Anal fissures are tears in the anal mucosa which extend from the anal verge towards the dentate line. They can occur at any age, but most commonly present in teenagers and young adults. 

The current leading hypothesis on why anal fissures occur proposes that trauma due to passage of hard stools creates an acute anal fissure. Reflex hypertonia of the internal anal sphincter causes ischaemia of the anoderm which in turn leads to non-healing and development of chronic fissures. People with previous history of anal surgery are thought to be particularly at risk as scarring from  surgery can cause stenosis or tethering of the anal canal, which makes it more susceptible to trauma from hard stool.¹ The posterior anal commissure (midline posterior) is the most poorly perfused part of the anal canal. In patients with hypertonic internal anal sphincters the blood supply is further compromised, rendering the posterior midline of the anal canal most at risk of developing fissures.²

The hallmark of acute anal fissures is severe pain after defecation lasting up to several hours, often  with a preceding history of constipation. The pain reoccurs with every bowel movement and can lead to a vicious cycle of worsening constipation, further tearing and aggravation of pain. A further frequently associated symptom is small amounts of bright red blood per rectum noted either on toilet paper or as small drops in the toilet bowel. Larger volumes of blood or dark blood including melena should alert one to a different diagnosis. 

Furthermore, it is essential to exclude a rectal tumour which may also present with pain on defecation and rectal bleeding. Thorough examination of the perineum and digital rectal examination (DRE) may reveal a sentinel anal tag or increased anal tone in patients with anal fissures. As patients with anal fissures are often in excruciating pain when the anal canal is stretched, they may refuse or be unable to undergo DRE. 

Acute anal fissures

In the acute phase, most anal fissures respond well to conservative management and indeed these should be trialled prior to specific medical or surgical management.³ Such management aims to stop the vicious cycle of pain and constipation, reduce recurrent trauma to the mucosa and allow relaxation of internal sphincter, thereby improving blood supply and healing potential of the mucosa. 

Warm water sitz baths help in soothing pain and relaxing the spasm of the internal sphincter for some time.⁴ This can be further aided by the use of simple analgesics and stool softener which should ideally be taken regularly initially to ensure painless defecation. Patients should also be advised to take plenty of oral fluids. 

The application of local anaesthetic creams may help further by alleviating the discomfort associated with defecation. There are many different preparations available which contain a variety of local anaesthetics at different concentrations. They also frequently contain agents to reduce local inflammation and aid healing. These may include steroidal agents such as prednisolone or hydrocortisone. Possible complications of these topical treatments are local irritations including allergic reactions to the anaesthetic agents. 

Chronic anal fissures

Most acute anal fissures resolve after four to six weeks of management as described, while others fail conservative management and go on to become chronic anal fissures. These have similar symptoms to acute anal fissures, with frequent additional physical findings of a sentinel tag at the external apex, exposed internal sphincter muscle and hypertrophied anal papilla at the internal apex. 

Typical chronic anal fissure as a result of non-healing acute fissure should be distinguished from atypical fissures in which there is a more chronic and sometimes infectious underlying cause. 

Atypical anal fissures which are recurrent or fail to respond to conservative management, especially in the setting of associated diarrhoea rather than constipation, should alert one to the possibility of Crohn’s disease. There are various reports suggesting that perianal Crohn’s disease can be treated successfully with topical ointments, metronidazole, prednisone or sulfasalazine.^5-7 For these patients the underlying disease process and symptomatic fissure have to be treated concomitantly to avoid possible complications such as abscess formation. 

Other atypical anal fissures may be associated with human immunodeficiency virus (HIV) infection, syphilis, tuberculosis, chemotherapy, trauma and neoplastic lesions. If suspected, the underlying cause should be diagnosed, and early specialist opinion obtained. 

Treatment

Medical treatment of chronic anal fissures

Once the diagnosis of typical chronic anal fissure is confirmed, management is aimed at reducing internal sphincter spasm, improving mucosal blood supply and healing capability. Nitric oxide (NO) donors undergo cellular metabolism to release NO, which works as an inhibitory neurotransmitter in the internal anal sphincter resulting in sphincter relaxation.⁸ This effect has been shown to last for up to 60 minutes after application without the risk of development of tolerance.⁹

A recent Cochrane Review demonstrated marginally but statistically significant better healing rates for patients receiving glyceril trinitrate (GTN) treatment versus placebo at 48.9% versus 35.5% (p = 0.0009).¹⁰  

The most common side-effect identified with NO donors is headaches, which can range from mild to debilitating.¹¹ Others include orthostatic hypotension and syncopal attacks. Also, patients should be advised that the use of GTN ointment should be avoided within 24 hours of erectile dysfunction medication such as sildenafil.¹² The application of GTN patch can be as effective as local topical application for treatment of anal fissures.¹³ 

Calcium channel blockers (CCBs) cause relaxation of smooth muscle and can abolish tone and spontaneous activity of the internal anal sphincter.¹⁴ Both oral and topical nifedipine have been shown to lower mean resting anal pressure.¹⁵ Diltiazem has been used with similar effect, although it appears to be more effective in the topical form rather than orally.¹⁶

In a recent prospective randomised double blind trial diltiazem gel was found to be superior to GTN ointment due to significantly higher healing rate and fewer side-effects.¹⁷ There are also studies to suggest the use of nifedipine in the treatment of acute anal fissures may prevent their evolution to chronicity.¹⁸ The use of oral diltiazem for treatment of chronic anal fissures has a further advantage of being limited to taking 60mg tablets twice daily with healing of the fissure in 38% of cases. 

However, these patients suffer from more side-effects and have lower response rates when compared to topical treatment which can give up to 65% healing after eight weeks.¹⁶ Similar to GTN, side-effects of CCB include: headaches, postural hypotension and gastrointestinal upset (abdominal pain, nausea, vomiting and diarrhoea). 

The internal anal sphincter is stimulated by adrenergic innervation and is inhibited by cholinergic innervation from the sacral parasympathetic fibres. Bethanechol is a muscarinic agonist which has been used with some success in reducing internal anal sphincter tone and aid in healing of anal fissures.^19,20 While muscarinic agonists have a better side-effect profile than NO donors and CCB, the studies evaluating their efficacy have had small number of patients and suggest lower healing rates.^19,20 Indoramin, an adrenergic antagonist has also been shown to reduce internal anal sphincter resting pressure, however studies have demonstrated little benefit in its therapeutic use for treatment of anal fissures.²¹ Similarly the use of minoxidil, a smooth muscle relaxant, in combination with local anaesthetics has shown no difference in healing rates compared to local anaesthetics alone.²²

Most recently the use of angiotensin converting enzyme (ACE) inhibitors in topical form have been shown to reduce mean internal anal sphincter resting pressure.²³ However, their use in the treatment of anal fissures remains to be established. 

Botulinum toxin (botox)  

Clostridium botulinum is an anaerobic bacteria which produces a variety of toxins that target presynaptic proteins. These toxins digest proteins in the plasma membrane (syntaxin and SNAP 25) and synaptic vesicle (synaptobrevin), thereby blocking the release of the neurotransmitter acetylcholine. The result of this is flaccid paralysis of the affected muscle and reduced activity of parasympathetic and sympathetic cholinergic synapses.¹² 

The use of botulinum toxin for treatment of anal fissures fills a gap between medical and surgical treatment. While most recent studies confirm healing rates similar to those achieved with CCB, botulinum toxin may still be used after failed medical therapy due to its low rate of incontinence compared to surgical intervention.^24,25 Various methods of injection have been described, including injection into single or multiple sites and at different doses, but no one method has shown to be clearly superior to the other. Relaxation of the internal anal sphincter occurs within days of treatment and lasts two to four months.²⁶

Although free of the complications associated with CCB and GTN, recurrence rates after botulinum toxin treatment can be as high as 50% after one year.²⁷ The risk of incontinence is, however, very rare, and the most common complaint post-treatment is local pain, which is generally short-lived.²⁶ 

Surgical treatment of anal fissures 

Similar to medical management of chronic anal fissures, surgical treatment aims to reduce internal anal sphincter tone, thereby increasing blood flow and allowing healing of the fissure. This is generally achieved by causing some degree of tearing to the internal sphincter fibres by various methods. 

Although effective at reducing internal sphincter tone, due to their inherent invasive nature the main problems with these surgical techniques are risk of incontinence and post-operative pain. The gold standard for treatment of anal fissures remains lateral internal sphincterotomy (LIS), which achieves reduced internal sphincter tone by surgically splitting or cutting the sphincter fibres.^28-31 The good results achieved with LIS are associated with an overall continence disturbance rate of 14% which can range from flatus incontinence (9%) to incontinence of solid stools (0.83%).³² Particular caution must be used in women of child-bearing age due to the potential added risk of sphincter damage during child birth.

The surgical option of anal dilation is now largely abandoned due to the unpredictable nature of the result and possible incontinence after. 

Anal dilation is now largely replaced by injection of botulinum toxin, with patients who fail this treatment going for LIS. Anal fissure excision, where the edges of the fissure are excised and the healthy tissue sewn over, is frequently employed as an alternative to LIS. Excision of the fissure alone often causes a painful defect which can take a long time to heal. For this reason, excision is often performed with an advancement flap. This procedure has the advantage of complete preservation of the internal sphincter and therefore lower risk of incontinence. 

Recent studies comparing LIS to anal advancement flap demonstrate comparable results, however LIS remains the gold standard.^33-35 While proponents of the advancement flap technique advocate its use in treatment of all chronic fissures, it shows particular usefulness in treatment of fissures with normal or hypotonic internal sphincters.³⁶

Conclusion

Anal fissures are a common problem with many treatment options. 

Once the diagnosis of simple chronic anal fissure is confirmed, the treatment should be tailored to the individual to provide best possible chance of healing with minimum risk of complication. Failed conservative and medical management is an indication to proceed to surgery.  

References

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