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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Anal fissure

and .

Department of Surgery, University Hospital, Nottingham, UK

Introduction

An anal fissure is a linear tear in the skin of the distal anal canal below the dentate line. It is a common condition affecting all age groups but particularly common in young adults; men and women are equally affected. The classical symptoms are of anal pain during or after defaecation and the passage of bright red blood per anus. The pain is often severe and may last for a few minutes or for several hours after defaecation. Bleeding from an anal fissure is usually modest and any significant loss of fresh blood may be from another source such as haemorrhoids as these two conditions commonly co-exist. Pruritus ani may also accompany anal fissures. Symptoms from fissures cause considerable discomfort and reduction in quality of life.

On examination the fissure may be apparent as a linear or pear-shaped split in the lining of the distal anal canal as the buttocks are parted, but there is often marked spasm of the anal canal which obscures the view. The combination of spasm and pain often precludes a digital rectal or proctoscopic examination but a typical history supported by clinical findings of anal spasm makes the diagnosis of anal fissure highly likely. If visualized an acute fissure will have sharply demarcated fresh mucosal edges and there may be granulation tissue in its base. With increasing chronicity there is induration of the margins of the fissure and a distinct lack of granulation tissue; horizontal fibres of the internal sphincter muscle may be seen in the base of the mucosal defect and secondary changes such as a sentinel skin tag, hypertrophied anal papilla or a degree of anal stenosis may be present.

The majority of anal fissures are probably acute and resolve either spontaneously or with simple dietary modification to increase fibre and laxatives where appropriate. The distinction between acute and chronic fissures is an arbitrary one, but fissures failing to heal within 6 weeks despite straightforward measures are generally designated as “chronic”. Although a proportion (less than 10%) of these chronic fissures will eventually resolve with conservative measures, most will require further intervention in order to heal. Fissures are usually single and posterior midline fissures are most common, but 10% of women and 1% of men have fissures in the anterior midline. Women who develop symptoms after childbirth usually have anterior fissures. Multiple fissures or those in a lateral position on the anal margin raise suspicion as there may be underlying inflammatory bowel disease, syphilis, or immunosuppression including HIV infection. However, it is important to recognize that most fissures arising in patients with inflammatory bowel disease are posterior and are also painful in at least one half of cases. Similarly, fissures that are resistant to treatment should prompt further investigation.

Pathogenesis

The pathogenesis of chronic anal fissure is poorly understood. In the past it was believed that the passage of a hard stool traumatized the anal mucosa. Although a plausible initiating factor, this does not explain why only one in four patients reports constipation and the onset of symptoms follows a bout of diarrhoea in 4 to 7% of instances. A dietary association may exist as people taking a diet low in fibre appear to be at increased risk of developing anal fissures.

There may be more than one pathogenic process leading to the development of chronic fissures:

Trauma during pregnancy

Up to 11% of patients with chronic anal fissures develop symptoms following childbirth and the risk increases with traumatic deliveries. Shearing forces from the foetal head on the anal mucosa may have significance in this group of patients. Postpartum, the anal mucosa may become tethered to the underlying muscle thereby rendering it more susceptible to trauma, and this has also been cited as a possible aetiological factor. Both theories on the mechanism of trauma are speculative and difficult to substantiate.

Anal spasm

The resting pressure in the anal canal is largely a function of the internal sphincter which is in a continuous state of partial contraction that is both nerve-mediated via α-adrenergic pathways and due to inherent myogenic tone. Relaxation of this smooth muscle occurs automatically in response to rectal distension, the so-called rectoanal inhibitory reflex. Acetylcholine via muscarinic receptors and β-adrenergic stimulation both mediate relaxation in isolated strips of internal sphincter. The same effect is observed in response to electrical field stimulation via a non-adrenergic, non-cholinergic neuronal pathway and nitric oxide has been demonstrated to be the neurotransmitter responsible.

Patients with chronic anal fissure generally have raised resting anal pressures due to hypertonicity of the internal anal sphincter, but the mechanisms of this are unclear. A long high pressure zone in the anal canal and ultraslow waves are seen more commonly in fissure patients than in healthy controls and there may be an abnormal rectoanal inhibitory reflex. The administration of pharmacological preparations that relax the internal anal sphincter, effectively reducing anal pressure, can lead to healing of chronic fissures. However, this effect on the muscle is reversible and resting pressures appear to return to original values once treatment is discontinued, even after the fissure has healed. These findings suggest that the anal spasm may predate the onset of the fissure. The internal sphincter spasm is probably not secondary to pain as the application of topical local anaesthetic to a fissure alleviates the pain but does not reduce the anal spasm.

In the presence of chronic anal fissure, the internal anal sphincter has been shown on histological examination to be fibrotic both in the base of the fissure and at remote sites. This finding has led to the suggestion of an underlying inflammatory process where myositis occurs early on in the condition with subsequent fibrosis. The fibrosis may in fact be secondary to ischaemia. However, despite various theories, the cause of the spasm associated with anal fissure remains obscure.

Local ischaemia

Chronic anal fissure has been described as an ischaemic ulcer. The distal anal canal receives its blood supply from the inferior rectal arteries, branches of the internal pudendal arteries. In cadaveric studies, angiography of the inferior rectal vessels has demonstrated a paucity of arterioles at the posterior commissure in 85% of cases, the site for which fissures appear to have a predilection. Blood flow to the distal anal canal, measured by laser doppler flowmetry is inversely correlated with anal pressure and increases as pressures fall. General anaesthesia, sphincterotomy, and the application of topical glyceryl trinitrate (GTN) ointment all lower resting anal pressure and simultaneously increase the local tissue perfusion in anal fissure. As lateral internal sphincterotomy and topical GTN successfully heal 90% and 70% of fissures respectively, the blood supply prior to treatment may have been inadequate for healing to occur. It is possible that blood vessels traversing the hypertonic internal sphincter en route to the anal mucosa may be compressed, resulting in compromised perfusion of the anal mucosa and fissure. Since the spasm in the anal canal in patients with chronic anal fissures appears to predate the fissure, this would support an ischaemic basis for chronic anal fissure, and imply that some people may be predisposed towards developing anal fissures.

Treatment

Acute fissure

Over 90% of acute anal fissures will heal spontaneously or with simple measures. A diet high in fibre (with an increased intake of water) is recommended, laxatives may be required to soften constipated stool, while warm sitz baths may offer symptomatic relief. Topical preparations of hydrocortisone and local anaesthetics have been compared with dietary bran supplements and probably confer no added benefit. These preparations may have adverse effects and a patient in one study found that topical steroid precipitated extensive anal herpes, previously occult. There is evidence that local anaesthetic significantly delays healing compared with bran supplements or topical hydrocortisone and may also lead to skin sensitisation. The use of lubricated anal dilators prior to defaecation gained popularity for a period of time, but fell out of favour as studies reported a high relapse rate among those initially cured. The majority of fissures responding to this treatment in the first instance were acute fissures.

Chronic fissure

A small number of chronic fissures heal without intervention but the vast majority do not. The treatment of chronic anal fissure is directed at reducing the spasm of the internal anal sphincter and hence, anal canal pressure. Traditionally this has been achieved surgically by sphincterotomy, where part of the internal anal sphincter is divided, but more recently various pharmacological agents have been shown to lower resting anal pressure and promote healing.

The recognition of nitric oxide as a neurotransmitter mediating relaxation of the internal anal sphincter has led to the use of exogenous nitric oxide from drug donors in the treatment of chronic anal fissure. Various preparations of isosorbide mononitrate, isosorbide dinitrate and glyceryl trinitrate have been shown to successfully heal chronic fissures.

Topical glyceryl trinitrate (GTN) ointment applied to the anal verge has now gained acceptance in many centers as an effective first line treatment for chronic fissures. GTN is metabolized at a cellular level to release nitric oxide which in turn mediates relaxation of the internal sphincter via the guanylate cyclase pathway. This effect has been coined a “chemical sphincterotomy”, and is reversed once treatment is stopped. The dose of GTN delivered depends upon the concentration and the volume of ointment applied. A regime using approximately 500 mg of 0.2% GTN ointment, applied twice daily to the anal verge, has been shown to heal 70 to 80% of chronic fissures. Fifty per cent of patients using GTN develop a headache which may be sufficiently severe to warrant discontinuing the drug. Anal pressures appear to return to pre-treatment levels within 3 months of GTN being stopped even after the fissure has healed and there is therefore the possibility of the fissure recurring. The long term follow up, by questionnaire, of 41 patients included in a randomized controlled trial using 0.2% GTN for chronic fissure reported a recurrence of symptoms in 11 patients within a median of 2 years; 8 resolved with further GTN and 3 underwent sphincterotomy. This illustrates that almost 93% of patients in the study avoided surgery for their fissures and demonstrated that topical GTN may be used effectively should fissures recur.

Botulinum toxin has also been used to treat chronic anal fissures. It is a potent neurotoxin, binding to presynaptic cholinergic nerve terminals and inhibiting the release of acetylcholine. Muscle paralysis occurs within hours and the effect remains for 3–4 months, until there has been axonal regeneration with the formation of new nerve terminals. There is some confusion in the literature about the optimal site of injection of the toxin. Studies including small numbers of patients where the toxin has been injected into the external anal sphincter have reported healing rates of over 80%. The internal sphincter has also been injected with botulinum toxin causing reduction in resting anal pressure and healing of 70–80% of fissures. In the external anal sphincter the toxin probably causes relaxation by inhibiting the release of acetylcholine from nerve terminals. However, acetylcholine mediates relaxation in the smooth muscle of the internal sphincter and so blockade of its release by botulinum toxin ought to increase anal tone. The mechanism by which botulinum reduces the tone in internal sphincter remains unclear. The treatment itself has the advantage of having a prolonged effect that is nonetheless reversible, avoiding the risk of permanent injury to the anal sphincter mechanism. On the other hand it is invasive and associated with complications such as perianal haematoma, sepsis, and pain during injection of the toxin. It is somewhat difficult to be certain as to precisely where the toxin has been injected and patients may find the procedure uncomfortable.

Pharmacological agents are employed as the first line treatment for chronic fissures in many centers, but failure of medical therapy in the presence of persistent symptoms warrants surgical intervention. The surgical approaches to chronic fissures have included anal stretch, posterior sphincterotomy through the base of the fissure later replaced by lateral internal sphincterotomy, and most recently advancement flaps to cover the mucosal defect. Anal stretch is a nonstandardized procedure and the resultant disruption to the sphincter mechanism, as demonstrated by endoanal ultrasonography may be significant and lead to permanent damage to the sphincter mechanism. Incontinence for flatus and soiling is reported in up to 39%, up to 16% have faecal incontinence and recurrence of fissure following anal stretch occurs in as many as 56.5%.

Sphincterotomy was initially performed at the site of the fissure usually in the posterior midline, and the fibres of the internal sphincter were divided in its base. However, posterior sphincterotomy wounds take noticeably longer to heal than lateral sphincterotomy sites, sepsis is more common in the former, and guttering of the posterior midline scar may occur in up to 28%. This so-called keyhole deformity sometimes leads to imperfect closure of the anal canal or trapping of faeces with resultant soiling.

Posterior sphincterotomy was then replaced by lateral internal sphincterotomy either performed using a closed technique or under direct vision, under local or general anaesthesia. Studies have shown the results of the open and closed techniques to be similar. The type of anaesthesia probably makes little difference to healing. The ideal length of the lateral sphincterotomy is undecided but most agree that it is wise to limit the incision to the length of the fissure. This procedure is complicated by varying degrees of incontinence in up to 35% of patients, that is more frequently encountered in women. One study using endosonography to assess the internal sphincter postoperatively revealed that the sphincterotomy was often more extensive than appreciated at the time of operation, particularly in female patients. To avoid complication in women with fissures in the puerperium, who may have sustained significant damage to the anal sphincter, for example severe tears or episiotomy, it is prudent to assess the integrity of the anal sphincter using anorectal ultrasound prior to surgical intervention. Where the internal sphincter is already compromised it may be more appropriate to perform an anal advancement flap to repair the mucosal defect rather than to risk impairing anal continence through iatrogenic injury to the sphincter.

Until the advent of topical GTN therapy, lateral internal sphincterotomy was the “gold standard” treatment for chronic fissures. In recent years topical 0.2% GTN ointment has become a useful first line pharmacological treatment. “Chemical sphincterotomy” is particularly suitable in patients with associated inflammatory bowel disease where sphincterotomy for anal fissure is generally contraindicated. Where pharmacological therapy fails lateral internal sphincterotomy is the surgical treatment of choice and the results are satisfactory so long as patients are carefully selected.

The future

Recent studies have demonstrated that there is a role for pharmacological agents in the treatment of chronic anal fissure. Preliminary data using calcium channel antagonists in volunteers and in patients with chronic anal fissure indicate that these drugs reduce resting anal pressure but their precise role in the treatment of fissures is yet to be determined. Bethanacol, a parasympathomimetic drug, has also been shown to lower pressures in the anal canal and by the same token shows similar promise. An obvious advantage of these alternative treatments is that they may be effective in the 30% of cases where GTN fails as they act via different pathways, so that ultimately surgery is avoided. In addition, there have not been significant associated side effects reported but patient selection is important. Calcium channel blockers, for example, may have deleterious effects in patients with existing cardiac abnormalities and can interact with other drugs. The precise role for these drugs in the treatment of chronic anal fissure remains to be seen based upon future studies.

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Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6878

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