Anorectal Disorders

Meet the patient

A 26-year-old man lowers himself into the outpatient chair very slowly and carefully. For three weeks he has had a tearing pain on defecation that he describes as "like passing glass", lasting two to three hours afterwards — bad enough that he has stopped opening his bowels, which has only made the stool harder and the tear deeper. There is a small smear of bright red blood on the toilet paper and none in the pan; no mass, no weight loss, no fever.[6]

The diagnosis is on the history before you examine him: a typical acute anal fissure, posterior midline, until proven otherwise. Hold the two questions that decide this stem — and every anorectal stem — and the whole topic slots into place: is the bleeding painful or painless? (painful is fissure; painless is piles, prolapse or cancer) and is the lesion typical or atypical? (a single posterior midline tear is fissure; anything lateral, multiple, painless or non-healing is Crohn, HIV, syphilis, TB or cancer until biopsy proves otherwise).[6]

The dentate line decides pain and spread

One embryological line — the dentate (pectinate) line — runs almost every clinical feature of every anorectal condition you will meet. Hindgut-derived columnar mucosa above meets ectoderm-derived squamous epithelium below at this line, the embryological union of the hindgut with the proctodeum, and the two territories behave like different countries.[3]

Above the line is visceral: autonomic innervation, so lesions are painless; lymph drains to the inferior mesenteric nodes. Below the line is somatic: somatic pain fibres, voluntary control, and lymph drains to the superficial inguinal nodes. So a haemorrhoid above the line bleeds silently; a fissure below the line hurts exquisitely; and anal cancer spreads to inguinal nodes if it sits below the line and to mesenteric nodes if above. Pain versus painlessness, the route of spread, the line of surgical excision — all decided by where the lesion sits relative to this single landmark.[3]

The seven conditions declare themselves to the surgeon in only three ways: with pain (fissure, abscess, thrombosed external pile), with bleeding (haemorrhoids, fissure, cancer), or with a lump or discharge (prolapse, fistula, pilonidal sinus, cancer). The triage question below tells you which path you are on within thirty seconds of the history.[3]

The key discriminator for haemorrhoids versus fissure is pain: haemorrhoids bleed painlessly unless they thrombose; fissures cause severe pain on defecation followed by a small smear of blood. For pruritus ani, exclude Candida, dermatophyte infection, pinworm, lichen sclerosus, and perianal Crohn — the last two change management entirely.[6]

Concentric folds = prolapse, radial folds = piles

The single bedside sign that separates rectal prolapse from prolapsing Grade IV haemorrhoids is the pattern of the mucosal folds: circumferential concentric folds are prolapse, radial folds are piles. Each of the seven conditions has its own management ladder, so classify by the primary disease process first, then walk the ladder.[3]

Who sits in your clinic, and why. Haemorrhoids affect roughly 4–5 percent at any time (lifetime prevalence near 75 percent), peak 45–65, driven by anything that raises intra-abdominal venous pressure — constipation, straining, pregnancy, chronic cough, heavy lifting, obesity, low-fibre diet. Portal hypertension does not cause haemorrhoids; it causes anorectal varices, a separate painless entity that must not be banded.[3]

Anal fissure peaks at 20–40 years (M equals F); the classic precipitant is a hard stool, with pregnancy, Crohn disease and prior anorectal surgery as add-ons. Abscess and fistula hit males 2:1 aged 30–50, cryptoglandular in 90 percent, with 30–50 percent of drained abscesses going on to fistula. Pilonidal sinus is the disease of the young (15–30), hirsute, often obese, sedentary male — drivers, barbers, desk workers, military recruits.[8][15]

Anal cancer is uncommon (incidence about 1–2 per 100,000) but rising on the back of HPV, with HIV/AIDS carrying a relative risk near 30 (especially at CD4 under 200). Rectal prolapse is overwhelmingly a disease of elderly women (F:M 6:1) — frail, multiparous, chronic constipation, pelvic floor weakness; in a child it suggests cystic fibrosis, malnutrition or chronic diarrhoea. Pruritus ani affects 1–5 percent, M greater than F, peak 40–60s, idiopathic in 25–75 percent.[12][14]

Posterior midline is 90 percent — the ischaemia cycle

A typical anal fissure sits at the posterior midline in 90 percent of patients because the posterior midline is a vascular watershed, and the reason it will not heal is ischaemia — not the stool that tore it. The word itself tells the story: fissure comes from the Latin fissura, a cleft or split. A hard stool splits the sensitive squamous anoderm, and what happens next is why the tear becomes chronic.[4][6]

The tear exposes the underlying internal anal sphincter, which reacts with sustained hypertonia, driving the maximum resting pressure up and the already-poor posterior midline perfusion down — the inferior rectal artery's posterior branches are anatomically deficient in 85 percent of people. The result is local ischaemia: the fissure cannot heal, hypertonia deepens, and the cycle self-perpetuates. Every effective fissure treatment works by lowering internal sphincter pressure and restoring perfusion — GTN, diltiazem, botulinum toxin, and lateral internal sphincterotomy all share one mechanism.[4][6]

The fissure triad of chronicity — what to look for at the verge

A chronic fissure (over 6 weeks) shows three stigmata: a sentinel pile (a skin tag at the distal end, at the anal verge), a hypertrophied anal papilla (at the proximal end, above the dentate line), and exposed white internal sphincter fibres at the base of the fissure. The sentinel pile is often mistaken for an external haemorrhoid; the hypertrophied papilla for a polyp. Both are reactions to chronicity, not the primary lesion. Acute fissure (under 6 weeks) is a superficial linear tear without these.[6]

The classic trap: an atypical fissure — lateral, multiple, painless, or non-healing despite eight weeks of correct topical therapy — is not a fissure until you have excluded Crohn disease, HIV, syphilis, tuberculosis and anal cancer by biopsy. Treating a Crohn fissure or an anal cancer with GTN ointment for two months is the recurring error that delays the real diagnosis by a semester.[6]

Everyone forgets: defecation pain that the patient describes as "like passing glass", with a small smear of blood on the paper and worsening constipation from bowel avoidance, is the fissure triad — and the constipation is both a cause and a consequence. Break the cycle with a stool softener or the fissure will not heal regardless of what you apply.[6]

Goodsall: anterior straight, posterior curved to midline

An anorectal abscess and a fistula-in-ano are the same disease at two moments — pus, then a persistent track — and both are cryptoglandular in origin. The word fistula is Latin for a pipe or tube; the track is the pipe left behind when an abscess drains. The anal glands of Hermann and Desfosses sit in the crypts of Morgagni at the dentate line, and when a gland duct obstructs the sequence is always the same: stasis, infection, pus spreading along the path of least resistance into the perianal, ischiorectal, intersphincteric or supralevator spaces.[8]

The abscess either points through the skin spontaneously or is drained surgically; in 30–50 percent a persistent epithelialised track remains between the internal opening at the diseased crypt and the external opening at the skin — and it will not heal, because it is continuously bathed in faecal organisms. That track is the fistula.[8]

The cryptoglandular theory in depth — why the dentate line is the origin

There are six to twelve anal glands (of Hermann and Desfosses) lying in the submucosa at the level of the dentate line, with ducts opening into the anal crypts (of Morgagni). Obstruction of a duct — usually by faecal material or oedema — traps bacteria within the gland, and the suppuration dissects along the path of least resistance: inward is rare, outward into the perianal space is commonest (60 percent), into the ischiorectal fossa in 20 percent, between the sphincters in 5 percent, and above the levator in 2.5 percent. The intersphincteric space is the highway connecting them. This is why every perianal abscess is a potential fistula in waiting, and why you always review a drained abscess at four to six weeks for a persistent track.[8]

The Goodsall rule (Goodsall and Miles, 1900) predicts where the internal opening lies from where the external opening sits. Draw an imaginary transverse line through the centre of the anus. An external opening anterior to that line runs on a straight radial track directly inward to the anal canal at the matching clock position; an external opening posterior to the line runs on a curved track to the posterior midline (6 o'clock). It is the single most examinable rule in anorectal surgery.[8]

A consultant confession on the exception: I check the 3-cm rule every single time, because the one anterior fistula that behaves as posterior is the one that ruins an examination under anaesthesia. The exception is that an anterior external opening more than 3 cm from the anal verge usually follows the posterior (curved) rule. Forget the exception and you will probe for an anterior internal opening that does not exist.[8]

Park classification of fistula tracks — named after Sir Alan Parks — sorts fistulas by how much sphincter they cross, which is what decides whether you can lay it open: intersphincteric (commonest, 70 percent), transsphincteric (25 percent), suprasphincteric, and extrasphincteric. The percentages are exam gold.[8]

Abscess presentation is constant, throbbing perianal pain with a tender, warm, fluctuant swelling, fever and malaise — continuous, unlike the defecation pain of a fissure, and worse on sitting or walking. Ischiorectal abscesses are larger and less acutely tender; supralevator abscesses may show minimal external signs and present with deep pelvic pain and urinary symptoms. A fistula presents with intermittent or continuous discharge of pus, blood or faeculent material from a perianal pit, with recurrent pain when the opening temporarily occludes.[8]

A nest of hair in the natal cleft — pilonidal sinus

Pilonidal disease is a foreign-body reaction to shed hair drawn into the natal cleft — and the name says it: pilus (hair) plus nidus (nest), a nest of hair. The Bascom theory, now widely accepted, is that shed hair from the back or the cleft itself is sucked into the midline pits by the vacuum effect of the deep natal cleft during sitting and rising. Hair acts as a foreign body, triggering a granulomatous inflammatory response and a sinus with chronic discharge and recurrent abscess.[15]

The midline pits are the source; the lateral openings are secondary. It is intensely linked to hirsute individuals with a deep natal cleft and friction from sedentary work — which is why it afflicts young drivers, barbers and military recruits, and why lifelong depilation of the cleft reduces recurrence after any operation. A young hirsute male presents either with an acute abscess (painful, fluctuant swelling in the natal cleft with fever) or a chronic sinus (one or more midline pits with recurrent discharge of pus, sometimes extruding hair). Recurrence is the rule without definitive surgery.[15]

Nigro made anal cancer a chemoradiation disease

Before 1974, anal cancer was treated with abdominoperineal resection and a permanent colostomy; after Nigro, it became a disease cured by chemoradiation with the sphincter preserved — one of the sharpest turning points in surgical oncology. Nigro's 1974 preliminary report showed that combined 5-FU, mitomycin C and radiotherapy could ablate the tumour, and fifty years later the regimen still defines first-line curative therapy.[11]

Anal squamous cell carcinoma is etiologically linked to high-risk HPV — type 16 in about 75 percent, type 18 in about 10 percent. The viral E6 and E7 oncoproteins inactivate p53 and Rb, permitting clonal expansion through anal intraepithelial neoplasia (AIN) to invasive carcinoma; immunosuppression from HIV or transplant impairs HPV clearance and accelerates the cascade. Most SCCs arise at the transformation zone at the dentate line; lower-third tumours behave like skin SCC. Lymphatic spread follows the dentate line rule — to inguinal nodes below the line, to inferior mesenteric and internal iliac nodes above.[12]

Presentation is insidious and often delayed because the bleeding, pain, mass, pruritus or altered habit is attributed to haemorrhoids. Any non-healing ulcer or atypical mass must be biopsied; a substantial minority present with enlarged inguinal nodes from metastatic spread. Diagnosis requires examination under anaesthesia with biopsy; staging is pelvic MRI, inguinal node assessment, and CT chest, abdomen and pelvis.[12]

The Nigro regimen doses in full — the viva numbers

External beam pelvic radiotherapy 50.4–55.8 Gy in 28–31 fractions over 5–6 weeks (a primary 45 Gy field plus a 9–14 Gy boost), with the inguinal nodes included for tumours below the dentate line or with positive nodes. 5-Fluorouracil 1000 mg/m²/day as a continuous IV infusion on days 1–4 and 29–32 of radiotherapy (two cycles). Mitomycin C 10–12 mg/m² IV bolus on days 1 and 29, acting as a radiosensitiser. The ACT II trial found cisplatin no better than mitomycin C and that maintenance chemotherapy added nothing. Complete response in 80–90 percent; local failure is managed by salvage abdominoperineal resection.[11][12]

Concentric folds in an elderly woman — rectal prolapse

Complete rectal prolapse is a true intussusception of the full-thickness rectum through the anal canal, and the bedside signature is concentric circumferential mucosal folds — never the radial folds of prolapsing piles. It is overwhelmingly a disease of elderly, frail, multiparous women (F:M 6:1) with pelvic floor weakness, a deep pouch of Douglas, redundant sigmoid, weak anal sphincters and often neurological comorbidity. Constant straining telescopes the rectal wall downward until it exteriorises, with progressive denervation of the external sphincter and faecal incontinence.[14]

The prolapse presents as a mass protruding on straining that initially reduces spontaneously and later needs manual reduction, with mucus discharge, faecal soiling and incontinence. Partial (mucosal) prolapse, by contrast, is radial rather than circumferential and is the pathophysiological cousin of prolapsing haemorrhoids. Surgical strategy is dictated by fitness for abdominal surgery and continence status — abdominal for the fit (lower recurrence), perineal for the frail (lower morbidity).[14]

The itch that will not stop — pruritus ani

Pruritus ani is a final common pathway of perianal itch from cutaneous nerve endings, idiopathic in 25–75 percent, and the itch–scratch–lichenification cycle is what thickens and damages the skin. Secondary causes cluster into four groups: anorectal disease (fissure, fistula, haemorrhoids, faecal soiling), infection (Candida in moist or diabetic skin, dermatophytes, pinworm especially nocturnal in children, STIs), dermatoses (psoriasis, lichen sclerosus, atopic eczema), and contact or irritant dermatitis from over-washing, scented soaps, baby wipes and topical anaesthetics. A focused history of cleansing products, topical agents, diabetes, sexual exposure and bowel pattern is essential — the cause is usually in the history.[3]

The bedside round — DRE first, always

Examination rarely makes the diagnosis, but the digital rectal examination is the one act that must never be skipped in any patient with rectal bleeding or an altered habit — and in anorectal disease it is the act that protects you from the catastrophic miss. Position the patient left lateral (Sims) or knee–chest (jack-knife), with a chaperone and good light, and work in three steps: inspect, palpate (PR), then proctoscopy or sigmoidoscopy.[3]

Inspection — gently separate the buttocks and look for the posterior midline linear tear of a fissure (90 percent), the sentinel pile and exposed sphincter fibres of chronicity, the small red papule or pit of a fistula external opening, the firm tender bluish lump of a thrombosed external pile, the midline natal-cleft pits of pilonidal disease, and any anal ulcer or mass. Ask the patient to strain: complete rectal prolapse shows concentric mucosal folds, unlike the radial folds of prolapsing haemorrhoids. Any atypical, lateral, multiple or non-healing lesion is biopsied.[12]

Apply the Goodsall rule at the bedside. Draw an imaginary transverse line through the centre of the anus: an anterior external opening tracks straight in; a posterior opening curves to the posterior midline; an anterior opening more than 3 cm from the verge behaves as posterior. Then palpate — assess sphincter tone (hypertonic in chronic fissure), feel for an indurated fistula track, a rectal mass, the prostate, or a high-riding abscess. Defer PR if the fissure is too painful — examination under anaesthesia is the safer route. A tender, boggy, fluctuant mass is an abscess needing drainage.[8]

Proctoscopy or rigid sigmoidoscopy visualises internal haemorrhoids above the dentate line, the internal opening of a fistula, a fissure or a tumour, and excludes proximal rectal pathology.[3]

Investigations — scope, map, biopsy

Most anorectal conditions are clinical diagnoses confirmed at the bedside or under anaesthesia; investigations are reserved for atypical, complex or malignant presentations. Choose the test by the question you are trying to answer.[8]

• Proctoscopy or rigid sigmoidoscopy — first-line for haemorrhoids, fissure and the internal opening of a fistula, and it excludes a rectal tumour or proctitis; perform gently in fissure or under anaesthesia.
• Endoanal ultrasound (EAUS) — maps the fistula track and the extent of sphincter involvement; essential before surgery for any complex or recurrent fistula and to detect occult sphincter defects.
• MRI pelvis — the gold standard for complex, recurrent or Crohn-related fistulas; it defines secondary tracks, supralevator extension and abscess cavities that EUA or EAUS may miss.
• Examination under anaesthesia (EUA) — for the painful acute fissure, for abscess drainage, and for definitive fistula mapping with dye injection, hydrogen peroxide or a probe.
• Biopsy — any atypical, multiple or non-healing ulcer or fissure (exclude anal cancer, AIN, Crohn, TB, HSV, syphilis); pilonidal sinus in long-standing disease to exclude the rare Marjolin squamous carcinoma.
• FBC, CRP, blood glucose, HIV serology — in abscess with systemic sepsis or atypical or complex disease; diabetes and HIV must be excluded.
• Colonoscopy — if Crohn is suspected (multiple fissures, complex fistula, diarrhoea), or in any patient over 45 with new bleeding to exclude colorectal cancer.

[3]

The emergency: anorectal sepsis and the strangulated pile

Most anorectal conditions are not resuscitation emergencies — but two are, and recognising them in the first hour is what separates a surgeon from a clerk. The time-critical scenarios are anorectal sepsis threatening Fournier gangrene, and a strangulated or thrombosed entity.[8]

The classic trap, played straight because lives depend on it: a diabetic or immunocompromised patient with perianal sepsis can progress to Fournier gangrene within hours. Crepitus, skin necrosis, bullae, severe pain out of proportion to the findings, or systemic sepsis are not findings to chart and review — they are the indication for immediate drainage, radical debridement, IV broad-spectrum antibiotics and critical-care support. Do not wait for fluctuation, do not wait for imaging, do not send the patient home. A missed Fournier is a preventable death.[8]

For abscess with systemic features, admit, give IV fluids, IV analgesia and IV antibiotics (co-amoxiclav 1.2 g IV TDS or metronidazole 500 mg IV TDS plus a cephalosporin), correct electrolytes and glucose, and take the patient to theatre for incision and drainage — antibiotics alone will not cure an abscess. For a strangulated Grade IV haemorrhoid or an acute thrombosed external haemorrhoid within 72 hours of onset, urgent assessment and excision under local anaesthesia is appropriate for the thrombosed external pile.[8][3]

The ladders, condition by condition

Haemorrhoids — band the prolapse, excise the irreducible

Management follows the grade, and lifestyle comes first — high-fibre diet 25–30 g/day, adequate fluids 2 L/day, avoid straining, bulk-forming laxatives such as ispaghula husk, and sitz baths. Then walk the ladder.[1][3]

[1] [2] [3]

The MacRae meta-analyses are the evidence every candidate names: RBL is the most efficacious office procedure for Grade II–III disease, with efficacy comparable to surgical haemorrhoidectomy but far less pain — so RBL is first-line for Grade II–III haemorrhoids.[1][2]

Anal fissure — drop the sphincter pressure, restore the perfusion

Treat the acute fissure (under 6 weeks) conservatively first; escalate only if it is chronic or non-healing. The principle is one mechanism: lower the internal sphincter pressure to restore perfusion.[4][5][6]

[4] [5] [6]

Chronic fissure (over 6 weeks, or failed 6–8 weeks of topical therapy, with sentinel pile and exposed sphincter fibres) moves to surgery:[7]

• Lateral internal sphincterotomy (LIS) — the gold standard. Through a small lateral (3 or 9 o'clock) incision, the lower one-third of the internal anal sphincter is divided (open or closed). It relieves hypertonia permanently, heals 90–95 percent, and carries a flatus-incontinence risk of about 5 percent. Avoid LIS in Crohn disease, in the elderly with weak sphincters, and after prior sphincter injury.[7]
• Fissurectomy plus Botox — the alternative when sphincterotomy is contraindicated (Crohn, weak sphincter, primiparous women).[7]
• Advancement flap — for the non-healing fissure after LIS, or for an atypical fissure with low resting pressure.

Anorectal abscess — drain it, culture the pus

[8]

Cruciate incision and drainage under general anaesthesia is the definitive treatment, and antibiotics alone do not cure an abscess. Reserve antibiotics for cellulitis extending beyond the abscess, immunocompromise, diabetes, valvular heart disease or systemic sepsis — never as a substitute for drainage, and always send pus for culture.[8]

Fistula-in-ano — fistulotomy for low, sphincter-sparing for high

The Goodsall rule guides surgical planning, and the amount of sphincter involved dictates the operation. A low fistula (subcutaneous, low intersphincteric, low transsphincteric) can be laid open without compromising continence; a high fistula must be managed by sphincter-sparing techniques. Never divide more than 30 percent of the external sphincter in one stage.[8]

[8]

The LIFT (ligation of intersphincteric fistula tract) procedure, first described by Rojanasakul, is now the workhorse sphincter-sparing option for transsphincteric fistulas, with success rates of 70–95 percent and minimal incontinence.[8][9][10]

Pilonidal sinus — drain the abscess, off-midline the closure

[15] [16]

The Cochrane review of pilonidal wound closure (Cai 2024) is the evidence that off-midline closure — Karydakis, Bascom cleft-lift, Limberg flap — is superior to midline closure in both healing time and recurrence; the natal cleft is best obliterated, not recreated. Wiinblad's 2025 systematic review confirms no single technique is universally superior, but flap-based off-midline reconstructions dominate for recurrent disease, and lifelong depilation of the cleft reduces recurrence after any procedure.[15][16]

Anal cancer — Nigro chemoradiation first, APR for salvage only

Squamous cell carcinoma of the anal canal is treated first-line with the Nigro protocol — concurrent chemoradiation. Radical surgery (abdominoperineal resection, APR) is reserved for local failure after chemoradiation or for patients who cannot tolerate it. The Nigro protocol (1974) transformed anal cancer from a surgical disease treated by APR into a radiocurable disease treated by chemoradiation, with sphincter preservation in 70–80 percent. ACT II confirmed mitomycin C-based chemoradiation as standard and showed no benefit to maintenance chemotherapy; colostomy-free survival at five years exceeds 70 percent and overall survival approaches 75 percent. APR is reserved for local failure.[11][12][13]

Rectal prolapse — abdominal for the fit, perineal for the frail

The Cochrane review (Tou 2015) found no clear winner between abdominal and perineal approaches on aggregate, but abdominal rectopexy has the lowest recurrence and is preferred for fit patients; perineal procedures are reserved for the frail and elderly.[14]

Pruritus ani — find the cause, break the cycle

A stepped approach: (1) exclude and treat any cause — Candida with topical clotrimazole 1% BD, dermatophyte with terbinafine 1% OD, pinworm with mebendazole 100 mg PO as a single dose repeated at two weeks, lichen sclerosus with ultra-potent topical steroid clobetasol 0.05% OD for a short course, perianal Crohn by treating the underlying disease. (2) Eliminate irritants — stop scented soaps, wet wipes, over-the-counter anaesthetic creams and excessive wiping (use water or moist cotton wool). (3) Perianal hygiene — gentle washing with water and patting dry, dry with a hairdryer on the cool setting, cotton underwear. (4) Symptom relief — topical hydrocortisone 1% for a short course only (chronic steroid thins skin), oral antihistamine at night (hydroxyzine 25 mg) for sedation and itch-cycle interruption. (5) Intradermal methylene blue for refractory idiopathic pruritus ani (chemical denervation of perianal skin nerve endings — a specialist-centre option).[3]

The special groups that change the plan

Quick-fire scenarios — hide and self-test

• HIV patient with non-healing anal ulcer — biopsy for AIN or SCC; anal cancer is AIDS-defining.[12]
• Painless bright-red bleeding in a 50-year-old — exclude colorectal cancer by colonoscopy before attributing to haemorrhoids.
• Multiple atypical fissures in a young man — HIV test, syphilis serology, swab for HSV, biopsy.
• Complex recurrent fistula — MRI pelvis, EUA, consider Crohn (colonoscopy and biopsy), anti-TNF if confirmed.
• Acute thrombosed external haemorrhoid under 72 h — excision under local anaesthesia; over 72 h, conservative (warm baths, analgesia, stool softener).
• Diabetic with perianal sepsis — admit, IV antibiotics, urgent drainage, watch for Fournier gangrene.
• Strangulated Grade IV haemorrhoid — urgent excisional haemorrhoidectomy within 72 h (or conservative with later elective surgery).
• Pregnant with fissure — diltiazem 2% (avoid GTN — hypotension); avoid Botox and LIS; defer surgery to the post-partum period.
• Elderly frail woman with complete rectal prolapse — perineal Delorme or Altemeier, not abdominal.
• Child with rectal prolapse — sweat chloride test for cystic fibrosis; usually managed by reduction, manual pressure, treating constipation.

Perianal Crohn disease deserves special attention — fistulas and fissures in Crohn may be the presenting feature of the intestinal disease. The principles are non-negotiable: avoid sphincterotomy (high incontinence risk), preserve the sphincter with loose setons, and treat the underlying bowel disease (azathioprine; anti-TNF with infliximab 5 mg/kg at weeks 0, 2 and 6 then 8-weekly, or adalimumab 160 mg then 80 mg then 40 mg every other week). Infliximab closes perianal Crohn fistulas in 50–70 percent. Surgery is for drainage of sepsis and seton placement, not cure.[8]

Hidradenitis suppurativa is an important mimic of complex fistula-in-ano and pilonidal sinus — it affects the axilla, groin, buttocks and perineum with chronic recurrent sinuses and scars, and it is managed by dermatology and wide local excision rather than fistula surgery. HIV-related perianal disease spans the full spectrum — AIN, SCC, atypical ulceration (HSV, syphilis, CMV), large condylomata (HPV) and complex fistulas — and biopsy is mandatory for any chronic lesion, with a low threshold for EUA.[8][12]

Pregnancy — haemorrhoids and fissures are common (constipation, venous engorgement, progesterone slowing the gut); conservative management first, diltiazem 2% preferred over GTN (hypotension concern), defer Botox and LIS to the post-partum period; most improve after delivery. Paediatrics — rectal prolapse in a child demands a sweat chloride test for cystic fibrosis (the cannot-miss diagnosis); also consider malnutrition, chronic diarrhoea and pertussis. The elderly — perineal Delorme or Altemeier for prolapse, faecal incontinence frequently coexists, avoid lateral sphincterotomy in weak sphincters, and exclude colorectal cancer in any new bleeding.[6][14]

Named traps — the recurring trainee errors

These are the errors that delay diagnosis, sacrifice continence, or kill the patient. Name them and you will not make them.[3]

• Attributing rectal bleeding to haemorrhoids without a DRE — and without a scope in anyone over 40. Piles are common and coexist with cancer; the bleed you are reassuring the patient about may be the tumour.
• Treating an atypical fissure as a typical one — a lateral, multiple, painless or non-healing fissure is Crohn, HIV, syphilis, TB or cancer until biopsy says otherwise.
• Diabetic or immunosuppressed perianal sepsis sent home on oral antibiotics — crepitus, necrosis or systemic sepsis is Fournier gangrene until proven otherwise; admit, drain, debride.
• Fistulotomising a high fistula — dividing more than 30 percent of the external sphincter in one stage sacrifices continence. Always map with EUA plus EAUS or MRI first; if in doubt, seton.
• Performing a lateral sphincterotomy in Crohn disease — high risk of a non-healing wound and incontinence.
• Closing a pilonidal wound in the midline — higher recurrence than off-midline closure; the natal cleft must be obliterated, not recreated.
• Banding below the dentate line — excruciating pain; remove the band immediately.
• Missing the 3-cm Goodsall exception — an anterior external opening more than 3 cm from the verge curves to the posterior midline.

[3]

Complications — by disease and by operation

The disease harms the patient directly, and the operation harms them too — both lists are examinable.[3]

• Untreated abscess — spontaneous rupture, recurrent abscess, fistula formation, septicaemia, Fournier gangrene in the diabetic or immunosuppressed, anal stenosis from chronic fibrosis.
• Strangulated Grade IV haemorrhoid — thrombosis, ulceration, gangrene.
• Chronic fissure — sentinel pile, hypertrophied papilla, anal stenosis from chronic spasm.
• Untreated anal cancer — inguinal and pelvic node metastasis, obstruction, fistulation.
• Chronic pilonidal sinus — squamous cell carcinoma (Marjolin ulcer, rare), chronic recurrent sepsis, sinus extension into the sacrum.
• Complete rectal prolapse — faecal incontinence from sphincter denervation, rectal ulceration, bleeding, incarceration.

[3]

Procedure-related complications:[3]

• Rubber band ligation — severe pain (band too low; remove immediately), secondary haemorrhage 7–10 days post-op, vasovagal, rare pelvic sepsis (report any fever or dysuria after banding).
• Haemorrhoidectomy — significant post-op pain (the main driver of stapled and THD adoption), urinary retention, anal stenosis (do not excise more than the three primary cushions; preserve anoderm bridges), incontinence from injudicious sphincter division, recurrence.
• Lateral internal sphincterotomy — flatus incontinence about 5 percent, rare solid-stool incontinence, recurrence if division is insufficient.
• Fistulotomy of a high fistula — incontinence; the cardinal sin. Never divide more than 30 percent of the external sphincter in one stage.
• Seton — pain, drainage, and incontinence from a cutting seton.
• Pilonidal excision — wound infection, dehiscence (especially with midline closure), recurrence 5–50 percent depending on technique.
• Chemoradiation for anal cancer — perianal skin desquamation, diarrhoea, cytopenias (mitomycin rarely causes haemolytic–uraemic syndrome), late anal stenosis, vaginal stenosis in women, small-bowel obstruction.

[3]

Prognosis — the numbers that close the viva

Acute anal fissure: 50–70 percent heal on topical GTN or diltiazem; recurrence 15–40 percent over five years. Chronic fissure heals in 90–95 percent after lateral sphincterotomy, with 5 percent minor incontinence.[6][7]

Anorectal abscess: drain; 30–50 percent develop a fistula needing definitive surgery; diabetic and immunocompromised patients need admission and aggressive management. Low fistula: 70–90 percent cure with fistulotomy. High or complex fistula: lower cure rates; LIFT, advancement flap and seton give 60–95 percent healing with 10–30 percent recurrence per procedure.[8][9][10]

Pilonidal sinus: recurrence 10–50 percent after excision, lowest with off-midline flap reconstruction; lifelong depilation reduces recurrence. Anal cancer (SCC): with Nigro chemoradiation, complete response in 80–90 percent, five-year overall survival about 75 percent, colostomy-free survival 70–80 percent; prognosis is stage-dependent — T1N0 five-year survival 90 percent, node-positive 50–60 percent, distant metastatic 20 percent. HIV does not by itself worsen outcome provided CD4 is maintained. Rectal prolapse: recurrence 5–15 percent (lowest after abdominal rectopexy); faecal incontinence improves in about half but not all. Pruritus ani: idiopathic cases improve in 80 percent with hygiene measures; secondary resolves with treatment of the cause; chronic lichenified cases may be refractory.[12][13][14][15][16]

Evidence, guidelines and regional differences

The mantra, and the mnemonics

[3] [8] [6]

The mantra: the dentate line decides pain and spread — posterior midline is the fissure, anterior straight and posterior curved is the fistula, concentric folds are the prolapse, and a diabetic perianal abscess is Fournier until proven otherwise.[3][8]

Ward-round test — three stems

Stem 1 — 'like passing glass' in a 26-year-old (answer)

A 26-year-old man has three weeks of tearing defecation pain lasting hours afterwards, a small smear of bright blood on the toilet paper, and worsening constipation from bowel avoidance. What is the diagnosis, the first treatment with dose, and the single feature that would make you biopsy? Model: This is a typical acute anal fissure — posterior midline, the commonest pattern at 90 percent. First treatment is a stool softener (lactulose 15–30 mL or ispaghula husk) plus GTN 0.4% ointment, a pea-sized amount to the anal verge BD for six to eight weeks, warning the patient about headache and to sit after applying to avoid hypotension; diltiazem 2% is the headache-free alternative. The single feature mandating biopsy is atypicality — a lateral, multiple, painless or non-healing fissure, which is Crohn, HIV, syphilis, TB or anal cancer until histology proves otherwise. Do not accept an atypical fissure as a typical one.[6]

Stem 2 — the diabetic with throbbing perianal pain and fever (answer)

A 68-year-old diabetic man has 24 hours of severe throbbing perianal pain, fever, a tender perianal swelling, and on examination you note crepitus and dusky overlying skin. What is the diagnosis, and what do you do in the next hour? Model: This is a perianal abscess complicated by early Fournier gangrene in a diabetic — a surgical emergency, not a clinic complaint. In the next hour: admit, take cultures, give IV fluids and IV broad-spectrum antibiotics (piperacillin–tazobactam 4.5 g IV TDS plus gentamicin, with clindamycin to suppress toxin), optimise glucose, and take the patient to theatre for immediate incision, drainage and radical debridement of all necrotic tissue. Do not delay for imaging in an unstable patient. Crepitus, skin necrosis, bullae, pain out of proportion, or systemic sepsis are the indications for debridement now. Antibiotics alone will not cure an abscess, and a delayed debridement in a diabetic is a preventable death.[8]

Stem 3 — the external opening and the Goodsall rule (answer)

At examination under anaesthesia you find a fistula with an external opening at the 10 o'clock position, 1 cm from the anal verge, anterior to a transverse line through the anus. Where does the internal opening lie, and which operation is appropriate if the track involves less than 30 percent of the external sphincter? Model: By the Goodsall rule, an anterior external opening less than 3 cm from the verge runs on a straight radial track to the internal opening at the matching clock position — so the internal opening is at 10 o'clock in the anal canal. Because the track involves less than 30 percent of the external sphincter, it is a low fistula and a fistulotomy is safe: lay the track open along a probe, curette the granulation tissue, and leave it to heal by secondary intention, with an expected cure rate of 70–90 percent. If the track involved more than 30 percent of the external sphincter, you would place a loose seton and plan a sphincter-sparing definitive procedure (LIFT or advancement flap) — never a fistulotomy. The one exception to remember: an anterior opening more than 3 cm from the verge curves to the posterior midline.[8][10]

References

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