Anal Fissure

An anal fissure is a longitudinal tear in the mucosa of the anal canal, typically at the posterior midline, causing severe pain during defecation and minor rectal bleeding.

Exam domain	One-glance essentials
Definition / diagnosis	*Longitudinal tear in anoderm distal to the dentate line, usually extending toward the anal verge ^[1] Acute* fissure is superficial; chronic fissure is non-healing with sentinel pile, hypertrophied papilla and exposed IAS fibres ^[1]
Epidemiology / risks	*Constipation, hard stool and straining* are key precipitating factors ^[1] Diarrhoea, pregnancy/vaginal delivery and local anal trauma also increase risk ^[1] *Posterior midline accounts for about 90%; anterior fissures are more common in women* ^[1]
Core mechanism	Trauma causes a tear, followed by pain-induced internal anal sphincter spasm ^[1] IAS spasm worsens posterior anoderm ischaemia, impairing healing ^[1] Pain-related stool avoidance causes constipation and re-trauma: the vicious cycle ^[1]
Clinical picture	*Sharp, tearing pain at the start of defaecation, often persisting afterwards ^[1] Small-volume bright-red bleeding* on paper or stool surface; pruritus may occur ^[1] Typical: single midline lesion; multiple, lateral, deep, painless or non-healing lesions suggest secondary disease ^[1]
Investigations	*Clinical diagnosis: spread the buttocks and inspect; avoid acute DRE/proctoscopy because they are painful* ^[1] EUA is appropriate when examination is intolerable or another lesion is suspected ^[1] Atypical fissure or red flags require endoscopy, biopsy and targeted testing for IBD, infection or malignancy ^[1]
Management	*Initial treatment: fibre/bulk agents, stool softeners, topical anaesthetic, sitz baths and dietary modification* ^[1] Persistent disease: topical GTN or a calcium-channel blocker to relax the IAS; GTN commonly causes headache ^[1] Refractory disease: botulinum toxin or lateral internal sphincterotomy; choose sphincter-sparing surgery if continence risk is high ^[1]
Complications	Failure to heal produces chronic fissure with sentinel pile, hypertrophied papilla and exposed IAS fibres ^[1] Deep disease may progress to perianal abscess and fistula, especially with Crohn disease ^[1] LIS trades high healing efficacy for flatus/faecal incontinence risk; urinary retention, bleeding and infection are postoperative risks ^[1]
Prevention / follow-up	*Maintain soft, regular stools with fibre, adequate fluids and stool softeners when needed* ^[1] Avoid straining, prolonged toilet sitting and recurrent local trauma ^[1] Treat persistent diarrhoea or underlying Crohn disease/infection to reduce recurrence and non-healing ^[1]
Exam traps	Constant throbbing pain, fever or swelling suggests abscess, not a simple fissure ^[1] *Atypical position or multiple fissures should prompt investigation for secondary causes, particularly Crohn disease* ^[1] *Do not perform routine acute DRE; always consider colorectal neoplasm in significant or red-flag PR bleeding* ^[1] Avoid Lord four-finger stretch because of sphincter injury and incontinence risk ^[1]

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p42–45)

A split (tear) in the anoderm at the dentate line ^[1]. Let's break the name down: "anal" = relating to the anus; "fissure" from Latin fissura = a cleft or crack. So quite literally, it is a crack in the lining of the anal canal.

More precisely, an anal fissure is a longitudinal tear in the squamous epithelium (anoderm) of the anal canal, located distal to the dentate line ^[1]^[2]. It is one of the most common anorectal conditions encountered in clinical practice. The tear typically extends from the dentate line to the anal verge.

Key Distinction: Acute vs Chronic

Acute anal fissure: A superficial tear resembling a paper cut; typically heals within 6 weeks with conservative management ^[2].
Chronic anal fissure: Persists beyond 6–8 weeks; fails conservative management; characterised by a triad of the fissure itself + sentinel pile + hypertrophied anal papillae, with visualization of the internal sphincter muscle fibres at the base of the fissure ^[1]^[3].

Extremely common: One of the most frequent causes of anal pain and fresh per-rectal bleeding presenting to primary care and surgical outpatients.
Age: Peak incidence in young adults (20–40 years), though can occur at any age including infants.
Sex: Affects males and females roughly equally. However, anterior midline fissures are more common in women (10% of women have anterior fissures, often post-partum) ^[1].
Posterior predominance: 90% occur at the posterior midline ^[1]. This is critical to understand and is directly related to blood supply (explained below).
Lifetime prevalence is estimated at ~11% in the general population.
In Hong Kong, the high prevalence of low-fibre diets, sedentary lifestyles, and constipation contributes significantly.

The risk factors overlap heavily with those for haemorrhoids and other anorectal pathology, because they all share the common final pathway of increased anal canal pressure and/or local trauma ^[1]^[4]:

Category	Risk Factors
Bowel habit	Constipation, straining at stool, prolonged diarrhoea ^[1]^[4]
Diet	Low fibre diet, inadequate fluid intake ^[1]^[4]
Obstetric	Pregnancy, vaginal delivery (especially anterior fissures) ^[1]^[4]
Genetic / Familial	Family history (possibly related to inherited sphincter tone or connective tissue characteristics) ^[4]
Iatrogenic / Trauma	Anal instrumentation, anal intercourse
Hypertonic sphincter	Young patients with high resting internal anal sphincter (IAS) tone
Secondary causes	IBD (especially Crohn's), HIV, TB, syphilis, malignancy (see Aetiology)

Anatomy and Function

Understanding the anatomy of the anal canal is essential for understanding why fissures occur where they do, why they hurt, why they bleed, and how we treat them.

The anal canal measures approximately 4 cm in length from the anal verge to the anorectal junction ^[2]. The critical anatomical landmark is the dentate (pectinate) line, which divides the canal into upper two-thirds and lower one-third.

Feature	Above Dentate Line	Below Dentate Line
Embryology	Endoderm (hindgut)	Ectoderm (proctodeum)
Epithelium	Columnar epithelium	Stratified squamous epithelium (anoderm)
Nerve supply	Autonomic (visceral — inferior hypogastric plexus) → insensate to sharp pain	Somatic (inferior rectal nerve, branch of pudendal nerve, S2–S4) → exquisitely sensitive to pain
Venous drainage	Superior rectal vein → portal system	Middle & inferior rectal veins → systemic (IVC)
Lymphatic drainage	Internal iliac & inferior mesenteric nodes	Superficial inguinal nodes
Cancer type	Adenocarcinoma	Squamous cell carcinoma

Why Does an Anal Fissure Hurt So Much?

Anal fissures occur below the dentate line in the anoderm, which is innervated by somatic nerves (inferior rectal nerve). This area has the same pain sensitivity as skin — think of a paper cut on your finger. That's why a small tear causes excruciating, disproportionate pain. By contrast, internal haemorrhoids above the dentate line are painless because they are innervated by visceral autonomic nerves.

Internal anal sphincter (IAS): Thickened continuation of the circular smooth muscle of the rectum. It is involuntary and responsible for ~70–85% of resting anal tone. This is the key muscle involved in fissure pathophysiology — its spasm perpetuates the fissure ^[3].
External anal sphincter (EAS): Skeletal muscle under voluntary control (innervated by the inferior rectal nerve and perineal branch of S4). Responsible for voluntary squeeze pressure.
Conjoint longitudinal muscle: Between IAS and EAS; transmits fibrous septa.

The anal canal is supplied by:

Superior rectal artery (terminal branch of IMA) — supplies above the dentate line
Middle rectal artery (from internal iliac) — variable contribution
Inferior rectal artery (from internal pudendal artery) — supplies below the dentate line

Critically, anatomical studies have shown that the anoderm at the posterior midline has the least blood flow compared to other quadrants of the anal canal ^[2]^[3]. The posterior commissure is a relative "watershed zone" where the terminal branches of the inferior rectal artery provide the poorest perfusion. This explains:

Why 90% of fissures occur at the posterior midline ^[1]
Why increased sphincter pressure (IAS spasm) further compromises this already tenuous blood supply
Why the posterior fissure is the most resistant to healing

High Yield: The posterior midline is a watershed area of blood supply. IAS spasm → ↓ perfusion → ischaemia → impaired healing. This is the pathophysiological basis for the entire condition and the rationale for all treatments.

Aetiology

Anal fissures can be classified aetiologically into primary and secondary causes ^[2]:

These result from local trauma to the anal canal ^[2]:

Passage of hard stools (constipation) — the single most common cause ^[1]^[4]
Prolonged diarrhoea — liquid stool can be just as traumatic due to repeated passage and chemical irritation
Vaginal delivery — particularly causes anterior fissures
Anal intercourse
Straining at defaecation ^[1]^[4]

The common thread is mechanical trauma to the anoderm that exceeds its capacity to stretch.

These should be suspected when fissures are atypical in position (non-midline), multiple in number, recurring, non-healing, unusually deep or wide, or painless ^[1]^[3]:

Category	Specific Causes
Inflammatory bowel disease	Crohn's disease (most important — always suspect perianal Crohn's disease if atypical features ^[3]); Ulcerative colitis (less common)
Infections	Tuberculosis, syphilis, HIV infection, CMV ^[1]
Granulomatous disease	Extrapulmonary TB, Sarcoidosis
Malignancy	Squamous cell carcinoma of the anus, Leukaemia
Sexually transmitted diseases	HIV, Syphilis, Chlamydia, Herpes simplex (HSV)

When to Suspect Secondary Causes

Atypical position and multiple in number should immediately raise suspicion for: inflammatory bowel disease, tuberculosis, syphilis, HIV infection, CMV ^[1]. In Hong Kong, TB is an important consideration given higher prevalence. A single posterior midline fissure in a young patient with constipation = primary. Multiple off-midline fissures with deep ulceration in a patient with diarrhoea = think Crohn's, TB, or HIV.

Pathophysiology

This is the core of understanding anal fissure. It is a vicious cycle — and every treatment we use targets a specific point in this cycle.

Let's walk through this step by step:

Initiating event: Hard stool or local trauma stretches the anal mucosa beyond its capacity → a tear forms in the anoderm, most often at the posterior midline (least perfused area) ^[1]^[3].
Pain: The anoderm below the dentate line is richly innervated by somatic sensory nerves (inferior rectal nerve). The exposed nerve endings in the tear cause severe, sharp, tearing pain during and after defaecation.
IAS spasm: The pain triggers a reflex spasm of the internal anal sphincter ^[3]. This is the key pathological event. The IAS goes into sustained contraction, which:
- Pulls the edges of the fissure apart → prevents apposition of wound edges → impairs healing ^[2]
- Compresses the blood vessels traversing through the sphincter → further reduces perfusion to the already ischaemic posterior midline ^[2]^[3]
Ischaemia: The posterior midline already has the least blood flow ^[1]^[3]. IAS spasm worsens this by compressing the terminal branches of the inferior rectal artery. Ischaemia impairs tissue repair and perpetuates the wound.
Avoidance behaviour: The patient begins to avoid defaecation due to fear of pain → this leads to further constipation → harder stools → re-traumatisation of the fissure ^[3].
Chronicity: If this cycle is not broken within ~6 weeks, the fissure becomes chronic. Chronic changes develop:
- Fibrosis of the fissure edges (raised, rolled edges)
- Sentinel pile (skin tag) at the distal (external) end of the fissure — this represents failed healing with formation of a hypertrophied skin tag ^[3]
- Hypertrophied anal papillae at the proximal (internal) end of the fissure ^[1]^[3]
- Exposed internal sphincter muscle fibres visible as white, horizontally-oriented fibres at the base of the fissure ^[1]^[2]

Understanding the Pathophysiology = Understanding the Treatment

Every treatment for anal fissure targets this vicious cycle:

Fibre supplements, stool softeners, laxatives → soften stool → reduce trauma
Sitz baths → relax IAS, improve blood flow
Topical vasodilators (GTN, nifedipine) → relax IAS smooth muscle → reduce spasm → improve blood flow
Botulinum toxin → chemically paralyse IAS → break spasm
Lateral internal sphincterotomy → surgically divide IAS → permanently reduce tone

To reiterate this critical point because it is extremely high yield:

The aetiology of posterior midline predominance is threefold ^[1]^[3]:
1. Hard stool + tight internal anal sphincter → maximal shearing force at the posterior midline during defaecation (biomechanical studies show the posterior midline bears the greatest mechanical stress)
2. Ischaemia of the overlying anoderm at the posterior midline — the posterior commissure is the furthest point from the main arterial supply ^[1]
3. The posterior midline has the thinnest support from the external sphincter (the EAS is deficient posteriorly in the upper anal canal, offering less structural support)

Classification

Feature	Acute Fissure	Chronic Fissure
Duration	< 6 weeks	> 6–8 weeks
Appearance	Superficial tear, resembles a "paper cut", fresh laceration ^[2]	Deep ulcer with fibrotic raised/rolled edges ^[2]
Sentinel pile	Absent	Present (distal end) ^[1]^[3]
Hypertrophied papilla	Absent	Present (proximal end) ^[1]^[3]
Sphincter fibres visible	No	Yes — white horizontally oriented fibres of IAS at base ^[1]^[2]
Pathognomonic feature	Superficial tear ^[2]	Hypertrophied with skin tags or papillae ^[2]
Management	Conservative (medical)	Surgical if fails 8 weeks medical Rx

	Typical	Atypical
Position	Posterior midline (90%) or anterior midline (10%, especially women) ^[1]	Off-midline, lateral
Number	Single	Multiple
Depth	Superficial to moderate	Unusually deep or wide
Healing	Responds to treatment	Non-healing, recurring
Pain	Present	May be painless
Implication	Primary (idiopathic)	Suspect secondary cause (Crohn's, TB, HIV, syphilis, CMV) ^[1]

High Yield: Typical features = single posterior or anterior fissure without evidence of Crohn's disease. Atypical features = multiple, recurring, non-healing, deep or wide, painless, and at off-midline locations → suggests secondary causes ^[2].

Primary (idiopathic): Related to local trauma, constipation, high sphincter tone
Secondary: Related to underlying systemic or local disease (IBD, infections, malignancy)

Clinical Features

Symptom	Pathophysiological Basis
Severe pain on defaecation — sharp, tearing, "cutting" quality ^[2]^[3]	The tear exposes somatic nerve endings (inferior rectal nerve) in the anoderm below the dentate line. Passage of stool mechanically stimulates these exposed nerves. The pain may persist for minutes to hours after defaecation due to sustained IAS spasm.
Pain associated with the start of defaecation ^[5]	As stool begins to pass through the anal canal, it mechanically stretches and re-opens the fissure. This distinguishes it from other causes of anal pain (e.g., perianal abscess causes constant throbbing pain).
Fresh bright red per-rectal bleeding (PRB) — typically small amount on toilet paper or surface of stool ^[2]^[3]	The tear disrupts small submucosal vessels in the anoderm. Bleeding is typically minor because the vessels below the dentate line are small terminal branches. Blood is bright red (arterial/capillary) because it is fresh and has not been oxidised.
+/- Mucus discharge ^[3]	Chronic fissures with associated sentinel pile and hypertrophied papilla may produce mucus from the irritated anal mucosa.
Perianal pruritus (itching) or skin irritation ^[2]	Chronic discharge, moisture from the wound, and sentinel skin tags cause local skin maceration and irritation.
Fear/avoidance of defaecation ^[3]	Due to severe pain → patients consciously or subconsciously avoid going to the toilet → worsening constipation → harder stools → further trauma (feeds the vicious cycle).

Classic History

The classic patient is a young adult who says: "Every time I go to the toilet, I get a sharp, tearing pain in my bottom that lasts for an hour afterwards. There's a small amount of bright red blood on the toilet paper. I've been putting off going to the toilet because I'm so afraid of the pain, which makes my constipation worse."

Sign	Description & Pathophysiological Basis
Visible tear on inspection	Most fissures can be identified simply by gentle parting of the buttocks (without need for DRE in many acute cases). The fissure appears as a linear tear, most commonly at the posterior midline (6 o'clock in lithotomy position) ^[1].
Acute fissure appearance	Superficial tear — looks like a fresh "paper cut" with clean, sharp edges ^[2]. The base may show healthy granulation tissue.
Chronic fissure triad ^[1]^[3]	1. The fissure itself — deep, with fibrotic raised/rolled edges; white horizontally-oriented fibres of the internal anal sphincter muscle visible at the base ^[1]^[2]. 2. Sentinel pile (skin tag) at the distal/external end — represents failed healing with hypertrophic skin tag formation ^[1]^[3]. 3. Hypertrophied anal papillae at the proximal/internal end ^[1]^[3].
Sphincter spasm	On gentle examination, the IAS is in sustained spasm — the anus appears "tight" and the patient will resist any attempt at digital examination due to pain.
DRE may be too painful to perform	Examination under anaesthesia (EUA) may be required ^[3]. The examiner should NOT force a DRE in a patient with a suspected acute fissure — it is extremely painful and not necessary for diagnosis if the fissure is visible on inspection.

Do NOT Perform Lord's Four-Finger Stretch

Avoid Lord's four-finger stretch ^[3]. This was a historical procedure involving forceful dilatation of the anus with four fingers to reduce IAS tone. It is now considered obsolete because it causes uncontrolled tearing of the sphincter and carries an unacceptably high risk of faecal incontinence. It has been replaced by controlled lateral internal sphincterotomy.

Condition	Character of Pain	Timing
Anal fissure	Sharp, tearing, cutting	Associated with start of defaecation ^[5], persists after
Perianal abscess	Constant, throbbing, progressive	Not specifically related to defaecation
Thrombosed external haemorrhoid	Acute, severe, constant	Sudden onset, may worsen with sitting
Proctalgia fugax	Sudden, severe, cramping	Occurs at night, not related to defaecation
Internal haemorrhoids	Usually painless bleeding	Related to defaecation but without the sharp pain

This is worth emphasising separately because it is a common exam question and has important clinical implications:

Always suspect perianal Crohn's disease if ^[3]:

Non-midline position
Recurring fissures
Multiple fissures
Unusually deep or wide
Perianal hypertrophic skin tags

Other secondary causes to consider with atypical features: HIV, TB, STD (syphilis, CMV) ^[1]

In any patient with atypical fissure features, the workup must include:

Assessment for systemic symptoms (weight loss, chronic diarrhoea, fever, joint pain, eye symptoms)
Sigmoidoscopy/colonoscopy to evaluate for Crohn's disease
Appropriate serological testing (HIV, syphilis, CMV)
Biopsy of the fissure edge if indicated (granulomas → Crohn's or TB)

High Yield Summary

Definition: A tear in the anoderm below the dentate line; 90% posterior midline, 10% anterior (women).
Pathophysiology — the vicious cycle: Trauma → tear → pain → IAS spasm → ischaemia (posterior midline is the least perfused area) → impaired healing → chronicity. Fear of pain → avoidance → constipation → re-trauma.
Acute vs Chronic: Acute = superficial "paper cut" (< 6 weeks). Chronic = triad of fissure + sentinel pile + hypertrophied anal papillae with visible IAS fibres at the base.
Typical vs Atypical: Typical = single, midline. Atypical = multiple, off-midline, deep, wide, painless, non-healing → suspect Crohn's, TB, HIV, syphilis, CMV.
Clinical features: Sharp pain on defaecation + small amount of bright red PR bleeding + perianal pruritus. DRE often too painful — EUA may be required.
Why posterior midline?: (a) Least blood supply (watershed zone), (b) greatest mechanical shearing force, (c) poorest EAS support posteriorly.
Every treatment targets the vicious cycle: Soften stool (fibre/laxatives), relax IAS (GTN/nifedipine/botox/LIS), improve blood flow (vasodilators/sitz bath).

Active Recall - Anal Fissure (Definition, Epidemiology, Anatomy, Aetiology, Pathophysiology, Clinical Features)

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p42–45) ^[2] Senior notes: felixlai.md (Anal fissures section) ^[3] Senior notes: maxim.md (Anal fissure section) ^[4] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p24 — Etiology) ^[5] Senior notes: maxim.md (Table — Anal fissure: Hx of constipation, sharp pain a/w start of defaecation)

Differential Diagnosis of Anal Fissure

The presentation of anal fissure — pain on defaecation + fresh per-rectal bleeding (PRB) — overlaps with several other anorectal and colorectal conditions. The differential diagnosis can be thought of in two clinical scenarios:

"Painful anal/perianal condition" — what else causes pain in this area?
"Fresh PR bleeding (outlet-type)" — what else causes bright red blood separate from stool?

A good clinician must systematically consider and exclude these before settling on a diagnosis of anal fissure. Let's remember what the lecture slides emphasise: common anorectal conditions are mostly benign but colorectal neoplasm needs to be excluded ^[1].

Differential Diagnosis Table

I'll organise this by the two cardinal symptoms of anal fissure and explain how each differential mimics or differs from it.

Condition	Key Distinguishing Features	Why It Mimics Fissure	How to Tell It Apart
Thrombosed external haemorrhoid (perianal haematoma)	Sudden onset of a painful bluish perianal mass ^[6]; constant pain, worse with sitting	Both cause acute anal pain	Haemorrhoid presents as a visible bluish, tense, tender lump at the anal verge. Pain is constant, not specifically at the start of defaecation. No linear tear visible.
Perianal abscess	Constant throbbing pain not necessarily associated with bowel movements; fever, malaise; tender fluctuant swelling ^[8]	Both cause perianal pain	Abscess pain is constant and progressive, with systemic features (fever). There is a palpable tender swelling with warmth and erythema — not a linear tear.
Anorectal fistula	Intermittent perianal discharge (purulent) + pain that decreases with drainage ^[1]^[9]; palpable cord-like tract on PR exam	Both cause pain on defaecation and PRB	Fistula has a visible external opening with discharge. Pain improves when pus drains (opposite to fissure where pain persists). History of previous perianal abscess. PR exam: induration with cord-like structure ^[1].
Anal carcinoma	Painful PR bleeding, pruritus, palpable mass ^[10]; risk factors include HPV, HIV, smoking	Can mimic chronic fissure with pain + bleeding	Mass is palpable on DRE; often in older patients or immunocompromised. Non-healing ulcer that doesn't respond to fissure treatment. Biopsy is diagnostic.
Proctalgia fugax	Brief attacks of severe rectal pain at night, unrelated to defaecation ^[10]	Both cause severe anal pain	Proctalgia fugax occurs in young anxious men, lasts only minutes, occurs at night, and is completely unrelated to defaecation — no bleeding, no visible pathology.
Perianal Crohn's disease	Non-midline, multiple, deep, wide fissures + perianal hypertrophic skin tags + may have fistulae/abscesses ^[1]^[3]^[11]	Can present as anal fissure(s)	Look for associated GI symptoms (chronic diarrhoea, abdominal pain, weight loss) and extra-intestinal manifestations (joints, eyes, skin). Fissures are atypical in position and number.
Perianal herpes simplex (HSV)	Painful vesicles/ulcers in the perianal region; may be multiple shallow ulcers	Painful perianal lesions + bleeding	Vesicular appearance, clustering of lesions, history of sexual contact, may have systemic viral prodrome. Viral swab/PCR is diagnostic.

Condition	Key Distinguishing Features	Why It Mimics Fissure	How to Tell It Apart
Haemorrhoids	Fresh outlet-type bleed, perianal mass/pain, constipation ^[5]; typically painless unless thrombosed	Both cause bright red PRB associated with defaecation	Haemorrhoid bleeding is classically painless (internal haemorrhoids are above dentate line → visceral innervation). Blood drips into toilet bowl or is on paper. Prolapsing mass may be noted.
Colorectal carcinoma (CRC)	Constitutional symptoms, change in bowel habits, change in stool calibre, tenesmus, IO symptoms, family history ^[5]	Both can cause PRB	CRC bleeding is typically mixed with stool (not outlet-type), associated with weight loss, altered bowel habit, tenesmus. Older age group. Must always be excluded ^[1].
Solitary rectal ulcer syndrome	A benign ulcer on the anterior rectal wall, associated with straining and rectal prolapse ^[2]	Both cause PRB and pain on defaecation	Usually presents with mucus discharge, straining, and sensation of incomplete evacuation. Diagnosis is on proctoscopy/sigmoidoscopy — ulcer is on the anterior rectal wall, not at the anal verge.
Diverticular disease	Painless profuse haematochezia ^[5]^[7]	Both cause PRB	Diverticular bleeding is painless and profuse — a completely different clinical picture from fissure. Occurs in older patients. Right-sided diverticula more common in Asian populations ^[7].
Angiodysplasia	Usually anaemic symptoms, associated with aortic stenosis and vascular malformations ^[5]	Both cause PRB	Bleeding is typically occult (chronic iron deficiency anaemia) or painless. In older patients ( > 65). Diagnosed on colonoscopy/angiography.
IBD (Ulcerative Colitis)	Joint, liver, eye, skin manifestations ^[5]; bloody diarrhoea with mucus	Both cause PRB	UC presents with bloody diarrhoea (blood mixed with stool), urgency, tenesmus, and systemic features. Continuous mucosal inflammation on colonoscopy.
Infective colitis	Fever, chills/rigors, recent antibiotic usage (C. diff), TB exposure, travel history ^[5]	Both cause PRB	Acute onset with diarrhoea, fever, systemic toxicity. Stool culture is diagnostic.
Rectal polyp / low colorectal polyp	Painless bleeding, may be palpable on DRE	Both cause outlet-type PRB	Bleeding is painless. Polyp may be palpable on DRE or visible on proctoscopy. Common cause of painless PRB in children (juvenile polyps) ^[12].
Rectal prolapse	Protruding mass through anus with circumferential folds, mucous discharge, faecal incontinence ^[6]	Both can cause PRB and perianal symptoms	Prolapse presents with a visible circumferential mass (unlike the radial folds of prolapsed haemorrhoids). Associated with incomplete evacuation and incontinence.

The Cardinal Rule

Colorectal neoplasm needs to be excluded ^[1]. Even if the clinical picture is classic for anal fissure, any patient over 40 (or younger with red flag features — weight loss, family history, change in bowel habit, anaemia) should have lower GI investigation (sigmoidoscopy or colonoscopy) to exclude malignancy. The lecture slides are very clear on this point.

Once you've identified that the lesion is indeed an anal fissure, the next question is: is this primary (idiopathic) or secondary to an underlying disease?

Atypical position and multiple in number should prompt investigation for ^[1]:

Inflammatory bowel disease (especially Crohn's)
Tuberculosis
Syphilis
HIV infection
CMV

The perianal examination in IBD is critical — the lecture slides on IBD specifically state that physical examination should include: perianal region: skin tags, fissures, fistulas, abscess, PR exam ^[11].

Feature	Primary Fissure	Secondary Fissure
Position	Posterior (90%) or anterior (10%) midline	Off-midline, lateral
Number	Single	Multiple
Depth	Shallow to moderate	Unusually deep/wide
Healing	Responds to conservative Rx	Non-healing, recurring
Associated features	Constipation history	Systemic symptoms (diarrhoea, weight loss, fever, other organ involvement)
What to do	Treat conservatively	Investigate: colonoscopy, biopsy, HIV/syphilis serology, TB workup

In practice, diagnosis is by spreading the buttocks to reveal the fissure ^[1]. Rectal examination and proctoscopy are painful and not indicated in the acute setting ^[1]. So how do we differentiate?

History is king:
- Hx of constipation, sharp pain associated with start of defaecation ^[5] → classic fissure
- Constant throbbing pain + fever → abscess
- Painless bleeding with prolapsing mass → haemorrhoids
- Constitutional symptoms + change in bowel habit → CRC
- Intermittent discharge + prior abscess → fistula
Inspection (gentle separation of buttocks):
- Linear posterior midline tear → fissure
- Bluish tense lump → thrombosed external haemorrhoid
- External opening with discharge → fistula
- Erythematous fluctuant swelling → abscess
- Hard irregular mass → carcinoma
DRE — only when tolerable or under anaesthesia:
- Cord-like induration → fistula
- Palpable mass → carcinoma, polyp
- Boggy fluctuance → abscess
Investigations (when indicated):
- EUA when DRE is too painful ^[3]
- Proctoscopy ^[3] — when fissure has healed or under anaesthesia
- Sigmoidoscopy / Colonoscopy — to exclude CRC and evaluate for IBD (especially with atypical features) ^[2]
- Biopsy — if non-healing ulcer (exclude carcinoma, Crohn's, TB)

Letter	Differential
F	Fistula-in-ano
I	Inflammatory bowel disease (Crohn's perianal disease)
S	Solitary rectal ulcer syndrome
S	Sexually transmitted diseases (syphilis, HSV, HIV)
U	Ulcers (perianal ulcers/sores from various causes)
R	Rectal/anal carcinoma
E	External thrombosed haemorrhoid

High Yield Summary — Differential Diagnosis of Anal Fissure

Two symptom axes to differentiate: (a) Anal pain — sharp at start of defaecation = fissure; constant/throbbing = abscess; unrelated to defaecation = proctalgia fugax. (b) Fresh PRB — outlet-type on paper = fissure/haemorrhoids; mixed with stool = CRC/IBD/colitis; profuse painless = diverticular.
Key differentials to always consider: Haemorrhoids (painless), thrombosed external haemorrhoid (painful mass), perianal abscess (constant pain + fever), anorectal fistula (discharge, cord-like tract), CRC (must always exclude), solitary rectal ulcer, anal carcinoma.
Atypical fissure features (off-midline, multiple, deep, non-healing) → investigate for Crohn's, TB, HIV, syphilis, CMV.
Diagnosis is clinical: spread buttocks to visualise the fissure. DRE and proctoscopy are painful and not indicated acutely. EUA if needed. Colonoscopy to exclude CRC and IBD.
Colorectal neoplasm needs to be excluded in any patient with PR bleeding — this is the most important differential to rule out.

Active Recall - Differential Diagnosis of Anal Fissure

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p42–46, p56, p77) ^[2] Senior notes: felixlai.md (Anal fissures — Differential diagnosis and Diagnosis sections) ^[3] Senior notes: maxim.md (Anal fissure section) ^[5] Senior notes: maxim.md (LGIB DDx table — Anal fissure, CRC, Haemorrhoids, IBD, Diverticular disease, Angiodysplasia) ^[6] Senior notes: maxim.md (Acute painful anal mass — Differential diagnosis) ^[7] Senior notes: felixlai.md (Lower GI bleeding — Differential diagnosis) ^[8] Senior notes: felixlai.md (Anorectal abscess — Clinical manifestation) ^[9] Senior notes: felixlai.md (Anorectal fistula — Clinical manifestation) ^[10] Senior notes: maxim.md (Proctalgia fugax; Anal carcinoma) ^[11] Lecture slides: Inflammatory bowel disease.pdf (p10 — Diagnosis: perianal region examination) ^[12] Senior notes: maxim.md (Paediatric GI bleed — colonic polyp)

Diagnostic Criteria, Diagnostic Algorithm & Investigations

Here's the thing about anal fissure — there are no formal laboratory-based or scoring-system diagnostic criteria like you'd see for, say, rheumatoid arthritis or SLE. Anal fissure is a clinical diagnosis, made primarily on history and visual inspection. The lecture slides are emphatic about this: diagnosis is by spreading the buttocks to reveal the fissure ^[1]. Rectal examination and proctoscopy are painful and not indicated ^[1] in the acute setting.

That said, there are well-established clinical diagnostic criteria that we use to confirm the diagnosis and classify it:

Clinical Diagnostic Criteria for Anal Fissure

Criterion	Details
1. Characteristic history	Pain on defaecation ^[1] — sharp, tearing, specifically at the start of defaecation; fresh rectal bleeding ^[1] — small amount on toilet paper or stool surface
2. Visual inspection	Spreading the buttocks reveals a linear tear in the anoderm ^[1], most commonly at the posterior midline (90%) or anterior midline (10% of women) ^[1]
3. Classification as Acute or Chronic	Acute: Superficial tear resembling a "paper cut" ^[2]. Chronic: Sentinel pile + hypertrophic papilla + visualization of internal sphincter muscles at the base of the fissure ^[1]
4. Typical vs Atypical determination	Typical: Single, midline, without evidence of Crohn's. Atypical: Multiple, off-midline, recurring, deep/wide, painless → suspect secondary cause ^[1]^[2]

The Diagnosis is Clinical — Full Stop

You do NOT need blood tests, imaging, or endoscopy to diagnose a straightforward primary anal fissure. The combination of (1) characteristic pain on defaecation + fresh PRB, and (2) a visible linear tear at the posterior midline on buttock separation, is sufficient. Investigations are reserved for atypical features, suspected secondary causes, exclusion of malignancy, and pre-operative planning.

Diagnostic Algorithm

Let me walk you through the systematic clinical approach from presentation to final diagnosis. This is how you should think in an exam or on the ward.

Let me explain each step from first principles:

The history alone often gives you the diagnosis. Key elements to elicit ^[3]^[5]:

Chief complaints: Bleeding, pain (fissure-in-ano: pain on defaecation), itching, swelling, tenesmus, discharge ^[3]
Pain character: Sharp/tearing at the START of defaecation → classic for fissure. Constant throbbing → abscess. Brief nocturnal episodes → proctalgia fugax.
Bleeding character: Outlet-type (separate from stool, on paper) → fissure/haemorrhoids. Mixed with stool → CRC/IBD. Fresh PRB → distal to splenic flexure; Dark PRB → proximal to splenic flexure ^[3].
Bowel habits: Constipation history, straining → supports primary fissure
Red flags for malignancy: Age > 40, family history CRC, weight loss, change in bowel habit, change in stool calibre, tenesmus, anaemia
Features suggesting secondary causes: Chronic diarrhoea, joint/eye/skin symptoms (IBD), immunosuppression, sexual history (STDs), TB exposure

Diagnosis is by spreading the buttocks to reveal the fissure ^[1].

Patient positioned in left lateral (Sims') position or prone jackknife position
Gently part the buttocks to expose the anal verge
Look specifically at the posterior midline (6 o'clock in lithotomy) and anterior midline (12 o'clock)
Identify the tear and classify:
- Acute: Superficial, clean-edged, resembles a paper cut ^[2]
- Chronic: Sentinel pile (distal), hypertrophic papilla (proximal), internal sphincter muscle fibres at base of fissure ^[1]

Critical Examination Point

Rectal examination and proctoscopy are painful and not indicated ^[1] when an acute anal fissure is visible. Forcing a DRE or proctoscope into a patient with an acute fissure causes unnecessary agony, provides no additional diagnostic information, and may worsen the tear. If examination is essential (e.g., to exclude other pathology), it should be done under EUA (examination under anaesthesia) ^[3]. AVOID Lord's four-finger stretch ^[3] — it is obsolete due to risk of uncontrolled sphincter damage and faecal incontinence.

Feature	Acute	Chronic
Duration	< 6 weeks	> 6–8 weeks
Pathognomonic finding	Superficial tear ^[2]	Hypertrophied with skin tags or papillae ^[2]
Base	Granulation tissue or exposed anoderm	White horizontally oriented IAS muscle fibres ^[1]^[2]
Edges	Sharp, clean	Raised, fibrotic, rolled
Sentinel pile	Absent	Present at distal end ^[1]
Hypertrophied papilla	Absent	Present at proximal end ^[1]

This is a crucial branch point because it determines whether you investigate further or proceed directly to treatment:

Typical: Single + posterior or anterior midline + no features of Crohn's → primary fissure → treat
Atypical: Multiple + off-midline + recurring + deep/wide + painless → suspect secondary cause → investigate ^[1]^[2]

Atypical position and multiple in number warrants investigation for: inflammatory bowel disease, tuberculosis, syphilis, HIV infection, CMV ^[1]

Most typical primary fissures need no investigations. Investigations are indicated for:

Atypical features (to identify secondary cause)
Red flag symptoms (to exclude CRC)
Pre-operative assessment (before surgical intervention)
When diagnosis is uncertain

Investigation Modalities

Aspect	Details
When	DRE too painful to perform in clinic ^[3]; need to assess the fissure in detail; suspicion of concurrent pathology (fistula, abscess)
What it involves	Under general or regional anaesthesia: thorough inspection of the fissure, DRE (assess sphincter tone, exclude mass/induration), proctoscopy, possible biopsy
Key findings	Depth of fissure, presence of chronic features (sentinel pile, papilla, IAS fibres), sphincter tone, concurrent pathology (fistula tract, abscess cavity)
Why it's useful	Eliminates pain as a barrier to complete examination. Allows assessment of the entire anal canal which is impossible in the awake patient with an acute fissure. Can combine with therapeutic procedure if needed.

EUA is Both Diagnostic and Therapeutic

In practice, if a patient is being taken to theatre for an EUA, the surgeon may combine the diagnostic assessment with a therapeutic procedure (e.g., botulinum toxin injection or lateral internal sphincterotomy) in the same anaesthetic session, avoiding the need for a second procedure.

Aspect	Details
When	After the fissure has healed or under EUA ^[3]; not indicated in acute fissure ^[1] (too painful)
What it involves	A rigid or disposable proctoscope is inserted into the anal canal to visualise the distal rectum and anal canal mucosa
Key findings	Visualise internal haemorrhoids, hypertrophied anal papillae, the fissure itself, rule out low rectal mass or polyp
Why from first principles	A proctoscope provides a direct view of the anal canal lining — it can confirm chronic fissure features and exclude other anal canal pathology (e.g., internal haemorrhoids, low rectal polyp, anal carcinoma) that wouldn't be visible on external inspection alone

Aspect	Details
When	(1) Atypical fissure features → evaluate for Crohn's disease ^[2]^[4]. (2) Symptoms suggestive of colorectal cancer (age > 40, red flags, family history) ^[2]. (3) Endoscopy to rule out Crohn's disease first before proceeding to surgery for chronic fissure ^[4].
What it involves	Flexible sigmoidoscopy (examines rectum + sigmoid + descending colon) or full colonoscopy (examines the entire colon to caecum + terminal ileum)
Key findings	For Crohn's: Skip lesions, cobblestoning, deep longitudinal ulcers, strictures, aphthous ulcers, terminal ileal involvement. For UC: Continuous mucosal inflammation from rectum proximally, pseudopolyps, loss of haustral pattern. For CRC: Mass, polyp, ulcerating lesion, stricture. For TB: Ileocaecal thickening, transverse ulcers.
Why it's important	The lecture slides state that investigations serve to exclude diseases in the proximal bowel and associated bowel problems (e.g., inflammatory bowel disease) ^[13]. You cannot see Crohn's disease of the terminal ileum by looking at the anus alone. If you're about to perform a lateral internal sphincterotomy on someone who actually has Crohn's, the wound may never heal — Crohn's patients have impaired wound healing and are at high risk of complications.

High Yield: Endoscopy to rule out Crohn's disease first ^[4] before surgical intervention for chronic fissure. This is a crucial pre-operative step.

Blood tests are not needed for diagnosis of the fissure itself, but are useful for:

Test	Indication & Rationale
Full blood count (FBC)	Assess for anaemia (iron deficiency from chronic blood loss; or anaemia of chronic disease if IBD). Raised WCC may suggest abscess or infection.
Inflammatory markers (CRP, ESR)	Elevated in IBD, infection, abscess. Normal in primary fissure.
HIV serology	If atypical fissure + risk factors (MSM, IVDU, high-risk sexual behaviour). HIV-associated anal ulcers are typically deep, atypical, and painful.
Syphilis serology (RPR/VDRL, TPHA/FTA-Abs)	If atypical perianal ulcer, especially painless ulcer (primary chancre can mimic fissure).
Iron studies, B12, Folate	If anaemia detected — helps distinguish cause (iron deficiency from bleeding vs B12/folate deficiency in Crohn's with ileal involvement).

Test	When & Why
STI screen (HIV, syphilis, HSV, chlamydia, gonorrhoea)	Atypical fissure in sexually active patient, especially with receptive anal intercourse history
TB workup (Mantoux/IGRA, CXR, sputum AFB)	Atypical fissure in TB-endemic area (relevant in Hong Kong). Perianal TB can present as non-healing fissure/fistula.
CMV serology / biopsy with immunohistochemistry	Immunocompromised patients (HIV, transplant). CMV causes perianal ulceration.
Stool cultures	If concurrent diarrhoea — exclude infective colitis mimicking IBD

Aspect	Details
When	Non-healing fissure despite adequate treatment; atypical features; suspicion of malignancy (anal carcinoma), Crohn's, or TB
What it involves	Incisional or punch biopsy of the fissure edge, performed under EUA
Key findings	Crohn's: Non-caseating granulomas, transmural inflammation. TB: Caseating granulomas with AFB on Ziehl-Neelsen stain. SCC: Malignant squamous cells, keratinisation. CMV: Inclusion bodies ("owl's eye" intranuclear inclusions).
Why from first principles	A fissure that doesn't heal after 8–12 weeks of appropriate treatment is NOT behaving like a typical fissure. The tissue needs histological examination to identify an underlying cause that is preventing healing.

Aspect	Details
When	Pre-operative assessment in selected patients, particularly those at high risk of incontinence (multiparous women, elderly, previous anal surgery)
What it measures	Resting anal pressure (reflects IAS tone) and squeeze pressure (reflects EAS function)
Key findings in fissure	Elevated resting anal pressure (confirming IAS hypertonia/spasm) — this is the physiological basis of the fissure
Why it matters	If a patient already has low sphincter pressures (e.g., from previous obstetric injury), performing a lateral internal sphincterotomy (which permanently reduces IAS tone) could cause faecal incontinence. Manometry helps guide surgical decision-making: sphincterotomy for hypertonic sphincters vs sphincter-sparing procedures (fissurectomy + advancement flap) for those at risk ^[4].

Aspect	Details
When	Pre-operative assessment; suspected sphincter defect; suspected concurrent fistula
What it shows	Integrity and thickness of IAS and EAS; presence of fistula tracts; scarring from previous surgery
Why useful	Identifies pre-existing sphincter defects that would make sphincterotomy risky. Can reveal occult fistula tracts not apparent on clinical examination.

Clinical Scenario	Investigations Needed
Typical acute fissure, young patient, no red flags	NONE — clinical diagnosis, treat conservatively
Chronic fissure failing 8 weeks of medical treatment	EUA + proctoscopy; consider anorectal manometry pre-operatively; endoscopy to rule out Crohn's disease first ^[4]
Atypical features (off-midline, multiple, deep, non-healing)	Colonoscopy (Crohn's, CRC); HIV/syphilis/CMV serology; TB workup; biopsy under EUA
Red flags for CRC (age > 40, weight loss, FHx, altered bowel habit)	Sigmoidoscopy or colonoscopy ^[2] to exclude CRC
Pre-operative (before LIS in high-risk patient)	Anorectal manometry ± endoanal ultrasound

High Yield Summary — Diagnosis of Anal Fissure

Anal fissure is a CLINICAL diagnosis — history + visual inspection by spreading the buttocks. No investigations needed for typical cases.
Diagnosis is by spreading the buttocks to reveal the fissure. Rectal examination and proctoscopy are painful and not indicated in acute fissure.
Acute fissure: superficial paper-cut tear. Chronic fissure: sentinel pile + hypertrophic papilla + IAS muscle fibres at base.
Typical = single, midline → primary → treat. Atypical = multiple, off-midline, deep, non-healing → secondary → investigate (colonoscopy, serology, biopsy).
Endoscopy to rule out Crohn's disease first before surgical intervention for chronic fissure.
Colorectal neoplasm must always be excluded in patients with PR bleeding and red flag features.
EUA is used when the examination is too painful, and can be combined with therapeutic intervention.
Anorectal manometry is used pre-operatively to assess sphincter function and guide choice between sphincterotomy vs sphincter-sparing surgery.

Active Recall - Diagnosis of Anal Fissure

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p42, p44, p45, p46) ^[2] Senior notes: felixlai.md (Anal fissures — Diagnosis section) ^[3] Senior notes: maxim.md (Anal fissure — Investigations section) ^[4] Senior notes: maxim.md (Anal fissure — Surgical management: endoscopy to rule out Crohn's) ^[5] Senior notes: maxim.md (Diseases of anal canal — History taking) ^[13] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p13 — Investigations)

Management of Anal Fissure

Before diving into specific treatments, let's ground ourselves in the pathophysiology, because every single treatment targets a specific point in the vicious cycle:

Trauma → Tear → Pain → IAS spasm → ↓ Blood flow (ischaemia) → Impaired healing → Chronicity
                  ↘ Fear → Avoidance → Constipation → Re-trauma ↗

Therapeutic Target	Treatment Modality
Reduce trauma / soften stool	Fibre supplements, stool softeners, laxatives, adequate fluid intake
Reduce pain	Topical anaesthetics (lidocaine), sitz baths
Relax IAS / reduce spasm	Topical GTN, topical nifedipine/diltiazem, botulinum toxin, lateral internal sphincterotomy
Improve blood flow	Topical vasodilators (GTN, CCBs), sitz baths
Mechanically break the cycle	Surgical division of IAS (sphincterotomy), fissurectomy + advancement flap

The overarching strategy follows a step-up approach: start conservative → escalate to pharmacological → escalate to surgical if medical treatment fails.

Step 1: Conservative / Supportive Management

This is the first-line treatment for all anal fissures, and is sufficient for the majority of acute fissures. The lecture slides group these as non-operative treatment: bulk agents, stool softeners and topical anaesthetics ^[1].

Measure	Mechanism (from first principles)	Details
Increased dietary fibre ^[1]^[2]^[3]	Fibre adds bulk to stool and retains water → softer, bulkier stool that passes more easily → less mechanical trauma to the anoderm	Aim for 25–30 g/day. Sources: vegetables, fruits, whole grains, psyllium husk (e.g., Metamucil). "Bulk agents" = fibre supplements.
Adequate fluid intake ^[2]^[3]	Water works synergistically with fibre — without adequate fluid, fibre can paradoxically worsen constipation (fibre needs water to swell and soften stool)	Aim for 1.5–2 L/day
Stool softeners / laxatives ^[1]^[2]^[3]	Osmotic laxatives (lactulose, macrogol/PEG) draw water into the bowel lumen → softer stool. Stool softeners (docusate) act as surfactants to allow water penetration into stool. Both reduce the need to strain.	Used as adjunct when dietary modification alone is insufficient
Avoid straining ^[2]	Straining increases intra-abdominal and intra-anal pressure → increases IAS tone → worsens ischaemia and re-opens the tear	Advise patients not to sit on the toilet for prolonged periods; go when there is an urge rather than forcing

Aspect	Details
What it is	Sitting in a basin of warm water (not hot) covering the perineum for 10–15 minutes, 2–3 times daily and after bowel movements
Mechanism	Warmth causes relaxation of the IAS smooth muscle → reduces spasm → reduces pain. Also causes local vasodilatation → improves blood flow to the ischaemic posterior midline → promotes healing ^[2]. Additionally provides soothing effect and helps keep the area clean.
Evidence	Simple, free, no side effects. Part of the standard conservative package for all fissures.

Agent	Mechanism	Details
Topical anaesthetics e.g. 5% lignocaine (lidocaine) jelly ^[1]^[3]	Lignocaine is an amide-type local anaesthetic that blocks voltage-gated sodium channels in sensory nerve endings → prevents depolarisation → blocks pain signal transmission from the exposed somatic nerves in the fissure	Applied before defaecation to reduce the sharp pain. Provides symptomatic relief but does NOT address the underlying IAS spasm or ischaemia — purely palliative. Important as an adjunct to allow more comfortable defaecation and break the avoidance/constipation cycle.

Conservative Measures Alone Heal ~50% of Acute Fissures

With dietary modification, stool softeners, sitz baths, and topical anaesthetics, approximately half of acute fissures will heal within 6 weeks. The key is breaking the constipation-trauma cycle and giving the anoderm time to re-epithelialise. If it doesn't heal → escalate to topical vasodilators.

Step 2: First-Line Medical Therapy — Topical Vasodilators

These are the newer topical agents to reduce internal sphincter pressure mentioned in the lecture slides ^[1]. They are the cornerstone of medical treatment for anal fissure.

Aspect	Details
Drug	0.2–0.4% nitroglycerin (glyceryl trinitrate / GTN) ointment ^[1]^[2]^[3]
Mechanism	GTN is a nitric oxide (NO) donor. NO activates guanylate cyclase in smooth muscle → increases cGMP → smooth muscle relaxation. Applied to the perianal skin, it is absorbed and causes: (1) Relaxation of the IAS smooth muscle → reduces resting anal pressure → breaks the spasm cycle. (2) Local vasodilatation → increases blood flow to the ischaemic posterior midline → promotes healing.
Application	Applied perianally (to the anal margin, NOT inserted into the canal) 2–3 times daily for 6–8 weeks
Efficacy	Healing rate ~50–68% (superior to placebo but inferior to surgery). Recurrence rate is significant (~50% at long-term follow-up).
Side effects	Headache ^[3] — the most common side effect (up to 20–60% of patients). This is because GTN is absorbed systemically and causes vasodilatation of cerebral vessels (the same reason IV GTN causes headaches in angina patients). Headache is dose-limiting and is the main reason for non-compliance. Also: dizziness, hypotension.
Contraindications	Concurrent use of PDE5 inhibitors (sildenafil etc.) — risk of severe hypotension. Severe hypotension/haemodynamic instability.
Indications	First-line pharmacological treatment for acute fissure not responding to conservative measures alone, and for chronic fissures

Aspect	Details
Drugs	Topical nifedipine ointment (0.2–0.5%) ^[1]^[2]^[3]; topical 0.5% diltiazem ^[3]
Mechanism	Nifedipine and diltiazem are calcium channel blockers (CCBs). They block L-type voltage-gated calcium channels in smooth muscle → prevent calcium influx → IAS smooth muscle cannot contract effectively → reduces IAS spasm and improves local blood flow. The name gives a clue: "nifedipine" → "-dipine" suffix = dihydropyridine CCB = primarily acts on vascular/smooth muscle.
Application	Applied perianally 2–3 times daily for 6–8 weeks
Efficacy	Similar to GTN (~65–70% healing rate). Some studies suggest slightly better tolerability due to fewer headaches.
Side effects	Much fewer headaches than GTN (main advantage). Mild local irritation. Theoretically: risk of incontinence ^[3] (any agent that reduces IAS tone can cause minor flatus incontinence, though this is rare with topical agents).
Indications	First-line alternative to GTN (especially if GTN not tolerated due to headache). Topical nifedipine or diltiazem can be used interchangeably as first-line.

GTN vs Nifedipine — Which to Choose?

Both are first-line options with similar efficacy. The practical choice often comes down to side effects:

GTN: Well-studied, widely available, but headache is a major problem (up to 60%). Many patients stop treatment because of this.
Nifedipine/Diltiazem: Fewer headaches, better tolerated. Increasingly preferred as first-line in many centres.

Both work by the same principle: reduce IAS pressure → break the spasm–ischaemia cycle.

Aspect	Details
Drug	Botulinum toxin (Botox) type A, 50 IU ^[1]^[3]
Mechanism	Botulinum toxin ("botulinum" from Latin botulus = sausage, because it was first identified in sausage food poisoning) is a neurotoxin produced by Clostridium botulinum. It cleaves SNARE proteins (specifically SNAP-25) at the neuromuscular junction → prevents acetylcholine release from presynaptic nerve terminals → chemical denervation of the IAS smooth muscle → muscle paralysis → reduces IAS spasm. Effect lasts ~3 months (until new nerve terminals sprout).
Administration	Injected directly into the internal anal sphincter under local or general anaesthesia (often during EUA). Usually injected at multiple sites around the IAS.
Efficacy	Healing rate ~60–80%. Can be repeated if first injection fails.
Side effects	Temporary flatus incontinence (usually mild and self-limiting as the toxin wears off). Very rarely: faecal incontinence (< 5%). Perianal haematoma at injection site.
Indications	Second-line medical therapy ^[3]: patients who fail 8 weeks of topical vasodilator therapy ^[2], or who cannot tolerate GTN/nifedipine. Also useful as a bridge in patients where surgery is relatively contraindicated (e.g., Crohn's disease).
Contraindications	Known allergy to botulinum toxin. Myasthenia gravis or other neuromuscular junction disorders (risk of systemic weakness). Active perianal sepsis.

High Yield: Botulinum toxin is positioned as a second-line option between topical vasodilators and surgery. It provides a reversible chemical sphincterotomy — unlike surgical sphincterotomy, which is permanent. This makes it particularly useful in patients at high risk of incontinence.

Step 4: Surgical Management

Indicated in patients who fail 8 weeks of initial medical treatment ^[2] (some sources say fail conservative management for 8 weeks overall ^[4]). Before ANY surgery: endoscopy to rule out Crohn's disease first ^[4] — this is a critical pre-operative step because operating on a Crohn's fissure without treating the underlying disease leads to disastrous wound healing.

Step	Details
Endoscopy to rule out Crohn's disease ^[4]	Sigmoidoscopy or colonoscopy before proceeding to surgery. Crohn's patients heal poorly and may develop non-healing wounds, fistulae, or abscesses after sphincterotomy.
Anorectal manometry (selected patients)	Assess resting IAS pressure and EAS squeeze pressure. Guides choice between sphincterotomy (if hypertonic) vs sphincter-sparing (if normal/low tone).
Stool softener	Start pre-operatively to reduce post-operative pain from hard stool ^[6]
Position	Prone jackknife or lithotomy position ^[6]
Anaesthesia	Perianal local anaesthesia / spinal anaesthesia / general anaesthesia ^[6]

This is the gold standard surgical treatment for chronic anal fissure.

Aspect	Details
What it is	Lateral internal sphincterotomy is the commonest surgery for anal fissure ^[1]. It involves a controlled, partial division of the internal anal sphincter at the lateral aspect (away from the fissure itself, which is usually posterior).
Why "lateral"?	The sphincterotomy is performed laterally (at the 3 o'clock or 9 o'clock position) rather than at the site of the fissure (posterior midline). Why? Because cutting the IAS at the posterior midline (where the fissure already is) would create a "keyhole deformity" — a gutter-like defect that causes soiling and mucus leakage. Lateral division avoids this.
Why "internal"?	Only the internal anal sphincter is divided (the involuntary smooth muscle responsible for ~80% of resting tone). The external sphincter (voluntary skeletal muscle) is preserved entirely. This is why continence is maintained.
How much to divide	The IAS is divided up to the level of the dentate line (approximately the length of the fissure, or roughly the distal 1/3 of the IAS). Over-division causes incontinence; under-division causes treatment failure.
Mechanism	By permanently reducing resting IAS tone, the surgery: (1) Eliminates the spasm component of the vicious cycle. (2) Allows wound edge apposition. (3) Restores blood flow to the posterior midline. The fissure then heals by secondary intention.
Technique	Can be performed open (small incision at the intersphincteric groove, IAS identified and divided under direct vision) or closed (blade inserted through a small stab incision and IAS divided — faster but less controlled).
Efficacy	Healing rate: 95% ^[1] — the most effective treatment available
Complications	Incontinence: 0–15%, most are minor with flatus incontinence ^[1]. This is the main risk. Breakdown: minor flatus incontinence is most common; significant faecal incontinence is rare (< 3%). Other complications: bleeding, haematoma, perianal abscess (rare).
Indications	Chronic fissure failing 8 weeks of medical treatment ^[2]^[4]; low risk of faecal incontinence ^[4] (young males, no prior sphincter injury)
Contraindications	High risk of incontinence (multiparous women, elderly, prior anal surgery, pre-existing sphincter damage, low resting pressures on manometry) ^[4]; active Crohn's disease (impaired healing); active perianal sepsis

LIS — Key Numbers to Remember

Healing rate: 95% ^[1]
Incontinence risk: 0–15% ^[1]
Most incontinence is minor = flatus incontinence ^[1]
Recurrence rate: < 5%
This is the MOST effective treatment for anal fissure — but the incontinence risk means it must be used judiciously.

Aspect	Details
What it is	Excision of the chronic fissure (including sentinel pile, hypertrophied papilla, and fibrotic tissue) WITHOUT cutting the IAS. The resulting defect is then covered with a V-Y advancement flap — a flap of perianal skin advanced to cover the wound and provide fresh, well-vascularised tissue.
Mechanism	By excising the chronic fibrotic fissure, you remove the unhealthy tissue that will never heal on its own. The advancement flap provides: (1) Well-vascularised tissue cover. (2) Reduces tension on wound edges. (3) Avoids the need to divide the IAS — hence "sphincter-sparing".
Efficacy	Healing rate ~85–90% (slightly lower than LIS, but avoids incontinence risk)
Complications	Flap failure/dehiscence, infection, recurrence (higher than LIS), but no risk of incontinence from the procedure itself
Indications	High risk of incontinence: e.g., multiparous women, older patients ^[4] — anyone in whom you cannot afford to reduce sphincter tone further. Also used for fissures associated with low sphincter pressures.
Contraindications	Active perianal sepsis, active Crohn's (relative)

Choosing Between LIS and Fissurectomy + Advancement Flap

Think of it simply:

LIS = most effective (95% healing) but trades off a small risk of incontinence. Best for young, healthy patients with high sphincter tone and no prior sphincter injury.
Fissurectomy + V-Y advancement flap = slightly less effective (~85-90%) but sphincter-sparing. Best for patients where any degree of incontinence would be unacceptable — multiparous women, older patients, those with pre-existing sphincter weakness ^[4].

These require treatment of the underlying cause rather than (or in addition to) standard fissure treatment:

Secondary Cause	Management Approach
Crohn's disease	Medical treatment of Crohn's is the priority (immunomodulators, biologics). Supportive fissure treatment (stool softeners, sitz baths, topical vasodilators). Avoid LIS — Crohn's patients have impaired wound healing and high risk of non-healing wound, fistula formation, and incontinence. Botulinum toxin may be used as a bridge. Fissurectomy + advancement flap only if absolutely necessary.
TB	Anti-TB chemotherapy (standard 6-month RIPE regimen). Supportive perianal care.
HIV	Antiretroviral therapy. Topical vasodilators for symptomatic relief. Biopsy to exclude CMV or other opportunistic cause.
Syphilis	Penicillin (standard treatment for syphilis). The "fissure" (chancre) heals with treatment of the infection.
CMV	Ganciclovir or valganciclovir (especially in immunocompromised patients).
Malignancy	Treatment according to staging (wide local excision for T1N0 anal SCC; chemoradiation for higher stages).

Prevention of anal fissures ^[2]:

Measure	Rationale
High fibre diet and adequate fluids ^[2]	Maintains soft, bulky stool → reduces mechanical trauma
Avoid trauma to anus ^[2]	Self-explanatory — avoid anal intercourse or instrumentation during healing
Avoid straining during defaecation ^[2]	Straining increases IAS pressure → ischaemia → re-tear
Prompt treatment of diarrhoea ^[2]	Prolonged diarrhoea causes repeated passage of irritant liquid stool → re-traumatises healing anoderm
Proper anal hygiene ^[2]	Keep the anal area dry; wipe with soft moist cloth rather than rough toilet paper → reduces irritation to healing tissue

Step	Treatment	Healing Rate	When to Escalate
1. Conservative	Fibre, stool softeners, sitz bath, topical anaesthetics	~50% (acute)	Failure after 6–8 weeks
2. First-line medical	Topical GTN or nifedipine/diltiazem + supportive	~50–70%	Failure after 8 weeks
3. Second-line medical	Botulinum toxin 50 IU injection	~60–80%	Failure or recurrence
4. Surgery	LIS (low incontinence risk) or Fissurectomy + V-Y flap (high incontinence risk)	95% (LIS) / ~85–90% (flap)	—

High Yield Summary — Management of Anal Fissure

All fissures: Start with conservative management — bulk agents, stool softeners, topical anaesthetics + sitz baths + dietary modification.
First-line pharmacological: Newer topical agents to reduce internal sphincter pressure — nitroglycerin, calcium channel blockers ^[1]. GTN causes headache; nifedipine/diltiazem better tolerated. Both relax IAS and improve blood flow.
Second-line: Botulinum toxin 50 IU injection into IAS ^[1]^[3]. Reversible chemical sphincterotomy. Good bridge option.
Surgery if fail 8 weeks of medical treatment ^[2]^[4]: Endoscopy to rule out Crohn's disease first ^[4].
- Low risk of incontinence → Lateral internal sphincterotomy (commonest surgery, healing rate 95%, incontinence 0–15% mostly flatus) ^[1].
- High risk of incontinence (multiparous women, older patients) → Fissurectomy + V-Y advancement flap (sphincter-sparing) ^[4].
Atypical/secondary fissures: Treat the underlying cause (Crohn's, TB, HIV, syphilis). Avoid sphincterotomy in Crohn's.
Prevention: High fibre, adequate fluids, avoid straining, proper hygiene, prompt treatment of diarrhoea.

Active Recall - Management of Anal Fissure

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p47, p48) ^[2] Senior notes: felixlai.md (Anal fissures — Treatment and Prevention sections) ^[3] Senior notes: maxim.md (Anal fissure — Management section) ^[4] Senior notes: maxim.md (Anal fissure — Surgical management: indications, endoscopy, risk stratification) ^[6] Senior notes: maxim.md (Haemorrhoidectomy section — pre-op preparation, position, anaesthesia)

Complications of Anal Fissure

Complications can be organised into two categories: (A) complications of the disease itself (what happens if the fissure is left untreated or doesn't respond), and (B) complications of treatment (side effects and adverse outcomes of medical and surgical therapy). Both are important for exams. Let's walk through each from first principles.

A. Complications of the Disease Itself

Aspect	Details
What happens	An acute fissure that fails to heal within 6 weeks becomes a chronic fissure — the single most common "complication" of an untreated or inadequately treated acute fissure ^[2]
Why it happens	The vicious cycle of pain → IAS spasm → ischaemia of the overlying anoderm at the posterior midline ^[1] → impaired healing perpetuates itself. Without intervention to break this cycle, the wound cannot close.
Pathological changes	The chronic fissure develops the characteristic triad: (1) Sentinel pile at the distal end ^[1], (2) Hypertrophic papilla at the proximal end ^[1], (3) Internal sphincter muscle fibres visible at base of fissure ^[1]. The edges become fibrotic and rolled. The base becomes indurated. These changes represent failed wound healing with progressive fibrosis.
Clinical significance	A chronic fissure will not heal with conservative measures alone — it requires pharmacological or surgical intervention. The fibrotic tissue at the fissure edges has poor vascularity and cannot re-epithelialise without the underlying IAS spasm being addressed.

Aspect	Details
What happens	A deep chronic fissure can extend through the anoderm into the intersphincteric space. Faecal bacteria colonise this space → suppuration → perianal or intersphincteric abscess
Why it happens	The base of a chronic fissure exposes the internal sphincter muscle fibres ^[1]. If the tear extends deep enough, it breaches the IAS entirely and communicates with the intersphincteric plane — a potential space that is vulnerable to infection. The warm, moist, bacteria-rich environment of the anal canal provides the inoculum.
Clinical features	Transition from pain purely on defaecation to constant, throbbing pain with swelling, erythema, and possibly fever/systemic symptoms. A tender fluctuant mass may become palpable perianally.
Management	Incision and drainage under GA. Antibiotics if surrounding cellulitis or immunocompromised ^[14]. Pus sent for culture and sensitivity.

Aspect	Details
What happens	A chronic deep fissure with associated abscess can spontaneously drain, forming an anorectal fistula — an abnormal epithelialised tract connecting the anal canal (internal opening) to the perianal skin (external opening)
Why it happens	This follows the cryptoglandular theory: infection spreads from the base of the fissure into the intersphincteric plane → abscess forms → pus tracks along the path of least resistance → eventually discharges to the perianal skin, creating a fistula tract. Essentially, fissure → abscess → fistula represents a continuum of the same pathological process (anorectal sepsis). In Crohn's disease, this progression is particularly common due to transmural inflammation predisposing to perianal disease — skin tags, anal fissures, perirectal abscess and anorectal fistulas ^[15].
Clinical features	Intermittent purulent perianal discharge, pain that improves when pus drains, palpable cord-like tract on PR examination
Management	Depends on fistula type (Parks classification) — ranges from fistulotomy for simple fistulas to seton placement or advancement flap for complex fistulas

The Anorectal Sepsis Continuum

Think of fissure → abscess → fistula as a spectrum of the same disease:

Fissure = initial tear
Abscess = acute suppuration when the fissure extends deep enough for bacterial invasion
Fistula = chronic tract that forms after the abscess drains

This continuum is why chronic non-healing fissures must be taken seriously — they can progress to much more complex surgical problems.

Aspect	Details
What happens	Repeated cycles of fissuring, fibrosis, and healing can lead to progressive fibrotic narrowing of the anal canal
Why it happens	Each episode of fissure → healing deposits scar tissue (fibrosis) in the anoderm and underlying sphincter. Over time, circumferential or extensive fibrosis contracts the anal canal lumen. This is analogous to how repeated oesophageal ulceration leads to oesophageal stricture.
Clinical features	Progressive difficulty passing stool, pencil-thin stools, worsening pain and constipation, a cycle of further trauma. On examination: a tight, fibrotic anal canal that barely admits a finger.
Management	Gentle anal dilatation (graduated dilators), fissurectomy with advancement flap, or rarely anoplasty for severe cases

Aspect	Details
What happens	The open wound of the fissure is continuously exposed to faecal flora → secondary bacterial infection of the wound
Why it happens	The anal canal is one of the most heavily colonised sites in the body. An open wound in this environment is a setup for infection. Normally the epithelial barrier provides protection, but a fissure removes this barrier.
Clinical features	Increased pain, perianal cellulitis (erythema, warmth, swelling extending beyond the fissure), purulent discharge, fever (if progresses to abscess)
Management	Antibiotics if cellulitis; I&D if abscess. Addressing the underlying fissure is essential.

Aspect	Details
What happens	Chronic, unremitting anal pain significantly impacts quality of life — patients develop anxiety about defaecation, avoidance behaviours, dietary restriction (eating less to produce less stool), and social withdrawal
Why it happens	The pain of anal fissure is among the most severe in clinical practice — the anoderm has the same density of somatic nerve endings as fingertip skin. Chronic pain → central sensitisation → pain may persist even after the fissure heals (though this is uncommon). The avoidance cycle (fear of defaecation → constipation → harder stool → more trauma) creates a self-reinforcing psychological component.
Clinical significance	Must be addressed holistically — reassurance, adequate analgesia, and definitive treatment of the fissure. Depression and anxiety screening may be warranted in chronic cases.

Aspect	Details
What happens	Chronic, repeated small-volume bleeding from the fissure over months to years can lead to iron deficiency anaemia
Why it happens	Although each episode produces only a small amount of blood (on toilet paper, surface of stool), cumulative daily losses eventually deplete iron stores → microcytic hypochromic anaemia. This is uncommon because the bleeding volume per episode is typically tiny, but can occur in chronic, neglected cases.
Clinical features	Fatigue, pallor, dyspnoea on exertion, palpitations
Investigation	FBC (low MCV, low Hb), iron studies (low ferritin, low serum iron, high TIBC)

B. Complications of Treatment

Treatment	Complication	Mechanism
Topical GTN (nitroglycerin) ^[1]^[3]	Headache ^[3]	GTN is a systemic NO donor — absorbed through perianal skin and enters systemic circulation → vasodilatation of cerebral vessels → headache. This is the same mechanism as the headache side effect of sublingual GTN for angina. Reported in up to 20–60% of patients; dose-limiting and the main cause of non-compliance.
Topical GTN	Dizziness / hypotension	Systemic vasodilatation → reduced SVR → postural hypotension
Topical nifedipine / diltiazem ^[1]^[3]	Minor local irritation	Local reaction to the ointment base. Systemic absorption is minimal, hence fewer headaches.
All topical vasodilators	Risk of incontinence ^[3]	Any agent that reduces IAS tone could theoretically impair the contribution of the IAS to resting continence. In practice, this is rare with topical agents and is typically limited to minor flatus incontinence.
All topical vasodilators	Recurrence	Topical agents have recurrence rates of ~40–50% after initial healing, because they provide temporary sphincter relaxation without permanently addressing the underlying hypertonic sphincter

Complication	Mechanism
Temporary flatus incontinence	Botulinum toxin paralyses the IAS → reduced resting anal tone → minor leakage of flatus. Self-limiting as the toxin wears off (~3 months when new nerve terminals regenerate).
Faecal incontinence (rare, < 5%)	Excessive or misdirected injection → over-weakening of IAS tone → cannot maintain continence. Usually temporary.
Perianal haematoma	Direct trauma from the injection needle to perianal vessels
Failure / recurrence	Insufficient dose, incorrect injection site, antibody formation (rare with single injection)

This is the most important section because LIS is the gold standard surgery, and its complications are high yield for exams.

Complication	Incidence	Mechanism & Explanation
Faecal incontinence	0–15% ^[1]	The IAS is responsible for ~70–85% of resting anal tone. Dividing it permanently reduces resting pressure. If too much IAS is divided, or if the patient has pre-existing sphincter weakness (e.g., previous obstetric injury, ageing), the remaining sphincter mechanism may be insufficient → incontinence. Most are minor with flatus incontinence ^[1] — meaning patients notice inability to control passage of gas, rather than frank leakage of liquid or solid stool. True faecal incontinence is rare (< 3%).
Urinary retention	Variable	Post-operative pain and reflex IAS/pelvic floor spasm → inhibition of the detrusor muscle via spinal reflex arcs → difficulty initiating micturition. Same mechanism as urinary retention after haemorrhoidectomy. Causes include: pain and anal spasm, fluid overload, rectal packing, drugs (narcotics, anticholinergics), pre-existing outflow tract obstruction ^[6]. Managed by leaving urinary catheter in situ for 24 hours ^[6].
Post-operative pain	Common	Surgical wound in the highly sensitive anoderm (somatic innervation). Pain is almost universal after anorectal surgery (~100% due to IAS spasm) ^[6]. Managed with analgesia (paracetamol, NSAIDs, opioids if needed), sitz baths, stool softeners.
Bleeding	Uncommon	Injury to branches of the inferior rectal artery during the sphincterotomy. Usually minor and self-limiting. Rarely requires return to theatre.
Anal stenosis	Rare	Excessive scarring and fibrosis at the sphincterotomy site → narrowing of the anal canal. More common if too much tissue is excised or if there is post-operative infection. Managed with graduated anal dilatation ^[6].
Perianal abscess / wound infection	Rare	Contamination of the surgical wound with faecal bacteria. The anal canal is a "dirty" surgical field by definition. Prophylactic antibiotics and meticulous wound care reduce this risk.
Keyhole deformity	If posterior	This is why LIS is performed laterally rather than posteriorly. A posterior sphincterotomy creates a gutter-like defect (keyhole) that allows mucus and stool to leak → soiling. The lateral approach avoids this.
Recurrence	< 5%	Incomplete division of the IAS → persistent spasm → recurrent fissure. Much lower recurrence than medical therapy.

The Trade-Off of Surgery

Lateral internal sphincterotomy: healing rate 95%, incontinence 0–15% ^[1]. This is the fundamental trade-off that every patient must be counselled about. You are PERMANENTLY dividing part of the IAS — this cannot be reversed. In young healthy patients with high sphincter tone, the risk is very low. In multiparous women, older patients ^[4], the risk is unacceptably high → choose fissurectomy + V-Y advancement flap (sphincter-sparing) ^[4] instead. Always assess pre-operative sphincter function (manometry ± endoanal USS) before committing to LIS.

Complication	Mechanism
Flap dehiscence / failure	The advancement flap separates from the wound bed due to tension, infection, or poor blood supply → wound breakdown → recurrence of the defect
Wound infection	Same principle as LIS — contaminated surgical field
Recurrence	Higher than LIS (~10–15%) because the underlying IAS hypertonia is NOT addressed (the sphincter is preserved) → the pathophysiological driver remains
No incontinence from the procedure itself	Key advantage — the IAS is not divided. However, pre-existing incontinence from other causes is not improved either.

Category	Complications
Disease complications	Chronicity (most common), perianal abscess, anorectal fistula, anal stenosis, secondary infection, chronic pain/psychosocial impact, iron deficiency anaemia (rare)
Topical vasodilator complications	Headache (GTN), dizziness, local irritation, minor incontinence risk, high recurrence
Botulinum toxin complications	Temporary flatus incontinence, haematoma, failure/recurrence
LIS complications	Faecal incontinence (0–15%, mostly flatus), urinary retention, pain, bleeding, anal stenosis, infection, keyhole deformity (if posterior), recurrence (< 5%)
Fissurectomy + flap complications	Flap dehiscence, infection, recurrence (10–15%), NO incontinence

High Yield Summary — Complications of Anal Fissure

Most common complication of the disease: Progression to chronicity — the fissure develops sentinel pile, hypertrophic papilla, and exposed IAS fibres at the base.
Fissure → Abscess → Fistula continuum: A deep chronic fissure can progress to perianal abscess and then anorectal fistula via the cryptoglandular mechanism. Especially common in Crohn's disease.
Anal stenosis: Repeated cycles of fissuring and fibrosis narrow the anal canal.
GTN side effects: Headache (most common, dose-limiting, up to 60%) due to systemic NO-mediated cerebral vasodilatation. Nifedipine/diltiazem have fewer headaches.
LIS complications: Healing rate 95%, incontinence 0–15% — most are minor with flatus incontinence. This is the key trade-off. Avoid LIS in high-risk patients (multiparous, elderly) → use sphincter-sparing fissurectomy + advancement flap instead.
Post-anorectal surgery complications: Pain (almost universal), urinary retention, bleeding, infection, anal stenosis, faecal incontinence.

Active Recall - Complications of Anal Fissure

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p42–48) ^[2] Senior notes: felixlai.md (Anal fissures — Overview, Pathogenesis, Treatment sections) ^[3] Senior notes: maxim.md (Anal fissure — Management section) ^[4] Senior notes: maxim.md (Anal fissure — Surgical management: risk stratification) ^[6] Senior notes: maxim.md (Haemorrhoidectomy — Complications: pain, urinary retention, incontinence, anal stenosis) ^[14] Senior notes: maxim.md (Anorectal abscess — Management) ^[15] Senior notes: felixlai.md (Crohn's disease — Perianal disease complications)

High Yield Summary

Definition: A tear in the anoderm below the dentate line; 90% posterior midline, 10% anterior (women).
Pathophysiology — the vicious cycle: Trauma → tear → pain → IAS spasm → ischaemia (posterior midline is the least perfused area) → impaired healing → chronicity. Fear of pain → avoidance → constipation → re-trauma.
Acute vs Chronic: Acute = superficial "paper cut" (< 6 weeks). Chronic = triad of fissure + sentinel pile + hypertrophied anal papillae with visible IAS fibres at the base.
Typical vs Atypical: Typical = single, midline. Atypical = multiple, off-midline, deep, wide, painless, non-healing → suspect Crohn's, TB, HIV, syphilis, CMV.
Clinical features: Sharp pain on defaecation + small amount of bright red PR bleeding + perianal pruritus. DRE often too painful — EUA may be required.
Why posterior midline?: (a) Least blood supply (watershed zone), (b) greatest mechanical shearing force, (c) poorest EAS support posteriorly.
Every treatment targets the vicious cycle: Soften stool (fibre/laxatives), relax IAS (GTN/nifedipine/botox/LIS), improve blood flow (vasodilators/sitz bath).

High Yield Summary — Differential Diagnosis of Anal Fissure

Two symptom axes to differentiate: (a) Anal pain — sharp at start of defaecation = fissure; constant/throbbing = abscess; unrelated to defaecation = proctalgia fugax. (b) Fresh PRB — outlet-type on paper = fissure/haemorrhoids; mixed with stool = CRC/IBD/colitis; profuse painless = diverticular.
Key differentials to always consider: Haemorrhoids (painless), thrombosed external haemorrhoid (painful mass), perianal abscess (constant pain + fever), anorectal fistula (discharge, cord-like tract), CRC (must always exclude), solitary rectal ulcer, anal carcinoma.
Atypical fissure features (off-midline, multiple, deep, non-healing) → investigate for Crohn's, TB, HIV, syphilis, CMV.
Diagnosis is clinical: spread buttocks to visualise the fissure. DRE and proctoscopy are painful and not indicated acutely. EUA if needed. Colonoscopy to exclude CRC and IBD.
Colorectal neoplasm needs to be excluded in any patient with PR bleeding — this is the most important differential to rule out.

High Yield Summary — Diagnosis of Anal Fissure

Anal fissure is a CLINICAL diagnosis — history + visual inspection by spreading the buttocks. No investigations needed for typical cases.
Diagnosis is by spreading the buttocks to reveal the fissure. Rectal examination and proctoscopy are painful and not indicated in acute fissure.
Acute fissure: superficial paper-cut tear. Chronic fissure: sentinel pile + hypertrophic papilla + IAS muscle fibres at base.
Typical = single, midline → primary → treat. Atypical = multiple, off-midline, deep, non-healing → secondary → investigate (colonoscopy, serology, biopsy).
Endoscopy to rule out Crohn's disease first before surgical intervention for chronic fissure.
Colorectal neoplasm must always be excluded in patients with PR bleeding and red flag features.
EUA is used when the examination is too painful, and can be combined with therapeutic intervention.
Anorectal manometry is used pre-operatively to assess sphincter function and guide choice between sphincterotomy vs sphincter-sparing surgery.

High Yield Summary — Management of Anal Fissure

All fissures: Start with conservative management — bulk agents, stool softeners, topical anaesthetics + sitz baths + dietary modification.
First-line pharmacological: Newer topical agents to reduce internal sphincter pressure — nitroglycerin, calcium channel blockers ^[1]. GTN causes headache; nifedipine/diltiazem better tolerated. Both relax IAS and improve blood flow.
Second-line: Botulinum toxin 50 IU injection into IAS ^[1]^[3]. Reversible chemical sphincterotomy. Good bridge option.
Surgery if fail 8 weeks of medical treatment ^[2]^[4]: Endoscopy to rule out Crohn's disease first ^[4].
- Low risk of incontinence → Lateral internal sphincterotomy (commonest surgery, healing rate 95%, incontinence 0–15% mostly flatus) ^[1].
- High risk of incontinence (multiparous women, older patients) → Fissurectomy + V-Y advancement flap (sphincter-sparing) ^[4].
Atypical/secondary fissures: Treat the underlying cause (Crohn's, TB, HIV, syphilis). Avoid sphincterotomy in Crohn's.
Prevention: High fibre, adequate fluids, avoid straining, proper hygiene, prompt treatment of diarrhoea.

High Yield Summary — Complications of Anal Fissure

Most common complication of the disease: Progression to chronicity — the fissure develops sentinel pile, hypertrophic papilla, and exposed IAS fibres at the base.
Fissure → Abscess → Fistula continuum: A deep chronic fissure can progress to perianal abscess and then anorectal fistula via the cryptoglandular mechanism. Especially common in Crohn's disease.
Anal stenosis: Repeated cycles of fissuring and fibrosis narrow the anal canal.
GTN side effects: Headache (most common, dose-limiting, up to 60%) due to systemic NO-mediated cerebral vasodilatation. Nifedipine/diltiazem have fewer headaches.
LIS complications: Healing rate 95%, incontinence 0–15% — most are minor with flatus incontinence. This is the key trade-off. Avoid LIS in high-risk patients (multiparous, elderly) → use sphincter-sparing fissurectomy + advancement flap instead.
Post-anorectal surgery complications: Pain (almost universal), urinary retention, bleeding, infection, anal stenosis, faecal incontinence.

Anal Fissure

Definition

Epidemiology

Risk Factors

Anatomy and Function

Anal Canal Anatomy

Anal Sphincter Complex

Blood Supply — Why Posterior Midline?

Aetiology

Primary (Idiopathic) Anal Fissures

Secondary Anal Fissures

Pathophysiology

The Vicious Cycle of Anal Fissure

Why Posterior Midline?

Classification

By Duration

By Position (Typical vs Atypical)

By Aetiology

Clinical Features

Symptoms

Signs

Distinguishing Fissure Pain from Other Causes of Anal Pain

Summary of Features Suggesting Secondary Causes

Active Recall - Anal Fissure (Definition, Epidemiology, Anatomy, Aetiology, Pathophysiology, Clinical Features)

References

Approach to Differential Diagnosis

Differential Diagnosis Table

A. Differentials for Anal/Perianal Pain

B. Differentials for Fresh Per-Rectal Bleeding

Differentiating Primary vs Secondary Fissure — A Critical Step

Approach to Excluding Differentials

Summary Mnemonic: "FISSURE" Differentials

Active Recall - Differential Diagnosis of Anal Fissure

Diagnostic Criteria

Diagnostic Algorithm

Step 1: Focused History

Step 2: Visual Inspection

Step 3: Classify the Fissure

Step 4: Determine If Typical or Atypical

Step 5: Decide on Investigations (If Needed)

Investigation Modalities

A. Examination Under Anaesthesia (EUA)

B. Proctoscopy

C. Sigmoidoscopy / Colonoscopy

D. Blood Tests (When Indicated)

E. Microbiological and Serological Tests

F. Biopsy

G. Anorectal Manometry (Specialised)

H. Endoanal Ultrasound (Specialised)

Summary: When to Investigate and What to Order

Active Recall - Diagnosis of Anal Fissure

Guiding Principles

Management Algorithm

Step 1: Conservative / Supportive Management

A. Dietary and Lifestyle Modification

B. Warm Sitz Bath

C. Topical Anaesthetics

Step 2: First-Line Medical Therapy — Topical Vasodilators

A. Topical Nitroglycerin (GTN) Ointment

B. Topical Calcium Channel Blockers

Step 3: Second-Line Medical Therapy — Botulinum Toxin

Step 4: Surgical Management

Pre-Operative Preparation

A. Lateral Internal Sphincterotomy (LIS)

B. Fissurectomy + V-Y Advancement Flap (Sphincter-Sparing)

Management of Secondary (Atypical) Fissures

Prevention of Recurrence

Summary of Treatment Step-Up Approach

Active Recall - Management of Anal Fissure

A. Complications of the Disease Itself

1. Chronicity (Acute → Chronic Fissure)

2. Perianal Abscess Formation

3. Anorectal Fistula Formation

4. Anal Stenosis (Stricture)

5. Secondary Infection

6. Chronic Pain and Psychosocial Impact

7. Iron Deficiency Anaemia (Rare)

B. Complications of Treatment

1. Complications of Topical Vasodilators

2. Complications of Botulinum Toxin Injection