Benign anorectal Flashcards
1
Q
What is an anal fissure? What is its pathogenesis?
A
An ulceration in the squamous lining of the anal canal, distal to the dentate line.
Two main contributors particularly to posterior fissures:
- passage of hard stool leads to trauma to anoderm
- affected pts present w int anal sphincter hypertonia (from decreased NO production) which enhances traumatic effect of hard stool & provokes relative tissue ischaemia w impaired blood supply & therefore healing of anal mucosa
- after initial tear get viscious cycle of non-healing & repeated trauma –> chronic deep fissure
- pts also postpone defaecation which leads to hard stools
- posterior triangular space is formed by peculiar arrangement of sphincter in posterior midline, where there is a ‘Y-shaped deficiency’ of fibres of the external sphincter
- this space = area where traumatic factors act most & where high resting anal pressures & decreased local perfusion are found
- branches of rectal artery at posterior commissure = less dense in subanodermal space & within the int anal sphincter in the posterior midline
Anterior fissures thought to be secondary to different mechanisms: high sphincter pressure seems less responsible for these eg postpartum injuries
Other things to consider are secondary causes
- complicated fissures may be due to Crohn’s, UC, TB, HIV, CMV, syphilis, herpes
- prev surgery eg haemorrhoidectomy or fistulectomy can lead to scarred anoderm w loss of elasticity; more likely to tear
- occasionally traumatic eg FB, anal intercourse, proctoscopy
2
Q
How are anal fissures classified?
A
-
Duration: acute <6wks, chronic >6wks
- acute fissure usu superficial w well demarcated edges, no muscle visible in base
- chronic fissure usu keratinised/indurated edges, deep w internal sphincter visible at base, classically a sentinel tag distally & hypertrophied anal papilla proximally
-
Appearance: superficial vs deep
- deep = deep, wide, pear-shaped, often w muscle at base & minimal granulation tissue - often persist/tend not to heal w/o intervention/recur
-
Location
- posterior 80-90% (in posterior triangular space)
- anterior (2.5-10%) - more frequent in women, usu assoc w occult ext anal sphincter injuries & impaired sphincter function
- other/unusual appearances - more likely to be secondary cause
-
Primary vs secondary
- primary = not caused by any underlying chronic disease
- secondary = assoc w other diseases eg IBD, HIV, TB, syphilis, some neoplasms (secondary usu multiple or in unusual positions
3
Q
Management of anal fissures
A
- General
- fluid intake, fibre, stool softeners, sitz baths for comfort, topical analgesia
- Medical/chemical treatments
- topical nitroglycerin 0.2-0.4% - applied BD/TDS
- acts through releasing int sphincter and increasing local blood flow through release of NO
- for 6-8wks to allow re-epithelialisation
- successful in 50-70%, recurrent in 50%
- side effects incl headaches, hypotension, burning on application
- topical diltiazem - TDS for 6wks
- CCB & vasodilator which increases blood flow to SM & relaxes muscle tone
- similar efficacy to GTN but less side effects
- topical nitroglycerin 0.2-0.4% - applied BD/TDS
- Surgery
- botox - protocols vary, 10-100U into intersphincteric groove or int sphincter at 3 and 9 o’clock
- as effective as topical but less side effects espec headaches & no compliance issues
- temporary incontinence (mainly flatus) in 5-10%
- higher costs & need GA
- up to 50% recur & need surgery
- anal stretch - no longer done, high incontinence rates
- fissurectomy
- excision of fibrotic edge of fissure, curettage of its base & excision of sentinel tag & assoc hypertrophied anal papilla
- +/- with other procedures eg botox or advancement flap
- 67% success rate with botox, up to 100% w flap
- lateral sphincterotomy - open or closed
- conventional - up to dentate line, or tailored up to apex of prox aspect of fissure (less incontinence but lower recurrence rates)
- successful in ~90% / 10% recur
- 30-45% initial alteration in continence; long term 9% flatus, soiling 6%, solid stool <1%
- contraindicated in impaired continence, chronic diarrhoeal states, known sphincter injuries
- mucosal advancement flap
- especially for those whose fissure isn’t assoc w hypertonia, also if impaired continence, female
- also good results for tx of chronic fissures (not just low pressure ones)
- bc decreased local pain, therefore helping relaxation of sphincter complex
- VY island, rotational
- frequently assoc w other procedures (botox, fissurectomy)
- similar efficacy to sphincterotomy
- especially for those whose fissure isn’t assoc w hypertonia, also if impaired continence, female
- botox - protocols vary, 10-100U into intersphincteric groove or int sphincter at 3 and 9 o’clock
4
Q
What are the considerations if an anal fissure recurs after sphincterotomy?
A
- can trial conservative measures w high fibre, ample fluid
- consider secondary causes, biopsy
- if painless doesn’t necessarily need further intervention
- consider USS to identify pts w low resting anal pressures/assess extent of previous sphincterotomy
- if doesn’t have hypertonic sphincter - consider fissurectomy + mucosal advancement flap
- if hypertonic sphincter & incomplete sphincterotomy - can complete or do sphincterotomy on opposite side
- if complete, fissurectomy & advancement flap
- anal fissures related to underlyling systemic illness eg Crohns best tx w aggressive medical mx of that illness
- after fissure heals ?or before, sigmoidoscopy to r/o IBD/ca
5
Q
How are perianal abscesses classified and what is their aetiology?
A
- Classification
- location: perianal 43%, submucosal 6%, supralevator 7%, intersphincteric 21%, ischioanal 23% +/- horseshoe
- primary (cryptoglandular, 90%) vs secondary
- Aetiology
- primary: cryptoglandular hypothesis
- infection begins in anal glands which are in the intersphincteric plane and usually discharge into the basal of the anal columns of Morgagni at the dentate line; but if blocked eg with stool or oedema from trauma or adjacent inflammation, can’t decompress into anal canal & abscess may develop in the intersphincteric plane
- pus from the abscess may discharge via the intersphincteric space (which may later result in an intersphincteric fistula), through the external anal sphincter (trans-sphincteric fistula) or above the sphincter complex (supra-sphincteric)
- extra-sphincteric fistulae don’t conform w the cryptoglandular hypothesis; these are either secondary to disease (cancer) or iatrogenic
- pts w DM/immunocompromised state most vulnerable
- secondary: manifestation of underlying disease process
- Crohn’s, anorectal ca, TB, HIV, fissure/haemorrhoids/surgery
- both aerobic and anaerobic bacteria; bacteroides, E coli, strep faecalis, staph, clostridium
- primary: cryptoglandular hypothesis
6
Q
Management of perianal abscess
A
- submucosal - drain into anal canal
- perianal - drain as close to anal verge as poss, curvilinear incision
- intersphincteric - drain into anal canal/rectum via internal sphincterotomy (if drain perianally will eg high fistula)
- make mucosal incision below dentate line & internal sphincter muscle is divided up to dentate line; abscess cavity then deroofed; then cut edge of mucosa and int sphincter muscle may be sutured (marsupialised) for haemostasis
- supralevator
- abscesses that form as an upward extension of an ishciorectal abscess should be drained through a skin incision
- abscesses originating from a pelvic process or as an upward extension of an intersphincteric abscess should be drained into rectum through incision in rectal wall or through a transanal drain to avoid creating an extrasphincteric fitula
- ischiorectal - subcut incision (as close to anus as poss) +/- malecot
- horseshoe abscess - multiple incisions better than one large incision, can place seton between 2 incisions
- most horseshoe abscesses originate from deep posterior anal space deep to external sphincter & inferior to levator ani muscle, before progressing into unilateral or bilateral ischiorectal spaces
- key to tx = adequate drainage of deep posterior anal space
- for isolated deep postanal space abscess, can make radial posterior incision midway between anus adn coccyx (but posterior incisions difficult to heal so slightly off midline is better alternative)
- dissect through subcut tissue and divide anococcygeal ligament at posterior midline to drain posterior anal infection
- most pts don’t present w isolated deep postanal space infection but w a unilateral (more common) or bilateral (rare) horseshoe abscess
- counter incisions can then be made on one or both sides to drain any extension of infection to the ischiorectal spaces from the postanal space
- draining seton can be placed, but often fistula tract is difficult to identify bc most pts present w the ischiorectal space inflamed and/or infected
- recurrence of abscess/fistula in 30%
7
Q
What is the classification and aetiology of fistula in ano?
A
Park’s classification - based on the cryptoglandular hypothesis & presence of intersphincteric sepsis, where ‘sphincteric’ relates to the external sphincter - 4 main groups
- Type 1 (45%): intersphincteric fistula that travels along the intersphincteric plane.
- Type 2 (30%): transsphincteric fistula that encompasses a portion of the internal and external sphincter.
- Type 3 (20%): suprasphincteric fistula that encompasses the entire sphincter apparatus.
- Type 4 (5%): extrasphincteric fistula that extends from a primary opening in the rectum, encompasses the entire sphincter apparatus, and opens onto the skin overlying the buttock.
- NB superficial (ie not related to anal sphincters) = not part of Park’s classification
Simple vs complex
-
Simple
- superficial fistula
- intersphincteric fistula
- low transsphincteric fistula (<30% sphincter complex)
-
Complex
- high transsphincteric fistula (>30% of sphincter complex)
- suprasphincteric
- extrasphincteric
- horseshoe fistula
- recurrent disease
- multiple tracts
- anterior fistula in women
- pre-existing incontinence
- prior radiation
- secondary (eg to Crohn’s, malignancy, TB, HIV)
Aetiology
- most as a sequelae of cryptoglandular abscess
- others: traumatic, iatrogenic, malignant, STI, IBD
8
Q
What do you want to establish on history and exam when assessing a patient with a fistula in ano?
A
History
- intermittent perianal pain/discharge
- GI sx suggestive of IBD
- PHx of abscess or perianal surgery
- continence/obstetric history
- previous colonoscopy
- risk factors for STI
Examine (may be under GA)
- location of internal opening
- location of external opening
- course of tract
- secondary tracts
- presence of any other diseases complicating the fistula
- presence of any sepsis, condition of sphincters
- note relative positions of int and ext openings indicate the likely course of the primary tract & presence of any palpable induration esp supralevator should alert surgeon to a secondary tract
9
Q
What is Goodsall’s rule?
A
A law that helps to predict the location of an internal opening in relation to an external opening within 3cm of the anal verge. An imaginary transverse line is drawn across the anus. An external opening anterior to this line predicts a radial tract. An external opening posterior to this line predicts a curved tract with the internal opening in the posterior midline.
An anterior opening >3cm from anal verge may have a long tract opening in the posterior midline.
Fistulas assoc w other diseases eg Crohn’s, malignancy, don’t follow this rule.
10
Q
How do you investigate a fistula in ano?
A
EUA.
Don’t do MRI routinely but can be useful if complex or recurrent disease
St James’ classification:
- grade 1 = simple intersphincteric tract
- grade 2 = intersphincteric w abscess/secondary fistulous tract
- grade 3 = transphincteric
- grade 4 = transphincteric + abscess or secondary tract within ischiorectal fossa
- grade 5 = supralevator and translevator disease
11
Q
What is the management of a fistula in ano?
A
* acutely: drain sepsis only (meta-analysis of trials looking at acute fistulotomy or seton found reduced risk of recurrence at final f/u but this was assoc w tendency to higher risk of flatus incontinence & soiling (RR 2.46)
* exception would be an obvious chronic tract in context of recurrent abscess formation * then early elective EUA
* define anatomy
* if simple fistula, fistulotomy
* in general, may lay open if encompasses
* half of ext sphincter posteriorly in a man, 1/3 in a woman
* 1/3 of ext sphincter ant in a man, never anteriorly in a woman
* if not simple, want sepsis eradicated & well-formed chronic tract; place seton
- Simple fistula
- fistulotomy (heals >90%, recurrence 7% in 3yrs)
- Complex fistula
- staged procedure - draining seton, wait >6 weeks, then choose sphincter-sparing procedure based on fistula anatomy & surgeon preference (or can leave seton indefinitely)
- Options as follows: (JB/UTD)
- intersphincteric: seton only, laying open of fistula or LIFT procedure
- trans-sphincteric: seton only, laying open of fistula is <30% involved, or LIFT procedure
- UTD says they do LIFT when the primary (internal) opening has migrated distal to dentate line or if pt has preexisting incontinence; and if internal opening is at dentate line, can do either endoanal advancement flap or LIFT
- supra-sphincteric: unlikely to heal with seton. Mucosal advancement flap with curettage of external opening (LIFT not an option bc there is no intersphincteric fistula tract). Refer to anorectal specialist
- extra-sphincteric: investigate for complex disease; typically not of cryptoglandular origin but caused by cancer or Crohn’s disease. Refer. Rare and difficult to treat; surgical options include proctectomy or faecal diversion
- horseshoe fistula: initially managed with drainage of the lateral sides with setons and a midline seton from the posterior primary opening to the deep postanal space. Lateral setons can be removed after 12wks, and the primary opening can be managed w an endoanal flap or a snug seton (ie modified Hanley procedure)
Other options - infill materials - glues & plugs
- biologic material to promote closure of fistulae w/o division of any sphincter muscle
- both plug & glue promote healing of track by providing an ECM that serves as a scaffolding, allowing ingrowth of host tissue for incorporation & remodeling (promotes healing through fibroblast migration & activation & formation of a collagen network)
- success rates ~40% (initially 80%)
Notes about after seton placement:
- principal role of loose seton = drain acute sepsis, allow inflammatory changes to settle facilitating safer definitive fistula tx, or ¯risk of abscess formation after administration of biologics in Crohn’s
- next step:
- if good healing both of wounds & around seton, can remove at 2-3mo on basis that the driving force of fistula in intersphincteric space has been removed (40-50% will heal)
- any suspicion of ongoing sepsis à repeat EUA
- w a loose seton in place, several options
- may be happy living w a controlled fistula w long-term draining seton
- sphincter-sparing procedure might be considered
- fistulotomy may be performed (setons tend to migrate a bit, so at repeat EUA 3-6mo later, ~75% of fistulae can be laid open
12
Q
What are haemorrhoids and what are their aetiology?
A
Normal:
- there are two arteriovenous plexuses - one in the upper anal canal (internal haemorrhoidal plexus) and one at the anal verge (external haemorrhoidal plexus)
- internal haemorrhoidal plexus, aka anal cushions, lie above the dentate line and are covered by columnar epithelial cells that have visceral innervation
- classically described as being in 4,7,11 o’clock in lithotomy
- average of 6 haemorrhoidal arteries originating from the superior rectal artery & reaching the haemorrhoidal zone
- int haemorrhoidal plexus drains into middle rectal veins & then into int iliac vessels
- cushions complement anal sphincter function in normal physiology by providing find control over continence of liquid gas (contribute up to 20% of resting anal pressure)
- cushions function normally when fixed to their proper sites within anal canal by fibromuscular ligaments, which are anal remnants of the longitudinal layer of muscularis propria from teh rectum (Treitz’s ligaments)
- external haemorrhoidal plexus lies below dentate line in subcut tissue at anal verge & drains via int rectal veins into pudendal vessels & then into int iliac vein
- these haemorrhoids are not normally visible & don’t really contribute to physiology of anal canal
- covered by anoderm that is comprised of modified squamous epithelium containing pain fibres
Abnormal: Anal cushion displacement theory
- haemorrhoidal disease affecting int haemorrhoids develops when tissues supporting the anal cushions (submucosal muscle fibres, Treitz’s ligaments) deteriorate, allowing them to slide down into the anal canal; this may occur due to prolonged and repeated downward stress from raised intra-abdominal pressure/straining
- with this downwards displacement of the cushions comes impairment of venous drainage, progressive venous engorgement, local stasis & transudation of fluid (‘soiling’) +/- prolapse
- once prolapse occurs, further engorgement of these vasc cushions –> pain & anal spasm which prevents reduction –> viscious cycle of prolapse & congestion
- microtrauma during defaecation produces small lacs of vessel wall & consequently bleeding
- local blood stasis also promotes venous thrombosis
- thrombosis of external haemorrhoids/perianal varix/haematoma
- spontaneous thrombosis of inferior haemorrhoid plexus = the precipitating event in ext haemorrhoid thrombosis
- internal haemorrhoids can prolapse chronically but becomem thrombosed when tissue becomes fixed outside the sphincter, impeding venous return
- usu a hx of straining/constipation w acute onset of pain after
- thrombosis of external haemorrhoids/perianal varix/haematoma
- Venous engorgement of the haemorrhoidal plexus is caused indirectly or directly with excessive straining and/or increased intra-abdominal pressure
- excess straining
- increased abdominal pressure
- hard stools/constipation
- pregnancy
- straining in labour
- defaecation in squatting position may also aggravate tendency to prolapse as this increases perineal descent and pressure
13
Q
How are haemorrhoids classified?
A
- internal vs external - based on physical exam
- external = distal to dentate line, arise from ectoderm and covered by squamous epithelium
- innervated by cutaneous nerves from the sacral plexus via pudendal nerve and sensitive to pain
- internal = arise from endoderm, thus covered w columnar epithelium
- external = distal to dentate line, arise from ectoderm and covered by squamous epithelium
- grading of internal haemorrhoids by degree of plexus prolapse
- 1st degree: bleeding after BM, no prolapse
- 2nd degree: anal cushions prolapse after BM but reduce spontaneously
- 3rd degree: anal cushions prolapse requiring manual reduction
- 4th degree: irreducible, can’t be reduced
14
Q
Management of haemorrhoids
A
- dietary - fibre supplements and increased fluid intake
- steroid ointments (eg ultraroct = steroid & LA) - useful when contraindications to more aggressive therapies? eg pregnancy, coag disorders, immmunosuppression
- sclerotherapy - for 1st & 2nd degree
- less frequently used now but can use if on anticoagulant
- 5% phenol in almond oil - 3mL into submucosa at anorectal junction/above each ‘cushion’ (around pedicle, at level of anorectal ring)
- causes local inflammation –> reduced blood flow, fibrosis which draws minor prolapse back into anal canal/strengthens anal cushions
- risks:
- bleeding (injection too superficial –> mucosal necrosis)
- inadvertently deep injections can cause perirectal fibrosis, prostatitis, infection, urethral irritation (prostatitis +/- severe sepsis)
- pain
- skin infection
- relapse - 40%
- rare but major complications eg impotence, fatal nec fasc & abdo compartment syndrome after sclerotherapy been reported
- banding
- technique of choice for grade 2 - initial relief in 80%, effective in 68% at 5yr f/u
- band above dentate line and redundant tissue sloughs away after 7-10 days forming scar that ‘re-suspends the haemorrhoid’
- may require several goes
- risks: pain/spasm, urinary retention (1%), bleeding, infection, recurrence, tenesmus
- relative contraindications: immunocompromised pts (chemo, HIV/AIDS), coagulopathy/anticoagulants
- Haemorrhoidectomy
- better long-term efficacy than banding espec for grade III
- but more pain, complications, time off work than banding, so banding preferred for grade 2
- indications:
- failure of non-operative measures to control bleeding
- (3rd or) 4th degree
- haemorrhoids complicated by strangulation, ulceration, fissure or fistula
- symptomatic external haemorrhoids
- pts on anticoagulants/bleeding disorders (ie can’t band but have signif dx)
- contraindications: Crohn’s, pregnancy
- options include
- Closed (Ferguson/Parkes technique): simultaneous excision of int & ext haemorrhoids; ellipse made encompassing complete haemorrhoidal column, ensuring enough anoderm preserved & preserving underlyling sphincter. Feeding vasc pedicle at prox point sutured & defect closed w a running absorbable suture.
- Open (Milligan-Morgan): differs in that excision site not closed & left open
- Open & Closed similar results re pain, complications, LOS
- Can use scissors, diathermy, Ligasure, Harmonic
- ligasure reduces postop pain & urinary retention, shorter op time, shorter LOS & quicker return to work
- Complications: pain (nerve block, GTN?, metro), urinary retention (up to 30%), faecal incontinence (2%), infection (1%), delayed haemorrhage (1%, peak day 6), stenosis (3-7%, usu presents 6wks postop)
- Main rationale for not undertaking emergency haemorrhoidectomy for acutely thrombosed haemorrhoids = 1) painful for about same amount of time as for natural healing and 2) benefits of surgery lessen as condition resolves. V rarely prolapsed int haemorrhoids w a gangrenous component may need excision. Perianal haematomas presenting v early may be drained with small ellipse.
- Stapled haemorrhoidopexy
- idea is that normal haemorrhoidectomy deals w sx alone by excising anal cushions but doesn’t deal with the descent of the anal cushions
- transanal circular stapling instrument; technique consists of a circumferential mucosectomy & mucosal lifting (haemorrhoidopexy); aims not to excise ‘diseased’ haemorrhoidal cushions but rather to reconstitute normal anatomy & physiology of haemorrhoidal plexus which in turn will decongest and shrink the engorged haemrrhoidal tissue (benefit of allowing haemorrhoidal cushions to remain & perform their role in continence)
- results in excision of a circumferential portion of lower rectal & upper anal canal mucosa & submucosa w a circular stapling device
- short term better than traditional haemorrhoidectomy w regard to postop pain, bleeding & LOS
- no better than ligasure however for range of measures
- compared to classic haemorrhoidectomy, increased recurrence of haemorrhoidal prolapse & anal skin tags
- also potential for serious morbidity/mortality - probably from a full- or near-full-thickness staple line & anastomotic leak
- haemorrhoidal arterial ligation
- non-excisional technique; based on occlusion of haemorrhoidal arterial flow that feeds the haemorrhoidal plexus by Doppler-guided identification & ligation of the terminal branches of the superior rectal artery using a specially designed proctoscope
- decreased blood flow to haemorrhoids –> shrinkage of anal cushions
- post-op pain 18.5%, recurrence 4.8% for 3rd degree and 26.7% for 4th degree but addition of mucosal plication (RAR?) reduced recurrence for 4th degree
- equal results w stapled haemorrhoidopexy but signif less post-op pain cf stapled
15
Q
AAST rectal injury scale
A
Grade I: contusion/haematoma w/o devascularisation +/- partial thickness lac
Grade II: lac ≤50% of circumference
Grade III: lack >50% of circumference
Grade IV: full-thicknes slac w extension into perineum
Grade V: devascularised segment
