Rectal Prolapse
Rectal prolapse is the protrusion of rectal mucosa or the full thickness of the rectal wall through the anal orifice.
"Procidentia" comes from Latin procidere = "to fall forward." That's literally what happens — the rectum falls forward and out through the anus.
Rectal prolapse is a full thickness protrusion of the rectum through the anal sphincters [1]. It is fundamentally a pelvic floor disorder in which the supporting structures of the rectum fail, allowing the rectal wall to telescope (intussuscept) and eventually protrude beyond the anal verge.
Key conceptual distinction [1][2]:
| Term | What prolapses | Key feature |
|---|---|---|
| Complete (full-thickness) rectal prolapse | All layers of the rectal wall (mucosa, submucosa, muscularis propria, serosa/adventitia) | Circumferential concentric mucosal rings visible at anus |
| Partial (mucosal) prolapse | Mucosa only | Radial folds (like spokes of a wheel), usually < 4 cm protrusion |
| Internal prolapse (internal intussusception) | Rectum intussuscepts but does not pass beyond the anus | Not visible externally; detected on defecography/dynamic MRI |
Exam Pearl — Concentric vs Radial Folds
Full-thickness rectal prolapse shows concentric rings (like a target). Mucosal prolapse and prolapsed haemorrhoids show radial folds (like spokes). This is the single most important clinical distinction on inspection.
- Occurs at any age but more commonly at extremes of life [1]:
- Elderly women (peak incidence in 7th–8th decade): the vast majority of adult cases
- Children (typically < 3 years): usually self-limiting mucosal prolapse
- Female predominance in adults — approximately 80–90% of adult patients are women, most > 50 years old [2]
- Male-to-female ratio roughly 1:6 in adults
- In children, roughly equal sex distribution; often resolves by age 5 with conservative management
- In Hong Kong, the ageing population and high prevalence of chronic constipation make this a clinically relevant condition in elderly patients presenting to colorectal surgery
Why predominantly elderly women?
- Cumulative pelvic floor injury from childbirth (pudendal nerve stretch, levator ani disruption)
- Postmenopausal decline in oestrogen → loss of connective tissue strength in pelvic floor supports
- Age-related sarcopenia of pelvic floor muscles
- Higher prevalence of chronic constipation and straining in this demographic
3. Anatomy & Function (Understanding the Supports of the Rectum)
To understand why the rectum prolapses, you need to understand what keeps it in place.
The pelvic floor (pelvic diaphragm) is a muscular sling that separates the true pelvis from the perineum. It is composed of:
- Levator ani — the key muscle group, comprising:
- Puborectalis — U-shaped sling around the anorectal junction; creates the anorectal angle (~80–90° at rest). Maintains continence by creating a "kink" at the anorectal junction.
- Pubococcygeus — runs from pubis to coccyx, supports pelvic viscera
- Iliococcygeus — the most posterior/lateral part; forms a horizontal shelf
- Coccygeus (ischiococcygeus) — posterior part of the pelvic floor
The rectum is held in place by:
- Lateral ligaments of the rectum (containing the middle rectal vessels and autonomic nerves)
- Mesorectal fascia (Waldeyer's fascia) — anchors the rectum to the presacral fascia of the sacrum
- Peritoneal reflection — the anterior peritoneum reflects off the rectum at the rectovesical pouch (males) or rectouterine pouch (Pouch of Douglas, females). A deep cul-de-sac (Pouch of Douglas) [1] means the peritoneum extends abnormally low, allowing a peritoneal sac (containing small bowel = enterocele) to herniate anteriorly and push the rectum down
- Puborectalis sling — maintains the anorectal angle
- Anal sphincter complex — internal anal sphincter (IAS, smooth muscle, involuntary) and external anal sphincter (EAS, striated muscle, voluntary)
- Pudendal nerve (S2–S4) — motor to EAS and sensory to perineum
- Chronic straining and stretch injury → pudendal neuropathy [1] → weakened EAS → faecal incontinence
- Autonomic (pelvic splanchnic) nerves — control IAS tone, rectal sensation
Why does the rectum prolapse?
Think of rectal prolapse as a "perfect storm" of anatomical failures: the pelvic floor muscles weaken (levator ani diastasis), the rectal attachments loosen (loss of rectal fixation), the sigmoid becomes redundant and heavy, the anal sphincter becomes patulous, and the pudendal nerves are damaged. No single factor is sufficient — it is multi-factorial.
4. Aetiology & Risk Factors
The following anatomical abnormalities are classically associated [1]:
| Abnormality | Explanation |
|---|---|
| Rectal intussusception | The rectum telescopes into itself — this is the initiating event; internal prolapse precedes external prolapse |
| Deep cul-de-sac (Pouch of Douglas) | Low peritoneal reflection allows a hernia sac to push the anterior rectal wall downward |
| Loss of rectal fixation | Weakened lateral ligaments and mesorectal fascia → rectum is no longer anchored to sacrum |
| Redundant sigmoid colon | Excess sigmoid length and mobility → increased weight bearing on the rectum; the sigmoid "pushes" the rectum down |
| Levator ani diastasis | Separation/weakening of the levator ani muscles → loss of pelvic floor support |
| Patulous anal sphincter | Chronically weakened, gaping anal sphincter → no resistance to prolapsing rectum |
| Pudendal neuropathy | Stretch injury to pudendal nerve → denervation of EAS → sphincter weakness and faecal incontinence |
Demographics [2]:
- Female sex
- Age > 40 (especially > 60)
Neurological disorders [1]:
- Stroke, dementia, spinal cord lesions, multiple sclerosis, cauda equina syndrome
- Mechanism: impaired voluntary sphincter control and pelvic floor coordination
Parity [1]:
- Multiparity, especially vaginal delivery [2]
- Mechanism: pudendal nerve stretch injury during labour; direct trauma to levator ani and anal sphincter
Constipation (25–50% of patients) [1]:
- Chronic straining → repetitive pelvic floor descent → pudendal nerve stretch injury → sphincter weakness → further prolapse
- Chronic faecal loading → sigmoid elongation and redundancy
Chronic diarrhoea [2]:
- Frequent defecation with straining → repetitive pelvic floor stress
Pelvic floor dysfunction [2]:
- Paradoxical puborectalis contraction (dyssynergic defecation) — puborectalis contracts instead of relaxing during defecation → obstruction → straining
- Non-relaxing puborectalis
- Abnormal perineal descent (> 3 cm descent during straining)
Pelvic floor anatomical defects [2]:
- Rectocele (posterior vaginal wall herniation)
- Cystocele (bladder prolapse)
- Enterocele (small bowel hernia into rectovaginal space)
- Uterine prolapse
- These often coexist → "multi-compartment pelvic organ prolapse"
Prior pelvic surgery [2]:
- Previous hysterectomy disrupts pelvic floor support structures
Childhood causes [1]:
- Cystic fibrosis — rectal prolapse may be the presenting feature in up to 20% of CF children (chronic cough → raised intra-abdominal pressure; malnutrition → loss of perirectal fat pad)
- Whooping cough (pertussis) — paroxysmal coughing → raised intra-abdominal pressure
- Developmental abnormalities (e.g., meningomyelocele → denervated pelvic floor)
- Malnutrition — loss of ischiorectal fat pad that normally supports the rectum
- Ehlers-Danlos syndrome and other connective tissue disorders
Childhood Rectal Prolapse & Cystic Fibrosis
In a child presenting with rectal prolapse, always consider cystic fibrosis — it should be excluded with a sweat chloride test. This is a classic exam question. The mechanism is multifactorial: chronic cough (↑ intra-abdominal pressure), steatorrhoea (bulky stools), and malnutrition (loss of perirectal fat).
5. Pathophysiology
Understanding the pathophysiology requires integrating the anatomical and aetiological factors above into a coherent sequence.
- Rectal prolapse is essentially a sliding hernia through the pelvic floor defect
- A peritoneal sac (hernial sac from the deep Pouch of Douglas) protrudes anteriorly, dragging the anterior rectal wall with it
- This explains why enteroceles (small bowel within the hernial sac) are frequently found within the prolapse
- Rectal prolapse begins as an internal intussusception (the rectum telescopes into itself)
- Over time, with repeated straining, the intussusception progresses distally until the leading edge passes through the anal canal → full external prolapse
- This is supported by defecography findings
| Symptom | Pathophysiological basis |
|---|---|
| Visible mass at anus | Full-thickness rectal wall protruding through anus |
| Faecal incontinence (up to 75%) | Chronic stretch of anal sphincter complex → sphincter weakness; pudendal neuropathy → EAS denervation; loss of anorectal angle due to puborectalis dysfunction |
| Constipation (15–65%) | Paradoxical puborectalis contraction; internal intussusception causes outlet obstruction; redundant sigmoid causes slow transit |
| Mucus discharge | Exposed rectal mucosa secretes mucus; chronic mucosal congestion and inflammation |
| Rectal bleeding | Mechanical trauma to exposed, congested mucosa; solitary rectal ulcer from ischaemic pressure of the leading point of intussusception |
| Pain | Mucosal ulceration; sphincter spasm; incarceration or strangulation of prolapse (acute presentation) |
| Incomplete evacuation / Tenesmus | Internal intussusception acts as a mechanical plug (outlet obstruction); the patient feels the intussuscepted mass in the rectum and strains more → vicious cycle |
| Need for digital manoeuvres | Patients push back the prolapse or digitally splint the rectovaginal septum/perineum to facilitate evacuation |
6. Classification
| Type | Description |
|---|---|
| Grade I (Internal intussusception / Occult prolapse) | Rectum intussuscepts but does not protrude beyond the anus. Not visible externally. Detected on defecography. |
| Grade II (External mucosal prolapse / Partial prolapse) | Only the mucosa protrudes beyond the anal verge (< 4 cm). Radial folds visible. |
| Grade III (Complete / Full-thickness prolapse) | All layers of the rectal wall protrude beyond the anus. Concentric rings visible. This is "true" rectal prolapse / procidentia. |
Used on defecography/dynamic MRI to grade internal intussusception:
| Grade | Description |
|---|---|
| I | Recto-rectal intussusception (rectum folds onto itself above the anal canal) |
| II | Recto-anal intussusception (intussusception reaches the anal canal) |
| III | Recto-anal intussusception with external protrusion (= overt rectal prolapse) |
In clinical practice, rectal prolapse is often simply described as:
- Reducible — can be manually replaced
- Irreducible (incarcerated) — cannot be pushed back → at risk of strangulation
- Strangulated — vascular compromise → ischaemia → necrosis → surgical emergency
7. Clinical Features
| Symptom | Pathophysiological Basis | Notes |
|---|---|---|
| Sensation of a mass / "something coming down" | Full-thickness rectal wall protruding through anus during straining; initially reduces spontaneously, later requires manual reduction, eventually irreducible | Most common presenting complaint |
| Abdominal discomfort [2] | Traction on mesentery and sigmoid colon; internal intussusception causing obstructive symptoms | Often vague, poorly localised |
| Mucus or stool discharge [2] | Exposed rectal mucosa secretes mucus continuously; patulous sphincter allows passive stool leakage | Causes perianal skin irritation and pruritus ani |
| Altered bowel habits [2] | — | — |
| — Constipation (15–65%) [2] | Internal intussusception → outlet obstruction; paradoxical puborectalis contraction; redundant sigmoid → slow transit | Constipation is both a cause AND a consequence |
| — Faecal incontinence (75%) [2] | Chronic sphincter stretch → mechanical sphincter damage; pudendal neuropathy → denervation of EAS; loss of anorectal angle; sampling reflex impaired by exposed mucosa | Very high prevalence; major driver of reduced quality of life |
| Incomplete bowel evacuation / Tenesmus [2] | Intussusception acts as a plug; the patient senses the mass as residual stool and strains further | Leads to a vicious cycle of straining |
| Straining to initiate or complete defecation [2] | Outlet obstruction from intussusception; dyssynergic defecation | — |
| Use of digital manoeuvres to aid defecation [2] | Patients manually reduce the prolapse or digitally splint perineum/posterior vaginal wall to overcome outlet obstruction | Important to ask about specifically in history |
| Pain [2] | Usually mild unless incarcerated/strangulated; mucosal ulceration; sphincter spasm | Severe pain = think incarceration or strangulation |
| Rectal bleeding (fresh blood per rectum) [2] | Mechanical trauma and friction on exposed, congested mucosa; associated solitary rectal ulcer | Usually minor; massive bleeding is rare |
| Seepage [2] | Passive leakage of mucus/stool through the patulous, incompetent sphincter | — |
| Sign | Pathophysiological Basis | Notes |
|---|---|---|
| Full-thickness protrusion of rectum with concentric rings [2] | All layers of rectal wall protruding; concentric ring appearance due to circumferential mucosal folds | Pathognomonic sign. Best demonstrated by asking the patient to strain on a commode/toilet |
| Patulous (gaping) anus at rest | Chronic stretch and denervation of sphincter complex | Anus does not "wink" on stroking perianal skin (absent anocutaneous reflex) |
| Reduced anal sphincter tone on DRE [2] | Sphincter damage (mechanical + neuropathic) | Important to document baseline tone and squeeze pressure |
| Attenuated sphincter tone [2] | As above — both resting tone (IAS) and voluntary squeeze (EAS) may be reduced | — |
| Palpable anorectal mass on DRE [2] | The intussuscepted rectum may be felt as a mass within the rectal lumen on digital examination | Especially in internal prolapse |
| Concomitant pelvic floor pathology [2] | Multi-compartment pelvic organ prolapse is common | Cystocele, rectocele, uterine prolapse — always examine for these |
| Mucosal oedema, congestion, ulceration | Venous and lymphatic congestion of the exposed, prolapsed mucosa; mechanical trauma | May progress to solitary rectal ulcer |
| Solitary rectal ulcer | The leading point of the intussusception is subjected to ischaemic pressure against the anal canal → mucosal ischaemia → ulceration | Found on the anterior rectal wall 6–10 cm from the anal verge |
| Perianal excoriation / dermatitis | Chronic mucus and stool soiling of perianal skin | Causes pruritus ani |
| Incarcerated prolapse | Prolapse that cannot be reduced → venous congestion → oedema → further swelling → vicious cycle → strangulation | Surgical emergency if strangulated |
| Incarcerated rectal prolapse: sugar application + manual reduction + surgery [3] | Granulated sugar (or salt) is applied to the oedematous prolapsed mucosa as an osmotic agent to draw out oedema fluid → reduces swelling → facilitates manual reduction | Classic bedside management technique |
Examining for Rectal Prolapse
If the prolapse is not visible on inspection, ask the patient to sit on a commode and strain (simulating defecation). Examining in the left lateral position alone may miss an intermittent prolapse. The prolapse must be seen to make the diagnosis — if it cannot be reproduced, consider defecography.
This is a critical clinical distinction [3]:
| Feature | Full-thickness Rectal Prolapse | Prolapsed Haemorrhoids |
|---|---|---|
| Mucosal folds | Concentric rings (circumferential) | Radial folds (spoke-like grooves between cushions) |
| Sulcus between prolapse and anal canal | Present (a groove exists between the prolapsing rectum and the anal canal) | Absent (haemorrhoids are in continuity with anal canal skin) |
| Layers involved | Full thickness (all layers) | Mucosa + submucosal vascular cushions only |
| Symmetry | Circumferential, symmetric | Segmental (classically at 3, 7, 11 o'clock in lithotomy) |
| Associated features | Faecal incontinence, solitary rectal ulcer | Bleeding, pruritus, rarely incontinence |
- Solitary rectal ulcer syndrome (SRUS): Found in 10–25% of patients with rectal prolapse. The intussuscepted anterior rectal wall is compressed against the anal canal → ischaemia → ulceration. Histology shows fibromuscular obliteration of the lamina propria.
- Multi-compartment pelvic organ prolapse: Cystocele, rectocele, enterocele, uterine prolapse — always assess all compartments
- Faecal incontinence: Present in up to 75% — both a consequence and a contributor to morbidity
- Obstructed defecation syndrome (ODS): Constipation and incomplete evacuation are both causes and consequences
- Cystic fibrosis in children: Rectal prolapse may be the first presentation
High Yield Summary
- Rectal prolapse = full-thickness protrusion of the rectum through the anal sphincters — internal prolapse is intussusception that does not pass beyond the anus.
- Bimodal age distribution: elderly women (commonest) and young children.
- Key anatomical abnormalities: rectal intussusception, deep cul-de-sac, loss of rectal fixation, redundant sigmoid, levator ani diastasis, patulous sphincter, pudendal neuropathy.
- Aetiological triad (adults): pelvic floor weakness + chronic straining + neurological/obstetric injury. In children: think cystic fibrosis, whooping cough, malnutrition.
- 25–50% associated with constipation; 75% have faecal incontinence.
- Pathophysiology: starts as internal intussusception → progresses to external prolapse → chronic sphincter stretch → incontinence.
- Concentric rings = full-thickness rectal prolapse; radial folds = prolapsed haemorrhoids — this is the key bedside distinction.
- Incarcerated rectal prolapse: sugar/salt osmotic application → manual reduction → surgery.
- Always assess for multi-compartment pelvic organ prolapse and exclude colorectal malignancy.
- In children, always exclude cystic fibrosis (sweat chloride test).
Active Recall - Rectal Prolapse: Definition, Epidemiology, Aetiology, Pathophysiology & Clinical Features
Differential Diagnosis of Rectal Prolapse
The differential diagnosis of rectal prolapse centres on one core clinical question: "There is something protruding from or visible at the anus — what is it?" The key differentials all present with a perianal mass, bleeding, discharge, or altered bowel habits. Your job is to distinguish them systematically using history, inspection, and examination.
The senior notes [2] list the following primary differentials for rectal prolapse:
- Prolapsed internal haemorrhoids
- Rectal mucosal prolapse (including occult rectal prolapse involving intussusception — telescoping of bowel on itself internally without protruding through the anal verge, and thus not a true rectal prolapse)
- Solitary rectal ulcer
Beyond these, a complete differential for "something protruding from/at the anus" or "anorectal mass with bleeding and altered bowel habits" also includes:
- Anal carcinoma
- Rectal carcinoma (low rectal polyp/tumour)
- Perianal Crohn's disease
- Anal fissure (shares the symptom of pain and PR bleeding)
- Incarcerated rectal prolapse vs thrombosed prolapsed haemorrhoids (acute painful anal mass differential) [3]
Detailed Differential Diagnosis
This is the most important differential and the most commonly confused condition.
What are haemorrhoids? Dilated submucosal arteriovenous vascular cushions in the anal canal. Internal haemorrhoids arise above the dentate line from the superior rectal venous plexus (portal drainage). They classically sit at 3, 7, and 11 o'clock positions in lithotomy (corresponding to the terminal branches of the superior rectal artery) [4].
Why can they be confused with rectal prolapse? Grade III and IV internal haemorrhoids prolapse through the anus and present as a protruding perianal mass — just like rectal prolapse.
How to distinguish:
| Feature | Full-thickness Rectal Prolapse | Prolapsed Haemorrhoids |
|---|---|---|
| Mucosal fold pattern | Concentric rings (circumferential, like a target) | Radial folds (spoke-like grooves between cushions) [3] |
| Sulcus between mass and anal canal | Present (a groove between prolapsing rectum and anal verge) | Absent (haemorrhoids are in continuity with perianal skin) |
| Symmetry | Circumferential, symmetric | Segmental — classically 3 separate cushions at 3, 7, 11 o'clock |
| Layers involved | All layers (mucosa, submucosa, muscularis, serosa) | Mucosa and submucosal vascular plexus only |
| Bleeding pattern | Usually minor, may have associated solitary rectal ulcer | Painless bright red outlet-type PR bleeding — blood drips into bowl, on paper [4] |
| Faecal incontinence | Very common (~75%) — due to chronic sphincter stretch/neuropathy | Rare |
| Pain | Usually painless unless incarcerated/strangulated | Usually painless unless thrombosed or incarcerated |
| Sphincter tone | Reduced (patulous anus) | Usually normal |
Exam Classic — Concentric vs Radial
The single most tested bedside distinction: concentric rings = rectal prolapse; radial folds = haemorrhoids. If you see circumferential concentric mucosal rings, it is full-thickness rectal prolapse regardless of what the patient calls it.
What is it? Only the mucosal layer of the rectum protrudes through the anus (unlike full-thickness prolapse where all layers protrude). The protrusion is typically < 4 cm.
Why does it happen? The mucosa becomes loosely attached to the underlying submucosa (lax submucosal attachments), often in the context of chronic straining. The muscularis propria stays in place — only the superficial layers slide out.
How to distinguish from full-thickness prolapse:
| Feature | Full-thickness Prolapse | Mucosal Prolapse |
|---|---|---|
| Length of protrusion | Often > 5 cm | Usually < 4 cm |
| Folds | Concentric rings | Radial folds (similar to haemorrhoids) |
| Thickness on palpation | Thick — you can feel the muscular wall between two fingers | Thin — no palpable muscular layer |
| Sulcus | Present between prolapse and anal verge | Absent |
| Digital examination | Can insert finger between prolapse and anal canal wall | Cannot — mucosa arises directly from anal canal |
Why this matters clinically: Mucosal prolapse is managed differently — it may respond to rubber band ligation or injection sclerotherapy (like haemorrhoids), whereas full-thickness prolapse requires surgical repair (rectopexy or perineal procedures).
What is it? Telescoping of bowel on itself internally without protruding through the anal verge and thus not a true rectal prolapse [2]. The rectum intussuscepts into itself but the leading point does not emerge externally.
Why does it matter? It causes obstructed defecation symptoms (incomplete evacuation, tenesmus, straining, need for digital manoeuvres) that mimic other causes of outlet obstruction. There is no visible external prolapse, so it is easily missed.
How to diagnose: Defecography (fluoroscopic or dynamic MRI) — this is the only reliable way to identify it. On defecography, you see the rectal wall telescoping during straining.
Clinical significance: Internal intussusception is thought to be the precursor to full-thickness external prolapse — it represents an earlier point on the same disease spectrum.
What is it? An ulcer (or sometimes a polypoid lesion) on the anterior rectal wall, typically 6–10 cm from the anal verge. Despite the name "solitary," there may be multiple ulcers.
Why does it occur? The leading point of the internal intussusception is subjected to repeated ischaemic pressure against the anal canal → mucosal ischaemia → ulceration. It is therefore strongly associated with internal rectal prolapse and rectal prolapse.
Clinical features:
- Rectal bleeding (fresh blood)
- Mucus discharge
- Straining and incomplete evacuation
- Perineal and rectal pain/pressure
Histology (characteristic): Fibromuscular obliteration of the lamina propria with smooth muscle fibres extending from the muscularis mucosae into the lamina propria, distorted crypt architecture [5].
Why it's a differential for rectal prolapse: It shares symptoms (bleeding, discharge, altered bowel habits) and is often found in association with rectal prolapse/internal intussusception. Importantly, it can mimic a rectal tumour on endoscopy — biopsy is essential.
When a patient presents with an acute painful anal mass, the differential is [3]:
- Thrombosed prolapsed internal haemorrhoids
- Thrombosed external haemorrhoids (a.k.a. perianal haematoma — present as painful bluish mass, form skin tag after 48 hours) [3]
- Incarcerated rectal prolapse (with circular folds) [3]
This is a critical distinction because management differs:
| Condition | Key distinguishing feature | Acute management |
|---|---|---|
| Thrombosed prolapsed internal haemorrhoids | Segmental, radial folds, usually 3 cushions visible | Hyperosmolar solution / sitz bath → urgent haemorrhoidectomy if < 72 h [3] |
| Thrombosed external haemorrhoid | Bluish, tender, localised perianal mass BELOW dentate line | Incision and evacuation if < 72 h; conservative if > 72 h [3] |
| Incarcerated rectal prolapse | Circumferential concentric folds | Sugar application + manual reduction + surgery [3] |
Why is it in the differential? A low rectal or anal tumour can present as a palpable/visible mass at the anus with bleeding, discharge, and altered bowel habits — similar to rectal prolapse.
Colorectal neoplasm needs to be excluded [1] in any patient presenting with anorectal symptoms.
Key distinguishing features:
- Hard, irregular, fixed mass (vs. soft, reducible prolapse)
- Constitutional symptoms (weight loss, anorexia, night sweats)
- Change in stool calibre, tenesmus [4]
- Palpable inguinal lymph nodes (if anal carcinoma below dentate line — drains to superficial inguinal nodes) [6]
- Risk factors: HPV infection (90%, especially HPV-16 & 18), HIV, smoking, immunocompromised [6]
Key investigation: Digital rectal examination to exclude other rectal lesions [1][7], proctoscopy, rigid or flexible sigmoidoscopy to exclude proximal bowel lesion [1][7], biopsy for histology.
Why is it a differential? Crohn's disease can cause perianal masses (skin tags, abscesses, fistulae), bleeding, discharge, and pain — mimicking prolapse-associated symptoms.
Always suspect perianal Crohn's disease if: non-midline fissures, recurring, multiple, unusually deep or wide, perianal hypertrophic skin tags [3].
Key distinguishing features:
- Associated systemic features (weight loss, diarrhoea, abdominal pain, oral ulcers, extraintestinal manifestations)
- Atypical fissures (off-midline, multiple)
- Complex fistulae
- Characteristic "violaceous" oedematous skin tags
Why is it a differential? Shares the symptoms of pain on defecation and fresh PR bleeding.
Anal fissure = tear in the mucosal lining below the dentate line [3]. Most at 6 o'clock (posterior midline) — the least perfused area [3].
How to distinguish: Fissure causes sharp, tearing pain during and after defecation with a visible linear tear on inspection. There is no protruding mass. Diagnosis is by spreading the buttocks to reveal the fissure — DRE and proctoscopy are painful and not indicated [1].
| Condition | Key Feature | Folds | Pain | Bleeding | Sphincter Tone | Distinguishing Investigation |
|---|---|---|---|---|---|---|
| Full-thickness rectal prolapse | All layers protrude circumferentially | Concentric | Usually painless (unless incarcerated) | Mild, mucosal trauma | Reduced (patulous) | Clinical inspection; defecography if occult |
| Prolapsed haemorrhoids | Submucosal vascular cushions prolapse | Radial | Painless (unless thrombosed) | Bright red, outlet-type | Normal | Proctoscopy |
| Mucosal prolapse | Only mucosa protrudes (< 4 cm) | Radial | Minimal | Mild | Normal | Clinical; thickness on palpation |
| Internal intussusception | Telescoping without external protrusion | Not visible | No | Variable | Variable | Defecography / dynamic MRI |
| Solitary rectal ulcer | Anterior wall ulcer 6–10 cm from verge | N/A | Rectal discomfort | Yes | Normal | Endoscopy + biopsy (fibromuscular obliteration) |
| Anal carcinoma | Hard, irregular, fixed mass | N/A | Yes | Yes | May be normal | Biopsy |
| Anal fissure | Linear mucosal tear, posterior midline | N/A | Sharp, on defecation | Bright red, small amount | IAS spasm (hypertonic) | Inspection (parting buttocks) |
| Perianal Crohn's | Atypical fissures, oedematous tags, fistulae | N/A | Variable | Variable | Variable | Colonoscopy + biopsy |
High Yield Summary
- The three named differentials from senior notes: prolapsed internal haemorrhoids, rectal mucosal prolapse (including occult internal intussusception), and solitary rectal ulcer.
- Concentric rings = rectal prolapse; radial folds = haemorrhoids/mucosal prolapse — the single most important bedside distinction.
- Acute painful anal mass "Big Three": thrombosed prolapsed internal haemorrhoids, thrombosed external haemorrhoid, incarcerated rectal prolapse (circular folds). Management differs for each.
- Incarcerated rectal prolapse: sugar application → manual reduction → surgery.
- Internal intussusception is occult — no visible external prolapse — diagnosed by defecography. It is the precursor to full-thickness prolapse.
- Solitary rectal ulcer: associated with internal intussusception; histology shows fibromuscular obliteration of lamina propria; can mimic tumour on endoscopy.
- Always exclude colorectal neoplasm — DRE + proctoscopy + sigmoidoscopy/colonoscopy.
- Atypical anal features (off-midline, multiple, deep fissures, hypertrophic skin tags) → suspect perianal Crohn's disease.
Active Recall - Differential Diagnosis of Rectal Prolapse
References
[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p28, p65–68, p77) [2] Senior notes: felixlai.md (Rectal prolapse section, pp. 761–763) [3] Senior notes: maxim.md (Acute painful anal mass differential; Rectal prolapse vs prolapsed haemorrhoid; Anal fissure section) [4] Senior notes: maxim.md (Haemorrhoids section — types, examination, DDx of LGIB) [5] Senior notes: felixlai.md (Ulcerative colitis differential diagnosis — solitary rectal ulcer syndrome; Anal fissure section) [6] Senior notes: maxim.md (Anal carcinoma section) [7] Senior notes: felixlai.md (Haemorrhoids — diagnosis: DRE, proctoscopy, sigmoidoscopy)
Diagnosis of Rectal Prolapse: Diagnostic Criteria, Algorithm & Investigations
Rectal prolapse is fundamentally a clinical diagnosis — you see it, you diagnose it. The challenge arises when the prolapse is intermittent or internal. That's when investigations become essential. The purpose of investigations is threefold: (1) confirm the diagnosis when clinical examination is equivocal, (2) characterise associated pelvic floor disorders to plan surgery, and (3) exclude sinister pathology (i.e., malignancy).
There is no formal "diagnostic criteria" checklist for rectal prolapse (unlike, say, Rome IV for IBS). Instead, diagnosis rests on demonstration of the prolapse — either clinically or radiologically.
The diagnosis of full-thickness rectal prolapse is made when:
- A circumferential, full-thickness protrusion of the rectal wall beyond the anal canal is directly visualised [1][2]
- The prolapsed tissue shows concentric rings (not radial folds) [2]
- All layers of the rectal wall are involved (mucosa, submucosa, muscularis propria) — palpably thick when compressed between two fingers
The diagnosis of internal prolapse (internal intussusception) is made when:
- The rectum intussuscepts but does not pass beyond the anus [1]
- Demonstrated on defecography or dynamic pelvic MRI — there is no way to diagnose this reliably on clinical examination alone [2]
Key Principle
If you can see concentric circumferential rings protruding through the anus, the diagnosis is made at the bedside. No further imaging is needed to confirm the prolapse itself. Investigations are then directed at pre-operative planning and excluding associated pathology.
2. Clinical Assessment — The Bedside Evaluation
The lecture slides [1] outline a systematic approach to anorectal disease assessment:
Physical examination [1]:
- General examination
- Abdominal examination
- Perianal examination
- Digital rectal examination
- Proctoscopy
Let's break down each step in the context of rectal prolapse.
Approach to anorectal diseases — History [1]:
- Present illness (anorectal symptoms: pain, bleeding, mass, prolapse) [1]
- Past health (medical diseases, previous surgery) [1]
- Family history [1]
- Sexual history [1]
Specific points to elicit for rectal prolapse:
- Mass protrusion: When does it come out? (straining, standing, coughing?) Does it reduce spontaneously or need manual reduction? Is it now irreducible?
- Incontinence [1] — passive soiling vs urge incontinence; use validated scoring systems (Wexner/Cleveland Clinic Continence Score)
- Constipation [1] — lifelong vs acquired; straining, incomplete evacuation, digital manoeuvres (important for surgical planning — may need sigmoid resection)
- Bleeding, Discharge [1]
- Sensation of incomplete emptying, Rectal pressure/tenesmus [1]
- Obstetric history: parity, vaginal deliveries, perineal tears
- Neurological history: stroke, dementia, spinal cord disease
- In children: respiratory symptoms (cystic fibrosis?), whooping cough, developmental history
Inspection (Perianal examination):
- Ask the patient to strain (ideally on a commode/toilet) — this is critical because the prolapse may only appear with Valsalva
- Look for: full-thickness protrusion with concentric rings, mucosal oedema/ulceration, perianal excoriation, patulous anus at rest
- Note: if the prolapse cannot be demonstrated in the left lateral position, have the patient squat or sit on a commode
Key findings on inspection:
- Full thickness protrusion of rectum — Concentric rings of rectum protruding through anus [2]
Digital rectal examination (DRE) [2]:
- Anal sphincter weakness — reduced resting tone (IAS dysfunction) and reduced voluntary squeeze (EAS dysfunction) [2]
- Attenuated sphincter tone [2]
- Anorectal mass — in internal intussusception, the intussuscepted rectum may be palpable as a mass in the rectal lumen [2]
- Concomitant pelvic floor pathology — Cystocele / Rectocele / Uterine prolapse [2] — always perform a bimanual/vaginal examination in women
Assessment [1]:
- Digital rectal examination (to exclude other rectal lesions) [1]
- Proctoscopy: for diagnosis and assessment of severity [1]
- Rigid or flexible sigmoidoscopy to exclude proximal bowel lesion [1]
Why DRE matters beyond just feeling the prolapse
DRE in rectal prolapse is about assessing sphincter function (which determines surgical approach and prognosis for continence recovery) and excluding other rectal lesions (especially low rectal carcinoma). Always document resting tone and squeeze pressure.
3. Investigation Modalities
The investigations can be organised into categories based on their purpose:
| Purpose | Investigation |
|---|---|
| Confirm prolapse (when not clinically demonstrable) | Defecography, Dynamic pelvic MRI |
| Characterise pelvic floor anatomy (multi-compartment assessment) | Dynamic pelvic MRI, Defecography |
| Assess sphincter function (predict continence outcomes) | Anorectal manometry, Endoanal USS, EMG, PNTML |
| Exclude other pathology (malignancy) | Colonoscopy, Sigmoidoscopy |
| Assess colonic transit (plan need for sigmoid resection) | Colonic transit study |
"Defeco-" = defecation; "-graphy" = imaging. You image the patient during simulated defecation.
What is it?
- Assessed by either traditional fluoroscopy or dynamic MRI [2]
- The patient's rectum is filled with barium paste (fluoroscopic) or ultrasound gel (MRI), and images are captured while the patient rests, squeezes, and strains on a commode
Why is it done?
- Reveals defects associated with rectal prolapse [2]
- It is the gold standard for demonstrating internal intussusception (occult prolapse) that cannot be seen clinically
- Also identifies enterocele, rectocele, cystocele, abnormal perineal descent, and paradoxical puborectalis contraction
Key findings and interpretation:
| Finding | Significance |
|---|---|
| Rectal wall infolding/telescoping during straining | Internal intussusception (Oxford Grade I–III) |
| Full-thickness rectal wall descending past the anal canal | External rectal prolapse confirmed |
| Anterior rectal wall indentation by small bowel | Enterocele (peritoneal sac herniating into rectovaginal space) |
| Posterior vaginal wall bulging into rectal lumen | Rectocele |
| Perineal descent > 3 cm below pubococcygeal line during straining | Abnormal perineal descent |
| Puborectalis impression on the posterior rectum not relaxing during straining | Paradoxical puborectalis contraction (dyssynergic defecation) |
| Incomplete rectal emptying | Obstructed defecation |
What is it?
- MRI sequences acquired dynamically (cine-MRI) while the patient rests and strains, ideally on an open-configuration MRI with a commode
- Provides the same functional information as fluoroscopic defecography but without radiation and with superior soft-tissue contrast
Indicated in patients for whom prolapse cannot be reproduced on physical examination or when symptoms are suggestive of additional pelvic floor disorder [2]
Key advantages over fluoroscopic defecography:
- Simultaneously visualises all three pelvic floor compartments (anterior = bladder/urethra, middle = uterus/vagina, posterior = rectum) → ideal for multi-compartment prolapse assessment
- No ionising radiation
- Better identification of levator ani diastasis and puborectalis morphology
Limitation: Some patients cannot strain effectively in a supine or semi-upright MRI → may miss prolapse. An upright/open MRI is preferable but not universally available.
3.3 Pelvic Physiology Studies [2]
Evaluation of faecal incontinence secondary to obstetrical injuries [2]. These are pre-operative tests that help predict functional outcomes after surgery and guide the choice of procedure.
What is it? A catheter with pressure sensors is inserted into the rectum and anal canal to measure pressures.
Key measurements and interpretation:
| Parameter | What it measures | Clinical significance in rectal prolapse |
|---|---|---|
| Resting anal pressure | IAS function (contributes ~80% of resting tone) | Low in rectal prolapse → chronic sphincter stretch → passive incontinence |
| Maximum squeeze pressure | EAS function (voluntary contraction) | Low → pudendal neuropathy or direct EAS injury → urge incontinence |
| Squeeze duration | EAS fatiguability | Shortened in neuropathic sphincter |
| Rectal sensation thresholds | First sensation, urge, maximum tolerable volume | May be elevated (reduced rectal sensitivity) in prolapse |
| Rectoanal inhibitory reflex (RAIR) | IAS relaxation in response to rectal distension | Present in rectal prolapse (absent in Hirschsprung disease — useful distinction in paediatric cases) |
| Rectal compliance | Ability of the rectal wall to stretch | May be abnormal |
Why this matters: If manometry shows very poor sphincter pressures pre-operatively, the surgeon knows that even a successful rectopexy may not fully restore continence — the patient should be counselled accordingly.
What is it? Needle or surface EMG electrodes assess electrical activity of the EAS and puborectalis muscles.
Key findings:
- Denervation changes (fibrillation potentials, reduced motor unit recruitment) → pudendal neuropathy
- Paradoxical puborectalis contraction during straining → dyssynergic defecation (outlet obstruction)
What is it? The pudendal nerve is electrically stimulated transrectally (St. Mark's pudendal nerve electrode), and the time for the signal to reach the EAS is measured.
Key findings and interpretation:
- Normal PNTML: ≤ 2.0 ms
- Prolonged PNTML: > 2.0 ms → pudendal neuropathy → predicts poorer recovery of continence after surgery
- Clinical significance: If PNTML is prolonged bilaterally, the chance of continence improvement after rectopexy is lower — important for patient counselling and surgical decision-making
Why does pudendal neuropathy occur in rectal prolapse? The pudendal nerve (S2–S4) courses through Alcock's canal along the lateral pelvic wall and is vulnerable to stretch injury during chronic straining (excessive perineal descent stretches the nerve around the ischial spine). This leads to denervation of the EAS → sphincter weakness → faecal incontinence.
What is it? A 360° rotating ultrasound probe is inserted into the anal canal to image the sphincter complex.
Key findings:
- Sphincter defects (tears/gaps in IAS or EAS) — important to identify especially in women with prior obstetric injury
- Sphincter atrophy (thinning)
Clinical significance: If a sphincter defect is identified, an overlapping sphincter repair may be considered at the time of prolapse surgery. If sphincter integrity is preserved but tone is low, the problem is likely neuropathic.
Detects other pathology such as malignancy [2]
Why is it essential?
- Colorectal neoplasm needs to be excluded [1] in any patient with anorectal symptoms — especially with PR bleeding, change in bowel habit, or new-onset symptoms in patients > 45 years
- Also identifies inflammatory bowel disease, diverticular disease, solitary rectal ulcer, and polyps
- In pre-operative assessment, identifies the state of the colon (redundant sigmoid, diverticulosis) which influences surgical planning
When to perform:
- All patients with rectal prolapse being considered for surgery should ideally have a colonoscopy as part of pre-operative workup
- Especially if: age > 45–50, PR bleeding, change in bowel habits, family history of CRC [4]
Performed for operative candidates that have a severe or lifelong history of constipation to determine if sigmoid colectomy is indicated to treat rectal prolapse [2]
What is it?
- The patient swallows radio-opaque markers (Sitzmarks) on Day 0, and abdominal X-rays are taken on Day 3 and Day 5
- Normal: ≥ 80% of markers passed by Day 5
- Slow transit constipation: markers retained throughout the colon (especially right colon)
- Outlet obstruction: markers accumulate in the rectosigmoid region
Why this matters for rectal prolapse surgery:
- If the patient has slow transit constipation (markers retained globally), a rectopexy alone may not improve constipation — adding a sigmoid resection (or even subtotal colectomy in severe cases) is indicated [2]
- If the patient has outlet obstruction only (markers retained in rectosigmoid), rectopexy alone may resolve the constipation by correcting the mechanical obstruction
- This is a critical investigation because constipation is the most common complaint after rectopexy if slow transit is not addressed pre-operatively
| Investigation | Indication | Key findings |
|---|---|---|
| Sigmoidoscopy (rigid or flexible) | Exclude proximal bowel lesion [1] — complement to DRE and proctoscopy | Rectal ulcer, polyp, mass; assess mucosal health |
| Sweat chloride test | Children with rectal prolapse — to exclude cystic fibrosis | Cl⁻ > 60 mmol/L = diagnostic of CF |
| Bloods (FBC, iron studies) | Any patient with PR bleeding | Iron deficiency anaemia from chronic blood loss |
| Stool cultures | If associated diarrhoea | Exclude infectious causes |
| Investigation | Purpose | Key Findings in Rectal Prolapse | When to Order |
|---|---|---|---|
| Perianal inspection + Straining | Confirm diagnosis | Concentric circumferential rings protruding through anus | Every patient — first-line |
| DRE [1][2] | Sphincter assessment, exclude mass | Reduced resting tone, reduced squeeze, palpable intussusception, exclude rectal tumour | Every patient |
| Proctoscopy [1] | Assess severity, mucosal health | Mucosal oedema, ulceration, exclude haemorrhoids | Every patient |
| Sigmoidoscopy [1] | Exclude proximal lesion | Solitary rectal ulcer, polyp, mass | Every patient |
| Colonoscopy [2] | Exclude malignancy and other pathology | Colorectal cancer, polyps, IBD, diverticulosis, redundant sigmoid | All surgical candidates; age > 45–50; PR bleeding |
| Defecography [2] | Confirm occult prolapse; assess pelvic floor dynamics | Internal intussusception, enterocele, rectocele, perineal descent, paradoxical puborectalis | Prolapse not demonstrable clinically; suspected internal intussusception |
| Dynamic pelvic MRI [2] | Multi-compartment pelvic floor assessment | As above + levator ani diastasis, cystocele, uterine descent | Cannot reproduce prolapse; suspected multi-compartment prolapse |
| Anorectal manometry [2] | Quantify sphincter function | Low resting pressure (IAS), low squeeze pressure (EAS), abnormal sensation | Pre-operative assessment |
| EMG [2] | Assess sphincter denervation | Denervation potentials, paradoxical puborectalis contraction | Pre-operative; suspected dyssynergia |
| PNTML [2] | Assess pudendal nerve integrity | Prolonged latency > 2.0 ms = neuropathy → poorer continence prognosis | Pre-operative assessment of incontinence |
| Endoanal USS | Image sphincter anatomy | Sphincter defects (tears), atrophy | Pre-operative; suspected obstetric sphincter injury |
| Colonic transit study [2] | Determine need for sigmoid resection | Slow transit (global marker retention) vs outlet obstruction (rectosigmoid retention) | Severe/lifelong constipation in surgical candidates |
| Sweat chloride test | Exclude CF in children | Cl⁻ > 60 mmol/L = CF | All children with rectal prolapse |
High Yield Summary
- Rectal prolapse is a clinical diagnosis — demonstrate the prolapse by asking the patient to strain, ideally on a commode. Look for concentric circumferential rings.
- Assessment triad from lectures: DRE (exclude other lesions, assess tone) → Proctoscopy (severity) → Sigmoidoscopy (exclude proximal lesion).
- If prolapse cannot be demonstrated clinically → Defecography or Dynamic pelvic MRI to identify internal intussusception or multi-compartment prolapse.
- Pelvic physiology studies (manometry, EMG, PNTML) are for pre-operative assessment — they predict continence outcomes and guide surgical planning, not diagnosis per se.
- Colonoscopy is mandatory in surgical candidates to exclude malignancy and characterise colonic anatomy.
- Colonic transit study is essential in patients with severe or lifelong constipation — determines whether sigmoid colectomy should be added to rectopexy.
- PNTML > 2.0 ms = pudendal neuropathy → poorer prognosis for continence recovery after surgery → counsel patient accordingly.
- In children, always perform a sweat chloride test to exclude cystic fibrosis.
Active Recall - Diagnosis of Rectal Prolapse
References
[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p3, p4, p7, p28, p65–69, p77) [2] Senior notes: felixlai.md (Rectal prolapse — Diagnosis section, pp. 762–763) [3] Senior notes: maxim.md (Acute painful anal mass; Incarcerated rectal prolapse management) [4] Senior notes: maxim.md (Haemorrhoids — Examination; indications for colonoscopy)
Management of Rectal Prolapse
The fundamental principle of rectal prolapse management is straightforward: surgery is the only definitive treatment for full-thickness rectal prolapse in adults. Conservative management has a limited role — it can manage symptoms but cannot fix the underlying anatomical defect. The real decision is which surgical approach to use, and that depends on the patient's fitness, anatomy, and predominant symptoms (constipation vs incontinence).
Abdominal or perineal approach are both available [2]. The choice between them is one of the most important decisions in rectal prolapse surgery.
Indicated in patients with sensation of mass from prolapsed bowel, fecal incontinence or constipation associated with rectal prolapse [2].
The two broad surgical approaches directly mirror the lecture slide categorisation [1]:
| Abdominal Repair [1] | Perineal Repair [1] | |
|---|---|---|
| Approach | Through the abdomen (open, laparoscopic, or robotic) | Through the perineum (no abdominal incision) |
| Recurrence rate | Lower (~3–9%) | Higher (~16–30%) |
| Functional outcomes | Better continence and constipation outcomes | Acceptable but inferior long-term function |
| Operative morbidity | Higher (general anaesthesia, abdominal access) | Lower (can be done under regional/spinal anaesthesia) |
| Best for | Fit patients, younger patients, those with significant constipation | Elderly/frail patients, high anaesthetic risk, recurrent prolapse after abdominal repair |
The Core Decision
Fit patient → abdominal approach (better long-term outcomes, lower recurrence). Frail/elderly/high-risk patient → perineal approach (lower operative morbidity, tolerable under regional anaesthesia). This is the single most important management principle to remember.
3. Conservative Management
Conservative management does not cure full-thickness rectal prolapse. It is reserved for:
- Children — most paediatric rectal prolapse resolves spontaneously by age 5
- Internal intussusception (without external prolapse) — trial of conservative therapy first
- Patients unfit for any surgery — symptom palliation only
- Perioperative optimisation — managing constipation and incontinence before and after surgery
| Measure | Rationale |
|---|---|
| High-fibre diet + adequate fluid intake | Softens stool → reduces straining → reduces repetitive pelvic floor descent |
| Stool softeners / Bulk-forming laxatives (e.g., psyllium, lactulose) | Same as above; prevents hard stools that require Valsalva |
| Avoidance of prolonged straining | Reduces further pudendal nerve stretch and pelvic floor descent |
| Toilet posture advice (feet on stool, slight forward lean) | Straightens the anorectal angle → facilitates evacuation without excessive straining |
- Biofeedback therapy: The patient uses manometric or EMG feedback to learn to relax the puborectalis during defecation and strengthen the EAS during holding
- Why it helps: In patients with paradoxical puborectalis contraction (dyssynergic defecation), biofeedback retrains the coordination of pelvic floor muscles → reduces outlet obstruction → reduces straining
- Evidence: Primarily used for internal intussusception and obstructed defecation; limited evidence for full-thickness external prolapse
Incarcerated rectal prolapse: sugar application + manual reduction + surgery [3]
Step-by-step approach:
- Osmotic reduction: Apply granulated sugar (or table salt) liberally to the oedematous, congested, prolapsed mucosa
- Why sugar? The hyperosmolar crystals draw interstitial fluid out of the oedematous tissue via osmosis → reduces swelling → makes the prolapse smaller and softer
- Leave in place for 15–20 minutes while gently compressing with gauze
- Manual reduction: Once oedema has reduced, gently push the prolapse back through the anus using steady circumferential pressure (start at the apex and work proximally)
- Assess viability: If mucosa is dusky/black/necrotic → suspect strangulation → do not attempt reduction → urgent surgery
- Definitive surgery: Plan elective surgery after successful reduction; if reduction fails or tissue is non-viable → urgent perineal procedure (typically Altemeier)
4. Surgical Treatment — Abdominal Approaches
The lecture slides [1] list the abdominal repair options as:
"Recto-" = rectum; "-pexy" = surgical fixation. You're fixing the rectum back to where it belongs.
Principle: Affix pararectal tissues to the presacral fascia or sacral periosteum in the sacral promontory using non-absorbable sutures or mesh [2]
Why does this work? The rectum has lost its normal fixation to the sacrum (loss of lateral ligaments, mesorectal fascia). Rectopexy restores this fixation by creating a fibrotic adhesion between the mobilised rectum and the presacral fascia at the level of the sacral promontory → the rectum can no longer slide down.
Types of rectopexy:
| Type | Description | Key features |
|---|---|---|
| Suture rectopexy | Sutures alone fix the lateral rectal stalks to the presacral fascia | Simple; lower cost; no foreign material; adequate for many patients |
| Mesh rectopexy (posterior) | A synthetic or biological mesh is placed posterior to the rectum and sutured to the sacral promontory (like the Ripstein or Wells procedure) | Promotes fibrosis; historically higher rates of constipation (mesh can kink or compress the rectum) |
| Laparoscopic ventral mesh rectopexy (LVMR) | Mesh placed on the anterior aspect of the rectum only, sutured to the sacral promontory; posterior rectal dissection is avoided | Currently the preferred technique [1] — see below |
Laparoscopic Ventral Mesh Rectopexy (LVMR) [1]
This is the modern "gold standard" for abdominal rectopexy and deserves special attention.
Technique: A biological or synthetic mesh is placed on the anterior wall of the rectum (in the rectovaginal/rectovesical septum), extending from the level of the Pouch of Douglas down to the perineal body, and fixed superiorly to the sacral promontory. The posterior aspect of the rectum is not mobilised.
Why ventral (anterior) rather than posterior?
- Avoids posterior rectal mobilisation → preserves the lateral ligaments and autonomic nerves → lower risk of new-onset constipation and sexual dysfunction
- Specifically addresses the deep cul-de-sac (obliterates the Pouch of Douglas) and supports the anterior rectal wall where intussusception typically begins
Systematic review in 2010 of 12 non-randomised studies — 728 patients [1]:
- Recurrence of 3.4% [1]
- Improvement in incontinence of 45% [1]
- Improvement in constipation of 24% [1]
Indications:
- Full-thickness rectal prolapse in fit patients
- Internal rectal prolapse (high-grade intussusception) refractory to conservative management
- Multi-compartment pelvic organ prolapse (simultaneously addresses enterocele/rectocele)
Contraindications (relative):
- Unfit for general anaesthesia / laparoscopy
- Previous extensive pelvic surgery with dense adhesions (relative)
- Active pelvic sepsis (absolute — mesh infection risk)
Why LVMR is the preferred abdominal approach
LVMR has emerged as the procedure of choice because it combines low recurrence (~3.4%), functional improvement in both constipation AND incontinence, avoids posterior dissection (preserving autonomic nerves), and can be performed laparoscopically with rapid recovery. It specifically targets the pathological anatomy — the deep cul-de-sac and anterior intussusception.
Resection of sigmoid colon in patients if it is redundant [2] Use as an adjunct to rectopexy to improve postoperative bowel function in patients with constipation [2]
Technique: The redundant sigmoid colon is resected and a colorectal anastomosis is performed, combined with rectopexy (= resection rectopexy, e.g., Frykman-Goldberg procedure).
Why add sigmoid resection?
- A redundant sigmoid [1] acts as a reservoir for stool → promotes constipation and provides the "weight" that pushes the rectum down
- In patients with slow transit constipation (confirmed on colonic transit study), removing the redundant sigmoid reduces the colonic reservoir → improves transit → reduces postoperative constipation
- Without sigmoid resection, constipation often worsens after rectopexy because the now-fixed rectum can no longer accommodate the slow-transit stool bolus
Indications:
- Rectal prolapse with significant constipation and redundant sigmoid
- Colonic transit study showing slow transit constipation
- Rectopexy alone would likely worsen constipation
Contraindications:
- Patients with predominant faecal incontinence (resection shortens the colon → looser stools → may worsen incontinence)
- Patients with diarrhoea-predominant symptoms
The Constipation vs Incontinence Decision
This is a critical surgical planning decision: If the main symptom is constipation → consider adding sigmoid resection. If the main symptom is incontinence → do NOT resect sigmoid (removing colon makes stools looser → worsens incontinence). Get a colonic transit study before deciding.
Listed on the lecture slides as an abdominal option [1]. This is rarely performed for rectal prolapse alone and is reserved for:
- Recurrent rectal prolapse after multiple failed repairs
- Concomitant rectal pathology (e.g., rectal cancer, severe radiation proctitis)
- Results in a permanent colostomy — significant quality of life implications
Suture, Mesh, Resection [1] — these can be combined in various permutations:
| Combination | When to use |
|---|---|
| Suture rectopexy alone | Prolapse without constipation; mesh not desired |
| Mesh rectopexy alone (posterior or ventral) | Prolapse, especially with multi-compartment involvement |
| Resection + suture rectopexy | Prolapse with constipation and redundant sigmoid |
| Resection + mesh rectopexy | Prolapse with constipation, multi-compartment prolapse, and redundant sigmoid |
Laparoscopic vs. open vs. robotic [1]:
- Laparoscopic approach is now standard — shorter hospital stay, less pain, faster recovery, equivalent recurrence rates
- Robotic approach increasingly used for LVMR — enhanced visualisation and dexterity in the pelvis; higher cost but similar outcomes
- Open approach reserved for patients with contraindications to laparoscopy (e.g., extensive adhesions, inability to tolerate pneumoperitoneum)
5. Surgical Treatment — Perineal Approaches
The lecture slides [1] list the perineal repair options as:
Full thickness resection [1] via the perineal route.
Technique: The prolapsed rectum is everted, and a full-thickness resection of the redundant rectosigmoid is performed through the perineum. A hand-sewn or stapled coloanal anastomosis is then created. A levatorplasty (plication of the levator ani muscles posterior to the rectum) is usually added to reinforce the pelvic floor.
Altemeier's operation (perineal rectosigmoidectomy) [3]
Why does it work?
- Removes the redundant, prolapsing bowel
- The subsequent fibrosis/scarring fixes the neo-rectum in place
- Levatorplasty narrows the levator hiatus → provides additional pelvic floor support
Indications:
- Elderly/frail patients unfit for abdominal surgery
- Incarcerated or strangulated prolapse requiring emergency surgery (can be performed without laparotomy)
- Recurrent prolapse after abdominal repair (avoids re-entering the abdomen)
- Can be performed under regional/spinal anaesthesia — major advantage in high-risk patients
Contraindications:
- Relative: young, fit patients (higher recurrence rate than abdominal approach)
Advantages: Low operative morbidity, can be done under regional anaesthesia, no abdominal incision Disadvantages: Higher recurrence rate (~16–30%), potential for anastomotic leak, may not address constipation
Mucosal resection with muscular reefing [1].
Delorme procedure: plication (folding) of sutures [3]
Technique: The mucosa of the prolapsed rectum is stripped off circumferentially, and the denuded muscularis propria is then plicated (folded/reefed) with serial sutures like an accordion. The mucosal edges are then re-anastomosed.
Why does it work?
- Mucosal stripping + muscular plication shortens and "thickens" the rectal wall
- Creates a bulky muscular cuff at the anorectal junction → acts as a physical barrier to re-prolapse
- The plication narrows the rectal lumen → improves continence by providing a better "plug"
Indications:
- Short prolapse (< 3–4 cm) — works best for smaller prolapses
- Elderly/frail patients (similar rationale to Altemeier)
- Mucosal prolapse (partial prolapse) rather than full-thickness
- Internal intussusception (selected cases)
Contraindications:
- Large, full-thickness prolapse (inadequate correction with plication alone)
Advantages: No bowel resection → no anastomotic leak risk; very low morbidity; can be done under local/regional anaesthesia Disadvantages: Highest recurrence rate of all procedures (~20–38%); less effective for large prolapses
Anal encirclement [1] — a wire, silastic band, or synthetic mesh strip is placed subcutaneously around the anal canal to narrow the anal orifice.
Technique: A circumferential subcutaneous suture or band is placed around the anal canal (outside the sphincter complex) to mechanically narrow the anal opening and prevent the rectum from prolapsing through it.
Why is it rarely used?
- It does not address the underlying pathology (the rectum is still intussuscepting — you've just narrowed the "exit")
- High complication rates: faecal impaction (too tight), infection, erosion through skin, breakage
- High recurrence rate once the encirclement fails or is removed
- Does not improve continence
Current indications:
- Extremely frail/moribund patients unfit for any other surgery — purely palliative
- Occasionally used as a temporary measure to prevent re-prolapse while awaiting definitive surgery
6. Special Populations
- Most childhood rectal prolapse resolves with conservative management by age 5
- Treatment: stool softeners, dietary fibre, avoidance of straining, treat underlying cause (CF, whooping cough, malnutrition)
- Manual reduction taught to parents — gentle, sustained pressure with lubricated gauze
- Surgery only if prolapse persists despite conservative management for > 1 year, or if it becomes recurrent and irreducible
- Procedures: submucosal injection sclerotherapy (creates fibrosis to fix mucosa), laparoscopic rectopexy (rare, for persistent cases)
- First-line: Conservative management — biofeedback, pelvic floor rehabilitation, dietary modifications, laxatives for constipation
- Surgery only if refractory to conservative measures and symptoms are significantly impacting quality of life
- Preferred procedure: Laparoscopic ventral mesh rectopexy [1] — addresses the intussusception and deep cul-de-sac while avoiding posterior dissection
| Procedure | Approach | Recurrence | Continence improvement | Constipation outcome | Best for | Anaesthesia |
|---|---|---|---|---|---|---|
| LVMR [1] | Abdominal (laparoscopic) | ~3.4% [1] | ~45% improvement [1] | ~24% improvement [1] | Fit patients; multi-compartment prolapse | GA |
| Suture rectopexy | Abdominal | ~3–9% | Moderate | May worsen (if posterior mobilisation) | Fit patients without constipation | GA |
| Resection rectopexy | Abdominal | ~2–5% | Good | Good (removes redundant sigmoid) | Prolapse + constipation + redundant sigmoid | GA |
| Altemeier [3] | Perineal | ~16–30% | Moderate (improved with levatorplasty) | Variable | Frail/elderly; emergency; recurrent after abdominal repair | Regional/Spinal |
| Delorme [3] | Perineal | ~20–38% | Moderate | Variable | Short prolapse; mucosal prolapse; frail patients | Regional/Local |
| Thiersch [1] | Perineal | Very high | None | May worsen (impaction) | Palliative only; extremely frail patients | Local |
| Issue | Details |
|---|---|
| Recurrence | Most common complication overall; higher with perineal approaches; counsel patient pre-operatively |
| New-onset/worsened constipation | Especially after posterior rectopexy (denervation of rectum during posterior mobilisation); mitigated by LVMR (no posterior dissection) or by adding sigmoid resection |
| Faecal incontinence persistence | May persist despite anatomical correction if pudendal neuropathy is severe (prolonged PNTML); biofeedback and pelvic floor rehab postoperatively |
| Mesh-related complications | Infection, erosion (into rectum or vagina), chronic pain, dyspareunia; use biological mesh to reduce erosion risk; avoid mesh in contaminated field |
| Anastomotic leak | Risk with Altemeier or resection rectopexy; presents with pelvic sepsis, fever, pain |
| Pelvic floor rehabilitation | Important adjunct to all surgical approaches — pelvic floor exercises, biofeedback, dietary advice continue postoperatively |
High Yield Summary
- Surgery is the definitive treatment for full-thickness rectal prolapse — conservative measures alone cannot fix it (except in children).
- Two broad approaches: Abdominal repair (lower recurrence, better function, needs GA) vs Perineal repair (higher recurrence, lower morbidity, can be done under regional anaesthesia).
- Abdominal options: Rectal fixation (suture/mesh), Sigmoid resection, Proctectomy, Combination of fixation + resection. Approach: laparoscopic vs open vs robotic.
- Perineal options: Full-thickness resection (Altemeier), Mucosal resection with muscular reefing (Delorme), Anal encirclement (Thiersch — rarely used).
- LVMR is the preferred abdominal technique — recurrence 3.4%, improvement in incontinence 45%, improvement in constipation 24%.
- Add sigmoid resection if patient has constipation with redundant sigmoid / slow transit on colonic transit study. Do NOT resect if predominant symptom is incontinence.
- Incarcerated rectal prolapse: sugar application → manual reduction → elective surgery. If strangulated → urgent perineal procedure.
- Rectopexy = affix pararectal tissues to presacral fascia/sacral periosteum at the sacral promontory using non-absorbable sutures or mesh.
- Frail/elderly patients → perineal approach (Altemeier or Delorme); fit patients → abdominal approach (LVMR or resection rectopexy).
Active Recall - Management of Rectal Prolapse
References
[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p65–66, p68–69, p72) [2] Senior notes: felixlai.md (Rectal prolapse — Treatment section, pp. 762–763) [3] Senior notes: maxim.md (Incarcerated rectal prolapse management; Altemeier; Delorme)
Complications of Rectal Prolapse
Complications of rectal prolapse can be divided into two broad categories: (A) complications of the disease itself (what happens if you leave the prolapse untreated or it progresses), and (B) complications of surgical treatment (what can go wrong after repair). Both are clinically important and frequently tested. Let's work through each systematically, always linking back to the underlying mechanism.
A. Complications of the Disease (Untreated Rectal Prolapse)
These are the natural consequences of a rectum that is chronically prolapsing through the anus. They progress over time if the prolapse is not addressed.
Incontinence [1] is the most functionally devastating complication and is present in up to 75% of patients with rectal prolapse [2].
Why does it happen? Three mechanisms work in concert:
| Mechanism | Explanation |
|---|---|
| Chronic mechanical sphincter stretch | The prolapsing rectal mass repeatedly dilates the anal sphincter complex → the sphincter becomes permanently patulous and loses resting tone |
| Pudendal neuropathy [1] | Chronic straining and excessive perineal descent stretch the pudendal nerve (S2–S4) around the ischial spine → denervation of the external anal sphincter → loss of voluntary squeeze |
| Loss of anorectal angle | Levator ani diastasis [1] and puborectalis weakening → loss of the normal ~90° anorectal angle → loss of the "flap-valve" continence mechanism |
Clinical significance: Even after successful surgical repair, incontinence may persist if pudendal neuropathy is severe (prolonged PNTML > 2.0 ms bilaterally). This is why pre-operative pelvic physiology studies are important for counselling.
Constipation [1] affects 15–65% of patients [2].
Why does it happen?
- The internal intussusception acts as a mechanical plug — the telescoped rectal wall obstructs the passage of stool (outlet obstruction)
- A redundant sigmoid [1] creates a long, tortuous colonic pathway → slow transit
- Paradoxical puborectalis contraction (dyssynergic defecation) — the puborectalis contracts instead of relaxing during defecation → functional outlet obstruction
- Patients compensate by straining harder → further pelvic floor descent → further pudendal nerve injury → a vicious cycle
Clinical significance: Constipation is both a cause and a consequence of rectal prolapse — treating one without the other leads to ongoing symptoms. This is why colonic transit studies are performed pre-operatively.
What is it? The prolapsed rectum cannot be manually reduced back through the anus. The prolapse becomes "trapped" outside.
Why does it happen? Once the rectum prolapses externally, venous and lymphatic drainage are obstructed by the constricting anal sphincter ring → oedema develops in the prolapsed tissue → the swollen tissue becomes too large to push back through the sphincter → a vicious cycle of congestion and swelling.
Management: Incarcerated rectal prolapse: sugar application + manual reduction + surgery [3]. Sugar draws out oedema fluid osmotically, shrinking the tissue enough to allow reduction.
What is it? This is the progression beyond incarceration. If an incarcerated prolapse is not reduced, arterial blood supply is eventually compromised → ischaemia → tissue necrosis (gangrene).
Why does it happen?
- Initially, only venous/lymphatic outflow is obstructed (the lower-pressure system) → congestion and oedema
- As oedema increases → compartment-like effect → eventually arterial inflow is also compromised
- Without arterial supply → mucosal then full-thickness ischaemia → gangrene → perforation → sepsis
Clinical features of strangulation:
- The prolapsed tissue becomes dusky, dark purple, or black (compared to the normal pink/red of a viable prolapse)
- Severe pain (ischaemic pain)
- Systemic signs: tachycardia, fever, leucocytosis
This is a surgical emergency. If the tissue is non-viable, do not attempt reduction (risk of reducing necrotic/perforated bowel into the abdomen → peritonitis). Proceed directly to urgent perineal resection (Altemeier procedure).
Incarceration → Strangulation Spectrum
This is analogous to any other hernia. Think of incarcerated rectal prolapse like a strangulated inguinal hernia — first venous congestion, then arterial compromise, then gangrene. The management principle is the same: reduce if viable, resect if non-viable. Never reduce gangrenous tissue back into the abdomen.
Bleeding [1] and Discharge [1]
Why does it happen?
- The exposed rectal mucosa is subjected to mechanical friction against clothing and the skin → traumatic erosion
- Venous and lymphatic congestion of the prolapsed segment → mucosal oedema → fragile, easily traumatised mucosa
- Solitary rectal ulcer syndrome (SRUS): the leading point of the intussusception is compressed against the anal canal during straining → localised mucosal ischaemia → ulceration (typically anterior rectal wall, 6–10 cm from anal verge)
Clinical features: Fresh PR bleeding (usually minor), mucus discharge, perianal soiling and excoriation.
This deserves separate mention as it is both a consequence and an associated condition.
Mechanism: Internal intussusception → the leading edge of the intussusceptum is repeatedly compressed against the anal canal → localised ischaemic pressure necrosis → mucosal ulceration. Additionally, direct digital trauma from patients using digital manoeuvres contributes.
Histology: Fibromuscular obliteration of the lamina propria (pathognomonic) — smooth muscle fibres from the muscularis mucosae extend upward into the lamina propria.
Clinical significance: Can mimic a rectal tumour on endoscopy → biopsy is essential to differentiate. Treating the underlying prolapse often resolves the SRUS.
Concomitant pelvic floor pathology — Cystocele / Rectocele / Uterine prolapse [2]
Why does it happen? Rectal prolapse is a manifestation of global pelvic floor weakness. The same levator ani diastasis and pudendal neuropathy that cause rectal prolapse also weaken the supports for the bladder (anterior compartment) and uterus/vaginal vault (middle compartment).
Clinical significance:
- Cystocele → urinary stress incontinence, urinary retention, recurrent UTIs
- Uterine prolapse → sensation of vaginal mass, dragging discomfort
- Enterocele → deep pelvic pressure, obstructed defecation (small bowel herniating into rectovaginal space pushes on rectum)
- Must be identified pre-operatively to plan multi-compartment repair (e.g., LVMR addresses the posterior compartment and obliterates the Pouch of Douglas)
Chronic mucus discharge and stool soiling → perianal maceration, excoriation, contact dermatitis, pruritus ani, and secondary fungal/bacterial infection of the perianal skin.
B. Complications of Surgical Treatment
Complications vary by approach (abdominal vs perineal) and specific procedure. Organised by timing:
| Complication | Mechanism | Relevant procedures | Management |
|---|---|---|---|
| Surgical site infection [5] | Contamination from bowel flora during rectal/sigmoid mobilisation or resection | All procedures | Wound care, antibiotics; I&D if abscess |
| Postoperative ileus [5] | Bowel handling, anaesthesia, electrolyte imbalance → temporary loss of coordinated peristalsis | Abdominal approaches | Conservative: NG tube, IV fluids, correction of electrolytes, early mobilisation |
| Urinary retention [4] | Pelvic dissection → oedema/inflammation near bladder and pelvic autonomic nerves; pain and opioid analgesia → detrusor inhibition | Both approaches; especially abdominal procedures with extensive pelvic dissection | Catheterisation for 24–48 hours |
| Haemorrhage / Reactionary bleeding | Presacral venous plexus injury (during posterior rectal mobilisation); mesenteric vessel injury | Abdominal rectopexy, resection rectopexy | Pressure, haemostatic agents, transfusion; reoperation if severe |
| Anastomotic leak [4][5] | Ischaemia at the anastomotic line, tension, poor technique, patient factors (malnutrition, steroids, diabetes) | Altemeier procedure (perineal coloanal anastomosis), Resection rectopexy (colorectal anastomosis) | Becomes apparent 5–7 days postoperatively [5]; signs: pain, fever, tachycardia, feculent/purulent drainage. Management: IV antibiotics, bowel rest, percutaneous drainage of collections, proximal faecal diversion if needed |
| Injury to neighbouring structures [4] | Iatrogenic damage during pelvic dissection | Abdominal approaches | — |
| — Autonomic nerve injury [4] | Damage to hypogastric nerves (sympathetic) or pelvic splanchnic nerves (parasympathetic) during posterior rectal mobilisation | Posterior mesh rectopexy, resection rectopexy | Sympathetic injury → ejaculatory dysfunction, incontinence. Parasympathetic injury → urinary retention, erectile dysfunction. This is why LVMR avoids posterior dissection |
| — Ureteral injury [4][5] | Left ureter runs close to the sigmoid mesentery and may be injured during sigmoid mobilisation/resection | Resection rectopexy | Intraoperative repair; ureteric stenting |
| Complication | Mechanism | Relevant procedures | Management |
|---|---|---|---|
| Recurrence of prolapse | The most common long-term complication overall. Failure of the repair to adequately fix the rectum. Risk factors: perineal approach, inadequate rectopexy, ongoing straining, severe pelvic floor weakness | All procedures — higher with perineal approaches (16–38%) than abdominal (~3–9%) | Repeat surgery; may switch approach (e.g., abdominal after failed perineal, or vice versa) |
| New-onset or worsened constipation | Posterior rectal mobilisation → division of lateral ligaments → denervation of rectum → impaired rectal motility. Mesh placed posteriorly can kink/compress the rectum. Fixed rectum can no longer accommodate stool bolus if sigmoid redundancy persists | Posterior mesh rectopexy (Ripstein, Wells); suture rectopexy without sigmoid resection | Laxatives, biofeedback. Prevention: use LVMR (avoids posterior dissection); add sigmoid resection if transit is slow |
| Persistent faecal incontinence | Pre-existing severe pudendal neuropathy does not recover even after anatomical correction. Irreversible sphincter damage | All procedures | Biofeedback, pelvic floor rehabilitation, sacral nerve stimulation; consider colostomy if refractory |
| Mesh-related complications | Foreign body → chronic inflammatory reaction → erosion into adjacent structures (rectum, vagina); infection; chronic pelvic pain; dyspareunia | Mesh rectopexy (posterior or ventral) | Mesh removal (difficult); antibiotics for infection. Use biological mesh to reduce erosion risk; avoid synthetic mesh in contaminated fields |
| Anastomotic stricture [4][5] | Excessive scarring/fibrosis at the anastomotic line → luminal narrowing | Altemeier procedure, resection rectopexy | Finger dilatation for low anastomosis; endoscopic balloon dilatation for high anastomosis [5] |
| Fistula [4][5] | Anastomotic breakdown → communication between bowel and adjacent structure | Altemeier, resection rectopexy | Enterocutaneous fistula: conservative management (most close spontaneously) [5]. Rectovaginal or rectourinary fistula: proximal faecal diversion [4][5] |
| Anal encirclement (Thiersch) specific | Band too tight → faecal impaction; band too loose → recurrence; infection; erosion through perianal skin; band breakage | Thiersch procedure | Removal of encirclement device; definitive surgical repair |
Why LVMR has fewer complications than posterior rectopexy
Posterior rectopexy requires mobilisation of the rectum posteriorly, which risks damage to the lateral ligaments (containing the middle rectal vessels and autonomic nerves) and the presacral venous plexus. This causes new-onset constipation (denervation) and haemorrhage. LVMR avoids posterior dissection entirely — the mesh is placed anteriorly in the rectovaginal/rectovesical septum — preserving autonomic innervation and reducing constipation. This is the fundamental reason for the shift toward ventral mesh rectopexy in modern practice.
| Procedure | Unique/Key Complications |
|---|---|
| LVMR [1] | Mesh erosion (into vagina/rectum), mesh infection, chronic pelvic pain, dyspareunia. Recurrence ~3.4% [1] |
| Posterior mesh rectopexy | New-onset constipation (posterior dissection), presacral haemorrhage, mesh complications |
| Resection rectopexy | Anastomotic leak, anastomotic stricture, fistula, ureteral injury, autonomic nerve injury |
| Altemeier [3] | Anastomotic leak (perineal), anastomotic stricture, recurrence (16–30%), pelvic sepsis |
| Delorme [3] | Highest recurrence (20–38%); mucosal dehiscence; minimal other complications |
| Thiersch [1] | Faecal impaction, infection, erosion, band breakage, very high recurrence |
Often overlooked but clinically significant:
- Social isolation: chronic faecal incontinence and soiling → embarrassment → withdrawal from social activities
- Depression and anxiety: particularly in elderly patients; multifactorial — incontinence, chronic pain, body image, functional limitation
- Sexual dysfunction: both from the disease itself (prolapse during intercourse, incontinence) and from surgery (autonomic nerve injury → erectile dysfunction, ejaculatory failure, dyspareunia from mesh erosion)
- Nutritional impact: patients may restrict food intake to reduce stool frequency and soiling → weight loss, malnutrition (especially in elderly)
High Yield Summary
- Complications of the disease: faecal incontinence (up to 75%), constipation/obstructed defecation, incarceration, strangulation/gangrene (surgical emergency), mucosal ulceration/bleeding, solitary rectal ulcer, multi-compartment pelvic organ prolapse, perianal skin complications.
- Incarceration → strangulation sequence: venous congestion → oedema → arterial compromise → gangrene. Manage with sugar application → manual reduction if viable; urgent perineal resection if non-viable.
- Surgical complications: recurrence (most common overall — higher with perineal approaches), new-onset constipation (posterior dissection), persistent incontinence (pudendal neuropathy), anastomotic leak/stricture/fistula, mesh erosion, autonomic nerve injury (sexual/urinary dysfunction), haemorrhage.
- Autonomic nerve injury during posterior rectal mobilisation → sympathetic damage (ejaculatory dysfunction) or parasympathetic damage (urinary retention, erectile dysfunction). LVMR avoids this by using an anterior-only approach.
- Anastomotic leak becomes apparent 5–7 days post-op; presents with pain, fever, tachycardia, feculent drainage.
- Mesh complications: erosion (into rectum/vagina), infection, chronic pain, dyspareunia. Use biological mesh to minimise risk.
- Recurrence rates: LVMR ~3.4%; abdominal suture/resection rectopexy ~3–9%; Altemeier ~16–30%; Delorme ~20–38%.
Active Recall - Complications of Rectal Prolapse
References
[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p65–66, p68–69, p72) [2] Senior notes: felixlai.md (Rectal prolapse — Clinical manifestation and Etiology sections, pp. 761–763) [3] Senior notes: maxim.md (Incarcerated rectal prolapse management; Altemeier; Delorme) [4] Senior notes: maxim.md (Post-operative complications of colorectal surgery — anastomotic leak, stricture, fistula, autonomic nerve injury) [5] Senior notes: felixlai.md (Complications of colorectal surgery — anastomotic complications, stoma complications, pp. 696, 706)
High Yield Summary
- Rectal prolapse = full-thickness protrusion of the rectum through the anal sphincters — internal prolapse is intussusception that does not pass beyond the anus.
- Bimodal age distribution: elderly women (commonest) and young children.
- Key anatomical abnormalities: rectal intussusception, deep cul-de-sac, loss of rectal fixation, redundant sigmoid, levator ani diastasis, patulous sphincter, pudendal neuropathy.
- Aetiological triad (adults): pelvic floor weakness + chronic straining + neurological/obstetric injury. In children: think cystic fibrosis, whooping cough, malnutrition.
- 25–50% associated with constipation; 75% have faecal incontinence.
- Pathophysiology: starts as internal intussusception → progresses to external prolapse → chronic sphincter stretch → incontinence.
- Concentric rings = full-thickness rectal prolapse; radial folds = prolapsed haemorrhoids — this is the key bedside distinction.
- Incarcerated rectal prolapse: sugar/salt osmotic application → manual reduction → surgery.
- Always assess for multi-compartment pelvic organ prolapse and exclude colorectal malignancy.
- In children, always exclude cystic fibrosis (sweat chloride test).
High Yield Summary
- The three named differentials from senior notes: prolapsed internal haemorrhoids, rectal mucosal prolapse (including occult internal intussusception), and solitary rectal ulcer.
- Concentric rings = rectal prolapse; radial folds = haemorrhoids/mucosal prolapse — the single most important bedside distinction.
- Acute painful anal mass "Big Three": thrombosed prolapsed internal haemorrhoids, thrombosed external haemorrhoid, incarcerated rectal prolapse (circular folds). Management differs for each.
- Incarcerated rectal prolapse: sugar application → manual reduction → surgery.
- Internal intussusception is occult — no visible external prolapse — diagnosed by defecography. It is the precursor to full-thickness prolapse.
- Solitary rectal ulcer: associated with internal intussusception; histology shows fibromuscular obliteration of lamina propria; can mimic tumour on endoscopy.
- Always exclude colorectal neoplasm — DRE + proctoscopy + sigmoidoscopy/colonoscopy.
- Atypical anal features (off-midline, multiple, deep fissures, hypertrophic skin tags) → suspect perianal Crohn's disease.
High Yield Summary
- Rectal prolapse is a clinical diagnosis — demonstrate the prolapse by asking the patient to strain, ideally on a commode. Look for concentric circumferential rings.
- Assessment triad from lectures: DRE (exclude other lesions, assess tone) → Proctoscopy (severity) → Sigmoidoscopy (exclude proximal lesion).
- If prolapse cannot be demonstrated clinically → Defecography or Dynamic pelvic MRI to identify internal intussusception or multi-compartment prolapse.
- Pelvic physiology studies (manometry, EMG, PNTML) are for pre-operative assessment — they predict continence outcomes and guide surgical planning, not diagnosis per se.
- Colonoscopy is mandatory in surgical candidates to exclude malignancy and characterise colonic anatomy.
- Colonic transit study is essential in patients with severe or lifelong constipation — determines whether sigmoid colectomy should be added to rectopexy.
- PNTML > 2.0 ms = pudendal neuropathy → poorer prognosis for continence recovery after surgery → counsel patient accordingly.
- In children, always perform a sweat chloride test to exclude cystic fibrosis.
High Yield Summary
- Surgery is the definitive treatment for full-thickness rectal prolapse — conservative measures alone cannot fix it (except in children).
- Two broad approaches: Abdominal repair (lower recurrence, better function, needs GA) vs Perineal repair (higher recurrence, lower morbidity, can be done under regional anaesthesia).
- Abdominal options: Rectal fixation (suture/mesh), Sigmoid resection, Proctectomy, Combination of fixation + resection. Approach: laparoscopic vs open vs robotic.
- Perineal options: Full-thickness resection (Altemeier), Mucosal resection with muscular reefing (Delorme), Anal encirclement (Thiersch — rarely used).
- LVMR is the preferred abdominal technique — recurrence 3.4%, improvement in incontinence 45%, improvement in constipation 24%.
- Add sigmoid resection if patient has constipation with redundant sigmoid / slow transit on colonic transit study. Do NOT resect if predominant symptom is incontinence.
- Incarcerated rectal prolapse: sugar application → manual reduction → elective surgery. If strangulated → urgent perineal procedure.
- Rectopexy = affix pararectal tissues to presacral fascia/sacral periosteum at the sacral promontory using non-absorbable sutures or mesh.
- Frail/elderly patients → perineal approach (Altemeier or Delorme); fit patients → abdominal approach (LVMR or resection rectopexy).
High Yield Summary
- Complications of the disease: faecal incontinence (up to 75%), constipation/obstructed defecation, incarceration, strangulation/gangrene (surgical emergency), mucosal ulceration/bleeding, solitary rectal ulcer, multi-compartment pelvic organ prolapse, perianal skin complications.
- Incarceration → strangulation sequence: venous congestion → oedema → arterial compromise → gangrene. Manage with sugar application → manual reduction if viable; urgent perineal resection if non-viable.
- Surgical complications: recurrence (most common overall — higher with perineal approaches), new-onset constipation (posterior dissection), persistent incontinence (pudendal neuropathy), anastomotic leak/stricture/fistula, mesh erosion, autonomic nerve injury (sexual/urinary dysfunction), haemorrhage.
- Autonomic nerve injury during posterior rectal mobilisation → sympathetic damage (ejaculatory dysfunction) or parasympathetic damage (urinary retention, erectile dysfunction). LVMR avoids this by using an anterior-only approach.
- Anastomotic leak becomes apparent 5–7 days post-op; presents with pain, fever, tachycardia, feculent drainage.
- Mesh complications: erosion (into rectum/vagina), infection, chronic pain, dyspareunia. Use biological mesh to minimise risk.
- Recurrence rates: LVMR ~3.4%; abdominal suture/resection rectopexy ~3–9%; Altemeier ~16–30%; Delorme ~20–38%.
Peritonitis
Peritonitis is inflammation of the peritoneum, typically caused by bacterial infection due to perforation of an abdominal viscus or contamination of the peritoneal cavity, presenting with severe abdominal pain, rigidity, and systemic sepsis.
Volvulus
Volvulus is the abnormal twisting of a segment of bowel around its mesenteric axis, leading to obstruction and potential vascular compromise with ischemia.