Anorectal Abscess

An anorectal abscess is a localized collection of pus in the perianal or perirectal tissue, most commonly arising from infection of the anal glands (cryptoglandular origin).

1. Definition

An anorectal abscess is an acute collection of purulent material (pus) that arises in the tissue spaces surrounding the anorectum ^[1]^[2]^[3]. It represents the acute phase of perianal sepsis; the corresponding chronic phase is the anorectal fistula (fistula-in-ano) ^[2].

Let's break the name down:

Ano- = relating to the anus (Latin: anus = ring)
Rectal = relating to the rectum (Latin: rectum = straight [intestine])
Abscess = from Latin abscessus = "a going away" — i.e., a walled-off collection of pus that has "gone away" from normal tissue

The abscess most commonly originates from infection of the anal crypt glands (cryptoglandular theory) ^[1]^[2]^[3]. These glands sit in the intersphincteric plane, and when their ducts become obstructed, bacteria proliferate in the trapped secretions, forming an abscess that can then track along tissue planes of least resistance into the various perianal and perirectal spaces ^[2]^[4].

Key Concept

Anorectal abscess = acute phase of perianal sepsis. Anorectal fistula = chronic phase of the same process. About 30–50% of anorectal abscesses will progress to a fistula-in-ano if the internal opening (infected crypt) persists.

2. Epidemiology & Risk Factors

Epidemiology

Incidence: ~1–2 per 10,000 population per year in Western literature; comparable rates in Hong Kong
Age: Peak incidence in the 3rd–4th decade of life (20–40 years old)
Sex: Male-to-female ratio approximately 2–3:1 — possibly related to greater density of anal glands in males and hormonal influences on gland secretion
The ischiorectal abscess is the most common type (60%), followed by perianal (20%) and intersphincteric (18%); supralevator is rare (2%) ^[1]^[2]

Risk Factors

Category	Specific Risk Factors	Mechanism
Local	Anal fissure, haemorrhoids, anal trauma, foreign body	Breach in mucosal barrier → bacterial entry
Inflammatory	Crohn's disease, ulcerative colitis	Transmural inflammation (Crohn's) creates fistulising tracts; disrupted mucosa allows bacterial invasion ^[1]^[3]
Infectious	Tuberculosis, actinomycosis, HIV, LGV (lymphogranuloma venereum)	Specific organisms cause granulomatous or chronic suppurative infection in perianal tissues ^[1]^[3]
Iatrogenic	Surgery (e.g., haemorrhoidectomy, post-sclerotherapy), episiotomy, radiation	Direct tissue injury opens a portal of entry ^[3]
Immunosuppression	Diabetes mellitus, HIV/AIDS, chemotherapy, chronic corticosteroids	Impaired neutrophil function → inability to contain crypt gland infection
Malignancy	Malignancies (rectal/anal carcinoma)	Tumour necrosis or obstruction of crypt glands ^[3]
Lifestyle	Obesity, smoking, poor hygiene	Obesity increases moisture/friction; smoking impairs microvascular perfusion

Hong Kong Context

In Hong Kong, be especially mindful of tuberculosis as a cause of perianal sepsis — TB remains more prevalent here than in many Western countries. A non-healing perianal abscess/fistula, especially with caseous material, should prompt AFB staining and TB culture. Also consider Crohn's disease, which, although historically less common in Asia, is rising in incidence in Hong Kong.

3. Anatomy & Function

Understanding anorectal abscess requires a solid grasp of the anal canal anatomy, the sphincter complex, the anal glands, and the perianal/perirectal tissue spaces. Think of the anatomy as a series of concentric tubes and the spaces between them.

3.1 The Anal Canal

Surgical anal canal: From the anal verge (where hair-bearing perianal skin begins) to the anorectal ring (the palpable upper border of the puborectalis/external sphincter complex) — approximately 4 cm long
Anatomical anal canal: From the dentate (pectinate) line to the anal verge — approximately 2 cm long
The dentate line is the key landmark:
- It is the junction of endoderm (above — columnar epithelium) and ectoderm (below — squamous epithelium)
- The crypts of Morgagni (anal crypts) are located at the dentate line — these are the openings into which the anal glands drain
- Arterial supply, venous drainage, lymphatic drainage, and nerve supply all differ above vs. below the dentate line

3.2 The Sphincter Complex

Structure	Type	Innervation	Function
Internal Anal Sphincter (IAS)	Smooth muscle (thickened continuation of the circular muscle layer of the rectum)	Autonomic (sympathetic = contraction, parasympathetic = relaxation)	Provides ~70–85% of resting anal tone — involuntary continence
External Anal Sphincter (EAS)	Skeletal (striated) muscle — encircles the IAS	Pudendal nerve (S2–S4) — somatic, voluntary	Provides voluntary squeeze pressure; crucial during coughing/straining
Puborectalis	Skeletal muscle — U-shaped sling around the anorectal junction	Pudendal nerve (S2–S4)	Maintains the anorectal angle (~80–90°); critical for gross continence

The intersphincteric groove (the sulcus between IAS and EAS) is palpable on digital rectal examination (DRE) and is the plane along which the anal glands reside — and along which pus first tracks.

3.3 The Anal Glands (Cryptoglandular Apparatus)

6–10 anal glands are present, clustered mainly in the posterior midline
Each gland opens via a duct into one of the crypts of Morgagni at the dentate line
The gland body lies in the intersphincteric plane (between IAS and EAS)
They secrete mucus to lubricate the anal canal
Why they matter: When a crypt duct becomes obstructed (by faecal matter, inspissated debris, or mucosal oedema), bacteria proliferate within the trapped glandular secretion → intersphincteric abscess forms → pus tracks along paths of least resistance into adjacent tissue spaces

3.4 Perianal & Perirectal Tissue Spaces

These are the potential spaces into which pus can spread. Think of them as compartments defined by the fascial planes and muscles:

Space	Location	Boundaries	Clinical Relevance
Perianal space	Immediately subcutaneous around the anal verge	Below the dentate line, superficial to the EAS	Most superficial abscess — easily visible and palpable externally
Intersphincteric space	Between IAS and EAS	Continuous superiorly with the rectal wall	The origin of cryptoglandular abscess; may not be visible externally; diagnosed on DRE (tender, boggy swelling)
Ischiorectal fossa	Lateral to the anal canal, below the levator ani	Medial = EAS; Lateral = obturator internus; Superior = levator ani; Inferior = transverse perineal muscles/skin	Large space → abscess can become very large before presenting; most common site (60%) ^[1]^[2]
Supralevator space	Above the levator ani, below the peritoneum	Between the levator ani and the pelvic peritoneum	Rare (2%) ^[1]^[2]; dangerous — may present with pelvic sepsis; drainage route must be chosen carefully to avoid creating an extrasphincteric fistula
Deep postanal space	Posterior to the anal canal, between the EAS and the anococcygeal ligament	Communicates with both ischiorectal fossae	Route for horseshoe abscess (bilateral ischiorectal spread)

Why is the ischiorectal fossa the most common abscess site?

The ischiorectal fossa is large and filled with loose fatty tissue that offers little resistance to the spread of infection. Once pus breaches the EAS from the intersphincteric plane, it can easily expand within this capacious space. The "path of least resistance" principle (Parks' theory) explains this preferential tracking ^[4].

4. Etiology

The etiology of anorectal abscess is dominated by the cryptoglandular theory, but always consider secondary causes, especially in Hong Kong where TB and rising IBD rates are relevant.

4.1 Cryptoglandular Infection (Most Common — ~90%)

Cryptoglandular infection ^[1]^[3] is the overwhelmingly predominant cause:

An anal crypt gland duct becomes obstructed (by faecal debris, mucosal inflammation, or inspissated secretions)
Bacteria proliferate within the sealed gland → intersphincteric abscess forms
Pus then extends along the path of least resistance into the various perianal/perirectal spaces

Microbiology: The organisms are typically a mixed flora of:

Gut organisms: E. coli, Bacteroides fragilis, Enterococcus spp. — these are the expected organisms when a fistula is present (communication with the bowel lumen)
Skin organisms: Staphylococcus aureus, Streptococcus spp. — when these predominate and gut flora is absent, a fistula is less likely

Pus Culture Predicts Fistula Risk

This is a clinically important pearl from the senior notes ^[4]: if pus culture shows gut flora → high likelihood of an associated fistula (internal communication with bowel). If only skin flora → less likely to have a fistula → reassurance. Always send pus for C/ST (culture and sensitivity testing) at the time of incision and drainage.

4.2 Other/Secondary Causes

Cause	Details	Hong Kong Relevance
Inflammatory bowel disease (IBD)	Crohn's disease is the classic culprit — transmural inflammation leads to fistulising perianal disease; UC rarely causes perianal sepsis ^[1]^[3]	IBD incidence rising in Hong Kong and East Asia; Crohn's disease may present with perianal abscess as the first manifestation
Tuberculosis	Perianal TB can present as chronic non-healing abscess, sinus, or fistula; caseous necrosis on histology; AFB staining positive ^[1]^[3]	TB remains endemic in Hong Kong — always consider in atypical/recurrent perianal sepsis
Actinomycosis	Caused by Actinomyces israelii; forms "sulfur granules"; typically in immunocompromised ^[1]^[3]	Uncommon but important differential
Foreign body	Rectal foreign bodies → mucosal laceration → abscess ^[1]^[3]	Consider in trauma, sexual practice, accidental ingestion
Surgery	Post-haemorrhoidectomy, post-sclerotherapy, post-episiotomy ^[3]^[4]	Iatrogenic cause — always take a surgical history
Malignancies	Anal or rectal carcinoma may present with secondary abscess due to tumour necrosis or obstruction ^[3]	Consider in older patients or atypical presentations
Radiation	Radiation proctitis following pelvic radiotherapy → mucosal breakdown → infection	Consider in patients with history of cervical/prostate/rectal cancer treatment
Lymphogranuloma venereum (LGV)	Chlamydia trachomatis serovars L1–L3; chronic lymphatic infection → inflammatory perirectal masses	Consider in MSM (men who have sex with men) — relevant in Hong Kong STI clinics
HIV/AIDS	Immunodeficiency → opportunistic infections, atypical organisms, poor healing	HIV testing should be considered in recurrent perianal sepsis
Diabetes mellitus	Not a direct cause, but significantly increases risk due to microvascular disease and impaired immune function	Very common comorbidity in Hong Kong; increases risk of complications (necrotising fasciitis)

5. Pathophysiology

5.1 The Cryptoglandular Sequence (Step-by-Step)

This is the core pathophysiological mechanism and ties together anatomy, microbiology, and clinical presentation:

Step 1 — Obstruction: The anal gland duct (which opens into a crypt of Morgagni at the dentate line) becomes blocked. This may be due to faecal material, inflammatory oedema, or inspissated mucus.

Step 2 — Infection: The obstructed gland becomes a closed space → bacteria (typically mixed gut and anaerobic flora) proliferate → acute suppurative infection develops.

Step 3 — Intersphincteric origin: Because the gland body lies in the intersphincteric plane (between IAS and EAS), the initial abscess always begins here ^[2]^[4]. This is why the intersphincteric abscess is considered the "origin" of all cryptoglandular abscesses.

Step 4 — Tracking: Pus does not respect fascial boundaries if the pressure is high enough. It follows the path of least resistance (Parks' theory ^[4]):

Inferiorly through the distal IAS → emerges at the perianal skin (perianal abscess)
Laterally through the EAS → fills the ischiorectal fossa (ischiorectal abscess)
Superiorly above the levator ani → enters the supralevator space (supralevator abscess)
Posteriorly through the deep postanal space → can cross to the contralateral ischiorectal fossa → horseshoe abscess

Step 5 — Spontaneous drainage or progression: If not drained, the abscess may:

Spontaneously drain through the perianal skin → if the internal opening (at the crypt) persists → a fistula forms (chronic tract connecting the internal opening to the external drainage site)
Progress to overwhelming local infection → cellulitis, necrotising fasciitis (Fournier's gangrene), or systemic sepsis

Why Do ~30–50% of Abscesses Become Fistulas?

When the abscess drains (spontaneously or surgically), the external opening heals but the internal opening (the original infected crypt) often remains patent. This creates a persistent communication between the anal canal lumen and the perianal skin — a fistula-in-ano. The tract becomes lined with granulation tissue and epithelium, preventing it from healing. This is why some surgeons advocate primary fistulotomy at the time of abscess drainage for simple, low fistulas — to address the internal opening and prevent recurrence ^[1].

5.2 Microbiology and Its Clinical Significance

Organism Type	Common Species	Implication
Gut flora	E. coli, Bacteroides fragilis, Enterococcus, Klebsiella	Suggests cryptoglandular origin with internal communication → high fistula risk
Skin flora	Staphylococcus aureus, Streptococcus pyogenes	Suggests superficial skin infection without internal communication → low fistula risk
TB	Mycobacterium tuberculosis	Chronic granulomatous abscess; AFB stain, culture, and tissue biopsy needed
Actinomyces	Actinomyces israelii	"Sulfur granules" on histology; prolonged antibiotic therapy required
Mixed anaerobes	Bacteroides, Peptostreptococcus, Fusobacterium	Common in deep abscesses; produce gas → subcutaneous crepitus if gas-forming infection

6. Classification

Anorectal abscesses are classified by their anatomical location, which determines clinical presentation, examination findings, and the surgical approach to drainage.

6.1 Classification by Anatomical Location

Type	Frequency	Location	Key Features
Perianal	20% ^[1]^[2]	Subcutaneous tissue at the anal verge, superficial to the EAS	Most superficial; easily visible and palpable as a tender, fluctuant swelling at the anal margin; the "classic" abscess that patients present with
Intersphincteric	18% ^[1]^[2]	Between the IAS and EAS (the intersphincteric groove)	May NOT be visible externally; diagnosed by DRE revealing a tender, boggy, fluctuant area in the anal canal wall; patient has severe anal pain without obvious external swelling
Ischiorectal	60% ^[1]^[2]	In the ischiorectal fossa, lateral to the anal sphincter complex, below the levator ani	Most common type; can become very large (the fossa is spacious and filled with fat); presents with diffuse buttock/perianal swelling, erythema, and induration; may be bilateral (horseshoe)
Supralevator	2% ^[1]^[2]	Above the levator ani muscle, below the pelvic peritoneum	Rarest but most dangerous; may present insidiously with pelvic/rectal pain and systemic sepsis without obvious perianal signs; drainage approach is critical — wrong approach can create an extrasphincteric fistula

6.2 Special Types

Horseshoe abscess: A bilateral ischiorectal abscess connected via the deep postanal space. The infection originates from a posterior midline crypt (where anal glands are most concentrated), tracks posteriorly into the deep postanal space, and then spreads laterally into both ischiorectal fossae. Requires drainage of both sides with counter-drainage of the postanal space.
Supralevator abscess — origin matters for drainage:
- If it originated from upward extension of an intersphincteric abscess → drain transanally (through the rectal wall) to avoid creating an extrasphincteric fistula ^[4]
- If it originated from upward extension of an ischiorectal abscess → drain through the ischiorectal fossa (buttock skin incision) ^[4]
- If it originated from intra-abdominal pathology (e.g., diverticular abscess, appendiceal abscess tracking down) → treat the primary intra-abdominal source

Supralevator Abscess Drainage — Critical Surgical Pearl

Draining a supralevator abscess via the WRONG route can create a devastating extrasphincteric fistula (a fistula that bypasses the entire sphincter complex). This is surgically very difficult to manage and risks faecal incontinence. Always determine the origin of the supralevator abscess before choosing the drainage approach:

Intersphincteric origin → drain transanally (internal sphincterotomy)
Ischiorectal origin → drain through buttock skin
Pelvic origin → treat the abdominal source

7. Clinical Features

7.1 Symptoms

Symptom	Pathophysiological Basis	Details
Pain ^[1]	Acute inflammation and distension of tissue by pus → stimulation of somatic pain fibres (especially below the dentate line, which is innervated by the inferior rectal nerve — somatic, very sensitive)	Constant, throbbing perianal pain that is exacerbated by sitting, walking, coughing, and defaecation. Intersphincteric abscess may cause deep, poorly localised anal pain. Supralevator abscess may cause vague pelvic or rectal pain.
Swelling ^[1]	Accumulation of pus and surrounding inflammatory oedema in the perianal tissues	Patient notices a lump near the anus. May be obvious in perianal/ischiorectal abscess but absent in intersphincteric/supralevator abscess.
Drainage/Discharge ^[1]	Spontaneous rupture of the abscess through the skin or mucosa → release of purulent material	Purulent (pus), serosanguinous, or foul-smelling discharge from the perianal area. Spontaneous drainage may provide temporary relief of pain but does not cure the underlying source.
Constipation ^[1]	Pain and sphincter spasm (the inflamed tissues cause reflexive tightening of the EAS) → patient avoids defaecation due to fear of worsening pain (proctalgia fugax-like mechanism)	Patient reports difficulty passing stool or deliberately delays defaecation.
Urinary difficulties ^[1]	Reflex urinary retention — the pudendal nerve (S2–S4) innervates both the EAS and the external urethral sphincter; severe perianal inflammation can cause reflex spasm of the urethral sphincter. Additionally, local swelling may mechanically obstruct the urethra in anterior abscesses.	Patient reports difficulty initiating micturition or incomplete voiding. This is more common with larger ischiorectal or supralevator abscesses.
Systemic symptoms	Bacteraemia from the abscess, systemic inflammatory response	Fever, rigors, malaise, tachycardia. More common with deep-seated (ischiorectal, supralevator) or large abscesses, and in immunocompromised patients (DM, HIV). Septic shock may occur if untreated.
Perianal itch/irritation	Chronic low-grade discharge irritating the perianal skin (more relevant in the transition from abscess to fistula)	May be present as a prodromal symptom before frank abscess formation.

7.2 Signs

Sign	Pathophysiological Basis	Details
Erythematous, fluctuant, tender mass	Localised pus collection with surrounding inflammatory hyperaemia → erythema (redness from vasodilation); fluctuance (fluid-filled cavity); tenderness (stimulation of nociceptors)	Palpable on inspection and/or DRE ^[4]. The classic finding for perianal abscess — a red, hot, tender, fluctuant swelling at the anal margin. For ischiorectal abscess — diffuse buttock swelling and induration.
Induration	Surrounding cellulitis and inflammatory oedema → tissue hardening	The tissues around the abscess feel firm and "woody" — this represents the zone of cellulitis surrounding the collection.
Digital rectal examination (DRE) findings	Intersphincteric abscess produces a tender, boggy, fluctuant area within the anal canal wall; ischiorectal abscess may be palpable laterally; supralevator abscess may be palpable as a tender fullness above the anorectal ring	DRE is critical for diagnosing deeper abscesses (intersphincteric, supralevator) that may not have external signs. However, DRE may be impossible due to pain — examination under anaesthesia (EUA) is often required.
Fever	Systemic inflammatory response to infection	Temperature > 38°C; more likely with larger or deep-seated abscesses.
Cellulitis	Spread of infection into the surrounding subcutaneous tissues and skin → diffuse erythema, warmth, and tenderness extending beyond the abscess	Important to note: antibiotics are indicated when there is surrounding cellulitis ^[1] (otherwise, the treatment is primarily surgical).
Crepitus	Gas-producing organisms (anaerobes, Clostridium spp.) in the soft tissues → subcutaneous emphysema	Red flag — suggests necrotising fasciitis (Fournier's gangrene). Requires emergency surgical debridement.
Absent or minimal external signs	Intersphincteric and supralevator abscesses are deep-seated → pus does not reach the skin surface	A patient with severe anorectal pain but no visible perianal swelling should raise suspicion for an intersphincteric or supralevator abscess. DRE +/- imaging (MRI, EUS) is essential.

Clinical Approach to Anorectal Pain Without Visible Swelling

A common exam pitfall: not all anorectal abscesses are visible externally! An intersphincteric abscess sits deep within the anal canal wall and may only be detected on DRE (tender, boggy mass in the anal canal). A supralevator abscess sits above the levator ani and may present with vague pelvic pain, rectal fullness, and systemic sepsis without any external perianal signs. When in doubt → EUA ± MRI pelvis.

7.3 Clinical Features by Abscess Type (Summary Table)

Feature	Perianal	Intersphincteric	Ischiorectal	Supralevator
Visible swelling	Yes — at anal margin	No — internal only	Yes — buttock/perianal	Usually no
Pain location	Localised perianal	Deep anal canal	Diffuse perianal/buttock	Vague pelvic/rectal
DRE finding	Tender superficial mass at verge	Tender boggy mass within canal wall	Lateral tender fullness	Tender fullness above anorectal ring
Systemic signs	Uncommon (unless large)	Variable	Common (large collections)	Common (deep sepsis)
Ease of diagnosis	Easy — visible	Difficult — DRE/EUA needed	Moderate — large but may be deep	Difficult — imaging often required

8. Investigations

Investigations serve three purposes ^[1]:

Help in the diagnosis and assess the severity of disease
Define anatomy of the pathological process (abscess and fistula)
Exclude diseases in the proximal bowel and associated bowel problems (e.g. inflammatory bowel disease)

8.1 Bedside

Investigation	Purpose
Digital rectal examination (DRE)	Palpate for intersphincteric/supralevator abscess; identify internal opening; assess sphincter tone
Proctoscopy / Anoscopy	Visualise the anal canal — identify inflamed crypts, internal openings, co-existing pathology (haemorrhoids, fissure, tumour)
Examination under anaesthesia (EUA)	Gold standard when pain precludes adequate bedside examination; allows thorough assessment of abscess extent, probing for fistula tracts, and drainage in one setting

8.2 Laboratory

Investigation	Purpose
CBC (FBC)	Leucocytosis (neutrophilia) — indicates active infection; degree correlates with severity
CRP / ESR	Inflammatory markers — elevated in infection; useful for monitoring response to treatment
Blood glucose / HbA1c	Screen for diabetes mellitus — a major risk factor for complicated perianal sepsis
Blood cultures	If systemically septic (fever, tachycardia, hypotension) — identify causative organism
Pus C/ST	Always send at time of I&D — gut flora suggests fistula; skin flora suggests no fistula ^[4]
Pus for AFB stain/TB culture	If TB is suspected (non-healing, caseous material, endemic setting — Hong Kong)
Tissue biopsy	If Crohn's disease, TB, actinomycosis, or malignancy suspected — send abscess wall for histopathology

8.3 Imaging

Investigation	Indication	Details
MRI pelvis	Deep-seated abscess (intersphincteric, supralevator); recurrent abscess; suspected complex fistula; Crohn's disease	Gold standard for mapping perianal sepsis — excellent soft tissue resolution; delineates abscess location, size, and relationship to sphincter complex; identifies occult collections and fistula tracts
Endoanal ultrasound (EUS)	Alternative to MRI; can be performed in clinic or theatre	Visualises the sphincter complex and intersphincteric collections; operator-dependent
CT pelvis	If MRI unavailable; suspected supralevator abscess from intra-abdominal source	Less soft tissue resolution than MRI but can identify collections and rule out intra-abdominal pathology (e.g., diverticular abscess tracking down)

8.4 Endoscopy

Investigation	Indication
Flexible sigmoidoscopy / Colonoscopy	Exclude diseases in the proximal bowel ^[1] — particularly Crohn's disease if recurrent or atypical perianal sepsis, young patient, or associated GI symptoms (diarrhoea, abdominal pain, weight loss)

High Yield Summary

Definition: Anorectal abscess = acute collection of pus in the perianal/perirectal tissue spaces; the acute phase of perianal sepsis (chronic phase = fistula-in-ano).

Aetiology: ~90% cryptoglandular infection. Secondary causes: Crohn's disease, TB, actinomycosis, foreign body, surgery, malignancy.

Anatomy: Anal glands sit in the intersphincteric plane, open at crypts of Morgagni (dentate line). Pus tracks along path of least resistance (Parks' theory) into perianal, intersphincteric, ischiorectal, or supralevator spaces.

Classification by frequency: Ischiorectal (60%) > Perianal (20%) > Intersphincteric (18%) > Supralevator (2%).

Clinical features: Pain (constant, throbbing, worse on sitting), swelling, drainage/discharge, constipation (pain avoidance), urinary difficulties (reflex retention). Signs: erythematous fluctuant tender mass, induration, fever, cellulitis.

Key exam pearls:

Intersphincteric abscess has NO visible external swelling — diagnosed on DRE.
Supralevator abscess may present with vague pelvic pain and systemic sepsis without perianal signs.
Pus C/ST: gut flora = fistula likely; skin flora = fistula unlikely.
Supralevator abscess drainage route depends on origin (intersphincteric → transanal; ischiorectal → buttock skin; pelvic → treat abdominal source).

Active Recall - Anorectal Abscess (Definition to Clinical Features)

1. What is the most common cause of anorectal abscess, and in which anatomical plane does the abscess initially form?

Your answer

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Cryptoglandular infection (~90%). Abscess initially forms in the intersphincteric plane (between IAS and EAS), where the anal gland bodies reside.

2. List the four types of anorectal abscess by anatomical location and their approximate frequencies.

Your answer

Show mark scheme

Ischiorectal (60%), Perianal (20%), Intersphincteric (18%), Supralevator (2%).

3. A patient presents with severe anorectal pain but no visible external perianal swelling. What type of abscess should you suspect, and how do you diagnose it?

Your answer

Show mark scheme

Intersphincteric abscess (or supralevator abscess). Diagnose by DRE (tender boggy mass in anal canal wall) or EUA +/- MRI pelvis.

4. Pus culture from an anorectal abscess grows E. coli and Bacteroides. What does this imply about fistula risk, and why?

Your answer

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Gut flora implies a communication (fistula) between the abscess and the bowel lumen (i.e., the internal opening at the crypt persists). High fistula risk. Skin flora only would suggest no internal communication and low fistula risk.

5. How should a supralevator abscess originating from an intersphincteric abscess be drained, and why?

Your answer

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Drain transanally (via internal sphincterotomy through the rectal wall). If drained through the ischiorectal fossa/buttock skin, it would create a track through the entire sphincter complex (extrasphincteric fistula), risking incontinence.

6. Why does anorectal abscess cause urinary difficulties?

Your answer

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Reflex urinary retention due to shared pudendal nerve innervation (S2-S4) of the EAS and external urethral sphincter. Severe perianal inflammation causes reflex spasm of the urethral sphincter. Mechanical obstruction from swelling may also contribute.

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p49–53) ^[2] Senior notes: felixlai.md (Anorectal abscess section) ^[3] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p49 — Etiology) ^[4] Senior notes: maxim.md (Anorectal abscess section)

Differential Diagnosis of Anorectal Abscess

When a patient presents with perianal pain, swelling, or discharge, you need a systematic differential diagnosis. The key is to think anatomically and pathophysiologically: What structures are in the perianal region, and what pathologies can affect them to produce a similar clinical picture?

The senior notes list three main differentials ^[2]:

Anorectal fistula
Internal haemorrhoid
Presacral epidermoid cyst

But in clinical practice (and for exams), the differential is broader. Let's work through it systematically, explaining why each condition mimics anorectal abscess and how to distinguish them.

Common anorectal conditions are mostly benign. Colorectal neoplasm needs to be excluded. Diagnosis can be usually made by careful history and examination. ^[1]

Approach to the Differential

The cardinal presenting features of anorectal abscess are:

Perianal pain (constant, throbbing)
Perianal swelling/mass
Discharge (purulent)
Systemic signs (fever)

The differential therefore covers conditions that present with one or more of these features. A useful way to organise this is by the dominant presenting complaint:

Differential Diagnoses — Detailed Comparison

1. Anorectal Fistula (Fistula-in-Ano)

This is the chronic phase of the same cryptoglandular process ^[2]^[5]. If a drained or spontaneously ruptured anorectal abscess leaves a persistent internal opening at the crypt, an epithelialised tract forms connecting the anal canal to the perianal skin.

Feature	Anorectal Abscess	Anorectal Fistula
Phase	Acute (active pus collection)	Chronic (persistent tract)
Pain	Constant, throbbing, severe	Intermittent — pain builds until pus discharges, then temporarily relieves ^[5]
Swelling	Fluctuant, tense mass	May have a small nodule at external opening
Discharge	Pus under pressure	Intermittent, malodorous purulent drainage ^[5]
Examination	Erythematous fluctuant tender mass	Palpable cord-like tract ^[5]; external opening appears as a dimple of granulation tissue that discharges on compression
Systemic signs	Fever, malaise common	Usually absent (unless superimposed abscess)
Timeline	Suspect fistula if anorectal abscess persists after 6–12 weeks ^[5]	Chronic, recurrent

Why it mimics abscess: A fistula can develop an acute exacerbation (the tract blocks, pus accumulates → essentially a recurrent abscess). The history of prior abscess drainage or recurrent perianal sepsis is the giveaway.

When to Suspect Fistula After Abscess Drainage

If perianal symptoms (discharge, intermittent pain) persist 6–12 weeks after abscess I&D, suspect a fistula-in-ano ^[5]. Send pus for C/ST at time of initial drainage — gut flora predicts fistula formation ^[4].

2. Thrombosed External Haemorrhoid (Perianal Haematoma)

Pathophysiology: An external haemorrhoid (venous plexus below the dentate line, covered by squamous epithelium) undergoes acute thrombosis → blood clot within the vein → sudden painful perianal lump
Why it mimics abscess: Acute onset of a painful perianal mass — just like a perianal abscess

Feature	Anorectal Abscess	Thrombosed External Haemorrhoid
Colour	Red, erythematous	Bluish/purple (visible clot through skin) ^[6]
Consistency	Fluctuant (fluid = pus)	Firm (solid = clot) — not fluctuant
Tenderness	Very tender, warm	Tender, but no warmth
Fever	Often present	Absent
Discharge	Purulent	None (unless spontaneous clot extrusion → dark blood)
Natural history	Does not resolve without drainage	Resolves spontaneously over 7–10 days → forms a skin tag ^[6]

Key distinguishing feature: The bluish discolouration and firm (non-fluctuant) consistency — because it contains clotted blood, not pus.

3. Thrombosed Prolapsed Internal Haemorrhoid

Pathophysiology: Grade III/IV internal haemorrhoid prolapses through the anal canal → becomes incarcerated (trapped by sphincter spasm) → venous congestion → thrombosis → acute pain and swelling
Why it mimics abscess: Acute painful perianal mass with swelling and oedema

Feature	Anorectal Abscess	Thrombosed Prolapsed Internal Haemorrhoid
History	May be first presentation	History of prolapsing haemorrhoids
Appearance	Erythematous fluctuant mass	Oedematous, congested, dark purple mass protruding from the anus; may be circumferential
Reducibility	N/A	Irreducible (incarcerated)
Mucosal folds	Absent	Radial mucosal folds visible (c.f. circular folds in rectal prolapse)
Fever	Common	Uncommon (unless secondary infection/gangrene)

4. Anal Fissure (Fissure-in-Ano)

Clinical features: pain on defaecation, fresh rectal bleeding. Diagnosis is by spreading the buttock to reveal the fissure. Rectal examination and proctoscopy are painful and not indicated. ^[1]

Pathophysiology: A tear in the anoderm distal to the dentate line → exposure of the internal sphincter beneath → sphincter spasm → ischaemia (especially posterior midline where blood supply is poorest) → impaired healing → chronic fissure ^[7]
Why it mimics abscess: Both cause severe perianal pain. An acutely inflamed chronic fissure with a sentinel skin tag can look like a small abscess.

Feature	Anorectal Abscess	Anal Fissure
Pain character	Constant, throbbing; not necessarily related to bowel movement ^[2]	Pain on defaecation — sharp, tearing, triggered by passing stool ^[1]^[7]
Bleeding	Purulent discharge, not typically blood	Fresh rectal bleeding — small amount on toilet paper/stool surface ^[1]^[7]
Examination	Fluctuant mass	Linear tear visible on spreading the buttocks; chronic fissure has sentinel pile + hypertrophied anal papilla
Swelling	Prominent	Absent (unless sentinel skin tag)
Fever	Common	Absent

Key distinguishing feature: Fissure pain is related to defaecation (tearing pain during bowel movement), while abscess pain is constant and independent of defaecation ^[2].

5. Pilonidal Sinus/Abscess

Pathophysiology: Infection and obstruction of a hair follicle in the natal cleft (intergluteal cleft) → foreign body reaction around hair → cavity formation → abscess ^[8]
"Pilonidal" = Latin: pilus = hair, nidus = nest → "nest of hair"
Why it mimics abscess: Presents as a painful, red, fluctuant mass in the sacrococcygeal/perianal region

Feature	Anorectal Abscess	Pilonidal Abscess
Location	At the anal verge or within the anal canal	Sacrococcygeal region / natal cleft — posterior and superior to the anus
Communication with anal canal	Yes (internal opening at crypt)	Does not continue into the anal canal ^[8]
Discharge	Purulent	Purulent, may contain hair
Risk factors	Cryptoglandular	Caucasian male, coarse dark body hair, prolonged sitting, increased sweating ^[8]
DRE	May reveal intersphincteric mass	Normal

Key distinguishing feature: Pilonidal sinus is located in the natal cleft, does not communicate with the anal canal, and may have visible hair protruding from the sinus opening.

6. Presacral Epidermoid Cyst (Dermoid Cyst)

This is a congenital cystic lesion in the presacral/retrorectal space, lined by squamous epithelium (hence "epidermoid" — epi- = upon, derm = skin, -oid = resembling). It can become secondarily infected, forming an abscess.

Feature	Anorectal Abscess	Presacral Epidermoid Cyst
Location	Perianal spaces	Presacral space (posterior to the rectum, anterior to the sacrum)
Age	Any age, peak 20–40	Often presents in young adults
Onset	Acute	Chronic mass, may become acutely painful if infected
DRE	Intersphincteric/ischiorectal mass	Smooth, well-defined posterior rectal mass on DRE
Imaging	Abscess with surrounding inflammation	Well-circumscribed cystic lesion on MRI, may have fat/calcification
Recurrence	After drainage → fistula	After drainage → recurs unless completely excised

Key distinguishing feature: A smooth, posterior rectal mass palpable on DRE, with cystic features on imaging, and no connection to the anal crypts.

7. Anal Carcinoma

Colorectal neoplasm needs to be excluded ^[1].

Pathophysiology: Malignant neoplasm of the anal canal — most commonly squamous cell carcinoma (80%), associated with HPV-16 & 18 ^[8]
Why it mimics abscess: Advanced tumours may undergo central necrosis → secondary abscess formation. Also presents with a painful anal mass and bleeding.

Feature	Anorectal Abscess	Anal Carcinoma
Age	20–40 years	Typically older (> 50), but can occur at any age
Pain	Acute, throbbing	Chronic, progressive
Mass	Fluctuant	Hard, fixed, irregular
Bleeding	Purulent discharge	Painful PR bleeding ^[8], may have mucoid or bloody discharge
Constitutional symptoms	Fever, malaise	Weight loss, anorexia
Lymphadenopathy	Absent	May have inguinal lymphadenopathy (if below dentate line → drains to inguinal nodes) ^[8]
Risk factors	Cryptoglandular	HPV, HIV, smoking, immunosuppression, Crohn's ^[8]

Key distinguishing feature: A hard, fixed, irregular mass that does not respond to antibiotics/drainage, especially in an older or immunocompromised patient. Always biopsy atypical or non-healing perianal lesions.

Red Flag — When to Suspect Malignancy

A perianal "abscess" that does not heal after adequate I&D, recurs repeatedly without an identifiable fistula, or is associated with a hard, irregular mass and weight loss should raise suspicion for anal carcinoma. Biopsy the abscess cavity wall at the time of drainage in any atypical case.

8. Perianal Crohn's Disease

Pathophysiology: Crohn's disease causes transmural inflammation → sinus tracts, fistulas, and abscesses as part of the fistulising phenotype. Perianal disease may be the first presentation of Crohn's in up to 10% of cases.
Why it mimics abscess: Can present with perianal abscess, fistula, or both

Feature	Simple Anorectal Abscess	Perianal Crohn's
Fistula pattern	Simple, usually single tract	Complex, multiple tracts, recurrent
Anal features	Single abscess	Multiple abscesses, multiple skin tags, anal fissures (often off-midline and painless — atypical) ^[7]
GI symptoms	Absent	Diarrhoea, abdominal pain, weight loss
Response to I&D	Usually curative	Recurs; requires immunosuppression (anti-TNF)
Histology	Acute suppuration	Non-caseating granulomas

9. Incarcerated Rectal Prolapse

A complete rectal prolapse that becomes irreducible and incarcerated — presents as a painful perianal/protruding mass
Distinguished by circular mucosal folds (vs. radial folds in prolapsed haemorrhoids) and the full-thickness nature of the prolapsing tissue ^[6]

10. Proctalgia Fugax

Benign, occur in young anxious men. Brief attacks of rectal pain at night, unrelated to defaecation. ^[8]
"Proctalgia" = proctos (Greek) = anus + algos = pain; "fugax" = fleeting
Distinguished from abscess by the episodic, brief, self-limiting nature with no physical findings on examination
No swelling, no discharge, no fever — examination is entirely normal between attacks

Summary Comparison Table

Condition	Pain Character	Mass	Discharge	Fever	Key Distinguishing Feature
Anorectal abscess	Constant, throbbing	Fluctuant, tender, red	Purulent	Yes	Fluctuant mass with erythema and systemic signs
Anorectal fistula	Intermittent, relieved by drainage	Cord-like tract	Intermittent, purulent	No	History of prior abscess; persistent discharge > 6–12 weeks
Thrombosed ext. haemorrhoid	Acute, at anal verge	Firm, bluish	None	No	Blue/purple firm lump (clot, not pus)
Anal fissure	On defaecation	No mass	Fresh blood	No	Pain related to defaecation; visible linear tear
Pilonidal abscess	Sacrococcygeal	Fluctuant, natal cleft	May contain hair	Possible	Located in natal cleft; no anal communication
Presacral cyst	Vague, deep	Smooth posterior mass on DRE	None (unless infected)	If infected	Well-circumscribed cystic lesion on MRI
Anal carcinoma	Chronic, progressive	Hard, fixed, irregular	Bloody/mucoid	No	Hard mass, inguinal LN, constitutional symptoms
Perianal Crohn's	Variable	Multiple abscesses, skin tags	Chronic discharge	Variable	Complex/multiple tracts, off-midline fissures, GI symptoms
Proctalgia fugax	Brief, nocturnal, episodic	None	None	No	Normal examination; fleeting pain

Diagnostic Approach to Differentiation

Investigations help in the diagnosis and assess the severity of disease, define anatomy of the pathological process (abscess and fistula), and exclude diseases in the proximal bowel and associated bowel problems (e.g. inflammatory bowel disease) ^[1].

Key Principles for DDx of Anorectal Abscess

Fluctuance = pus → Think abscess. Firm + blue → Think thrombosed haemorrhoid. Hard + fixed → Think malignancy.
Pain on defaecation → Think fissure. Constant pain independent of defaecation → Think abscess.
Natal cleft without anal communication → Think pilonidal sinus.
Recurrent, complex, atypical → Think Crohn's disease, TB, or malignancy — biopsy and scope.
Always exclude colorectal neoplasm ^[1] — especially in older patients or atypical presentations.

Active Recall - Differential Diagnosis of Anorectal Abscess

1. A patient presents with an acute painful perianal mass that is firm, non-fluctuant, and has a bluish discolouration. What is the most likely diagnosis and why?

Your answer

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Thrombosed external haemorrhoid (perianal haematoma). The bluish colour is due to clotted blood visible through the skin; it is firm (solid clot) rather than fluctuant (liquid pus). No fever or purulent discharge expected.

2. Name three features that differentiate anal fissure pain from anorectal abscess pain.

Your answer

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1) Fissure pain is triggered by defaecation (tearing on passage of stool); abscess pain is constant and independent of defaecation. 2) Fissure has fresh rectal bleeding on toilet paper; abscess has purulent discharge. 3) Fissure has a visible linear tear on spreading buttocks; abscess has a fluctuant mass.

3. A patient has recurrent perianal abscesses with multiple complex fistula tracts and off-midline anal fissures. What underlying condition should you suspect, and what investigations would you perform?

Your answer

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Crohn's disease (perianal Crohn's). Investigations: colonoscopy with biopsies (look for non-caseating granulomas, skip lesions), MRI pelvis (map fistula tracts), inflammatory markers (CRP/ESR), and consider anti-TNF therapy.

4. How do you distinguish a pilonidal abscess from an anorectal abscess on examination?

Your answer

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Pilonidal abscess is located in the natal cleft/sacrococcygeal region (posterior and superior to the anus), does NOT communicate with the anal canal, and may have visible hair in the sinus opening. Anorectal abscess is at the anal verge or within the anal canal and has an internal opening at the dentate line.

5. When should you suspect anal carcinoma rather than a simple anorectal abscess?

Your answer

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Suspect malignancy if: hard, fixed, irregular mass (not fluctuant); does not heal after adequate I&D; recurrent without identifiable fistula; associated with weight loss, inguinal lymphadenopathy, or chronic progressive pain. Risk factors include HPV, HIV, smoking, immunosuppression. Always biopsy atypical or non-healing perianal lesions.

6. What is proctalgia fugax and how does it differ from anorectal abscess?

Your answer

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Proctalgia fugax is a benign condition of brief, episodic rectal pain (typically nocturnal, in young anxious men), unrelated to defaecation, with completely normal examination between attacks. Anorectal abscess has constant pain with physical findings (fluctuant mass, erythema, fever). Proctalgia fugax has no swelling, discharge, or fever.

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p13, p46, p50, p77) ^[2] Senior notes: felixlai.md (Anorectal abscess — Clinical manifestation, Differential diagnosis) ^[4] Senior notes: maxim.md (Anorectal abscess) ^[5] Senior notes: maxim.md (Anal fistula); felixlai.md (Anorectal fistulas) ^[6] Senior notes: maxim.md (Acute painful anal mass — Differential diagnosis) ^[7] Senior notes: felixlai.md (Anal fissures) ^[8] Senior notes: maxim.md (Pilonidal sinus; Proctalgia fugax; Anal carcinoma)

Diagnostic Criteria, Diagnostic Algorithm & Investigation Modalities

1. Diagnostic Criteria

Anorectal abscess does not have formal diagnostic criteria in the way that, say, rheumatoid arthritis or SLE does. It is fundamentally a clinical diagnosis — you diagnose it by recognising the characteristic history and examination findings ^[1]^[2]^[4]. That said, we can define what constitutes a positive diagnosis:

1.1 Clinical Diagnostic Criteria (Practical Framework)

A diagnosis of anorectal abscess is made when ALL of the following are present:

Criterion	Explanation
1. Compatible symptoms	Pain (constant, throbbing, perianal/anorectal), ± swelling, ± drainage, ± constipation, ± urinary difficulties ^[1]
2. Compatible signs on examination	Erythematous, fluctuant, tender mass on inspection and/or DRE ^[4]; or a tender boggy mass palpable within the anal canal (intersphincteric) or above the anorectal ring (supralevator)
3. Collection of pus confirmed	Either by clinical fluctuance, aspiration of pus, imaging (MRI/CT/EUS showing a fluid collection), or at the time of incision and drainage

For superficial abscesses (perianal, most ischiorectal): the diagnosis is almost entirely clinical — you see it, you feel it, you drain it. No imaging is typically needed.

For deep-seated abscesses (intersphincteric, supralevator): the diagnosis may require additional investigation because there are no visible external signs — you rely on DRE findings and imaging.

Key Principle: Anorectal Abscess is a Clinical Diagnosis

Diagnosis can be usually made by careful history and examination ^[1]. The overwhelming majority of perianal and ischiorectal abscesses are diagnosed at the bedside. Reserve imaging (MRI, CT, EUS) for cases where the abscess is not palpable, is deep-seated, is recurrent, or when you suspect complex pathology (Crohn's, fistula, malignancy) ^[2].

1.2 When to Suspect an Anorectal Abscess (Clinical Triggers)

Think of this as the "screening criteria" — features that should make you actively look for an anorectal abscess:

Any patient with constant perianal pain, especially if worsened by sitting and not relieved by defaecation
Any patient with perianal swelling, redness, or warmth
Any patient with fever of unknown origin + perianal symptoms (even vague rectal discomfort) — especially if immunocompromised
Any patient with unexplained urinary retention + perianal/rectal pain
Immunocompromised patients (DM, HIV, chemotherapy, neutropaenia) with perianal symptoms — low threshold for imaging, as clinical signs may be attenuated (reduced inflammatory response → less erythema, less fluctuance, yet the abscess may be large)

Immunocompromised Patients — Beware

In neutropaenic or severely immunosuppressed patients, the classical signs of abscess (erythema, fluctuance, warmth) may be absent or minimal because the inflammatory response is blunted. These patients may present only with vague perianal pain and fever. Maintain a very low threshold for imaging (MRI pelvis) and examination under anaesthesia (EUA). Delayed diagnosis → necrotising soft tissue infection → mortality.

2. Diagnostic Algorithm

The algorithm follows a systematic approach: History → Examination → Bedside assessment → Targeted investigations → Definitive management. The branching points depend on whether the abscess is clinically obvious or occult.

The algorithm emphasises that most anorectal abscesses are diagnosed clinically and treated surgically without delay. Investigations are reserved for deep, occult, recurrent, or atypical cases. The mantra is: "If there is pus, let it out" — do not delay drainage waiting for imaging in an obvious abscess.

3. Investigation Modalities

Investigations serve three distinct purposes ^[1]:

Help in the diagnosis and assess the severity of disease
Define anatomy of the pathological process (abscess and fistula)
Exclude diseases in the proximal bowel and associated bowel problems (e.g. inflammatory bowel disease)

Let us organise investigations into bedside, laboratory, imaging, and endoscopic/procedural, explaining why each is done, what you expect to find, and how to interpret the results.

3.1 Bedside Investigations

Investigation	Purpose	Key Findings & Interpretation
Inspection of perianal region	Identify superficial abscess, external fistula openings, skin tags, fissures, scars	Erythematous, fluctuant, tender swelling at anal verge = perianal abscess. Diffuse buttock swelling/induration = ischiorectal abscess. Dimple of granulation tissue with discharge = external fistula opening.
Digital Rectal Examination (DRE)	Assess for deep abscess (intersphincteric, supralevator); evaluate sphincter tone; palpate for masses	Abscess can be felt in DRE if there is no findings on physical inspection ^[2]. Tender boggy mass in the anal canal wall = intersphincteric abscess. Tender fullness above the anorectal ring = supralevator abscess. Hard, fixed, irregular mass = suspect malignancy. Reduced sphincter tone may indicate prior surgery or neurological cause.
Proctoscopy / Anoscopy	Visualise the anal canal mucosa; identify inflamed crypt (internal opening); rule out co-existing pathology (haemorrhoids, fissure, tumour)	Inflamed, oedematous crypt at the dentate line = probable source. Purulent discharge from a crypt on gentle compression = confirms internal opening. May be too painful to perform in the acute setting → defer to EUA.
Assessment of vital signs	Detect systemic sepsis	Tachycardia, fever ( > 38°C), hypotension → suggests significant infection; may need resuscitation before theatre. In severe cases, consider Fournier's gangrene (necrotising fasciitis).

DRE — The Most Important Bedside Investigation

Never skip the DRE. An intersphincteric abscess is diagnosed only by DRE (or EUA) — it has no external signs. A supralevator abscess may also be first detected as a tender fullness on DRE. If the patient is in too much pain for bedside DRE, this itself is a strong indication for EUA in theatre.

3.2 Laboratory Investigations

Investigation	Purpose	Key Findings & Interpretation
Full blood count (CBC/FBC)	Assess for infection and its severity	Leucocytosis with neutrophilia = active bacterial infection. The WCC magnitude correlates loosely with severity. Neutropaenia in a chemotherapy patient = high risk of atypical presentation and fulminant sepsis — very low threshold for aggressive management.
C-reactive protein (CRP)	Quantify systemic inflammatory response; monitor response to treatment	Elevated CRP ( > 10 mg/L) supports active infection. Very high CRP ( > 100) raises concern for deep-seated collection or necrotising infection. Useful for serial monitoring after drainage — should trend downward.
Blood glucose / HbA1c	Screen for diabetes mellitus	Elevated glucose/HbA1c = previously undiagnosed or poorly controlled DM — a major risk factor for complicated perianal sepsis, poor wound healing, and necrotising fasciitis. Optimise glycaemic control perioperatively.
Blood cultures	Identify bacteraemia in systemically septic patients	Obtain before starting antibiotics if fever > 38°C, rigors, tachycardia, or hypotension. Positive blood cultures guide targeted antibiotic therapy. Most common isolates: E. coli, Bacteroides fragilis, Enterococcus.
Pus culture and sensitivity (C/ST)	Identify causative organisms; predict fistula risk	Culture shows skin flora: no fistula → reassurance. Culture shows gut flora: likely with fistula → treat as fistula after acute state ^[4]. Always send at time of I&D. Gut flora (E. coli, Bacteroides, Enterococcus) = internal communication with bowel lumen = high fistula risk (~50%). Skin flora only (Staph. aureus, Streptococcus) = no internal communication = low fistula risk. AFB positive = TB — send for culture (takes 6–8 weeks). Sulfur granules = Actinomycosis.
Pus for AFB stain + TB culture	Exclude tuberculosis (especially in Hong Kong)	Indicated if: non-healing abscess, caseous material, chronic/recurrent perianal sepsis, patient from TB-endemic area. AFB positive on Ziehl-Neelsen stain = TB. Culture on Löwenstein-Jensen medium takes 6–8 weeks but is definitive. Consider TB-PCR (GeneXpert) for rapid result.
Tissue biopsy (abscess wall)	Exclude Crohn's disease, TB, malignancy	Sent at time of I&D if atypical features. Non-caseating granulomas = Crohn's. Caseating granulomas = TB. Dysplasia/malignant cells = anal carcinoma. Sulfur granules with filamentous organisms = Actinomycosis.
HIV test	Screen for immunodeficiency	Consider in: recurrent perianal sepsis, atypical organisms, young patient with risk factors. HIV increases risk of perianal sepsis, atypical infections, and poor healing.
Inflammatory markers for IBD	Screen for Crohn's disease if suspected	Faecal calprotectin ( > 250 μg/g suggests active bowel inflammation); CRP/ESR elevated; ASCA positive (anti-Saccharomyces cerevisiae antibodies — more specific for Crohn's). These are adjuncts — definitive diagnosis requires colonoscopy + biopsy.

Pus C/ST — The Underappreciated Investigation

Many students forget the clinical significance of pus microbiology. It is not just about choosing the right antibiotic — the type of organism predicts fistula formation. Gut flora = fistula likely → plan for follow-up and possible fistula surgery. Skin flora = fistula unlikely → reassurance. This directly changes your management and counselling of the patient ^[4].

3.3 Imaging Investigations

Modality	Indication	Key Findings & Interpretation	Advantages & Limitations
MRI Pelvis	Non-palpable abscess ^[2]; deep-seated abscess (intersphincteric, supralevator); recurrent abscess; suspected complex fistula; perianal Crohn's disease	T2-weighted / STIR sequences: abscess appears as a high-signal (bright) fluid collection with surrounding oedema and rim enhancement on post-gadolinium T1. Fistula tracts appear as linear high-signal tracks on T2. Accurately maps the relationship of abscess/fistula to the sphincter complex and levator ani. Can identify occult secondary tracts and horseshoe extensions not apparent clinically.	Gold standard for perianal sepsis imaging. Excellent soft tissue resolution. Non-invasive. No radiation. Limitations: Expensive, time-consuming, may require sedation (claustrophobia), not universally available for emergency use.
Endoanal Ultrasound (EUS)	Alternative to MRI; can be performed in clinic or theatre; particularly useful for intersphincteric abscess	Abscess appears as a hypoechoic (dark) fluid collection. Can delineate the IAS, EAS, and intersphincteric plane with high resolution. Fistula tracts appear as hypoechoic linear tracks. Internal opening may be identified.	Good for imaging the sphincter complex and intersphincteric plane. Limitations: Operator-dependent; limited field of view (cannot assess supralevator space as well as MRI); may be painful in the acute setting.
CT Pelvis	If MRI unavailable; suspected supralevator abscess from intra-abdominal source (e.g., diverticular abscess, appendiceal abscess tracking down); to exclude pelvic pathology	Abscess appears as a rim-enhancing hypodense fluid collection with surrounding fat stranding. Can identify gas within the collection (concerning for gas-forming organisms / necrotising infection). Can assess the abdomen/pelvis simultaneously.	Fast acquisition (good for acutely unwell patients). Widely available. Good for excluding intra-abdominal sources. Limitations: Less soft tissue resolution than MRI for the sphincter complex and fistula tracts; radiation exposure; not first-line for perianal imaging.
Fistulography	Rarely used now; historical test for mapping fistula tracts	Contrast injected through external fistula opening → radiograph shows the tract.	Largely superseded by MRI which is non-invasive and provides superior anatomical detail. May still have a role in selected cases.

CT/MRI scan indicated in a non-palpable abscess ^[2]. Think of imaging as reserved for when your clinical examination cannot adequately define the problem.

3.4 Endoscopic & Procedural Investigations

Investigation	Indication	Key Findings & Interpretation
Examination Under Anaesthesia (EUA)	When bedside examination is too painful; to fully assess abscess extent; to probe for fistula tracts at time of I&D; to assess complex or recurrent perianal sepsis	The definitive investigation for anorectal abscess. Under GA/regional anaesthesia, the surgeon can: inspect the perianal region and anal canal thoroughly; perform DRE and proctoscopy without pain; incise and drain the abscess; probe the cavity to identify internal opening and fistula tracts (with caution — avoid creating false passages); assess sphincter integrity. EUA is both diagnostic and therapeutic.
Proctoscopy / Rigid Sigmoidoscopy	Visualise the anal canal and lower rectum; identify internal opening; exclude mucosal pathology	Inflamed crypt at dentate line (source). Purulent discharge from crypt on compression (internal opening identified). Mucosal ulceration, oedema, or nodularity may suggest IBD or malignancy.
Flexible Sigmoidoscopy / Colonoscopy	Exclude diseases in the proximal bowel and associated bowel problems (e.g. inflammatory bowel disease) ^[1]	Indicated when: recurrent/atypical perianal sepsis, young patient with GI symptoms (diarrhoea, abdominal pain, weight loss), suspicion of Crohn's disease, or to exclude colorectal malignancy. Findings in Crohn's: skip lesions, aphthous ulcers, cobblestoning, strictures, non-caseating granulomas on biopsy. Findings in malignancy: mass, ulcerated lesion, obstruction.
Fistula probing (at EUA)	Identify the course and complexity of an associated fistula	A malleable probe is gently passed through the external opening → follows the tract → emerges at the internal opening. Identifies the internal opening (usually at the dentate line at the site of the infected crypt). Determines if the fistula is simple (intersphincteric/low transsphincteric — < 30% EAS involvement) or complex (high transsphincteric, suprasphincteric, extrasphincteric, multiple tracts, Crohn's-related). Perform with extreme caution to avoid creating a false passage ^[5].
Goodsall's rule application (at EUA)	Predict the location of the internal opening based on the position of the external opening	Goodsall's rule: External opening anterior to the transverse anal line → fistula tract runs in a straight radial line to the nearest crypt (internal opening directly opposite). External opening posterior to the transverse anal line → tract curves to the posterior midline crypt (internal opening at 6 o'clock in lithotomy position). Exceptions: anterior external openings > 3 cm from the anal verge may still curve posteriorly. Crohn's fistulas often do not follow this rule.

Goodsall's Rule — A Useful but Imperfect Guide

Goodsall's rule helps predict where the internal opening of a fistula is located, which is critical for surgical planning. However, it is a guideline, not a law. Complex fistulas (especially Crohn's-related) frequently violate this rule. MRI is superior for mapping complex tracts.

3.5 Summary of Investigations — When and Why

Clinical Scenario	Investigations Needed	Rationale
Obvious perianal/ischiorectal abscess, first episode, otherwise healthy	FBC, CRP, blood glucose; pus C/ST at I&D; EUA for drainage and fistula assessment	Straightforward case — clinical diagnosis, surgical treatment, send pus to predict fistula risk
Deep abscess suspected (no external signs, severe pain)	As above + MRI pelvis (or EUS) before or concurrent with EUA	MRI indicated in a non-palpable abscess ^[2] — define anatomy before choosing drainage route (especially supralevator)
Recurrent perianal abscess	As above + MRI pelvis + colonoscopy + biopsy of abscess wall + AFB stain + HIV test	Exclude diseases in proximal bowel ^[1] — specifically Crohn's disease and TB; HIV testing for immunodeficiency
Immunocompromised patient (DM, HIV, neutropaenia)	As above + blood cultures + low threshold for MRI + aggressive monitoring	Attenuated clinical signs; higher risk of necrotising infection; blood cultures essential as bacteraemia more likely
Suspected Crohn's-related perianal sepsis	MRI pelvis + colonoscopy with biopsies + inflammatory markers (faecal calprotectin, CRP) + EUA	Crohn's perianal disease requires combined medical (anti-TNF) and surgical management; MRI maps complex fistula anatomy
Atypical/non-healing abscess — malignancy suspected	Biopsy of abscess cavity wall + MRI pelvis + colonoscopy + inguinal LN assessment (USS ± FNA)	Exclude anal carcinoma or rectal carcinoma with secondary abscess

4. Interpretation Framework — Putting It All Together

When you receive investigation results, interpret them systematically:

Finding	Interpretation	Next Step
Pus C/ST: gut flora	Internal communication with bowel → fistula likely ^[4]	Plan follow-up at 6–12 weeks; if persistent discharge → MRI + EUA for fistula assessment
Pus C/ST: skin flora only	No internal communication → fistula unlikely ^[4]	Reassurance; routine wound follow-up
Pus AFB positive	Tuberculosis	Start anti-TB therapy (RIPE regimen); tissue biopsy for confirmation; check CXR and sputum
Biopsy: non-caseating granulomas	Crohn's disease	Colonoscopy; gastroenterology referral; consider anti-TNF therapy
Biopsy: caseating granulomas	Tuberculosis	Anti-TB therapy
Biopsy: dysplasia/malignant cells	Anal carcinoma	Staging (MRI pelvis, CT TAP); MDT discussion; chemoradiation
MRI: rim-enhancing collection in intersphincteric plane	Intersphincteric abscess	Drain transanally at EUA
MRI: collection above levator ani	Supralevator abscess — determine origin	If from intersphincteric extension → drain transanally. If from ischiorectal extension → drain via buttock skin. If from pelvic source → treat abdominal pathology.
MRI: complex branching tracts with multiple collections	Complex fistula (likely Crohn's or recurrent cryptoglandular)	Seton drainage; consider anti-TNF if Crohn's; staged surgical approach
Blood cultures positive	Bacteraemia/sepsis	Targeted IV antibiotics based on sensitivities; ensure adequate source control (drainage)
HbA1c > 6.5% / Blood glucose elevated	Diabetes mellitus	Glycaemic optimisation; higher risk of wound complications — closer follow-up
Leucopaenia/neutropaenia	Immunosuppressed — attenuated clinical signs	Low threshold for imaging and EUA; broad-spectrum antibiotics; close monitoring

High Yield Summary — Diagnosis of Anorectal Abscess

1. Clinical diagnosis is the cornerstone. Most perianal and ischiorectal abscesses are diagnosed by history (constant perianal pain, swelling, discharge) and examination (erythematous fluctuant tender mass).

2. DRE is essential. An intersphincteric abscess has no visible external signs — only DRE (tender boggy mass in anal canal wall) can detect it. Supralevator abscess may also be detected as tenderness above the anorectal ring.

3. Imaging (MRI gold standard) is reserved for: non-palpable abscess, deep-seated abscess, recurrent abscess, suspected complex fistula, and Crohn's disease.

4. Always send pus C/ST at I&D. Gut flora = fistula likely; skin flora = fistula unlikely.

5. Investigate for underlying cause if atypical: Crohn's (colonoscopy), TB (AFB stain), malignancy (biopsy), HIV (serology).

6. Three purposes of investigations: (i) diagnose and assess severity, (ii) define anatomy, (iii) exclude proximal bowel disease.

Active Recall - Diagnosis of Anorectal Abscess

1. What are the three stated purposes of investigations in anorectal abscess according to the lecture slides?

Your answer

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1) Help in the diagnosis and assess the severity of disease. 2) Define anatomy of the pathological process (abscess and fistula). 3) Exclude diseases in the proximal bowel and associated bowel problems (e.g. inflammatory bowel disease).

2. Pus C/ST from an anorectal abscess grows Staphylococcus aureus only. What does this imply, and what do you tell the patient?

Your answer

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Skin flora only — suggests no internal communication with the bowel lumen. Fistula is unlikely. Reassure the patient that the abscess is likely superficial without a fistula tract, but advise to return if symptoms of persistent discharge develop.

3. When is MRI pelvis indicated in the workup of anorectal abscess? Name at least 4 indications.

Your answer

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1) Non-palpable/deep-seated abscess (intersphincteric or supralevator). 2) Recurrent abscess. 3) Suspected complex fistula. 4) Suspected perianal Crohn's disease. 5) To define anatomy of supralevator abscess before choosing drainage route. 6) Atypical presentation or non-healing abscess.

4. Describe Goodsall's rule and its clinical application.

Your answer

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Goodsall's rule predicts the internal opening of a fistula based on the external opening position. External opening ANTERIOR to the transverse anal line: fistula runs in a straight radial line to the nearest crypt. External opening POSTERIOR to the transverse anal line: tract curves to the posterior midline crypt (6 o'clock in lithotomy). Exception: anterior openings >3 cm from anal verge may curve posteriorly. Crohn's fistulas often violate this rule.

5. A patient with severe anorectal pain has no visible perianal swelling. DRE reveals a tender boggy area in the right lateral anal canal wall. What is the diagnosis, and what investigation would you perform next?

Your answer

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Intersphincteric abscess. Next step: Examination Under Anaesthesia (EUA) for definitive assessment and transanal drainage (internal sphincterotomy). MRI pelvis may be performed if available prior to EUA to map the collection, but should not delay surgical drainage.

6. What investigation findings on abscess wall biopsy would suggest: a) Crohn's disease, b) Tuberculosis, c) Anal carcinoma?

Your answer

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a) Non-caseating granulomas = Crohn's disease. b) Caseating granulomas (with or without AFB positive on stain) = Tuberculosis. c) Dysplastic or malignant cells (squamous cell carcinoma most common) = Anal carcinoma.

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p13, p50, p77) ^[2] Senior notes: felixlai.md (Anorectal abscess — Diagnosis) ^[4] Senior notes: maxim.md (Anorectal abscess — Pus C/ST interpretation) ^[5] Senior notes: felixlai.md (Anorectal fistulas — Diagnosis, EUA and fistula probing)

Management of Anorectal Abscess

1. Fundamental Principles

The management of anorectal abscess rests on a single, non-negotiable principle:

"If there is pus, let it out." Surgical drainage is the definitive treatment. An anorectal abscess will NOT resolve with antibiotics alone.

This is because an abscess is a walled-off collection of pus — antibiotics cannot penetrate the avascular abscess cavity in sufficient concentration to sterilise it. The cavity must be physically opened and drained to allow the immune system (and any antibiotics, if indicated) to clear the infection. The wound is then left open to heal by secondary intention (from the base upward), which prevents premature closure of the skin over an undrained cavity (which would lead to recurrence).

Treatment: incision and drainage of abscess ^[1].

2. Management Algorithm

3. Treatment Modalities

3.1 Surgical Management — Incision and Drainage (I&D)

This is the mainstay of treatment for ALL anorectal abscesses ^[1]^[4].

General Principles of I&D

Aspect	Details	Rationale
Setting	Operating theatre (preferred) or bedside (for small, superficial perianal abscesses in cooperative patients)	Theatre allows GA/regional anaesthesia for thorough drainage + EUA for fistula assessment
Anaesthesia	General anaesthesia (GA) or spinal/regional anaesthesia; local anaesthesia (LA) only for small superficial perianal abscess	Deep abscesses and EUA require adequate relaxation; LA is often insufficient and painful
Position	Prone jackknife or lithotomy	Provides optimal exposure of the perianal region
Incision	Cruciate or elliptical incision over the point of maximal fluctuance; excise a disc of skin (de-roofing)	An elliptical excision or cruciate incision prevents premature skin closure → the wound must drain from the base upward
Cavity exploration	Break all loculations digitally; irrigate with saline	Ensures complete evacuation of pus; undrained loculations = recurrence
Wound	Left open — heal by secondary intention ^[4]	Primary closure would trap residual infection → recurrence/re-accumulation
Packing	Wound may be lightly packed initially (alginate or ribbon gauze) to maintain patency; gradually reduced	Prevents premature skin closure; however, excessive tight packing is painful and counterproductive
Specimens	Pus for C/ST ^[4]; ± tissue biopsy of abscess wall if atypical	Culture guides antibiotic choice and predicts fistula risk; biopsy excludes Crohn's/TB/malignancy

Site-Specific Drainage Approach

This is critical — the wrong drainage approach can create an iatrogenic fistula that is worse than the original disease.

Abscess Type	Drainage Approach	Why This Approach?
Perianal	Skin incision ^[4] — cruciate/elliptical incision over the fluctuant area at the anal verge	The abscess is subcutaneous and superficial → direct skin incision is all that is needed. Make the incision as close to the anal verge as possible to minimise the length of any potential fistula tract.
Ischiorectal	Buttock skin incision → drain as close to sphincter complex as possible ^[4]	The abscess is in the ischiorectal fossa, lateral to the EAS. Incision is made in the buttock/perianal skin overlying the abscess. Draining as close to the sphincter as possible minimises the length of a potential fistula tract (a shorter tract is easier to manage surgically later).
Intersphincteric	Rectal incision (internal sphincterotomy) → drain transanally ^[4]	The abscess lies between the IAS and EAS. If you drain this through the perianal skin (outward through the EAS), you would create a transsphincteric or even extrasphincteric fistula — a surgical nightmare. Instead, you drain inward through the rectal mucosa and IAS (internal sphincterotomy) → the pus drains into the anal canal → no sphincter damage.
Supralevator (from intersphincteric extension)	Drain transanally ^[4]	Same logic — if you drain through the ischiorectal fossa/skin, the tract would traverse the entire sphincter complex + levator ani → extrasphincteric fistula. Transanal drainage keeps the tract within the intersphincteric plane.
Supralevator (from ischiorectal extension)	Drain via buttock skin (through ischiorectal fossa) ^[4]	The pus has already tracked through the EAS into the ischiorectal fossa and then extended upward. Draining back through the same route (ischiorectal fossa → skin) follows the existing path without creating new sphincter damage.
Supralevator (from pelvic/abdominal source)	Treat the primary abdominal pathology (e.g., CT-guided drainage of pelvic abscess; surgery for diverticular disease, appendicitis)	The perianal component is secondary — addressing it alone without treating the source leads to failure.
Horseshoe abscess	Drain both ischiorectal fossae + counter-drain the deep postanal space (modified Hanley procedure)	The horseshoe abscess connects via the deep postanal space — you must drain all three compartments (bilateral ischiorectal fossae + postanal space) for complete source control.

The Cardinal Rule of Supralevator Abscess Drainage

Determine the origin BEFORE choosing the drainage route. Draining a supralevator abscess via the wrong route creates an extrasphincteric fistula — the most devastating iatrogenic complication. Intersphincteric origin → transanal. Ischiorectal origin → through buttock skin. Pelvic origin → treat the abdomen. When in doubt, get an MRI pelvis before draining ^[4].

Primary Fistulotomy at Time of Abscess Drainage

?Primary fistulotomy ^[1] — the lecture slide deliberately includes a question mark, reflecting ongoing debate.

Aspect	Details
Concept	At the time of I&D, if a fistula tract is identified (by gentle probing), the surgeon may choose to lay open the tract simultaneously — this is "primary fistulotomy"
Rationale for	Treats the source (infected crypt) at the same time as draining the abscess → lower recurrence rate (reduces need for a second operation); studies show recurrence drops from ~30–50% (I&D alone) to ~5–10% (I&D + primary fistulotomy)
Rationale against	Risk of faecal incontinence if a significant portion of the EAS is divided; may create a false passage if probing is too aggressive; the fistula may not be clearly delineated in the acute inflamed state
Current consensus	Primary fistulotomy is appropriate only for simple, low fistulas (intersphincteric or low transsphincteric involving < 30% of EAS) identified at the time of drainage, performed by an experienced surgeon. It should NOT be performed for complex fistulas, high fistulas, or in Crohn's disease.

Fistulotomy/fistulectomy for simple low fistula. Risk of incontinence should be informed. ^[9]

3.2 Medical Management — Antibiotics

The role of antibiotics is adjunctive, not primary. Drainage is always the definitive treatment. Antibiotics alone cannot cure an abscess.

Little role for antibiotics except in patients with severe cellulitis, valvular heart disease, prosthetic heart valves and immunosuppression ^[1].

Indication for Antibiotics	Rationale	Regimen
Severe surrounding cellulitis ^[1]	Cellulitis = spreading soft tissue infection beyond the abscess cavity → antibiotics needed to control tissue-level infection that surgery alone cannot address	IV — Amoxicillin-clavulanate (Augmentin) 1.2g TDS, or Ceftriaxone + Metronidazole; step down to oral when improving
Valvular heart disease / Prosthetic heart valves ^[1]	Bacteraemia during I&D → risk of infective endocarditis (bacteria seeding damaged/prosthetic valves)	Antibiotic prophylaxis before procedure as per local endocarditis prophylaxis guidelines
Immunosuppression ^[1]^[4]	Impaired immune response → inability to contain infection after drainage; risk of fulminant sepsis. Includes: diabetes mellitus ^[4], HIV/AIDS, chemotherapy-induced neutropaenia, chronic corticosteroid use, organ transplant recipients	Broad-spectrum IV antibiotics covering gram-negatives and anaerobes (e.g., Piperacillin-tazobactam, or Ceftriaxone + Metronidazole); adjust based on C/ST results
Systemic sepsis	Fever, tachycardia, hypotension → bacteraemia/sepsis → antibiotics essential alongside surgical source control	Blood cultures → empirical broad-spectrum IV antibiotics → de-escalate based on sensitivities
Necrotising fasciitis (Fournier's gangrene)	Life-threatening emergency → aggressive antibiotics + emergency surgical debridement	Triple therapy: Meropenem (or Pip-Taz) + Vancomycin + Clindamycin (for toxin suppression); or per local protocol

When NOT to Give Antibiotics

A straightforward perianal or ischiorectal abscess in an otherwise healthy patient with no cellulitis does not need antibiotics. Drainage alone is curative. Unnecessary antibiotics expose the patient to side effects (C. difficile colitis, antibiotic resistance, allergic reactions) without benefit. The lecture slides specifically state little role for antibiotics except in the defined indications ^[1].

Antibiotic Choice — Principles:

Must cover gram-negative bacilli (E. coli, Klebsiella) and anaerobes (Bacteroides fragilis) — these are the dominant gut flora causing cryptoglandular abscesses
Common regimens:
- IV: Amoxicillin-clavulanate (Augmentin) 1.2g TDS; or Ceftriaxone 2g daily + Metronidazole 500mg TDS
- Oral step-down: Amoxicillin-clavulanate 625mg TDS; or Ciprofloxacin 500mg BD + Metronidazole 400mg TDS
Adjust based on C/ST results once available

3.3 Management of Associated Fistula

About 30–50% of anorectal abscesses will develop a fistula-in-ano. The management of the fistula is a separate (often staged) process after the acute abscess has been drained and the inflammation has settled.

Simple Fistula

Fistulotomy/fistulectomy for simple low fistula ^[9]:

Fistulotomy: Probe inserted from external to internal opening → all tissue overlying the probe is divided → tract is laid open to heal by secondary intention ± marsupialization (suturing the wound edges to the tract edges to speed healing) ^[10]
Indications: Simple fistula — Parks Type 1 (intersphincteric) or Type 2 (low transsphincteric involving < 30% of EAS) ^[10]
Risk of incontinence should be informed ^[9] — dividing sphincter muscle can impair continence

Complex Fistula

Complicated high fistula or transsphincteric fistula with significant amount of muscle involvement ^[9] — these require sphincter-sparing procedures because simple fistulotomy would divide too much sphincter muscle → incontinence.

Procedure	Mechanism	Indication
Seton (staged procedure) ^[9]^[10]	A loose (draining) seton (silastic vessel loop) is threaded through the fistula tract and left in place for ~6 weeks ^[10]. It keeps the tract open → prevents re-accumulation of pus → allows inflammation to settle. A cutting seton is gradually tightened to slowly cut through the sphincter while fibrosis occurs behind it (prevents gaping incontinence).	Complex/high fistula; first step before definitive sphincter-sparing surgery; also used in Crohn's perianal disease ^[10]^[11]
Endorectal advancement flap ^[9]^[10]	The internal opening is excised → a flap of rectal mucosa, submucosa, and circular muscle is advanced downward to cover the internal opening → the fistula tract heals with no internal communication	High transsphincteric, suprasphincteric fistulas ^[10]
Ligation of Intersphincteric Fistula Tract (LIFT) ^[9]^[10]	The fistula tract is identified in the intersphincteric plane → ligated and divided → both ends seal off. "LIFT" = you're literally lifting the tract out of the intersphincteric groove and tying it off.	High transsphincteric fistula, especially where internal opening is distal to the dentate line ^[10]
Anal fistula plug ^[9]	A bioabsorbable plug (e.g., collagen matrix) is inserted into the fistula tract from the internal opening → scaffold for tissue ingrowth → tract closure	High fistula; variable success rates (30–60%)
Fibrin sealant ^[10]	Fibrin glue injected into the tract → promotes healing by obliterating the dead space	Simple or complex fistula; low success rates (~15–40%) but minimal morbidity
Video-Assisted Anal Fistula Treatment (VAAFT) ^[12]	A fistuloscope is inserted into the tract → direct visualisation → electrocautery ablation of the tract lining from within → internal opening closed with a flap or stapler	Sphincter-sparing; newer technique
FiLaC (Fistula tract Laser Closure) ^[12]	Laser fibre inserted into the tract → thermal energy destroys the tract epithelium → promotes closure	Sphincter-sparing; newer technique
Permacol paste injection ^[12]	Acellular porcine dermal collagen paste injected into the tract → scaffold for tissue ingrowth	Experimental; newer technique
Stem cell treatment ^[12]	Mesenchymal stem cells injected into the tract → promotes healing and closure	Promising results in Crohn's perianal fistula (darvadstrocel/Alofisel); newer technique
Modified Hanley procedure ^[10]	For horseshoe fistula: drains the deep postanal space + bilateral ischiorectal extensions; counter-drainage ensures complete source control	Horseshoe fistula
Diversion / Proctectomy	Faecal diversion via colostomy; proctectomy if anorectal disease is unsalvageable	Refractory Crohn's perianal disease; extrasphincteric fistula (Parks Type 4) ^[10]

3.4 Management of Perianal Crohn's Disease

Perianal Crohn's disease requires a combined medical and surgical approach ^[11]^[13].

Perianal CD: ^[11]

Metronidazole/ciprofloxacin for infection control
Abscess — simple drainage
Simple fistula — fistulotomy
Complex fistula:
- Seton insertion for drainage
- Azathioprine
- Biologics
- Colostomy or proctectomy

The algorithm from the IBD lecture slides ^[13] is as follows:

Why biologics (anti-TNF) in Crohn's perianal disease?

TNF-α is a key pro-inflammatory cytokine driving the transmural inflammation and fistulising phenotype of Crohn's disease
Infliximab ("inflixi-" from "inflixing" a blow to TNF; technically a chimeric monoclonal anti-body against TNF-α) blocks TNF-α → reduces inflammation → promotes fistula healing
Adalimumab (a fully human anti-TNF-α monoclonal antibody; "adalim-" from "adaptive" + "immune") is used as second-line if infliximab fails

3.5 Post-operative Care and Follow-up

Aspect	Details
Wound care	Daily wound irrigation (shower/sitz bath); light packing initially → gradually reduce; wound should heal from the base upward over 4–8 weeks
Pain management	Regular paracetamol ± NSAIDs; avoid opioids if possible (cause constipation → straining → pain); warm sitz baths (relax sphincter, improve perfusion)
Stool management	High-fibre diet + adequate fluid intake + stool softeners (e.g., lactulose) → prevent hard stools → reduce pain on defaecation and trauma to healing wound
Follow-up timing	Review at 1–2 weeks post-drainage (wound check); then at 6–12 weeks (assess for fistula formation) ^[5]; C/ST results guide further management
Fistula surveillance	If pus C/ST showed gut flora → high fistula risk → clinical review ± MRI ± EUA if symptoms persist
Glycaemic control	Optimise blood glucose in diabetic patients → improves wound healing and reduces recurrence risk

3.6 Contraindications and Cautions

Intervention	Contraindication / Caution	Reason
Primary fistulotomy	Complex fistula (high transsphincteric, suprasphincteric, extrasphincteric); Crohn's disease; anterior fistula in females; pre-existing incontinence	Dividing a significant portion of the EAS → faecal incontinence; Crohn's fistulas are complex and require staged management
Cutting seton	Complex fistula with multiple tracts; Crohn's disease; patients with poor healing capacity	Risk of incontinence; Crohn's disease may not heal with cutting seton alone
Antibiotics without drainage	ALL anorectal abscesses	Antibiotics cannot penetrate the avascular abscess cavity → the abscess will not resolve; drainage is always required
Transanal drainage of ischiorectal abscess	Should NOT be done — this would create a fistula through the entire sphincter complex	The drainage route must respect the anatomical origin of the abscess
Buttock skin drainage of intersphincteric abscess	Should NOT be done — this would create a transsphincteric fistula	Same principle — drain along the path that does not traverse the sphincter
MRI with gadolinium	Severe renal impairment (eGFR < 30)	Risk of nephrogenic systemic fibrosis; use non-contrast MRI or EUS instead
EUA / surgery under GA	Uncorrected coagulopathy; patient unfit for anaesthesia	Risk of uncontrolled bleeding; optimise before theatre

4. Special Situations

4.1 Necrotising Fasciitis (Fournier's Gangrene)

Life-threatening emergency — perianal sepsis that progresses to necrotising soft tissue infection of the perineum and genitalia
Clinical clues: Pain out of proportion to examination findings, crepitus (gas-forming organisms), rapidly spreading erythema, skin necrosis, systemic toxicity (septic shock)
Management: Emergency surgical debridement (aggressive, wide, often requires multiple returns to theatre) + broad-spectrum IV antibiotics (Meropenem + Vancomycin + Clindamycin) + ICU support + possible faecal diversion (defunctioning colostomy)
Mortality: 20–40% even with treatment

4.2 Neutropaenic Patients

Anorectal abscess in neutropaenic patients (e.g., post-chemotherapy) may present with minimal external signs (attenuated inflammatory response)
Management: Low threshold for imaging (MRI/CT) → early drainage → broad-spectrum IV antibiotics → may require G-CSF to boost neutrophil count → close monitoring in haematology/oncology unit

4.3 Pregnancy

Perianal abscess is uncommon in pregnancy but can occur
Management: I&D under local or regional anaesthesia; avoid general anaesthesia if possible (especially first trimester); coordinate with obstetrics team

High Yield Summary — Management of Anorectal Abscess

1. Surgical I&D is the definitive treatment — antibiotics alone will NOT cure an abscess.

2. Site-specific drainage approach:

Perianal → skin incision
Ischiorectal → buttock skin incision (close to sphincter)
Intersphincteric → transanal (internal sphincterotomy)
Supralevator → depends on origin (intersphincteric → transanal; ischiorectal → buttock; pelvic → treat abdomen)

3. Antibiotics: limited role — only for cellulitis, valvular/prosthetic heart disease, immunosuppression, or systemic sepsis.

4. Always send pus for C/ST — gut flora predicts fistula; skin flora = reassurance.

5. Primary fistulotomy may be considered for simple, low fistulas at time of drainage, but never for complex fistulas or Crohn's.

6. Follow up at 6–12 weeks to assess for fistula formation.

7. Crohn's perianal disease = combined medical (antibiotics → azathioprine → biologics) + surgical (drainage → seton) approach.

Active Recall - Management of Anorectal Abscess

1. State the definitive treatment for anorectal abscess and explain why antibiotics alone are insufficient.

Your answer

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Incision and drainage (I&D) is the definitive treatment. Antibiotics cannot penetrate the avascular abscess cavity in sufficient concentration to sterilise it. The walled-off pus collection must be physically opened and drained. The wound is left open to heal by secondary intention.

2. Describe the correct drainage approach for an intersphincteric abscess and explain why you must NOT drain it through the perianal skin.

Your answer

Show mark scheme

Drain transanally via internal sphincterotomy (rectal mucosal incision). If drained through the perianal skin, the drainage tract would traverse the external anal sphincter, creating a transsphincteric or extrasphincteric fistula — risking faecal incontinence and making future surgical management much more difficult.

3. List four specific indications for antibiotics in the management of anorectal abscess.

Your answer

Show mark scheme

1) Severe surrounding cellulitis. 2) Valvular heart disease. 3) Prosthetic heart valves. 4) Immunosuppression (DM, HIV, neutropaenia). Also accept: systemic sepsis, necrotising fasciitis.

4. A patient with known Crohn's disease presents with a complex perianal fistula after abscess drainage. Outline the stepwise management approach.

Your answer

Show mark scheme

1) Antibiotics (metronidazole/ciprofloxacin) for infection control + azathioprine. 2) MRI pelvis + endoscopy to assess anatomy. 3) EUA with drainage and seton insertion. 4) Infliximab 5mg/kg at 0, 2, 6 weeks. 5) Remove seton at week 6. 6) Continue infliximab 8-weekly. 7) If partial response: continue infliximab and reassess 6-monthly. If no response: switch to adalimumab. If still refractory: consider colostomy or proctectomy.

5. What determines the drainage route for a supralevator abscess? Give the correct approach for each origin.

Your answer

Show mark scheme

The origin of the supralevator abscess determines the route. 1) Intersphincteric origin (upward extension): drain transanally. 2) Ischiorectal origin (upward extension): drain via buttock skin through the ischiorectal fossa. 3) Pelvic/abdominal origin (e.g. diverticular abscess tracking down): treat the primary abdominal pathology. Wrong route creates an extrasphincteric fistula.

6. Name four sphincter-sparing procedures for complex anal fistula.

Your answer

Show mark scheme

Any four of: 1) Loose (draining) seton + staged sphincter-sparing procedure. 2) Endorectal advancement flap. 3) LIFT (ligation of intersphincteric fistula tract). 4) Anal fistula plug. 5) Fibrin sealant. 6) VAAFT (video-assisted anal fistula treatment). 7) FiLaC (fistula tract laser closure). 8) Modified Hanley procedure (horseshoe fistula).

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p53 — Treatment) ^[4] Senior notes: maxim.md (Anorectal abscess — Management) ^[5] Senior notes: maxim.md (Anal fistula — suspect if abscess persists 6–12 weeks) ^[9] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p58 — Fistula treatment) ^[10] Senior notes: maxim.md (Anal fistula — Definitive treatment, sphincter-sparing procedures) ^[11] Lecture slides: Inflammatory bowel disease.pdf (p48 — Perianal CD) ^[12] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p61 — Other treatment modalities) ^[13] Lecture slides: Inflammatory bowel disease.pdf (p49 — Perianal CD algorithm)

Complications of Anorectal Abscess

Complications of anorectal abscess can be divided into those arising from the disease itself (if inadequately treated or left untreated) and those arising from the treatment (surgical complications). Think of it as a spectrum: the abscess is the acute event, and complications represent either progression of the disease or consequences of intervention.

1. Complications of the Disease (Untreated / Inadequately Treated Abscess)

1.1 Fistula-in-Ano (Anorectal Fistula) — THE Most Common Complication

This is the single most important complication and the natural chronic sequela of an anorectal abscess.

Incidence: 30–50% of anorectal abscesses will develop an associated fistula ^[2]^[4]^[5].

Pathophysiology (from first principles):

The anorectal abscess originates from an infected anal crypt gland → abscess forms in the intersphincteric plane → tracks outward
When the abscess is drained (surgically or by spontaneous rupture), the external opening (at the skin) heals
However, the internal opening — the original infected crypt at the dentate line — often remains patent
This creates a persistent communication between the anal canal lumen (internal opening at crypt) and the perianal skin (external opening where abscess drained)
The tract becomes lined with granulation tissue that eventually epithelialises → prevents spontaneous closure → chronic fistula

Anorectal fistula is the chronic phase of suppuration in this perirectal process ^[2].

Clinical presentation:

Intermittent perianal discharge (purulent, malodorous) + pain that builds until pus discharges, then temporarily relieves ^[5]
Palpable cord-like tract ^[5]
External opening visible as a dimple of granulation tissue
Suspect anal fistula if anorectal abscess persists after 6–12 weeks ^[5]

Classification — Parks Classification ^[5]:

Type	Name	Frequency	Description
I	Intersphincteric	45%	Tract between IAS and EAS
II	Transsphincteric	30%	Tract crosses through EAS into ischiorectal fossa
III	Suprasphincteric	20%	Tract loops above entire sphincter apparatus
IV	Extrasphincteric	5%	Tract bypasses sphincter entirely; opens into rectum

Why does this matter? The type of fistula determines the surgical approach:

Simple fistulas (Type I, low Type II) → fistulotomy/fistulectomy ^[9]
Complex fistulas (high Type II, Type III, IV) → seton drainage → staged sphincter-sparing procedures ^[9]^[10]

Predicting Fistula Risk from Pus Culture

Remember the pearl from earlier: Culture shows skin flora: no fistula → reassurance. Culture shows gut flora: likely with fistula → treat as fistula after acute state ^[4]. This makes biological sense — gut flora (E. coli, Bacteroides) in the pus means there is an internal communication with the bowel lumen, i.e., the infected crypt is still patent.

1.2 Recurrence of Abscess

Incidence: 10–30% after I&D alone (without primary fistulotomy); drops to ~5–10% if primary fistulotomy is performed for simple fistulas ^[1].

Why does recurrence happen?

The internal opening (infected crypt gland) is the source — if it is not addressed at the time of drainage, the crypt remains a portal for bacterial re-entry → new abscess forms
Inadequate drainage (undrained loculations, premature wound closure) → residual pus → re-accumulation
Underlying predisposing condition (Crohn's disease, TB, immunosuppression) not recognised or treated ^[3]

How to reduce recurrence:

Thorough drainage with breaking of all loculations
?Primary fistulotomy at time of I&D for simple, low fistulas ^[1]
Send pus for C/ST → if gut flora, plan for fistula follow-up at 6–12 weeks
Investigate and treat underlying causes (Crohn's, TB, DM, HIV) if atypical features

1.3 Progression to Adjacent Spaces (Extension of Abscess)

If an abscess is not drained promptly, pus continues to track along paths of least resistance (Parks' theory) ^[4]:

Starting Point	Extension	Resulting Abscess
Intersphincteric	Downward through IAS	Perianal abscess
Intersphincteric	Laterally through EAS	Ischiorectal abscess
Intersphincteric	Upward above levator ani	Supralevator abscess
Ischiorectal	Posteriorly via deep postanal space → contralateral ischiorectal fossa	Horseshoe abscess (bilateral ischiorectal)

A horseshoe abscess is a particularly challenging complication — it requires drainage of both ischiorectal fossae plus counter-drainage of the deep postanal space (modified Hanley procedure) ^[10].

1.4 Necrotising Fasciitis (Fournier's Gangrene)

This is the most feared and life-threatening complication.

Pathophysiology:

Perianal sepsis spreads from the localised abscess into the subcutaneous tissues and fascial planes of the perineum, genitalia, and abdominal wall
Synergistic polymicrobial infection (aerobic + anaerobic organisms) produces enzymes (collagenases, hyaluronidases, lipases) that destroy fascial planes → obliterative endarteritis of subcutaneous blood vessels → tissue ischaemia and necrosis → gas production by anaerobes → subcutaneous emphysema
The name: Fournier = Jean-Alfred Fournier, French venereologist who described the condition; gangrene = Greek gangraina = "eating sore" — tissue death

Risk factors: Immunosuppression (diabetes mellitus is the most common; also HIV, alcoholism, malignancy, chemotherapy) ^[1]^[4], delayed diagnosis or treatment

Clinical features:

Pain out of proportion to examination findings (early clue — the necrosis extends far beyond what is visible)
Rapidly spreading erythema, oedema, and skin discolouration (dusky, dark)
Crepitus (subcutaneous gas — palpable crackling under the skin)
Skin blistering, necrotic eschars
Systemic toxicity: high fever, tachycardia, hypotension, septic shock
Foul-smelling "dishwater" exudate

Management:

Emergency: This is a surgical emergency with mortality of 20–40%
Aggressive surgical debridement (wide excision of all necrotic tissue; often requires multiple returns to theatre)
Broad-spectrum IV antibiotics (Meropenem + Vancomycin + Clindamycin)
ICU support (fluid resuscitation, vasopressors, organ support)
Faecal diversion (defunctioning colostomy) may be needed to protect the wound
Vacuum-assisted closure (VAC) dressing for wound management
Delayed reconstruction (skin grafting) once infection controlled

Fournier's Gangrene — Never Miss

Any patient with perianal abscess who develops disproportionate pain, crepitus, rapidly spreading erythema, or systemic toxicity must be assessed for necrotising fasciitis immediately. Delayed surgical debridement is associated with exponentially increasing mortality. This is especially common in diabetic and immunocompromised patients.

1.5 Systemic Sepsis and Bacteraemia

Pathophysiology: Bacteria from the abscess cavity enter the systemic circulation (bacteraemia) → systemic inflammatory response syndrome (SIRS) → sepsis → septic shock → multi-organ dysfunction syndrome (MODS) if untreated.

Risk factors: Large or deep-seated abscesses (ischiorectal, supralevator), immunocompromised patients, delayed drainage.

Clinical features: Fever > 38°C, rigors, tachycardia, hypotension, confusion, oliguria.

Management: Blood cultures → empirical broad-spectrum IV antibiotics → urgent surgical drainage (source control) → ICU care if severe sepsis.

Rare but catastrophic extension: Septic portal pyaemia — bacteria from the perianal venous plexus enter the portal venous system → travel to the liver → pyogenic liver abscess formation. This is rare but well-described in the literature for any pelvic/abdominal septic source.

1.6 Anal Stenosis/Stricture

Pathophysiology: Repeated episodes of abscess formation and drainage → chronic inflammation → fibrosis and scarring of the anal canal → narrowing of the anal lumen (stenosis).

Clinical features: Difficulty passing stool, thin "ribbon-like" stools, straining, incomplete evacuation.

Management: Anal dilatation; may require anoplasty (surgical reconstruction of the anal canal) in severe cases.

2. Complications of Treatment (Surgical Complications)

2.1 Faecal Incontinence

The most important surgical complication to understand and prevent.

Pathophysiology:

The sphincter complex (IAS + EAS + puborectalis) is responsible for maintaining continence
Any surgical procedure that divides sphincter muscle risks incontinence:
- Fistulotomy for simple fistula: divides the overlying sphincter muscle to lay open the tract → if the tract involves a significant portion of the EAS ( > 30%), fistulotomy risks incontinence
- Incorrect drainage route: e.g., draining an intersphincteric abscess through the perianal skin (creating a transsphincteric tract) or draining a supralevator abscess through the wrong route → extrasphincteric fistula → devastating incontinence
- Cutting seton: gradually cuts through sphincter muscle; if not done carefully, excessive muscle division occurs

Risk of incontinence should be informed ^[9].

Prevention:

Choose the correct drainage route for each abscess type ^[4]
Perform fistulotomy only for simple, low fistulas (Parks Type I, low Type II) ^[9]
Use sphincter-sparing procedures (seton, advancement flap, LIFT) for complex fistulas ^[9]^[10]
Pre-operative assessment of sphincter function (manometry, EUS) in patients with any pre-existing incontinence

Continence Mechanism	Contribution	Implication
IAS (smooth muscle)	~70–85% of resting tone	Damage during internal sphincterotomy (for intersphincteric abscess drainage) may cause minor soiling/urgency
EAS (skeletal muscle)	Voluntary squeeze pressure	Damage during fistulotomy → inability to defer defaecation; urgency; incontinence to formed/liquid stool
Puborectalis	Anorectal angle (80–90°)	Damage → loss of gross continence; rare with standard procedures

Complication	Pathophysiology	Details
Delayed wound healing	The wound is left open to heal by secondary intention → healing depends on granulation from the base → if impaired (DM, malnutrition, smoking, immunosuppression), healing is prolonged	Average healing time: 4–8 weeks for perianal abscess; longer for ischiorectal. Optimise glycaemic control, nutrition, and smoking cessation.
Premature wound closure	The skin edges close before the deep cavity has granulated → trapped cavity → recurrent abscess	Why we excise an ellipse of skin (de-roofing) rather than making a simple linear incision — this prevents premature closure. Daily wound care and packing keep the wound open.
Wound infection / Secondary infection	Despite drainage, secondary bacterial contamination of the open wound (proximity to anus) → local infection	Wound care, sitz baths, and hygiene; antibiotics only if cellulitis develops.

2.3 Bleeding

Pathophysiology: The perianal and anorectal region has a rich blood supply (branches of the inferior and superior rectal arteries; internal pudendal artery). Surgical incision → vessel injury → bleeding.

Usually minor and self-limiting (controlled by pressure, packing, or cautery)
Rarely significant; massive haemorrhage is uncommon
Risk increased with: coagulopathy, anticoagulant/antiplatelet therapy, deep abscesses near major vessels

2.4 Urinary Retention (Post-Operative)

Pathophysiology: Same mechanism as the pre-operative symptom — reflex urinary retention via shared pudendal nerve innervation (S2–S4). Post-operative pain, local swelling, the effects of anaesthesia (especially spinal/epidural), opioid analgesics, and rectal packing all contribute to urethral sphincter spasm.

Management: Remove rectal packing; adequate analgesia (avoid excessive opioids); trial of micturition → if unable to void, insert urinary catheter for 24 hours ^[6].

2.5 Iatrogenic Extrasphincteric Fistula

Pathophysiology: Created when a supralevator abscess is drained via the wrong route:

Intersphincteric origin drained through buttock skin → tract now traverses the entire sphincter complex from the supralevator space through the ischiorectal fossa to the skin → extrasphincteric fistula ^[4]
This is a Parks Type IV fistula — the most difficult to manage, often requiring faecal diversion (colostomy) or even proctectomy ^[10]

This complication is entirely preventable by determining the origin of the supralevator abscess before choosing the drainage route.

2.6 False Passage Creation During Fistula Probing

Pathophysiology: At EUA, a fistula probe is passed through the tract to identify the internal opening. If too much force is applied, the probe can perforate the tract wall → creates a false passage — a new, iatrogenic tract through healthy tissue (potentially through the sphincter) ^[5].

Prevention: Gentle probing; never force the probe; use malleable probes; consider hydrogen peroxide injection or MRI to map the tract before probing.

When the anorectal abscess is secondary to an underlying condition (rather than simple cryptoglandular infection), additional complications may arise from the primary disease:

3.1 Crohn's Disease — Perianal Complications

Perianal disease in Crohn's can include ^[14]:

Abscess — simple drainage ^[11]
Fistula — simple (fistulotomy) or complex (seton insertion for drainage, azathioprine, biologics, colostomy or proctectomy) ^[11]
Anorectal stricture — chronic inflammation → fibrosis → narrowing → obstructed defaecation
Skin tags — large, oedematous, "elephant-ear" skin tags characteristic of Crohn's
Anal fissures — often off-midline, painless, multiple (atypical features compared to primary fissures)
Rectovaginal fistula — tract from the rectum to the vagina → passage of flatus/faeces through vagina

Perianal Crohn's disease is a marker of aggressive, fistulising phenotype and is an adverse prognostic factor that warrants early introduction of immunomodulators and biologics ^[14].

3.2 Tuberculosis — Chronic Non-Healing Fistula

TB-related perianal abscess may lead to a chronic, non-healing fistula with caseous discharge
Failure to diagnose TB means ongoing active infection → repeated recurrence → complex fistula tracts → anal stenosis
Requires anti-TB therapy (RIPE regimen) for cure; surgery alone will not resolve TB fistulas

3.3 Malignancy — Missed Diagnosis

An anorectal abscess may be the first presentation of anal carcinoma or low rectal carcinoma
Tumour necrosis or obstruction of a crypt gland by tumour → secondary abscess
If the abscess cavity wall is not biopsied, the underlying malignancy may be missed
Colorectal neoplasm needs to be excluded ^[1]

4. Summary Table — Complications at a Glance

Category	Complication	Incidence / Likelihood	Key Mechanism	Prevention / Management
Disease	Fistula-in-ano	30–50%	Persistent internal opening at infected crypt → chronic tract	Pus C/ST; follow-up 6–12 weeks; primary fistulotomy for simple fistulas
Disease	Abscess recurrence	10–30%	Undrained source (crypt) persists	Complete drainage; primary fistulotomy if appropriate; treat underlying cause
Disease	Extension to adjacent spaces	Variable	Pus tracks along path of least resistance	Timely drainage
Disease	Necrotising fasciitis	Rare but catastrophic	Synergistic polymicrobial infection → fascial necrosis	Early drainage; identify immunocompromised patients; emergency debridement
Disease	Systemic sepsis	Uncommon	Bacteraemia from abscess	Blood cultures; empirical antibiotics; urgent drainage
Disease	Anal stenosis	Late complication	Chronic fibrosis from repeated inflammation	Avoid repeated surgical trauma; treat underlying cause
Treatment	Faecal incontinence	Variable (0.6–12%)	Sphincter division during fistulotomy or incorrect drainage route	Correct drainage approach; sphincter-sparing procedures for complex fistula
Treatment	Delayed wound healing	Common (4–8 weeks)	Open wound healing by secondary intention	Optimise DM, nutrition, smoking; proper wound care
Treatment	Premature wound closure → recurrence	Moderate	Skin heals before deep cavity → trapped collection	De-roofing; daily wound care; packing
Treatment	Urinary retention	Common post-operatively	Reflex via pudendal nerve; anaesthesia; opioids	Adequate analgesia; early mobilisation; catheter if needed
Treatment	Iatrogenic extrasphincteric fistula	Rare but devastating	Wrong drainage route for supralevator abscess	Determine abscess origin before drainage
Treatment	False passage	Rare	Forceful fistula probing	Gentle probing; MRI guidance
Underlying disease	Crohn's perianal complications	In Crohn's patients	Transmural inflammation, fistulising phenotype	Biologics; seton; multidisciplinary management
Underlying disease	Missed malignancy	Rare	Tumour → secondary abscess; no biopsy taken	Biopsy abscess wall if atypical; colonoscopy

High Yield Summary — Complications of Anorectal Abscess

1. Fistula-in-ano is the most common complication (30–50%). It represents the chronic phase of the cryptoglandular process — a persistent tract from the internal opening (crypt) to the external opening (skin). Predicted by gut flora on pus culture. Managed by fistulotomy (simple) or seton + sphincter-sparing procedures (complex).

2. Recurrence occurs in 10–30% if the internal opening is not addressed. Reduced by primary fistulotomy for simple fistulas and treating underlying causes.

3. Necrotising fasciitis (Fournier's gangrene) is the most feared complication — life-threatening, 20–40% mortality. High risk in DM and immunosuppression. Requires emergency debridement + broad-spectrum antibiotics + ICU care.

4. Faecal incontinence is the most important surgical complication — caused by sphincter damage from fistulotomy or incorrect drainage route. Prevented by correct surgical approach and sphincter-sparing techniques.

5. Always biopsy the abscess wall if atypical — to exclude Crohn's disease, TB, and malignancy.

Active Recall - Complications of Anorectal Abscess

1. What is the most common complication of anorectal abscess, what is its incidence, and what is the underlying pathophysiology?

Your answer

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Fistula-in-ano, occurring in 30-50% of cases. Pathophysiology: after abscess drainage or spontaneous rupture, the external opening heals but the internal opening (infected crypt at the dentate line) persists, creating a chronic tract lined by granulation tissue connecting the anal canal to the perianal skin.

2. A diabetic patient with a perianal abscess develops rapidly spreading erythema, crepitus, and septic shock. What is the diagnosis, and what are the three key components of emergency management?

Your answer

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Necrotising fasciitis (Fournier's gangrene). Emergency management: 1) Aggressive surgical debridement of all necrotic tissue. 2) Broad-spectrum IV antibiotics (e.g. Meropenem + Vancomycin + Clindamycin). 3) ICU support (fluid resuscitation, vasopressors, organ support). Also consider faecal diversion (defunctioning colostomy).

3. How does incorrect drainage of a supralevator abscess lead to an iatrogenic extrasphincteric fistula, and how is this prevented?

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If a supralevator abscess of intersphincteric origin is drained through the buttock skin (through the ischiorectal fossa), the drainage tract traverses the entire sphincter complex and levator ani, creating a Parks Type IV extrasphincteric fistula. Prevention: determine the abscess origin before choosing the drainage route. Intersphincteric origin should be drained transanally.

4. List three factors that contribute to post-operative urinary retention after anorectal abscess drainage.

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1) Reflex urethral sphincter spasm via shared pudendal nerve innervation (S2-S4) due to perianal pain and inflammation. 2) Effects of spinal/general anaesthesia. 3) Opioid analgesics (reduce detrusor contractility). Also accept: rectal packing, fluid overload, pre-existing outflow tract obstruction.

5. Why is Crohn's-related perianal disease considered an adverse prognostic factor, and what is the general management approach for complex perianal fistula in Crohn's?

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Perianal Crohn's indicates aggressive, fistulising disease phenotype warranting early immunomodulator and biologic therapy. Management: antibiotics (metronidazole/ciprofloxacin) for infection control; EUA with seton insertion for drainage; azathioprine; biologics (infliximab then adalimumab if refractory); colostomy or proctectomy if all else fails.

6. What are two strategies to reduce the recurrence rate of anorectal abscess after initial I&D?

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1) Primary fistulotomy at the time of I&D for simple, low fistulas (addresses the internal opening/source). 2) Identify and treat underlying predisposing conditions (Crohn's disease, TB, diabetes mellitus, HIV). Also accept: thorough drainage with breaking of all loculations; pus C/ST to predict fistula and plan follow-up.

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p49, p53, p77) ^[2] Senior notes: felixlai.md (Anorectal abscess — Overview) ^[3] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p49 — Etiology) ^[4] Senior notes: maxim.md (Anorectal abscess — Management, drainage approaches) ^[5] Senior notes: maxim.md (Anal fistula — definitions, clinical features, classification); felixlai.md (Anorectal fistulas) ^[6] Senior notes: maxim.md (Haemorrhoidectomy complications — urinary retention management) ^[9] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p58 — Fistula treatment) ^[10] Senior notes: maxim.md (Anal fistula — Definitive treatment, sphincter-sparing procedures) ^[11] Lecture slides: Inflammatory bowel disease.pdf (p48 — Perianal CD) ^[14] Senior notes: felixlai.md (Crohn's disease — complications, perianal disease management)

Anorectal Abscess

Active Recall - Anorectal Abscess (Definition to Clinical Features)

Active Recall - Differential Diagnosis of Anorectal Abscess

Active Recall - Diagnosis of Anorectal Abscess

Active Recall - Management of Anorectal Abscess

Active Recall - Complications of Anorectal Abscess

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