort using visual or auditory feedback from anorectal manometry sensors or surface EMG electrodes. Typically 4–6 sessions over 2–3 months. The patient watches a screen showing anal pressure in real-time and learns to reduce it while increasing rectal (push) pressure simultaneously. | Most effective treatment for dyssynergia — response rates 70–80% in RCTs (vs ~20–30% for laxatives alone). Durable benefit at 1–2 years. Superior to PEG, sham biofeedback, and diazepam. First-line in all guidelines (AGA 2024, ACG 2021, BSG 2023). |
| Defecation posture training | Footstool to elevate knees above hips → straighten anorectal angle | Adjunctive; simple and free |
| Laxatives as adjunct | Continue PEG or osmotic laxative to keep stool soft (even a perfectly coordinated pelvic floor cannot expel rock-hard stool) | Adjunctive to biofeedback; not sufficient alone |
| Botulinum toxin injection into puborectalis | Chemo-denervation of the paradoxically contracting puborectalis muscle | Limited evidence; may be considered in biofeedback failures; effect wears off (3–6 months) |
| Posterior myectomy of puborectalis (rare) | Surgical division of part of the puborectalis muscle | Last resort; risk of incontinence; rarely performed |
| Condition | Treatment | Rationale |
|---|---|---|
| Rectocele ( > 2 cm with stool trapping) | Transanal/transvaginal rectocele repair (surgical); posterior colporrhaphy | Repairs the structural defect that allows stool to pocket into the rectocele instead of being evacuated. Only indicated if rectocele is symptomatic (incomplete evacuation, need for vaginal splinting, stool trapping on defecography) |
| Rectal prolapse | Rectopexy (affix rectum to sacral promontory) ± sigmoid resection (if sigmoid is redundant and patient has constipation) [6] | Rectopexy prevents prolapse recurrence; adding sigmoidectomy improves constipation in those with a redundant sigmoid |
| Rectal intussusception | Conservative first (biofeedback, laxatives); surgery (STARR procedure — Stapled Transanal Rectal Resection) if refractory | Addresses the internal intussusception that creates outlet obstruction |
| Enterocele | Sacrocolpopexy or other pelvic floor reconstruction | Corrects small bowel herniation into rectovaginal septum |
| Anal fissure | Conservative: ↑fibre and water, warm sitz baths, topical GTN (0.2–0.4%) or topical diltiazem (2%); refractory: botulinum toxin injection or lateral internal sphincterotomy [6] | Topical GTN/diltiazem relax the IAS → ↓resting anal pressure → ↑blood flow to fissure → promotes healing. Sphincterotomy is definitive but carries small risk of incontinence. |
| Anal stricture | Anal dilation (finger or endoscopic balloon); anoplasty if severe | Relieves mechanical outlet obstruction |
6. Special Populations
- Constipation affects up to 40% of pregnant women (progesterone-mediated smooth muscle relaxation + iron supplementation + mechanical compression by gravid uterus)
- First-line: dietary fibre + ↑fluid + exercise
- Second-line: Bulk-forming agents (psyllium — safe); osmotic agents (PEG — Category C but widely used; lactulose — long safety record in pregnancy)
- Avoid: stimulant laxatives in first trimester (theoretical uterotonic risk — senna and bisacodyl can stimulate uterine smooth muscle, though evidence of harm is minimal); mineral oil (↓fat-soluble vitamin absorption); castor oil (can stimulate uterine contractions)
- Lubiprostone is contraindicated (Category C; potential teratogenicity in animal studies)
- High prevalence (up to 50–75%)
- Multifactorial: polypharmacy (opioids, anticholinergics, CCBs [1]), immobility, ↓fluid intake, ↓dietary fibre, co-morbidities
- First-line: PEG (safest osmotic; no electrolyte disturbance at standard doses)
- Avoid: Mg salts (renal impairment risk); phosphate enemas (hyperphosphataemia risk); lactulose (excessive bloating may cause discomfort)
- Beware of hypokalaemia causing constipation in the elderly patient on diuretic treatment [1] — check K⁺ before adding more laxatives!
- Always check for and disimpact faecal impaction before starting maintenance regimen
- Regular toileting schedule, adequate hydration, review medications
- Constipation is common post-stroke (immobility, altered consciousness, medications, neurogenic bowel)
- High fibre diet + stool softener (NOT laxative) → avoid constipation, fecal impaction, soiling [24]
- Bowel care protocol: regular suppositories/enemas on scheduled days if unable to achieve spontaneous BMs
- Constipation is one of the most common non-motor symptoms (Lewy body pathology in the enteric nervous system)
- Constipation: common, consider high-fibre diet, bulk/osmotic laxative, ↑fluid intake/exercise [14]
- PEG is first-line laxative
- Prucalopride may be considered for refractory cases
- Avoid anticholinergics (worsen PD symptoms)
- Prophylactic laxative should ALWAYS be co-prescribed when starting opioids — the only opioid side effect that does NOT develop tolerance
- First-line: senna + docusate (stimulant + softener combination)
- Second-line: add PEG or lactulose
- Third-line: PAMORAs (naloxegol PO, methylnaltrexone SC) if conventional laxatives fail
- Lubiprostone is also licensed for OIC
| Step | Treatment | Target Population | Duration Before Escalation |
|---|---|---|---|
| 0 | Correct secondary cause (stop drug, replace K⁺/Ca²⁺/thyroid, disimpact, treat structural cause) | All patients with identifiable secondary cause | Ongoing |
| 1 | Lifestyle: ↑fibre 25–30 g/d, ↑fluid 1.5–2 L/d, exercise, bowel routine, posture | All patients | 2–4 weeks |
| 2a | Add bulk-forming laxative (psyllium) | Mild constipation | 2–4 weeks |
| 2b | Add osmotic laxative (PEG first-line; lactulose alternative) | Moderate constipation or failed 2a | 4–8 weeks |
| 2c | Add stimulant laxative (senna or bisacodyl) as rescue PRN or scheduled | Failed 2b; also prophylactic with opioids | Ongoing as adjunct |
| 3 | Physiological testing → subtype-directed therapy: biofeedback (dyssynergia), prucalopride (STC), secretory agents (linaclotide/lubiprostone for CIC or IBS-C) | Refractory to Step 2 | Ongoing |
| 4 | Surgery: subtotal colectomy + IRA (proven colonic inertia only); structural repair (rectocele, prolapse) | Failed all medical therapy with confirmed indication on physiological testing | Last resort |
High Yield Summary — Management of Constipation
-
Treat the cause first: stop offending drugs, correct metabolic disturbances (hypoK, hyperCa, hypothyroid), disimpact if impacted, treat structural/psychiatric causes.
-
Lifestyle modification is the foundation for all patients: ↑fibre (25–30 g/d), ↑fluid (1.5–2 L/d), exercise, bowel routine, proper posture, don't ignore the urge.
-
First-line laxative: PEG/macrogol (best evidence osmotic agent) ± psyllium (bulk-forming). PEG is preferred over lactulose (less bloating, more predictable).
-
Stimulant laxatives (senna, bisacodyl): useful as rescue PRN; safe for intermittent use; chronic abuse can cause melanosis coli and cathartic colon.
-
Refractory cases require physiological testing → subtype-directed treatment:
- Dyssynergic defecation → biofeedback therapy (first-line, 70–80% response rate)
- Slow-transit constipation → prucalopride (5-HT₄ agonist); surgery (subtotal colectomy + IRA) only as last resort after excluding defecatory disorder and pan-GI dysmotility
- IBS-C → linaclotide (GC-C agonist, also reduces visceral pain) or lubiprostone (ClC-2 activator)
-
Opioid-induced constipation: prophylactic laxatives with EVERY opioid prescription; PAMORAs (naloxegol, methylnaltrexone) if conventional laxatives fail.
-
Special populations: pregnancy (avoid stimulants in 1st trimester, avoid lubiprostone); elderly (PEG first-line, check K⁺, avoid Mg salts/phosphate enemas in CKD); stroke/PD (fibre + stool softener + osmotic laxative).
Active Recall - Management of Constipation
References
[1] Lecture slides: murtagh merge.pdf (Chronic constipation, p30–31) [3] Senior notes: Ryan Ho GI.pdf (Section 3.2.1 — IBS management: dietary fibre, PEG, lubiprostone, linaclotide, antispasmodics, TCA, SSRI, psychological treatment, p118–119) [6] Senior notes: felixlai.md (Rectal prolapse — rectopexy, sigmoid resection; Anal fissure — conservative and surgical treatment) [14] Senior notes: Ryan Ho Neurology.pdf (p121 — Parkinson's disease non-motor symptoms: constipation management) [22] Senior notes: maxim.md (AROU management — treat constipation with fleet enema, alpha blocker, TWOC) [23] Senior notes: Ryan Ho Urogenital.pdf (p168 — AROU management: treat reversible causes including constipation) [24] Senior notes: Ryan Ho Neurology.pdf (p82 — Stroke: bowel output management: high fibre diet + stool softener)
Complications of Constipation
Constipation is often dismissed as a trivial complaint, but untreated or chronic constipation can produce a cascade of complications — some merely uncomfortable, others genuinely life-threatening. The key to understanding these complications is recognising that constipation creates two fundamental pathological states: (1) hard, retained stool that directly damages the anorectal mucosa and accumulates in the colon, and (2) chronic straining that generates persistently raised intra-abdominal pressure. Nearly every complication flows from one or both of these mechanisms.
1. Local Anorectal Complications
These arise from the direct mechanical effect of hard stool on the anal canal and perianal tissues, and from the repeated straining that accompanies difficult evacuation.
- Mechanism: Chronic straining → ↑intra-abdominal pressure → ↑venous engorgement of the anal vascular cushions (located at 3, 7, 11 o'clock in lithotomy position). Simultaneously, repeated shearing forces during passage of hard stools cause degeneration of the supporting fibroelastic tissue and smooth muscle (Treitz's muscle) → the cushions displace caudally → prolapse and further engorgement [25]
- Clinical presentation: painless bright red PR bleeding (blood coating stool or on toilet paper — "outlet-type" bleeding), prolapsing perianal mass, pruritus ani from mucous discharge. Pain occurs only with thrombosis or strangulation of prolapsed haemorrhoids [25]
- Grading (internal haemorrhoids) [25]:
- Grade I: bleed but do not prolapse
- Grade II: prolapse on defecation but reduce spontaneously
- Grade III: prolapse and require manual reduction
- Grade IV: permanently prolapsed, irreducible
- Prevention: treating the constipation (↑fibre, ↑fluid, avoid straining) is the single most important measure to prevent haemorrhoidal disease
"Bleeding suggests cancer, haemorrhoids, diverticular disorder and inflammatory bowel disease" [1]. Always consider haemorrhoids in a constipated patient with PR bleeding — but never assume bleeding is "just haemorrhoids" without excluding more serious causes.
- Mechanism: passage of a large, hard stool → mechanical tearing of the anoderm (the delicate squamous epithelium below the dentate line) → acute fissure. The tear then causes reflex spasm of the internal anal sphincter (IAS) → ↓blood flow to the posterior midline (watershed zone) → ischaemia → impaired healing → the fissure becomes chronic [26]
- This creates a vicious cycle: fissure → pain on defecation → fear-avoidance (patient delays defecation) → stool accumulates and hardens further → next defecation tears the fissure open again → worsening pain → more avoidance
- Location: posterior midline in ~90% of cases (because the posterior commissure has the poorest blood supply — the terminal branches of the inferior rectal artery reach this area last) [26]
- Chronic fissure features: raised edges exposing white fibres of IAS at base, hypertrophied anal papilla proximally, sentinel skin tag distally [26]
- "Hx of constipation → severe sharp pain upon defecation" [4] — a classic association
- Mechanism: chronic straining → repetitive ↑intra-abdominal pressure → weakening of the pelvic floor muscles (levator ani, particularly puborectalis) and their fascial attachments → the rectum "slides" through the pelvic floor and protrudes through the anus [6]
- Types: partial (mucosal only) vs complete (full-thickness, circumferential)
- Once prolapse occurs, it further compromises the anal sphincter mechanism → faecal incontinence (75% of patients with rectal prolapse) and paradoxically worsening constipation (obstructed defecation from the prolapsing tissue) [6]
- Risk factors include chronic straining, chronic constipation, elderly females, multiparity, pelvic floor dysfunction [6]
- Mechanism: chronic straining and excessive pelvic floor contraction → direct mucosal trauma from repeated forceful contact of the anterior rectal wall against the contracted puborectalis muscle, combined with ischaemia from mucosal prolapse and compression
- Histology: characteristic thickened mucosal layer, fibromuscular obliteration of the lamina propria, distortion of crypt architecture
- Clinical features: rectal bleeding, mucus discharge, tenesmus, and perineal pain — often misdiagnosed as IBD or malignancy until biopsy clarifies
- Strongly associated with dyssynergic defecation and rectal intussusception
2. Colonic and Intestinal Complications
These arise from the chronic accumulation of faecal matter within the colon and the ↑intraluminal pressure generated by straining against a loaded, non-propulsive colon.
- Mechanism: chronic constipation → large, hard faecal mass accumulates in the rectum → the rectum distends chronically → rectal stretch receptors accommodate (desensitise) → the patient loses the urge to defecate → more stool accumulates → the mass becomes rock-hard and too large to evacuate voluntarily
- Overflow incontinence (paradoxical diarrhoea): liquid stool from above the impacted mass seeps around the obstruction and leaks out of the anus → the patient reports "diarrhoea" when they are actually severely constipated
- Populations at risk: elderly, demented, bedbound, institutionalised patients; psychiatric patients; children with behavioural constipation (encopresis)
- Complications of impaction itself:
- Stercoral ulceration: pressure necrosis of the colonic mucosa from a hard faecal mass → mucosal ulceration, typically in the sigmoid or rectum. Can progress to stercoral perforation — a surgical emergency with high mortality (~30–50%)
- Intestinal obstruction: massive faecal impaction can cause complete large bowel obstruction [15]
- Urinary retention (AROU): faecal loading in the rectum compresses the bladder neck and prostatic urethra → precipitates urinary retention, particularly in men with background BPH [22][23]
Constipation as a Precipitant of AROU
Constipation is listed as a common precipitating factor for acute retention of urine [22][23]. In men with background prostatic enlargement, the loaded rectum presses against the posterior bladder wall and prostatic urethra, tipping a borderline situation into frank retention. "Treat reversible causes: stop offending drugs, treat constipation (e.g. fleet enema) and UTI" [22]. Relieving constipation can restore voiding without further intervention.
- Acquired megacolon [1] — a complication of longstanding chronic constipation
- Mechanism: years of faecal retention → progressive colonic dilatation → loss of effective peristalsis (Laplace's law: as radius ↑, wall tension ↑ for the same pressure, but the ability to generate propulsive pressure ↓ because muscle fibres are overstretched beyond optimal length). Simultaneously, chronic rectal distension → rectal hyposensitivity → ever-larger volumes needed to trigger defecation urge → vicious cycle
- Defined as colonic diameter > 6.5 cm on imaging (or rectum > 6.5 cm on lateral radiograph)
- Consequences: intractable constipation refractory to medical therapy; may require subtotal colectomy in severe cases
- Distinguished from congenital megacolon (Hirschsprung disease) by the presence of ganglion cells on biopsy and absence of a transition zone
- Mechanism: chronic faecal overloading from constipation → elongation and dilatation of the sigmoid colon → the already redundant sigmoid (with its narrow mesenteric attachment) becomes even more mobile → predisposed to twisting around its mesenteric axis [6][27]
- Constipation is one of the most important modifiable risk factors for sigmoid volvulus [27]
- Once torsion exceeds 180°, there is luminal obstruction; beyond 360°, there is mesenteric vascular occlusion → ischaemia → gangrene → perforation [27]
- Clinical features: acute onset colicky abdominal pain, massive abdominal distension, absolute constipation (obstipation), vomiting (late) [27]
- AXR: classic coffee bean sign — dilated ahaustral sigmoid loop arising from the pelvis, with 3 lines of sigmoid wall converging to the site of obstruction [27]
- Risk factors: bedbound, high-fibre diet (bulky stool), chronic constipation, laxative abuse [27]
- Mechanism: bowel weakening with aging + increased intraluminal pressure (from chronic straining with constipation) → outpouching of mucosa and submucosa at the weakest points of the colonic wall (where vasa recta penetrate the circular muscle) → formation of false diverticula [10]
- The sigmoid colon is most commonly affected in Western populations because it has the narrowest lumen → generates the highest intraluminal pressure by Laplace's law [10]
- Constipation both causes diverticulosis (through ↑intraluminal pressure) and results from complicated diverticular disease (through fibrotic stricture formation from chronic diverticulitis)
- Complications of diverticular disease [10][28]:
- Diverticulitis: clinical triad of lower abdominal pain (RLQ in Asia) + fever + leucocytosis [10]
- Diverticular bleeding: painless massive PR bleeding (rupture of vasa recta) [10]
- Perforation → peritonitis (classified by Hinchey staging) [28]
- Abscess formation [28]
- Fistula: most commonly colovesical (pneumaturia, faecaluria, recurrent dysuria) [10][28]
- Intestinal obstruction: LBO from fibrosis and stricture [10]
- Severe faecal impaction can cause large bowel obstruction — this is a distinct entity from mechanical obstruction by tumour or stricture
- Mechanism: the faecal mass becomes so large and hard that it physically occludes the colonic lumen, typically in the rectosigmoid
- Clinical features mirror those of any LBO: colicky abdominal pain, abdominal distension, vomiting (late), absolute constipation [15]
- On AXR: multiple faecal densities throughout colon/rectum [15]
- Management: disimpaction (manual + enemas + high-volume PEG washout), NOT surgical unless peritonitis/perforation suspected
3. Extra-Intestinal Complications
Chronic constipation and the associated ↑intra-abdominal pressure have systemic effects that extend well beyond the GI tract.
- Mechanism: chronic straining → ↑intra-abdominal pressure → overwhelms the lower oesophageal sphincter (LES) → gastric content refluxes into the oesophagus [9]
- Constipation is listed as a contributing factor to GERD alongside pregnancy, obesity, and chronic cough [9]
- Over time, this can lead to oesophagitis, Barrett's oesophagus, and peptic stricture
| Complication | Mechanism |
|---|---|
| Acute retention of urine (AROU) | Faecal loading compresses the bladder neck/prostatic urethra, particularly in men with BPH → precipitates retention [22][23]. "Constipation is usually NOT a standalone aetiology of AROU but more often a precipitating factor with background prostatic enlargement" [23] |
| Urinary incontinence (stress type) | Chronic straining → ↑intra-abdominal pressure → can overwhelm a weakened urethral sphincter, particularly in women with pelvic floor laxity → stress urinary incontinence [29] |
| Urinary tract infection | Faecal impaction → incomplete bladder emptying (mechanical compression) → urinary stasis → bacterial colonisation |
| Recurrent UTI in children | Constipation is one of the most common causes of recurrent UTI in children — the loaded rectum compresses the bladder, impairing complete emptying |
- Mechanism: chronic straining → ↑intra-abdominal pressure → forces peritoneal contents through weak points in the abdominal wall [12]
- Constipation is a well-recognised risk factor for inguinal hernia, femoral hernia, and incisional hernia [12]
- Inguinal hernia specifically: ↑pressure pushes abdominal contents through the inguinal canal (indirect) or through Hesselbach's triangle (direct)
- Mechanism: chronic straining → ↑intra-abdominal pressure → transmitted retrograde to the lower limb venous system → ↑venous pressure → progressive dilatation of superficial veins with valvular incompetence [13]
- Increased abdominal pressure such as chronic cough and constipation is listed as a risk factor for varicose veins [13]
- Mechanism: chronic straining → repetitive ↑intra-abdominal pressure + weakening of pelvic floor muscles and fascia → descent of pelvic organs: uterine prolapse, cystocele, rectocele, enterocele
- Bidirectional relationship: constipation causes pelvic floor weakening → prolapse occurs → prolapse worsens constipation (rectocele traps stool, cystocele alters pelvic dynamics)
4. Metabolic and Systemic Complications
- Mechanism: constipation in a patient with cirrhosis is particularly dangerous because it increases the intestinal transit time → ↑time for colonic bacteria to produce ammonia (NH₃) from dietary protein and urea → ↑NH₃ absorption into the portal circulation → the cirrhotic liver cannot metabolise the NH₃ via the urea cycle → NH₃ crosses the blood-brain barrier → astrocyte swelling and neurotoxicity → hepatic encephalopathy (HE)
- Constipation is listed as a precipitating factor for hepatic encephalopathy [30]
- This is why lactulose (a laxative) is the first-line treatment for HE — it works by two mechanisms: (1) osmotic laxative effect → ↑frequency of bowel movements → ↓transit time → ↓NH₃ production and absorption; (2) acidification of colonic pH → converts NH₃ (absorbable) to NH₄⁺ (non-absorbable, trapped in the lumen and excreted) [30]
- Clinical pearl: the target for lactulose in HE is 2–4 soft bowel movements per day — too little is ineffective, too much causes dehydration and hypokalaemia
Constipation Precipitates Hepatic Encephalopathy
In a cirrhotic patient who becomes confused or drowsy, always check for constipation as a precipitating factor [30]. The management is straightforward: oral lactulose (or lactulose enema if unable to take orally) titrated to 2–4 stools/day + identify and treat any other precipitants (GI bleeding, infection, over-diuresis, drugs). This is a high-yield exam scenario.
- Mechanism: patients who self-treat constipation with excessive laxatives (particularly stimulant laxatives) can develop:
- Hypokalaemia: stimulant laxatives ↑colonic K⁺ secretion + watery diarrhoea from overdosing → K⁺ loss [31]
- Hyponatraemia: excessive water loss in stool relative to Na⁺ in severe diarrhoea from laxative overuse
- Metabolic acidosis: loss of HCO₃⁻ in stool (the colon secretes HCO₃⁻ in exchange for Cl⁻)
- Dehydration: excessive fluid loss in stool
- Stimulant laxative: hypoNa/K, metabolic acidosis, chronic constipation, melanosis coli [31]
- A vicious cycle: laxative abuse → electrolyte derangement (especially hypokalaemia) → hypokalaemia itself causes constipation → patient takes more laxatives → worsening derangement
- Chronic constipation significantly impairs quality of life — comparable to other chronic conditions like diabetes and heart disease
- Patients report anxiety about bowel habits, social embarrassment, restricted activities, reduced productivity
- Bidirectional relationship with depression [1]: constipation worsens mood, and depression worsens constipation
- In the elderly, chronic constipation is associated with increased healthcare utilisation, nursing home placement, and ↑mortality (likely a marker of overall frailty rather than a direct cause)
5. Complications in Special Populations
- Encopresis: faecal soiling (involuntary passage of stool into underwear) in children > 4 years, most commonly due to overflow incontinence from chronic constipation with faecal impaction
- Mechanism: chronic faecal retention → megarectum → rectal hyposensitivity → child loses awareness of urge → liquid stool leaks around the impacted mass
- Consequences: social stigma, bullying, school avoidance, anxiety, depression — significant psychosocial impact on the child and family
- Management: disimpaction first (PEG at high dose), then maintenance (PEG at low dose for ≥6 months), behavioural modification (regular toilet sitting after meals, positive reinforcement), and gradual weaning
- The most severe and lethal complication of Hirschsprung disease [5]
- Mechanism: aganglionic segment → functional obstruction → faecal stasis → bacterial overgrowth → bacterial translocation through oedematous mucosa → enterocolitis → can progress to toxic megacolon, perforation, septic shock, and death [5]
- Can occur before surgery, in the immediate postoperative period, or years after definitive repair [5]
- Risk factors: delayed diagnosis of HD > 1 week, longer aganglionic segment, Trisomy 21, associated anomalies [5]
- Management: IV fluids, IV antibiotics, repeated rectal irrigations with saline, diverting ileostomy/colostomy if refractory [5]
- Bowel output: high fibre diet + stool softener (NOT laxative) → avoid constipation, fecal impaction, soiling [24]
- Untreated constipation in stroke patients can lead to faecal impaction → overflow incontinence → skin breakdown (perineal dermatitis) → pressure sores → infection
- Autonomic dysreflexia in patients with spinal cord injury above T6: faecal impaction or rectal distension can trigger a dangerous hypertensive crisis through uncontrolled sympathetic reflex below the level of the lesion
| Complication | Mechanism | Key Clinical Features | Prevention/Management |
|---|---|---|---|
| Haemorrhoids | ↑IAP + degeneration of supporting tissue | Painless PR bleed, prolapse, pruritus | ↑Fibre, avoid straining; rubber band ligation, haemorrhoidectomy |
| Anal fissure | Hard stool tears anoderm → IAS spasm → ischaemia | Sharp pain on defecation, small amount of bright blood | Stool softening; topical GTN/diltiazem; sphincterotomy if refractory |
| Rectal prolapse | Chronic straining → pelvic floor weakening | Protruding mass, incontinence, obstructed defecation | Treat constipation; rectopexy ± sigmoidectomy |
| Faecal impaction | Chronic retention → rock-hard mass → rectal desensitisation | Overflow diarrhoea, abdominal distension, palpable mass on DRE | Disimpaction (manual + enemas + PEG); then maintenance laxative |
| Stercoral ulceration/perforation | Pressure necrosis of mucosa from hard faecal mass | Acute abdomen, peritonitis (if perforated); mortality 30–50% | Prevent impaction; urgent surgery if perforation |
| Acquired megacolon | Years of faecal retention → progressive colonic dilatation | Intractable constipation, massive distension | Aggressive laxative regimen; subtotal colectomy if refractory |
| Sigmoid volvulus | Faecal overloading → elongated sigmoid → torsion | Coffee bean sign on AXR; acute LBO | Endoscopic decompression; elective sigmoidectomy for recurrence |
| Diverticular disease | ↑Intraluminal pressure → mucosal herniation | Bleeding, diverticulitis, perforation, fistula, stricture | ↑Fibre; avoid straining; manage complications appropriately |
| GERD | ↑IAP → overwhelms LES → reflux | Heartburn, regurgitation | Treat constipation; standard GERD management |
| AROU | Faecal loading compresses bladder neck/prostatic urethra | Inability to void, suprapubic pain, distended bladder | Fleet enema, treat constipation; catheterisation for AROU |
| Hernias | ↑IAP → forces contents through abdominal wall defects | Groin/abdominal bulge with cough impulse | Treat constipation; surgical repair of hernia |
| Varicose veins | ↑IAP → ↑lower limb venous pressure → dilatation | Dilated tortuous leg veins; heaviness, aching | Treat constipation; compression; surgery if needed |
| Hepatic encephalopathy | ↑Transit time → ↑NH₃ production/absorption in cirrhotics | Confusion, asterixis, drowsiness → coma | Lactulose (2–4 stools/day); rifaximin; identify/treat all precipitants |
| Electrolyte disturbance | Laxative abuse → K⁺/Na⁺ loss, metabolic acidosis | Weakness, arrhythmia, worsening constipation | Gradual laxative withdrawal; switch to osmotic agents; replace electrolytes |
| Psychosocial | Chronic symptoms → anxiety, depression, ↓QoL | Social withdrawal, ↓productivity, healthcare burden | Effective constipation treatment; psychiatric support if needed |
High Yield Summary — Complications of Constipation
Local anorectal: haemorrhoids (↑IAP + tissue degeneration), anal fissure (hard stool tears anoderm → IAS spasm → ischaemia → vicious cycle), rectal prolapse (pelvic floor weakening from chronic straining), solitary rectal ulcer syndrome.
Colonic: faecal impaction → overflow incontinence (paradoxical diarrhoea in elderly), stercoral ulceration/perforation (high mortality), acquired megacolon, sigmoid volvulus (faecal overloading elongates sigmoid), diverticular disease (↑intraluminal pressure at vasa recta penetration points).
Extra-intestinal: GERD (↑IAP), AROU (faecal loading compresses bladder neck in men with BPH), hernias (↑IAP), varicose veins (↑IAP), pelvic organ prolapse.
Metabolic/systemic: hepatic encephalopathy (↑NH₃ in cirrhotics), electrolyte disturbances from laxative abuse (hypoK, hypoNa, metabolic acidosis), psychosocial impact.
Special: encopresis in children (overflow incontinence from impaction), HAEC in Hirschsprung disease (lethal enterocolitis from stasis), autonomic dysreflexia in spinal cord injury.
The two fundamental mechanisms: (1) hard retained stool directly damages mucosa and causes impaction; (2) chronic straining raises intra-abdominal pressure → haemorrhoids, fissure, prolapse, hernia, GERD, varicose veins.
Active Recall - Complications of Constipation
References
[1] Lecture slides: murtagh merge.pdf (Chronic constipation, p30–31) [4] Senior notes: Ryan Ho Fundamentals.pdf (p283 — Anal fissure: Hx of constipation, severe sharp pain upon defecation) [5] Senior notes: felixlai.md (Hirschsprung disease — HAEC: most severe complication, risk factors, management) [6] Senior notes: felixlai.md (Rectal prolapse — risk factors including chronic constipation and straining; sigmoid volvulus — chronic faecal overloading) [9] Senior notes: Ryan Ho GI.pdf (p57 — GERD: ↑intra-abdominal pressure from constipation) [10] Senior notes: maxim.md (Diverticular disease — pathophysiology: bowel weakening + increased intraluminal pressure; complications) [12] Senior notes: felixlai.md (Hernia — risk factors including chronic constipation) [13] Senior notes: felixlai.md (Varicose veins — risk factors including increased abdominal pressure from constipation) [15] Senior notes: Ryan Ho GI.pdf (p136 — AXR findings in IO: faecal impaction, 3-6-9 rule) [22] Senior notes: maxim.md (AROU — treat constipation with fleet enema as reversible cause) [23] Senior notes: Ryan Ho Urogenital.pdf (p165 — Constipation as precipitating factor for AROU; p168 — management) [24] Senior notes: Ryan Ho Neurology.pdf (p82 — Stroke complications: high fibre diet + stool softener to avoid constipation) [25] Senior notes: felixlai.md (Haemorrhoids — pathophysiology, grading, risk factors including constipation) [26] Senior notes: felixlai.md (Anal fissure — pathophysiology, clinical features, posterior midline location) [27] Senior notes: maxim.md (Volvulus — risk factors including chronic constipation; coffee bean sign; management) [28] Senior notes: felixlai.md (Diverticulitis complications — abscess, fistula, obstruction, perforation) [29] Senior notes: Ryan Ho Urogenital.pdf (p161 — Urinary incontinence: stress type from ↑IAP including constipation) [30] Senior notes: felixlai.md (Hepatic encephalopathy — constipation as precipitant; lactulose mechanism) [31] Senior notes: Ryan Ho Psychiatry.pdf (p216 — Stimulant laxative complications: hypoNa/K, metabolic acidosis, chronic constipation, melanosis coli)
High Yield Summary
Key Points for Constipation (Pre-DDx/Dx/Mx):
-
Definition: Always clarify what the patient means — constipation is subjective. Rome IV criteria define functional constipation (≥2 of 6 symptoms for ≥3 months).
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Epidemiology: ~10–15% global prevalence; more common in females, elderly, institutionalised. In HK, CRC is the #1 cancer — always exclude malignancy in new-onset constipation > 40 years.
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Three functional subtypes: Normal-transit (most common), slow-transit, and defecatory disorder (outlet obstruction). Often overlap.
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Secondary causes (must exclude): Drugs (most common reversible cause: opioids, anticholinergics, CCBs, iron, TCAs, SSRIs, benzodiazepines, aluminium antacids), hypothyroidism, hypercalcaemia, hypokalaemia, diabetes, spinal dysfunction, depression, anorexia nervosa, CRC.
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Drug-induced constipation is extremely common and reversible — always take a thorough drug history.
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Alarm features: Rectal bleeding, new constipation > 40 years, family history of CRC, weight loss, anaemia, palpable mass, progressive worsening.
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Key examination: Abdominal palpation + rectal examination (loaded rectum? mass? tone? dyssynergia?) + perianal sensation + anal reflex + sigmoidoscopy.
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Key basic investigations: FBE, ESR, occult blood in stool, serum Ca²⁺, K⁺, TFTs, CEA. Colonoscopy if alarm features present.
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Constipation causes other problems: ↑IAP → GERD, haemorrhoids, hernia, varicose veins, rectal prolapse; faecal loading → sigmoid volvulus, diverticular disease; precipitates AROU (especially in males with BPH).
High Yield Summary — Differential Diagnosis of Constipation
Murtagh's Framework [1]:
- Probability diagnosis: Simple constipation (low fibre/fluid/lifestyle), slow-transit constipation, IBS-C
- Serious not to miss: CRC (intrinsic neoplasia), extrinsic malignancy (lymphoma, ovarian CA), Hirschsprung (children)
- Pitfalls: Impacted faeces (overflow diarrhoea!), anal fissure, drug/purgative abuse, hypokalaemia (elderly on diuretics!), depressive illness, acquired megacolon, diverticular disease
- Masquerades: Depression, Diabetes, Drugs, Thyroid (hypothyroidism), Spinal dysfunction
- Psychosocial: "Is the patient trying to tell me something?" — depression, anorexia nervosa
Additional important DDx [2]: IO (mechanical), cord compression/cauda equina, pseudo-obstruction (Ogilvie's), Parkinson's disease
First priorities: Exclude alarm features → investigate for CRC. Exclude reversible secondary causes (drugs, metabolic, neurological). Only then classify as primary/functional.
High Yield Summary — Diagnosis of Constipation
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Rome IV criteria define functional constipation: ≥2 of 6 symptoms for ≥3 months. Key exclusion: if prominent abdominal pain → consider IBS-C instead.
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History and examination are paramount: "stool consistency, frequency, ease of evacuation, pain on defecation, blood or mucus, dietary and drug history" [1]. DRE is non-negotiable — it identifies impaction, mass, tone, and dyssynergia.
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Basic investigations: FBE/ESR, occult blood in stool, serum Ca²⁺, K⁺, TFTs, ± CEA [1]. These exclude the common reversible secondary causes (hypothyroidism, hypercalcaemia, hypokalaemia, CRC).
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Colonoscopy is the gold standard for excluding CRC — indicated when alarm features present, age > 40 with new-onset constipation, positive FIT, or FHx CRC.
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Physiological testing (transit study + anorectal manometry + balloon expulsion test ± defecography) is reserved for refractory cases to subclassify into NTC, STC, or defecatory disorder.
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Anorectal manometry: absent RAIR = Hirschsprung; paradoxical anal contraction during defecation = dyssynergia. Balloon expulsion test: failed expulsion > 3 min = defecatory disorder.
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Sitz marker transit study: > 5/24 markers retained at Day 5 = slow transit. Markers clustered in rectosigmoid = outlet obstruction pattern.
High Yield Summary — Management of Constipation
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Treat the cause first: stop offending drugs, correct metabolic disturbances (hypoK, hyperCa, hypothyroid), disimpact if impacted, treat structural/psychiatric causes.
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Lifestyle modification is the foundation for all patients: ↑fibre (25–30 g/d), ↑fluid (1.5–2 L/d), exercise, bowel routine, proper posture, don't ignore the urge.
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First-line laxative: PEG/macrogol (best evidence osmotic agent) ± psyllium (bulk-forming). PEG is preferred over lactulose (less bloating, more predictable).
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Stimulant laxatives (senna, bisacodyl): useful as rescue PRN; safe for intermittent use; chronic abuse can cause melanosis coli and cathartic colon.
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Refractory cases require physiological testing → subtype-directed treatment:
- Dyssynergic defecation → biofeedback therapy (first-line, 70–80% response rate)
- Slow-transit constipation → prucalopride (5-HT₄ agonist); surgery (subtotal colectomy + IRA) only as last resort after excluding defecatory disorder and pan-GI dysmotility
- IBS-C → linaclotide (GC-C agonist, also reduces visceral pain) or lubiprostone (ClC-2 activator)
-
Opioid-induced constipation: prophylactic laxatives with EVERY opioid prescription; PAMORAs (naloxegol, methylnaltrexone) if conventional laxatives fail.
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Special populations: pregnancy (avoid stimulants in 1st trimester, avoid lubiprostone); elderly (PEG first-line, check K⁺, avoid Mg salts/phosphate enemas in CKD); stroke/PD (fibre + stool softener + osmotic laxative).
High Yield Summary — Complications of Constipation
Local anorectal: haemorrhoids (↑IAP + tissue degeneration), anal fissure (hard stool tears anoderm → IAS spasm → ischaemia → vicious cycle), rectal prolapse (pelvic floor weakening from chronic straining), solitary rectal ulcer syndrome.
Colonic: faecal impaction → overflow incontinence (paradoxical diarrhoea in elderly), stercoral ulceration/perforation (high mortality), acquired megacolon, sigmoid volvulus (faecal overloading elongates sigmoid), diverticular disease (↑intraluminal pressure at vasa recta penetration points).
Extra-intestinal: GERD (↑IAP), AROU (faecal loading compresses bladder neck in men with BPH), hernias (↑IAP), varicose veins (↑IAP), pelvic organ prolapse.
Metabolic/systemic: hepatic encephalopathy (↑NH₃ in cirrhotics), electrolyte disturbances from laxative abuse (hypoK, hypoNa, metabolic acidosis), psychosocial impact.
Special: encopresis in children (overflow incontinence from impaction), HAEC in Hirschsprung disease (lethal enterocolitis from stasis), autonomic dysreflexia in spinal cord injury.
The two fundamental mechanisms: (1) hard retained stool directly damages mucosa and causes impaction; (2) chronic straining raises intra-abdominal pressure → haemorrhoids, fissure, prolapse, hernia, GERD, varicose veins.
Chest Pain
Chest pain is a symptom of discomfort or distress in the thoracic region that may originate from cardiac, pulmonary, gastrointestinal, musculoskeletal, or psychogenic causes, requiring prompt evaluation to exclude life-threatening conditions.
Cough
Cough is a protective reflex involving forceful expulsion of air from the lungs to clear the airways of irritants, secretions, or foreign particles.