Anorectal Fistula

• Surgical anal canal: From anal verge to anorectal ring (~4 cm).
• Dentate (pectinate) line: Located ~2 cm from the anal verge. This is the watershed landmark:
  • Above: columnar epithelium, visceral nerve supply (painless), superior rectal artery, internal haemorrhoidal plexus, lymphatic drainage to internal iliac nodes.
  • Below: squamous epithelium, somatic nerve supply (painful!), inferior rectal artery, external haemorrhoidal plexus, lymphatic drainage to inguinal nodes.

• At the dentate line sit 6–14 anal columns (columns of Morgagni) with intervening crypts of Morgagni (anal crypts).
• Anal glands (4–10 in number) open into these crypts. Their ducts penetrate through the internal anal sphincter (IAS) and terminate in the intersphincteric plane (between IAS and EAS).
• This is why the intersphincteric plane is "ground zero" for cryptoglandular infection — infection begins in the gland, spreads to the intersphincteric space, and then tracks along paths of least resistance ^[1][2].

Infection (and therefore fistula tracts) can spread through these spaces:

This is the dominant cause. The mechanism:

1. Obstruction of an anal gland duct → stasis.
2. Bacterial overgrowth within the obstructed gland (mixed flora: E. coli, Bacteroides, Enterococcus).
3. Abscess formation in the intersphincteric space (this is the primary site because the gland terminates here).
4. Pus tracks along the path of least resistance — this determines the type of abscess and the subsequent fistula tract.
5. If the abscess drains (spontaneously or surgically) but the internal opening persists and the tract epithelialises → fistula.

Why does the internal opening persist? Because the infected crypt continues to seed bacteria into the tract, preventing healing. This is the rationale for identifying and treating the internal opening in fistula surgery.

This is the cornerstone — understand it step-by-step:

Anal crypt gland obstruction
        ↓
Intersphincteric gland infection
        ↓
Intersphincteric abscess (primary)
        ↓
Pus tracks along path of least resistance
        ↓
Secondary abscess formation
(perianal / ischiorectal / supralevator)
        ↓
Spontaneous rupture or surgical drainage
        ↓
Persistent internal opening + granulation-lined tract
        ↓
FISTULA-IN-ANO

Why does it become chronic?

• The internal opening (at the infected crypt) continuously seeds bacteria.
• The tract becomes lined with granulation tissue and eventually partly epithelialised, preventing spontaneous closure.
• The ongoing faecal contamination from the anal canal keeps the inflammatory cycle going.

• Transmural inflammation is the hallmark of Crohn's — inflammation penetrates the full thickness of the bowel wall.
• This leads to microperforations and abscess formation, which then track to form fistulae.
• Crohn's fistulae are often complex (multiple tracts, horseshoe configurations, rectovaginal).
• Fistulising disease accounts for ~20% of Crohn's disease ^[3][4].

• If the abscess is adequately drained AND the internal opening heals → no fistula.
• Pus culture showing gut flora (e.g., E. coli, Bacteroides) suggests communication with the anal canal lumen → higher likelihood of fistula formation ^[3].
• Pus culture showing skin flora (e.g., Staphylococcus) → less likely to form a fistula (infection was superficial) ^[3].

This is THE classification. It describes the fistula tract's relationship to the external anal sphincter (EAS).

Not included in Parks: Superficial fistula — does not involve the sphincter at all (subcutaneous/submucosal tract). Easy to treat ^[3].

This classification determines surgical strategy — simple fistulae can usually be laid open safely; complex ones cannot.

Simple fistula:

• Superficial fistula
• Intersphincteric (Type I)
• Low transsphincteric (Type II) involving < 30% of EAS ^[2][3]

Complex fistula:

• High transsphincteric (Type II) involving ≥ 30% of EAS ^[2][3]
• Suprasphincteric (Type III)
• Extrasphincteric (Type IV)
• Horseshoe fistulas
• Multiple tracts
• Recurrent fistula
• Fistula associated with Crohn's disease ^[2][3]
• Fistula related to TB, HIV, radiation ^[2]
• Women with anterior fistulas / rectovaginal fistulas (thinner anterior sphincter in females → higher incontinence risk) ^[3]
• Patients with pre-existing anal incontinence ^[2]

• Low fistula: Below the dentate line / involving minimal sphincter → can usually fistulotomy safely.
• High fistula: Above the sphincter complex or involving significant sphincter → need sphincter-sparing techniques.

This is a clinical "rule of thumb" to predict the location of the internal opening based on the position of the external opening.

• Draw an imaginary transverse line across the anus (through the ischial spines/tuberosities).
• External opening ANTERIOR to the transverse line → fistula tracks in a straight (radial) line to the nearest crypt at the dentate line.
• External opening POSTERIOR to the transverse line → fistula follows a curved track to open at the posterior midline of the anal canal.

Goodsall's rule has higher reliability when the external opening is within 3 cm of the anal verge ^[3]. Beyond 3 cm, the rule is less reliable (the tract is more likely to be complex).

Why does this pattern occur? The posterior midline is where the anal glands are most concentrated. Additionally, the posterior anal canal has a relatively avascular area (the "posterior commissure"), which provides a path of least resistance for infection to track through.

When evaluating a patient with a fistula, always look for features suggesting an underlying cause:

• Crohn's disease: multiple fistulae, skin tags ("elephant ear" tags), fissures away from the midline, oral ulcers, abdominal pain, diarrhoea, weight loss, perianal disease preceding intestinal disease.
• TB: chronic non-healing fistula, constitutional symptoms (night sweats, weight loss), granulomata on histology (caseating).
• Malignancy: hard, irregular edges of fistula, bloody discharge, weight loss, change in bowel habit.
• HIV/immunosuppression: unusual organisms, poor healing.

Examination under anesthesia (EUA) is required before surgery to trace the fistula tract ^[3]. This is the most important investigation because it combines diagnostic confirmation with therapeutic planning — and is often performed immediately before definitive surgery.

What happens during EUA:

1. Visual inspection of perianal area (external opening, scarring, Crohn's features).
2. DRE with relaxed sphincter — assess internal opening, induration, sphincter integrity.
3. Proctoscopy — identify internal opening (may see pus draining from a crypt at the dentate line).
4. Fistula probing ^[2]:
   • A fistula probe (malleable metal probe) is gently inserted into the external opening and passed along the tract towards the internal opening.
   • Determine whether the fistula is simple or complex based on the extent of anal sphincter muscle involvement ^[2].
   • Performed with caution to avoid creating a false passage by penetrating the fistula wall ^[2].
5. Injection of hydrogen peroxide or methylene blue through external opening — helps visualise the internal opening (dye emerges at the crypt).
6. Assessment of sphincter bulk around the tract — the surgeon palpates how much muscle lies between the probe and the skin to decide if fistulotomy is safe.

These are adjunctive — no fistula will heal with conservative measures alone (except some Crohn's fistulae with biologics), but they support surgical healing.

Lifestyle modification ^[2]:

• Avoid constipation — hard stools traumatise the healing wound and internal opening. Use fibre supplementation, adequate fluid intake, stool softeners.
• Maintain proper anal hygiene — reduce bacterial load around the wound. Sitz baths (warm water soaks) after defecation promote wound cleanliness and comfort.

Crohn's perianal fistulae are a special category — the approach is fundamentally medical-first, with surgery playing a supportive/drainage role ^[5][8][9].

Perianal CD management ^[8][9]:

Step 1: Control Infection

• Metronidazole/ciprofloxacin for infection control ^[9]
  • Why antibiotics? Reduce the bacterial load driving the inflammatory process. Metronidazole and ciprofloxacin penetrate well into pelvic/perianal tissue. Used as bridge therapy until immunomodulators/biologics take effect.
  • From CD medical notes: Antibiotics are indicated in perianal diseases such as fistula ^[10].

Step 2: Drain Any Abscess

• Abscess — simple drainage ^[9]
  • I&D under GA. Do NOT perform definitive fistula surgery at this stage — tissue is inflamed, anatomy distorted.

Step 3: Manage the Fistula Based on Complexity

• Simple fistula — fistulotomy ^[9]
• Complex fistula ^[9]:
  • Seton insertion for drainage — loose seton to control sepsis and maintain drainage.
  • Azathioprine — immunomodulator to reduce Crohn's inflammation ^[8][9].
  • Biologics — Anti-TNF +/- AZA and/or seton drainage ^[8]. Give biologics after drainage of pus to close the fistula tract ^[5].
    • Why biologics after drainage? If you give biologics (which suppress immune response) while there is an undrained abscess, you risk uncontrolled sepsis. Drain first → control sepsis → then introduce biologics to promote fistula closure.
    • Must screen for TB with CXR/QuantiFERON-TB Gold + HBV with HBsAg before starting anti-TNF ^[10].
  • Colostomy or proctectomy — if all else fails ^[9].
    • If failed, consider surgery (defunctioning stoma ± proctectomy) ^[5].

Enterocutaneous Fistula in Crohn's — uses the SNAP principle ^[2][10]:

• Sepsis control: Antibiotics + abscess drainage ^[11]
• Nutrition support: High vs low output assessment, TPN aids closure ^[11]
• Anatomy: CTE or MRE to delineate anatomy ^[11]
• Procedure: Medication adjustment, closure with biological agents, en-bloc resection of involved bowel and fistula ^[11]

Since abscess and fistula are the same disease at different time points, managing the abscess correctly can prevent or set up proper management of the subsequent fistula.

Treatment of anorectal abscess ^[1][4]:

• Incision and drainage of abscess ^[1]
• Little role for antibiotics except in patients with severe cellulitis, valvular heart disease, prosthetic heart valves, and immunosuppression ^[1]
• ? Primary fistulotomy ^[1] — if a fistula is clearly identified at the time of abscess drainage (e.g., probe passes easily from abscess to internal opening), some surgeons will perform a primary fistulotomy at the same sitting. This is controversial and typically only done for simple, low fistulae with clearly identified anatomy.
• Drainage approach by site ^[4]:
  • Perianal abscess: skin incision close to the anal verge.
  • Ischiorectal abscess: buttock skin incision → drain as close to sphincter complex as possible to minimise the length of a potential fistula tract.
  • Intersphincteric abscess: rectal incision (internal sphincterotomy) → drain transanally to avoid creating an extrasphincteric fistula ^[4].

Mechanism: The fistula maintains a persistent communication between the anal canal lumen (via the internal opening at the infected crypt) and the perianal tissues. Faecal bacteria continuously seed the tract → intermittent accumulation of pus → cyclical abscess formation ^[2][3].

• This is the most common complication of an untreated fistula.
• Each recurrence can extend the septic process into new tissue planes → the fistula becomes progressively more complex (new secondary tracts, horseshoe extensions).
• Can expand into adjacent tissues including ischiorectal and supralevator space or even progress into generalised systemic infection ^[2].

Why does this matter? Each cycle of abscess → drainage → recurrence creates more scarring and fibrosis around the sphincter complex, making eventual definitive surgery more difficult and increasing the risk of incontinence from the surgery itself.

Mechanism: Undrained or inadequately drained sepsis tracks along paths of least resistance through perianal/perirectal tissue planes. Over time:

• A simple intersphincteric fistula can extend through the EAS → becomes transsphincteric.
• Pus can track through the deep postanal space (behind the anal canal) from one ischiorectal fossa to the other → horseshoe fistula.
• Multiple secondary tracts develop → complex fistula with multiple external openings.

The more complex the fistula becomes, the harder it is to treat surgically without damaging the sphincter, and the higher the recurrence rate.

Mechanism: If the external opening blocks and there is no adequate drainage path, pus accumulates under pressure. This can progress to:

• Cellulitis of the perianal skin and perineum.
• Necrotising fasciitis of the perineum (Fournier's gangrene) — a life-threatening surgical emergency. Polymicrobial infection spreads rapidly through subcutaneous tissues and fascial planes. Particularly dangerous in immunocompromised patients (diabetes, HIV, on immunosuppressants) and those with perianal Crohn's disease.
• Bacteraemia / sepsis — the perianal region is richly vascular; uncontrolled infection can seed the bloodstream.

Mechanism: Persistent discharge from the external opening causes:

• Chronic dermatitis and maceration of the perianal skin — from continuous moisture and irritant contact with pus/faecal material.
• Pruritus ani — secondary to chronic skin inflammation and excoriation ^[2].
• Scarring and fibrosis — repeated cycles of inflammation and healing lead to thickened, indurated perianal skin.

Mechanism: Chronic inflammation over many years (typically > 10 years of untreated fistula) can lead to squamous cell carcinoma or mucinous adenocarcinoma arising in the fistula tract. This is analogous to other chronic inflammatory conditions that predispose to malignancy (e.g., Marjolin's ulcer in chronic wounds, cholangiocarcinoma in PSC).

• Extremely rare but well-documented in case reports.
• Should be suspected in any long-standing fistula that suddenly changes character — increased pain, harder tissue, bloody rather than purulent discharge, rapid growth.
• Always send fistula tract curettings for histology at the time of surgery to exclude occult malignancy.

Crohn's perianal fistulae carry additional disease-specific complications due to the transmural inflammatory nature of the underlying disease ^[12][8]:

• Fistula formation (additional types beyond perianal) ^[12]:
  • Enteroenteric fistula → palpable mass ^[12]
  • Enterovesical fistula → urinary symptoms due to UTI (pneumaturia = air in urine, faecaluria = faeces in urine) ^[12][13]
  • Enterovaginal fistula → passage of gas or faeces through vagina ^[12][13]
  • Enterocutaneous fistula → drainage of bowel contents to surface of skin ^[12][13]
  • Retroperitoneal fistula → psoas abscess or ureteral obstruction with hydronephrosis ^[12]
• Abscess formation — sinus tracts may lead to abscess → acute localised peritonitis with fever, abdominal pain, and tenderness → perforation can lead to diffuse peritonitis ^[12].
• Perianal disease — formation of skin tags, anal fissures, perirectal abscess, and anorectal fistulas ^[12]. 83% of perianal Crohn's patients required surgery ^[8].
• Anal stenosis / stricture — chronic fibrosis from repeated inflammation narrows the anal canal.

This is the most feared complication of fistula surgery and the primary reason complex fistulae require sphincter-sparing approaches rather than fistulotomy.

Risk of incontinence should be informed before any fistula surgery ^[1].

Mechanism: Division of the anal sphincter muscle during surgery → loss of the sphincter's ability to maintain closure → involuntary leakage of gas, liquid stool, or solid stool.

Risk factors for incontinence after fistula surgery:

• Pre-existing sphincter damage (previous obstetric injury, prior fistula surgery, prior lateral internal sphincterotomy for fissure).
• Female sex — thinner, shorter anterior sphincter.
• Anterior fistula in women — even a small division of the anterior EAS can cause incontinence.
• Recurrent fistula surgery — each operation removes more sphincter tissue; cumulative damage.
• Older age — reduced baseline sphincter tone due to age-related muscle atrophy and pudendal neuropathy.

This is the second most common complication. Recurrence rates vary significantly by procedure:

Common reasons for recurrence:

1. Failure to identify the internal opening — if the cryptoglandular source is not addressed, the infection cycle restarts. The most critical step is to identify and curette the internal opening ^[2].
2. Missed secondary tracts — undrained extensions continue to harbour infection. This is why MRI is essential for complex fistulae.
3. Inadequate drainage of associated abscess — residual sepsis prevents healing.
4. Underlying Crohn's disease not treated medically — ongoing transmural inflammation drives recurrence regardless of surgical technique. More complicated courses of fistula tract in Crohn's ^[8].
5. Creation of false passage during probing → new iatrogenic tract that is not addressed.

Complications: sphincter injury ^[3].

Even when patients do not report overt incontinence, fistula surgery can cause subclinical sphincter damage detectable on endoanal ultrasound or anorectal manometry. This may only become clinically significant later in life when age-related sphincter degeneration further reduces continence reserves.

Fistulotomy wounds heal by secondary intention (from the base up, without primary closure). This creates specific wound-related issues:

• Delayed wound healing: Fistulotomy wounds in the perianal region take 6–12 weeks to heal fully. The perineum is a moist, contaminated environment (faecal bacteria, constant movement from sitting/walking), which slows healing.
• Wound infection: Despite the wound being intentionally left open, secondary bacterial overgrowth can cause wound cellulitis or a new abscess.
• Bleeding: Minor postoperative bleeding from the granulating wound bed is common. Significant bleeding (reactionary or secondary) is uncommon but may require return to theatre for haemostasis.
• Anal stenosis / stricture: Excessive fibrosis during wound healing can narrow the anal canal → difficulty with defecation, thin stools, straining. More common with extensive fistulotomy (large wound) or circumferential wounds. May require finger or endoscopic balloon dilatation ^[14].

Mechanism: During EUA, if the fistula probe is forced through the tract wall rather than following the true tract, a new iatrogenic passage is created through tissue that was previously uninvolved ^[2].

• Performed with caution to avoid creating a false passage by penetrating the fistula wall ^[2].
• This can convert a simple fistula into a complex one, or create a new fistula in addition to the original one.
• Avoided by: gentle probing, using a malleable (not rigid) probe, never forcing the probe.

For extrasphincteric fistulae (Type IV), refractory Crohn's perianal disease, or salvage procedures, a defunctioning stoma may be created. This carries its own set of complications ^[2][14]:

Early ( < 30 days):

• Stomal bleeding
• Stomal necrosis (ischaemia of the bowel stoma — appears dark/dusky)
• Stomal retraction (stoma sinks below skin level → appliance leakage)
• Mucocutaneous separation (dehiscence of the stoma-skin junction)
• Skin irritation and dermatitis (especially ileostomy — high-output alkaline enzymatic effluent is highly corrosive to skin)

Late ( > 30 days):

• Parastomal hernia (bowel herniates through the fascial defect around the stoma)
• Stomal prolapse
• Stomal stenosis