Haemorrhoids and Fissures

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Presentation transcript:

Haemorrhoids and Fissures What is the pathogenesis of haemorrhoids? How can haemorrhoids be classified? How can haemorrhoids be managed? What is the pathogenesis of fissures? What are the options for managing fissures?

HAEMORRHOIDS

What are haemorrhoids? Varicose veins? Vascular hyperplasia? Degeneration of supportive tissue (the sliding anal theory)? Thompson in 1975 preformed an anatomical and clinical study 95 cadaveric anorectal specimens 80 consecutive patients Results: No evidence that the arterial or venous system was responsible as the cause for haemorrhoids The anal cushions….. NO evidence that the branching pattern of the superior rectal artery is responsible for the position of piles around the anal circumference The dilatations of veins of the haemorrhoidal venous plexus are constant and normal structures

AETIOLOGY Derived from anal cushions Discontinuous series of cushions, 3 main: left lateral, right anterior and right posterior positions Normal structures in the anal canal consisting of mucosa, submucosal fibroelastic connective tissues and smooth muscles in an arteriovenous channel system Held in place by submucosal smooth muscle and elastic fibres (Treitz’s muscle) Fragmentation of supporting submucosal fibres (by prolonged downward stress)  cushions no longer restrained from engorging excessively with blood  bleeding and prolapse Veins that traverse anal sphincter are blocked, arterial inflow continues  haemorrhoidal congestion

PATHOGENESIS Implicated factors in pathogenesis Age Constipation (not supported in large epidemiologic study) Diarrhoea Heredity Erect posture Absence of valves within the haemorrhoidal plexus and draining veins Portal hypertension Pregnancy Pelvic tumours

ANATOMY AND NOMENCLATURE External = dilated vascular plexuses located below the dentate line (covered by squamous epithelium) Internal = symptomatic arteriovenous channels above the dentate line (covered by transitional and columnar epithelium) Divided into subcategories in order of severity Management depends on degree of severity

CLINICAL Bleeding Prolapse Pain (thrombosed haemorrhoid) Pruritis Faecal soilage

MANAGMENT Can coexist with other conditions such as rectal cancer or IBD  investigate appropriately Anal cushions are normal functional anatomical structures contributing to anal continence  treatment reserved for ‘haemorrhoidal diseases’ that are abnormal and cause symptoms Therapeutic strategies depend upon symptoms and the amount of haemorrhoidal tissue prolapsing beyond the anal verge

External Hemorrhoids (Perianal Haematoma) Dilated vascular plexuses Below the dentate line Covered by squamous epithelium Pain occurs due to acute thrombosis Bleeding uncommon Can incise if early (24-48 hours) but most resolve in 5 days If untreated  skin tags

Internal Haemorrhoids DEGREE DEFINITION MANAGEMENT First Bleeding, no prolapse Stool softeners Toilet re-education Local creams (no evidence) Second Prolapse but spontaneously reducible RBL Sclerotherapy Electrocoagulation (Haemorrhoidectomy) Third Prolapse requiring manual reduction Fourth Irreducible prolapse Haemorrhoidectomy

MANAGEMENT Non-Operative Banding Sclerotherapy Diet, fibre, water, toilet re-eductation Banding Up to 3 bands at a time Painless if above the dentate line 60-80% effective depending on proper selection 2-5% risk of secondary haemorrhage Sclerotherapy Sclerosant agent injected into submucosa around the pedicle at the level of the anorectal ring Sclerosant  inflammation  reduced blood flow Sclerosant  fibrosis  draws minor prolapse back into anal canal 70% effective Deep injections  perirectal fibrosis, infection, urethral irritation

MANAGEMENT Haemorrhoidectomy Milligan-Morgan (open) or Hills-Fergusson (closed) Ligasure Stapled Less pain, higher long-term risk of recurrence and symptoms of prolapse Suitable for circumferential 3rd degree haemorrhoids Complications Pain (Rx botox or GTN) Urinary retention Bleeding Incontinence Stricture Infection Doppler-guided haemorrhoidal artery ligation Increased risk of prolapse recurrence Milligan-Morgan – grasp and evert haemorrhoid, dissecting off anal sphincter, tie pedicle, wound left open Ferguson – haemorrhoid exposed in anoscope, excision and ligation performed in anatomical position, wound closed with continuous suture Stapled hemorrhoidectomy (stapled hemorrhoidopexy) — An intraluminal circular stapling device has been developed as an alternative to conventional surgical hemorrhoidectomy. The device excises a circumferential column of mucosa and submucosa from the upper anal canal, thus reducing the hemorrhoids back into the anal canal and fixing them in position. It also interrupts part of the hemorrhoidal blood supply thereby decreasing vascularity [47-49]. It is not appropriate for treatment of external hemorrhoids. Ligasure appears as effective and associated with less post-operative pain

ANAL FISSURE

ANAL FISSURE Common problem Fissure = benign superficial ulcer or tear within the anal canal (beyond the anoderm, distal to the dentate line) Chronic fissure = persistence for more than 6 weeks despite adequate medical therapy Signs of chronicity = sentinel skin tag, intra-anal fibroepithelial polyp May result from local trauma or secondary to underlying medical/surgical problem

PATHOGENESIS Superfical tear of mucosa  pain  defecation avoidance  hardened stool Pain also causes spasm of IS and high anal pressure  reduced anodermal perfusion  ischaemia  poor healing Raised resting anal pressure from internal sphincter hypertonia Pharmacological agents to relax IS  fissure healing but resting pressure returns to pretreatment levels once fissure has healed Local ischaemia Paucity of arterioles in the posterior commisure Postpartum Anterior fissures IS hypertonia and anal spasm predate onset of the fissure

AETIOLOGY Primary Secondary Local trauma Previous anal surgical procedures IBD Granulomatous diseases Malignancy Communicable diseases

CLINICAL PAIN Bleeding Presence of a skin tag Predominant symptoms Pain on defecation, persisting to minutes  hours afterwards Bleeding Presence of a skin tag Elicit symptoms of altered bowel habit, exclude proximal colonic lesion Ex Skin tag (sentinel pile) Usually single and at 6 o’clock If multiple or eccentrically located? HIV, IBD, TB, syphilis

MEDICAL TREATMENT Stool softener GTN Diltiazem Botulinum A toxin Optimal healing in up to 70% with minimal adverse effects Diltiazem Lower side-effect rate Similar effectiveness and recurrence rate with GTN Botulinum A toxin Reduces resting anal pressure, promotes healing in 70-96% of patients Risk of incontinence Mode of action unclear Botox, CCB and GTN are significantly better than placebo Medications are safe and side-effects are not serious and are reversible with cessation of therapy Late recurrence higher with medical therapy Surgery reserved to treatment failures NO as a neurotransmitter mediating relaxation of internal sphincter

SURGICAL MANAGEMENT Clasical Lateral Sphincterotomy Division of IS to level of the dentate line Tailored Sphincterotomy IS divided to highest point of fissure only Skin tag and fibrous polyp can be removed Many variations of technique, none shown to be superior Healing rates 85-95% Incontinence to flatus and faecal soilage reported in up to 35% of patients

RECURRENT OR ATYPICAL FISSURES Consider Crohn’s or immunosuppressive conditions if not anterior or posterior midline Investigate with anal manometry and anal sphincter mapping (endo-anal ultrasound)