Chronic Anal Fissure

Fig. 16.1
Algorithm for management of chronic anal fissure

The various components of the algorithm are explained below.

Medical Management of Sphincter Spasm

Topical Creams: Nitric Oxide Donors and Calcium Channel Blockers

Primary therapy for chronic anal fissure consists of a topical agent combined with a stool softener.

The first pharmacological treatments developed were the nitric oxide donors. These cause vasodilation and smooth muscle relaxation and are long established in the management of coronary artery disease. Topical glyceryl trinitrate (GTN) causes relaxation of the internal sphincter [13] and is the most studied of all medical therapies for anal fissure. The usual course is 0.2 %, applied directly to the anus two or three times daily, for 8 weeks. The Cochrane meta-analysis published in 2008 included 15 randomised trials (1,190 patients) and reported an overall fissure healing rate of 48.6 % for GTN paste versus 37 % for placebo [13]. This was statistically significant. The principal side effect of GTN is headache which may occur in up to 50 %.

Direct comparison of trials is complicated by the different dosages of GTN used, the criteria used for distinguishing chronic and acute fissures and the duration of symptoms prior to treatment. However, GTN is still considered first-line therapy in many centres as it is easily available and its safety is undisputed. However, as half of patients treated with GTN will not respond [13], the downside for the patient is 6–8 weeks of persistent symptoms and possibly headache with the ultimate need for second-line treatment. There are few data on whether these patients should be scheduled for surgery after treatment failure or whether further medical therapy confers any benefit.

Despite its frequent use, the role of topical GTN in chronic anal fissure remains uncertain. Although it showed early promise in healing fissure, initial enthusiasm has been tempered somewhat by concerns over medium-term relapse, headache and tachyphylaxis. As a topical preparation, there are inevitable difficulties with regulating dose, and non-compliance may also be common.

There are probably additional explanations for the shortfall in healing rates with GTN. Pitt et al. followed 64 patients treated with GTN with the aim of identifying independent risk factors for treatment failure. Failure to heal was more likely in the presence of a sentinel tag (p < 0.035) and in fissures present for more than 6 months (p < 0.05) [14]. This suggests an inability of medical therapy to heal fissures at the truly chronically established end of the spectrum. There is also a subgroup of patients with chronic fissure who fail to exhibit reductions in resting pressure in response to topical GTN, and healing seems unlikely in these patients [15]. Furthermore, patients with low or normal resting anal pressures may also fail GTN therapy as sphincter spasm is probably not the principal underlying reason for persistence of the fissure in these patients.

Calcium channel blockers, such as diltiazem and nifedipine, lower resting anal pressure by causing smooth muscle relaxation. As with GTN, there is also a vasodilator effect, hence the established role of these drugs as antihypertensives. For anal fissure, topical calcium channel blockers are applied for 6–8 weeks. Four trials with heterogenous methodologies, comparing calcium channel blockers with GTN, were included in a Cochrane Review [13]. These studies are limited by small sample size or short follow-up, but there was no significant difference in healing rates between GTN and calcium channel blockers, whereas side effects such as headache are more common with GTN. In the United Kingdom, anal fissure is at present an unlicensed indication for topical diltiazem although it may be used in patients who have not responded to topical nitrates.

A study of 64 patients comparing topical 0.5 % nifedipine with lateral sphincterotomy reported healing rates of 96.7 % at 8 weeks and 93.3 % at 19 months in the nifedipine group, which was not significantly less than the 100 % in the lateral sphincterotomy group [16]. Overall side effects were higher with nifedipine (headache 15.6 % vs 0 %; flushing 15.6 % vs 0 %; anal irritation 18.7 % vs 6.2 %), but 12.5 % of patients in the sphincterotomy group developed permanent flatus incontinence as contrasted by 0 % in the nifedipine group [16].

Whilst the efficacy of topical medical therapies remains in question, and the side effects are well documented, there are no concerns regarding long-term safety. Therefore, we believe that primary therapy for chronic anal fissure should be with a topical agent. We use GTN as the first-line therapy, reserving diltiazem for those who are intolerant to GTN.

A course of topical therapy is also useful in identifying those patients who may have low or normal pressure fissures and would be less likely to respond to escalation of treatments aimed at reducing resting pressure (e.g. botulinum toxin and internal sphincterotomy). It is not practical to perform anal manometry in every patient with chronic anal fissure, so response to topical therapy is used to select those patients in which manometry is likely to be helpful. For example, a patient who is fully compliant with an 8-week course of topical therapy, yet does not respond at all, should go on to have anal manometry studies for measurement of sphincter pressures, whereas a patient who partially responds, or responds and relapses, probably has a high pressure fissure. Reasons for persistence or recurrence of these fissures may include chronic fibrosis, poor compliance or the reduction in resting pressure being inadequate or not sustained for long enough.

Botulinum Toxin A

Botulinum toxin A (BTX), a neurotoxin produced by Clostridium botulinum, is established in cosmetic medicine and for hypertonic skeletal muscle disorders. In skeletal muscle it inhibits the release of acetylcholine at the neuromuscular junction, but its action on the smooth muscle of the internal sphincter is less clear. A study using a porcine model found that BTX reduces myogenic tone and contractile response to sympathetic stimulation, either directly on smooth muscle or indirectly on the nerves, perhaps through acetylcholine [17]. When injected into muscle, BTX produces a paralysis of predictable duration (2–4 months). The aim of its use in treating chronic anal fissure is to cause a sustained reduction in resting anal pressure but for a temporary period to allow fissure healing without compromising long-term continence.

BTX is supplied in powder form which requires reconstitution with normal saline. Injection may be done in the outpatient clinic or under general anaesthesia. A total of 20–40 units of Botox™ or 100–200 units of Dysport™ is injected into the internal sphincter or the intersphincteric space on either side of the anterior or posterior midline with a fine-bore (27-G) needle. A number of alternative methods of injection, including unilateral injection, more than two injection sites and injection into the external sphincter, have been reported.

A placebo-controlled double-blind randomised trial of 30 patients published in 1998 demonstrated BTX to be considerably more effective than saline injection [18]. Patients in the intervention group were treated with a total of 20 units of Botox™ injected into the internal sphincter adjacent to the fissure on both sides. Fissure healing rates were 53 and 73 % at 1 and 2 months, respectively, in the BTX group. In the control group, only 13 % were healed at 2 months (p = 0.003). No continence disturbances occurred in the BTX group. One patient in the control group suffered temporary flatus incontinence [18].

As well as placebo, BTX has been compared with GTN and lateral internal sphincterotomy in randomised trials presented in a meta-analysis by the Cochrane Collaboration [13]. With the exclusion of three outlying studies, the Cochrane Review found BTX to be superior to placebo, equivalent to GTN and inferior to surgical sphincterotomy, with an overall healing rate with BTX of 65 % [13].

For several reasons, BTX injection has distinct advantages over other current medical therapies. BTX is administered by one-off injection, which seems to be well tolerated, thus eliminating non-compliance issues. A single injection into the internal sphincter produces a reduction in resting pressure of a similar order to that obtained with GTN. However, BTX produces a constant reduction in resting pressure sustained over a 2–3-month period which should translate to improved healing. Side effects such as temporary minor incontinence, urgency and perianal haematoma are infrequent and not sustained. Its major disadvantage is its cost, though this can be set against the cost of surgical therapy.

We use BTX in patients who have partially responded to topical agents, in those who have responded and relapsed and in those who did not respond but have high resting pressure on anal manometry (Fig. 16.1). In the absence of a sentinel tag, and in chronic fissures present for less than 6 months, BTX is injected under local anaesthetic anal block (10 mL 0.5 % bupivacaine and 10 mL 1 % lignocaine) in an outpatient setting. If there are signs of chronic fibrosis, BTX injection is combined with fissurectomy under general anaesthesia (see below).

Management of Chronic Fissure Fibrosis

Pitt et al. identified the presence of a sentinel tag and persistence for more than 6 months as independent risk factors for poor healing [14]. Chronic fibrosis cannot be treated by medical therapy, hence the failure to heal despite adequate treatment of the internal sphincter spasm.

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Feb 26, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Chronic Anal Fissure
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