Rectal Prolapse

"Procidentia" comes from Latin procidere = "to fall forward." That's literally what happens — the rectum falls forward and out through the anus.

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1. Definition

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]:

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2. Epidemiology

• 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

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3. Anatomy & Function (Understanding the Supports of the Rectum)

To understand why the rectum prolapses, you need to understand what keeps it in place.

3.1 The Pelvic Floor

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

3.2 Fixation of the Rectum

The rectum is held in place by:

1. Lateral ligaments of the rectum (containing the middle rectal vessels and autonomic nerves)
2. Mesorectal fascia (Waldeyer's fascia) — anchors the rectum to the presacral fascia of the sacrum
3. 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
4. Puborectalis sling — maintains the anorectal angle
5. Anal sphincter complex — internal anal sphincter (IAS, smooth muscle, involuntary) and external anal sphincter (EAS, striated muscle, voluntary)

3.3 Relevant Innervation

• 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

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4. Aetiology & Risk Factors

4.1 Anatomical Abnormalities Associated with Rectal Prolapse

The following anatomical abnormalities are classically associated ^[1]:

4.2 Risk Factors (Organised by Category)

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

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5. Pathophysiology

Understanding the pathophysiology requires integrating the anatomical and aetiological factors above into a coherent sequence.

5.1 The "Sliding Hernia" Theory (Moschcowitz, 1912)

• 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

5.2 The "Intussusception" Theory (Broden & Snellman, 1968) — Currently Favoured

• 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

5.3 Integrated Pathophysiological Sequence

5.4 Why Specific Symptoms Occur (linked to pathophysiology)

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6. Classification

6.1 By Degree of Prolapse

6.2 Oxford Classification of Internal Rectal Prolapse (Defecographic)

Used on defecography/dynamic MRI to grade internal intussusception:

6.3 Practical Clinical Classification

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

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7. Clinical Features

7.1 Symptoms

7.2 Signs

7.3 Distinguishing Rectal Prolapse from Prolapsed Haemorrhoids

This is a critical clinical distinction ^[3]:

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8. Associated Conditions

• 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

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Active Recall - Rectal Prolapse: Definition, Epidemiology, Aetiology, Pathophysiology & Clinical Features

1. Name the key anatomical abnormalities associated with rectal prolapse (at least 5 from the lecture slides).

Your answer

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Rectal intussusception, deep cul-de-sac (Pouch of Douglas), loss of rectal fixation, redundant sigmoid colon, levator ani diastasis, patulous anal sphincter, pudendal neuropathy. (Any 5 for full marks)

2. How do you clinically distinguish full-thickness rectal prolapse from prolapsed haemorrhoids on inspection?

Your answer

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Full-thickness rectal prolapse shows concentric (circumferential) mucosal rings; prolapsed haemorrhoids show radial folds with grooves between cushions. Full-thickness prolapse also has a sulcus between the prolapse and the anal canal, is circumferentially symmetric, and involves all layers of the rectal wall.

3. Why is cystic fibrosis an important differential in a child presenting with rectal prolapse?

Your answer

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Rectal prolapse may be the presenting feature in up to 20% of CF children. Mechanism: chronic cough raises intra-abdominal pressure, steatorrhoea produces bulky stools requiring straining, and malnutrition leads to loss of the perirectal fat pad that normally supports the rectum. A sweat chloride test should be performed.

4. Explain why up to 75% of patients with rectal prolapse have faecal incontinence, linking pathophysiology to anatomy.

Your answer

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Three mechanisms: (1) Chronic mechanical stretch of the anal sphincter complex by the prolapsing rectum leads to sphincter weakness. (2) Pudendal nerve stretch injury (neuropathy) causes denervation of the external anal sphincter. (3) Loss of the anorectal angle due to puborectalis dysfunction removes the flap-valve mechanism of continence.

5. What bedside technique is used to reduce an incarcerated rectal prolapse, and what is the mechanism?

Your answer

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Application of granulated sugar (or salt) to the oedematous prolapsed mucosa. Mechanism: osmotic effect draws interstitial fluid out of the congested tissue, reducing oedema and swelling, thereby facilitating manual reduction. This is followed by definitive surgical repair.

6. A patient with rectal prolapse complains of incomplete evacuation and tenesmus but has no visible external prolapse. What is the likely diagnosis, and how would you confirm it?

Your answer

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Internal rectal prolapse (rectal intussusception) - the rectum telescopes but does not protrude beyond the anus. Confirmed by defecography (either fluoroscopic or dynamic pelvic MRI), which will show the intussusception during straining.

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References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p65–67) ^[2] Senior notes: felixlai.md (Rectal prolapse section, pp. 761–763) ^[3] Senior notes: maxim.md (Rectal prolapse and prolapsed haemorrhoid distinction; incarcerated prolapse management)

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.

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Overview of Key Differentials

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]

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Detailed Differential Diagnosis

1. Prolapsed Internal Haemorrhoids [2][3]

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:

2. Rectal Mucosal Prolapse (Partial Prolapse) [2]

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:

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).

3. Occult Rectal Prolapse (Internal Intussusception) [2]

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.

4. Solitary Rectal Ulcer (Syndrome) [2][5]

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.

5. Acute Painful Anal Mass — The "Big Three" [3]

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:

6. Anal / Low Rectal Carcinoma [6]

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.

7. Perianal Crohn's Disease [3][5]

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

8. Anal Fissure [3]

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].

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Diagnostic Approach — Mermaid Flowchart

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Summary Table of Key Differentials

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Active Recall - Differential Diagnosis of Rectal Prolapse

1. Name the three key differentials for rectal prolapse listed in the senior notes, and explain how each is distinguished from full-thickness rectal prolapse.

Your answer

Grade

Show mark scheme

1. Prolapsed internal haemorrhoids - radial folds, segmental (3/7/11 o'clock), no sulcus, mucosa+submucosa only. 2. Rectal mucosal prolapse / occult internal intussusception - mucosa only, thin, less than 4 cm, radial folds; internal intussusception has no external protrusion. 3. Solitary rectal ulcer - ulcer on anterior rectal wall associated with internal intussusception, histology shows fibromuscular obliteration.

2. A patient presents with an acute painful irreducible perianal mass with circumferential concentric folds. What is the diagnosis and immediate bedside management?

Your answer

Grade

Show mark scheme

Incarcerated rectal prolapse. Immediate management: apply granulated sugar to the oedematous prolapsed mucosa (osmotic effect draws out oedema fluid), then attempt gentle manual reduction. Definitive management is surgical repair.

3. Why is solitary rectal ulcer syndrome associated with rectal prolapse, and what is the characteristic histological finding?

Your answer

Grade

Show mark scheme

The leading point of the intussuscepting rectum is compressed against the anal canal during straining, causing ischaemic pressure on the anterior rectal wall mucosa leading to ulceration. Histology: fibromuscular obliteration of the lamina propria with smooth muscle fibres extending from muscularis mucosae into the lamina propria, and distorted crypt architecture.

4. List the three causes of an acute painful anal mass and one key distinguishing feature for each.

Your answer

Grade

Show mark scheme

1. Thrombosed prolapsed internal haemorrhoids - segmental with radial folds. 2. Thrombosed external haemorrhoid - localised bluish mass below dentate line, forms skin tag after 48 hours. 3. Incarcerated rectal prolapse - circumferential with concentric (circular) folds.

5. What clinical features should make you suspect perianal Crohn's disease rather than a simple anal fissure?

Your answer

Grade

Show mark scheme

Non-midline fissures, recurring fissures, multiple fissures, unusually deep or wide fissures, perianal hypertrophic skin tags. Also consider if associated with systemic symptoms of Crohn's (abdominal pain, diarrhoea, weight loss, oral ulcers, extraintestinal manifestations).

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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).

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1. Diagnostic Criteria

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]

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2. Clinical Assessment — The Bedside Evaluation

The lecture slides ^[1] outline a systematic approach to anorectal disease assessment:

Physical examination ^[1]:

1. General examination
2. Abdominal examination
3. Perianal examination
4. Digital rectal examination
5. Proctoscopy

Let's break down each step in the context of rectal prolapse.

2.1 History

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

2.2 Anorectal Examination [2]

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]

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3. Investigation Modalities

The investigations can be organised into categories based on their purpose:

3.1 Defecography [2]

"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:

3.2 Dynamic Pelvic MRI [2]

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.

3.3.1 Anorectal Manometry [2]

What is it? A catheter with pressure sensors is inserted into the rectum and anal canal to measure pressures.

Key measurements and interpretation:

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.

3.3.2 Electromyography (EMG) [2]

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)

3.3.3 Pudendal Nerve Terminal Motor Latency (PNTML) [2]

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.

3.3.4 Endoanal Ultrasonography (EAUS)

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.

3.4 Colonoscopy [2]

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]

3.5 Colonic Transit Study [2]

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

3.6 Additional/Adjunctive Investigations

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4. Diagnostic Algorithm

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5. Summary of Investigations with Key Findings

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Active Recall - Diagnosis of Rectal Prolapse

1. What is the gold standard investigation for diagnosing internal rectal prolapse (internal intussusception) and why is it needed?

Your answer

Grade

Show mark scheme

Defecography (fluoroscopic or dynamic MRI). It is needed because internal intussusception does not protrude beyond the anus and therefore cannot be seen on clinical inspection. Defecography images the rectum during simulated straining and can demonstrate the telescoping of the rectal wall.

2. List the three-step assessment outlined in the lecture slides for anorectal disease, and state the purpose of each step.

Your answer

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1. DRE - to exclude other rectal lesions and assess sphincter tone. 2. Proctoscopy - for diagnosis and assessment of severity. 3. Rigid or flexible sigmoidoscopy - to exclude proximal bowel lesion.

3. Why is a colonic transit study performed in patients with rectal prolapse who have severe constipation, and how does it change surgical management?

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It determines whether constipation is due to slow transit (global marker retention) or outlet obstruction (rectosigmoid retention). If slow transit constipation is identified, sigmoid resection should be added to rectopexy to address constipation; if outlet obstruction only, rectopexy alone may suffice.

4. What does a prolonged PNTML indicate, what is the normal value, and why is it clinically important in rectal prolapse?

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PNTML > 2.0 ms indicates pudendal neuropathy (normal is 2.0 ms or less). It predicts poorer recovery of continence after surgical repair of rectal prolapse because the denervated external anal sphincter is less likely to regain function. Important for patient counselling pre-operatively.

5. A 3-year-old child presents with rectal prolapse. What specific investigation should be performed and why?

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Sweat chloride test to exclude cystic fibrosis. Rectal prolapse may be the presenting feature in up to 20% of children with CF due to chronic cough (raised intra-abdominal pressure), steatorrhoea (bulky stools), and malnutrition (loss of perirectal fat pad). Chloride > 60 mmol/L is diagnostic.

6. What is the advantage of dynamic pelvic MRI over fluoroscopic defecography in evaluating rectal prolapse?

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Dynamic pelvic MRI simultaneously visualises all three pelvic floor compartments (anterior - bladder, middle - uterus/vagina, posterior - rectum) without ionising radiation and with superior soft-tissue contrast. It can identify levator ani diastasis and puborectalis morphology. Ideal for multi-compartment pelvic organ prolapse assessment.

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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).

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1. General Principles

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]:

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2. Management Algorithm

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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

3.1 Dietary and Lifestyle Modifications

3.2 Pelvic Floor Rehabilitation / Biofeedback

• 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

3.3 Management of Incarcerated Rectal Prolapse (Emergency)

Incarcerated rectal prolapse: sugar application + manual reduction + surgery ^[3]

Step-by-step approach:

1. 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
2. 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)
3. Assess viability: If mucosa is dusky/black/necrotic → suspect strangulation → do not attempt reduction → urgent surgery
4. Definitive surgery: Plan elective surgery after successful reduction; if reduction fails or tissue is non-viable → urgent perineal procedure (typically Altemeier)

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4. Surgical Treatment — Abdominal Approaches

The lecture slides ^[1] list the abdominal repair options as:

• Rectal fixation (suture/mesh) ^[1]
• Sigmoid resection ^[1]
• Proctectomy ^[1]
• Combination of rectal fixation and sigmoid resection ^[1]
• Laparoscopic vs. open vs. robotic ^[1]

4.1 Rectopexy [2]

"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:

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)

4.2 Sigmoid Resection [1][2]

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

4.3 Proctectomy [1]

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

4.4 Other Abdominal Approaches [1]

Suture, Mesh, Resection ^[1] — these can be combined in various permutations:

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)

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5. Surgical Treatment — Perineal Approaches

The lecture slides ^[1] list the perineal repair options as:

• Full thickness resection ^[1]
• Mucosal resection with muscular reefing ^[1]
• Anal encirclement ^[1]

5.1 Altemeier Procedure (Perineal Rectosigmoidectomy) [1][3]

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

5.2 Delorme Procedure [1][3]

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

5.3 Anal Encirclement (Thiersch Procedure) [1]

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

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6. Special Populations

6.1 Children

• 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)

6.2 Internal Intussusception (Without External Prolapse)

• 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

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7. Comparison of Surgical Procedures — Summary Table

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8. Postoperative Considerations

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Active Recall - Management of Rectal Prolapse

1. Name the abdominal and perineal surgical options for rectal prolapse as listed in the lecture slides.

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Abdominal: Rectal fixation (suture/mesh), Sigmoid resection, Proctectomy, Combination of rectal fixation and sigmoid resection. Perineal: Full-thickness resection (Altemeier), Mucosal resection with muscular reefing (Delorme), Anal encirclement (Thiersch).

2. What is laparoscopic ventral mesh rectopexy, and what outcomes were reported in the 2010 systematic review cited in the lecture slides?

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LVMR involves placing mesh on the anterior (ventral) aspect of the rectum, extending from the Pouch of Douglas to the perineal body, fixed to the sacral promontory. Posterior dissection is avoided. 2010 systematic review of 12 non-randomised studies, 728 patients: recurrence 3.4%, improvement in incontinence 45%, improvement in constipation 24%.

3. A frail 85-year-old woman presents with an incarcerated, oedematous rectal prolapse. Describe the stepwise emergency management.

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1. Apply granulated sugar to the prolapsed mucosa (osmotic effect to reduce oedema). 2. Gently attempt manual reduction once swelling decreases. 3. Assess mucosal viability - if necrotic/strangulated, do not reduce, proceed to urgent surgery. 4. If successfully reduced, plan elective surgery (perineal approach preferred given frailty - e.g. Altemeier procedure). If unsuccessful, urgent perineal rectosigmoidectomy.

4. When should sigmoid resection be added to rectopexy, and when should it be avoided? Explain the rationale.

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Add sigmoid resection when: constipation is the predominant symptom, sigmoid is redundant, and/or colonic transit study shows slow transit constipation. Rationale: redundant sigmoid acts as a stool reservoir promoting constipation; removing it improves transit. Avoid when: predominant symptom is faecal incontinence. Rationale: removing sigmoid shortens the colon, producing looser and more frequent stools, which would worsen incontinence.

5. Compare the Altemeier and Delorme procedures in terms of technique, recurrence rate, and ideal patient.

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Altemeier (perineal rectosigmoidectomy): full-thickness resection of redundant rectosigmoid via perineum with coloanal anastomosis plus levatorplasty. Recurrence 16-30%. Best for frail patients, emergency (incarcerated/strangulated), larger prolapses. Delorme: mucosal stripping with plication (reefing) of the denuded muscularis. No bowel resection. Recurrence 20-38%. Best for shorter prolapses (less than 3-4 cm), mucosal prolapse, very frail patients. Both can be done under regional anaesthesia.

6. Why is posterior rectal mobilisation avoided in laparoscopic ventral mesh rectopexy, and what is the clinical benefit?

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Posterior mobilisation risks damaging the lateral ligaments of the rectum and the autonomic (pelvic splanchnic) nerves that run in them. This can cause new-onset or worsened constipation (rectal denervation impairs motility) and sexual dysfunction. By using a ventral (anterior-only) approach, LVMR preserves these structures, resulting in better functional outcomes for both constipation and continence.

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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.

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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.

1. Faecal Incontinence

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:

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.

2. Chronic Constipation and Obstructed Defecation

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.

3. Incarceration

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.

4. Strangulation and Gangrene

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).

5. Mucosal Ulceration and Bleeding

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.

6. Solitary Rectal Ulcer Syndrome (SRUS)

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.

7. Multi-Compartment Pelvic Organ Prolapse

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)

8. Perianal Skin Complications

Chronic mucus discharge and stool soiling → perianal maceration, excoriation, contact dermatitis, pruritus ani, and secondary fungal/bacterial infection of the perianal skin.

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B. Complications of Surgical Treatment

Complications vary by approach (abdominal vs perineal) and specific procedure. Organised by timing:

Early Complications (< 30 days)

Late Complications (> 30 days)

Procedure-Specific Complication Summary

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C. Psychological and Quality-of-Life Impact

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)

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Active Recall - Complications of Rectal Prolapse

1. Explain the pathophysiological sequence from incarceration to strangulation in rectal prolapse, and state the key management principle for each stage.

Your answer

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Incarceration: prolapse cannot be reduced, anal sphincter ring compresses venous and lymphatic drainage causing oedema, which further prevents reduction (vicious cycle). Management: sugar application to osmotically reduce oedema then manual reduction. Strangulation: progressive oedema eventually compromises arterial inflow causing ischaemia then gangrene. Management: do NOT attempt reduction of non-viable tissue. Proceed to urgent perineal resection (Altemeier).

2. Why does new-onset constipation occur after posterior mesh rectopexy, and how does LVMR avoid this?

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Posterior mobilisation of the rectum damages the lateral ligaments containing autonomic nerves, causing rectal denervation and impaired motility. Mesh placed posteriorly can also kink or compress the rectum. LVMR avoids posterior dissection entirely by placing mesh on the anterior (ventral) aspect only, preserving the lateral ligaments and autonomic innervation.

3. List three mechanisms by which rectal prolapse causes faecal incontinence.

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1. Chronic mechanical stretch of the anal sphincter complex by the prolapsing rectum causes sphincter weakness. 2. Pudendal neuropathy from chronic straining and perineal descent causes denervation of the external anal sphincter. 3. Loss of the anorectal angle due to levator ani diastasis and puborectalis weakening removes the flap-valve continence mechanism.

4. What is solitary rectal ulcer syndrome, why does it occur in rectal prolapse, and what is the pathognomonic histological finding?

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SRUS is an ulcer (typically on the anterior rectal wall 6-10 cm from the anal verge) caused by the leading point of the internal intussusception being repeatedly compressed against the anal canal during straining, causing localised ischaemic pressure necrosis. Pathognomonic histology: fibromuscular obliteration of the lamina propria with smooth muscle fibres extending from the muscularis mucosae into the lamina propria.

5. Compare the recurrence rates of LVMR, Altemeier, and Delorme procedures, and explain why perineal approaches have higher recurrence.

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LVMR: approximately 3.4%. Altemeier: 16-30%. Delorme: 20-38%. Perineal approaches have higher recurrence because they do not address the fundamental intra-abdominal anatomical defects (loss of rectal fixation to the sacrum, deep cul-de-sac, redundant sigmoid). They remove or plicate the prolapsing tissue but do not restore the normal anatomical supports. Abdominal rectopexy directly fixes the rectum to the sacral promontory, addressing the root cause.

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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)