Anal Fissure



Fig. 5.1
Acute anal fissure



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Fig. 5.2
Chronic anal fissure



5.1 Etiology


The precise etiology of anal fissures is likely multifactorial. Most would agree that trauma to the mucosa of the distal anal canal and anoderm likely plays an instrumental role in the pathophysiology of anal fissures. However, while fissures may often result from passage of a large, firm stool bolus commonly associated with constipation, many patients develop fissures after episodes of intractable diarrhea. Trauma from anoreceptive instrumentation or intercourse may also play a role. However, despite the proposed role of trauma as a precursor in the pathogenesis of anal fissures, many patients present without a history of antecedent trauma. Additionally, some patients who develop an acute fissure will heal very quickly without any specific treatment, while others will have persisting symptoms even after prolonged efforts at conservative management. Clearly, there seem to be factors besides local trauma that play a role in the development and persistence of anal fissures.

One of the most widely accepted contributing factors to the development of anal fissures, besides trauma, is elevated resting hypertonia of the internal anal sphincter (IAS). Resting anal pressure is maintained by tonic contraction of the IAS, which is mediated by both α-adrenergic innervation and inherent myotonic tone [6, 7]. Patients with both acute and chronic anal fissures have been shown to have higher maximal and mean resting anal pressures (MRAP) than normal control subjects [8, 9]. It has been proposed that IAS hypertonia may contribute to the persistence or nonhealing of anal fissures by two mechanisms: (1) spasm or lack of relaxation of the IAS during defecation, leading to continued trauma to the fissure, and (2) reduced blood flow to the fissure, leading to decreased tissue perfusion and poor healing.

The role of ischemia in the persistence of anal fissures was first proposed by Gibbons and Read in 1986 [10]. Normal resting anal canal pressure in healthy volunteers ranges from 80 to 100 mmHg, which may approach the intra-arterial systolic pressure in the inferior mesenteric artery. With increased IAS tone, IAS pressure may exceed systolic pressure and blood flow may be impeded, resulting in an area of relative ischemia and a superficial ischemic ulcer [11, 12]. In addition to increased IAS tone, the inherent microvascular anatomy of the anus may play a role in chronic fissures. Angiography performed postmortem has been shown to demonstrate decreased perfusion in the posterior midline of the distal anal canal, where a large proportion of fissures are located [13]; this has also been corroborated using Doppler laser flowmetric studies [12]. Additionally, an inverse relationship has been shown to exist between posterior midline anodermal blood flow and maximum resting anal pressure [12]; this mechanism may be responsible for delaying or preventing healing of anal fissures.

Other factors that may contribute to the development of anal fissures include reduced support of the anoderm by the underlying sphincter complex (leading to shear injury), diets lacking adequate fiber, and trauma during childbirth. Anal fissures that occur postpartum and atypical fissures associated with other disease processes typically are not associated with elevated resting IAS pressures. The presence of an anal fissure in a child without a history of constipation should alert the clinician to the possibility of sexual abuse.


5.2 Symptoms and Diagnosis


The diagnosis of anal fissure is usually suggested by the patient’s history. Patients often present either with a self-diagnosis of “hemorrhoids” or are diagnosed by their primary care provider as having hemorrhoids based simply on the presence of anal pain and bleeding, when they actually have an anal fissure. The “classic” description of symptoms includes sharp pain during and immediately after defecation. Patients usually describe the pain with defecation as a sensation of passing “broken glass” or “razor blades.” Pain after defecation often transitions to a dull, throbbing pain that is intense and may last for several hours after a bowel movement; in some patients this post-defecatory pain can last for up to 24 h. Patients may also complain of rectal bleeding with bowel movements. While this usually consists of a minimal amount of bright red blood seen on the toilet tissue, occasionally patients will report more significant bleeding. Blood mixed with the stool is not typical for patients with anal fissures and should be further evaluated to rule out other conditions. There is often an antecedent history from the patient of passage of a large, firm bowel movement or an episode of constipation and straining prior to the initial onset of symptoms.

The pain experienced by patients afflicted with an anal fissure during bowel movements often creates significant anxiety surrounding the act. This can lead to failure of the sphincter muscles to relax appropriately or spasms in the sphincter muscles with attempts to defecate. In turn, this may lead to “self-imposed” constipation, as the patient learns all too well the pain he/she can expect during bowel movements. These factors often initiate a cascade or self-perpetuating cycle of worsening symptoms due to failure to heed the call to defecate, leading to larger and more traumatic bowel movements that exacerbate the fissure and prevent appropriate healing.

Diagnosis of anal fissure is usually made by simple visual inspection. Proper positioning (either kneeling or Sims’ position) and lighting are critical. Gentle bimanual retraction of the buttocks and effacement of the anal verge will usually reveal the fissure in the distal anal canal, often just crossing over the anal verge. A sentinel skin tag or hypertrophied papilla may be visualized in close approximation with the fissure. Once the diagnosis has been confirmed, there is no need to exacerbate symptoms further by performing a digital rectal examination or anoscopy during the initial evaluation. It is critical to evaluate the anal canal at some point, either after treatment commences and symptoms resolve or at the time of surgical intervention if conservative measures ultimately fail. When dealing with atypical fissures that are either multiple, painless, or located off the midline, an exam under anesthesia should be strongly considered to exclude other pathology.


5.3 Nonsurgical Management



5.3.1 Fiber, Diet, and Anti-inflammatory Agents


More than half of acute anal fissures will heal, either with no specific measures or with increased fiber and fluid intake in order to create softer, bulkier stool; however, up to one-third of these can be expected to recur. The addition of sitz baths or warm soaks along with topical agents, such as anti-inflammatory agents or local anesthetics, may offer some contribution to healing as well. In a randomized trial comparing topical lignocaine, topical hydrocortisone, and sitz baths in combination with unprocessed bran, Jensen reported no significant differences in symptomatic relief amongst the three groups [14]. Furthermore, at 1-year follow-up, fissure recurrence was experienced by 16 % of patients receiving 15 g of unprocessed bran daily, compared with 60 % of patients receiving 7.5 g daily and 68 % of those receiving placebo [15]. Shub et al. also demonstrated a 44 % healing rate in patients with anal fissures treated with psyllium and sitz baths, though the recurrence rate during a 5-year follow-up period was 27 % [16]. Hanahel and Gordon reported initial healing in 44 % of patients with anal fissures treated with bulking agents and sitz baths, though recurrences were seen in 18.6 % [5].

The advantages of utilizing increased fiber/fluid intake and soaks/sitz baths as an initial management strategy for acute anal fissures are that it is inexpensive and moderately effective and there is essentially no risk of adverse effects. Despite the widespread availability and use of a number of hydrocortisone or other anti-inflammatory preparations, either alone or with the addition of topical anesthetics, there is little convincing evidence to suggest that they contribute significantly to the healing of anal fissures.


5.4 Case 1



5.4.1 Acute Fissure


A 45-year-old female presents with a 2-week history of severe anal pain with defecation as well as bright red blood on the toilet tissue after bowel movements. She describes the pain as sharp and stabbing during defecation, transitioning to a dull, achy discomfort that lasts for a few hours afterwards. She reports having had a very large, painful bowel movement prior to the onset of symptoms. Her primary care physician diagnosed her as having hemorrhoids and prescribed topical hydrocortisone 2.5 %, which has not improved her symptoms.

On examination, she has an acute-appearing posterior midline fissure in ano. She is counseled regarding increased fiber intake (20–25 g/day), increased fluid intake, and warm soaks/sitz baths. She is also prescribed 0.2 % NTG for topical use three times daily. After a few days, she calls complaining of severe headaches; NTG is discontinued and she is instead prescribed 5 % diltiazem for topical use three times daily.

At 6-week follow-up, her symptoms have improved significantly, though on examination, the fissure has not fully healed. She is instructed to continue with the current regimen. Two weeks later she returns to the office with worsening symptoms and on examination, the fissure appears worse. She subsequently undergoes BTX injection, and 6 weeks later she is pain-free. Examination at that time reveals that the fissure has completely healed; digital rectal examination and anoscopy reveal no other abnormalities. Her continence is normal.


5.4.2 Topical Nitrates


The main goal of therapy in patients afflicted with an acute fissure that has failed to heal with initial attempts at conservative measures is centered around the principles of managing IAS hypertonia, reducing resting anal pressure, and increasing blood flow to the fissure to facilitate healing. While the “gold standard” in the operative management of chronic anal fissures has long been considered internal anal sphincterotomy, a multitude of oral, topical, and injectable agents are often utilized to effect a “chemical sphincterotomy” and avoid surgery along with the inherent risk of altered postoperative continence.

The first class of pharmacologic agents to be used in this regard was topical nitrates, including nitroglycerin [NTG], glyceryl trinitrate [GTN], and isosorbide dinitrate [ISDN]. Nitric oxide (NO) is the predominant non-adrenergic, non-cholinergic neurotransmitter in the IAS. It stimulates guanylate cyclase, leading to the formation of cGMP, which then activates protein kinases that dephosphorylate myosin light chains, resulting in muscle fiber relaxation [17]. The use of exogenous nitrates has been shown to release nitric oxide in vivo, thus serving as nitric oxide donors and resulting in reduced resting anal pressure.

Guillemot et al. first studied the effect of topical application of perianal NTG in patients with constipation, both with and without anal sphincter hypertonicity, as well as in a control group, and found that topical application of NTG resulted in a significant reduction in MRAP in all three groups [18]. Loder et al. also investigated the effect of topical nitrates on anal sphincter function, reporting a 27 % reduction in MRAP after topical application of 0.2 % GTN [19]. Shortly thereafter, Gorfine published one of the first case series utilizing topical nitrates in the clinical management of anal fissure, in which he reported healing in 77 % of patients after 8 weeks of therapy with topical 0.3 % NTG ointment [20].

A number of randomized trials investigating the use of topical nitrates in the management of anal fissures soon followed. In a randomized, prospective placebo-controlled trial, Lund and Scholefield showed healing rates of 68 % after 8 weeks with the use of topical 0.2 % GTN compared with 8 % using placebo. They also demonstrated increased anodermal blood flow via laser Doppler flowmetry after application of GTN [21]. Bacher et al. reported healing rates of 80 % after 1 month of treatment using 0.2 % NTG compared with 40 % using 2 % lidocaine; manometric studies after 1 month of treatment also showed a 20 % reduction in MRAP in patients treated with 0.2 % NTG [22]. Carapeti et al. similarly published a randomized controlled trial that showed a healing rate of 67 % in patients treated with topical GTN compared with 32 % in those treated with placebo, though they found a significant recurrence rate [23]. Additional randomized controlled trials published by Kennedy et al. and Chaudhuri et al. reported similar trends [24, 25]. A Cochrane Database review found that GTN was significantly better than placebo in terms of healing rates (48.9 % vs. 35.5 %, p < 0.0009), though late recurrences were seen in 50 % [26]. More recently, Berry et al. compared the use of 0.4 % NTG with placebo for the treatment of chronic anal fissures, also administering acetaminophen to patients in both treatment groups prior to NTG application in order to control for the confounding effects of analgesics; they reported that pain was significantly reduced in the NTG group compared with placebo [27].

Other studies investigating the utility of topical nitrates for the treatment of anal fissures have reported contradictory results. Altomare et al. randomized patients with anal fissure to receive either 0.2 % GTN or placebo and found no difference in pain reduction or healing, despite demonstrating improved anodermal blood flow with GTN treatment [28]. Another multicenter, prospective, double-blinded study of 304 patients randomized to receive either placebo or NTG at concentrations of 0.1, 0.2, and 0.4 % found healing rates of 50 % in all groups, though 0.4 % NTG was associated with a more significant reduction in average pain intensity than other treatment arms [29].

The most widely reported adverse effect encountered with the use of topical nitrates is headache, occurring in as many as 90 % of patients. These headaches tend to be transient and often subside within 15 min of application. Starting with a lower dose and gradually escalating therapy over a 4–5-day period can often mitigate the occurrence and severity of headaches. The use of gloves or finger cots to limit systemic absorption, application in a recumbent position, and remaining recumbent for 15 min after application have also been reported to minimize headache severity [30, 31]. Despite these measures, in 10–15 % of patients, the headache associated with topical nitrate use is disabling enough to result in cessation of treatment [3234]. Perez-Legaz et al. found a lower incidence of headaches in patients randomized to receive endoanal as opposed to perianal application of 0.4 % GTN (23 vs. 54 %, p = 0.003); they also reported an improved healing rate at 24 weeks with endoanal application compared with perianal application (77 % vs. 62 %, p < 0.05) [35]. Orthostatic hypotension is also a reported adverse effect associated with the use of topical nitrates, due to the potential for vasodilation if systemic absorption occurs.

Other studies have investigated the use of higher concentrations of topical nitrates. In the study by Carapeti et al. previously mentioned, the authors investigated the use of an escalating dose of GTN, starting with 0.2 % and increasing the dose by 0.1 % weekly to a maximum of 0.6 %; they found no difference in healing rates after 8 weeks of treatment when compared with a standard dose of 0.2 % [23]. In a randomized controlled trial comparing placebo to 0.1, 0.2, and 0.4 % GTN, Scholefield et al. found no difference in any of the GTN groups compared with placebo. However, a secondary analysis excluding fissures without secondary criteria for chronicity found statistically higher healing rates for the 0.1 % GTN, 0.4 % GTN, and GTN group as a whole compared with placebo, suggesting that the use of higher concentrations of topical GTN may be more beneficial for patients with chronic fissures [36]. Unfortunately, the use of higher concentrations of topical nitrates is associated with more frequent and severe headaches, as well as a higher incidence of orthostatic hypotension .

The length of treatment has also been studied as a predictor for successful treatment with topical nitrates. Gaglairdi et al. randomized patients to either 40 days or 80 days of treatment with 0.4 % GTN and found that both pain at defecation and healing improved significantly until 40 days (p < 0.001), while the difference between 40 and 80 days was not significant [32]. In contrast, Lund and Scholefield reported that extending the use of 0.2 % GTN from 4 to 6 weeks increased healing rates from 36 to 85 % [37].

More recent studies have also examined the efficacy of L-arginine, an endogenous nitric oxide donor, in the treatment of anal fissure. L-arginine has been shown to lower MRAP and improve anodermal blood flow [38, 39], and in a phase II clinical trial, topical L-arginine was found to have a 62 % healing rate for anal fissure after 18 weeks, with no patients experiencing headache as a side effect [40].

Besides the increased incidence of headaches, the other major drawback to the use of topical nitrates is the rate of fissure recurrence, which has been reported to be as high as 67 % [41]. The reduction in MRAP induced by topical nitrate application is transient, meaning that IAS pressure may return to pretreatment levels with cessation of treatment, which can predispose to a relapse.


5.4.3 Calcium Channel Blockers


Calcium channel blockers (CCBs), such as nifedipine and diltiazem, act by inhibiting voltage-dependent calcium channels in the cell membranes of smooth muscle cells, thus decreasing intracellular calcium concentrations and interfering with calcium-mediated signal transduction and phosphorylation; this ultimately results in decreased muscle contraction and subsequent smooth muscle relaxation [17]. Chyrsos et al. demonstrated a reduction in MRAP by approximately 30 % after administration of sublingual nifedipine, establishing a basis for the potential therapeutic effect of CCBs in the management of anal fissures [42]. Factors that often limit the use of topical nitrates, such as severe headaches and systemic hypotension, are seen infrequently with CCBs, often making them a more attractive alternative.

Early reports established the clinical efficacy of both topical and oral nifedipine in the management of anal fissures. Antropoli published a series of 283 patients randomized to receive either topical 0.2 % nifedipine gel or placebo twice daily for 3 weeks; healing was seen in 95 % of the nifedipine-treated patients compared with 50 % of controls (p < 0.01) [43]. In another prospective randomized trial, Perrotti randomized patients to receive either topical 0.3 % nifedipine ointment or 1 % hydrocortisone (both groups also received 1.5 % lidocaine) and found healing in 94.5 % of the nifedipine-treated patients compared with 16.4 % of controls (p < 0.001) [44]. Another study by Cook et al. found that 20 mg of nifedipine taken orally twice daily reduced MRAP in patients with anal fissure by 36 %; this resulted in healing in 60 % and resolution of symptoms in 80 % of patients [45]. Agaoglu et al. also reported healing rates of 60 % with the use of 20 mg of oral nifedipine taken twice daily [46]. Agrawal randomized 90 patients to conventional treatment (psyllium, stool softeners, sitz baths, lidocaine ointment), oral nifedipine, or topical nifedipine and found that pain relief was significantly better in the group treated with topical nifedipine than in the other two groups, while the use of oral and topical nifedipine was found to result in comparable healing rates [47].

Further studies demonstrated similar findings with diltiazem. Carapeti et al. treated patients suffering from chronic anal fissure with topical 2 % diltiazem gel and found significant reductions in pain scores and MRAP, with a 67 % healing rate [48]. Knight et al. reported a 75 % healing rate with the use of 2 % diltiazem topical gel for 3 months; 47 % of the patients that did not heal after 3 months of treatment healed after an additional 8-week course of treatment [49]. In a randomized, controlled trial comparing the effectiveness of both oral (60 mg) and topical 2 % diltiazem, Jonas et al. reported that, after 8 weeks of treatment, healing was seen in 38 % of the patients treated via the oral route, compared with 65 % in those treated topically. Additionally, side effects (including rash, headache, nausea, vomiting, reduced smell and taste) were seen in 33 % of those treated orally, while those treated topically experienced no adverse reactions [50]. In a separate study, the same authors reported that the use of topical 2 % diltiazem resulted in healing of fissures in 49 % of patients that had failed to previously respond to a complete course of topical GTN [51].

As with topical nitrates, the major concerns regarding the use of CCBs center on long-term efficacy and recurrence once treatment is stopped and MRAP returns to baseline. Nash et al. followed 112 patients treated with topical diltiazem for an average of 2 years and found that, while more than two-thirds reported initial success, 59 % required further treatment (either medical or surgical) during the follow-up period [52].


5.4.4 Botulinum Toxin


Botulinum toxin (BTX) is an endopeptidase exotoxin synthesized by Clostridium botulinum that binds to the presynaptic nerve terminals at the neuromuscular junction of α-motor neurons, γ-neurons in muscle spindles, and all parasympathetic and cholinergic postganglionic sympathetic neurons, thus blocking acetylcholine release and causing temporary paralysis [17]. This effect can persist for as long as 3–4 months, until axonal regeneration occurs with the formation of new nerve terminals [53]. The exact mechanism of BTX in smooth muscle has not been fully elucidated, as smooth muscle fibers, unlike skeletal muscle fibers, lack neuromuscular synapses. However, injection of BTX into both the external anal sphincter (skeletal muscle) and IAS (smooth muscle) has been shown to produce sphincter relaxation [54, 55]. This temporary chemodenervation produces a “chemical sphincterotomy” without the risk of possible long-term alterations in fecal continence as can be seen with surgical sphincterotomy.

Early studies by Jones et al. using a porcine model demonstrated decreased MRAP after localized intrasphincteric injection of BTX; examination of strips of treated sphincter muscle found that the mostly likely mechanism of action on the IAS is via sympathetic blockade [56]. One of the earliest clinical studies evaluating the use of BTX in the treatment of anal fissures was reported by Gui et al., who prospectively studied the effect of injection of a total of 15 U of BTX into the IAS of ten patients with chronic anal fissure (two lateral injections and one posterior injection, five U each) and found healing of the fissure in seven patients at 2 months’ follow-up [57].

A number of subsequent studies further evaluated the safety and efficacy of BTX in the management of anal fissures. Maria et al. [58] conducted a double-blind, placebo-controlled study of BTX injection (20 U) for the treatment of chronic anal fissure and reported 73.3 % (11 of 15) healing at 2 months in the BTX group, compared with 13.3 % (2 of 15) in the control (saline injection) group (p = 0.003). The four patients in the BTX group with a persistent fissure at 2 months were retreated with another injection of BTX (25 U), and all had healed by 2 months after reinjection, with no relapses during an average follow-up of 16 months. Colak et al. demonstrated the superiority of BTX to topical lidocaine, reporting healing in 70.6 % of patients treated with BTX compared with 21.4 % in patients treated with lidocaine (p = 0.006) [59]. Lindsey et al. performed BTX injection (20 U) in 40 patients with chronic anal fissures who had failed prior treatment with 0.2 % GTN; they reported healing in 43 % and symptomatic improvement in 73 %, while 18 % experienced symptoms of mild, transient incontinence [60]. Jost and Shrank reported that a repeat injection of BTX in patients who did not heal after an initial BTX injection was effective in 63 % of patients [61].

A number of studies have sought to determine the optimal dose for BTX injection. Minguez et al. compared groups treated with 10 U (5 U on each side of the IAS), 15 U (5 U on each side of the IAS and 5 U beneath the fissure), and 21 U (7 U on each side of the IAS and 7 U beneath the fissure); they found that the groups treated with a higher dose demonstrated better pain relief, a more significant reduction in MRAP, and a lower likelihood to require reinjection for persistent symptoms. The need for surgery was similar in the first 2 groups (17 and 19 %) but significantly lower in the third group (5 %) [62]. Brisinda et al. randomized patients to receive BTX injections of 20 U (and retreatment with 30 U for persistent symptoms) or 30 U (and retreatment with 50 U for persistent symptoms), and they found that the higher dose resulted in a higher rate of healing (87 % vs. 73 %), though the higher dose was associated with a higher incidence of mild, transient incontinence to flatus [63].

Other studies have sought to determine the most effective injection technique or location(s). Maria et al. found that injection of the IAS in the anterior midline resulted in improved lowering of MRAP and produced an earlier healing scar, compared with injection in the posterior midline [64]. Othman compared two separate BTX injections of 20 U each into each side of the IAS with a single posterior midline injection of 25 U and found equivalent outcomes in terms of healing and time to pain relief [65].

Some investigators have combined BTX injection with other modalities in the management of anal fissures in an attempt to improve rates of healing. Lysy et al. reported that daily application of ISDN after BTX injection was more effective than BTX alone [66]. Jones et al. randomized patients to receive either BTX injection plus topical GTN paste or BTX injection plus placebo paste; there was a non-statistically significant trend towards better outcomes in the group treated with GTN, though healing rates in both groups were poor (47 % vs. 27 %) [67]. Two small case series describing BTX injection in combination with fissurectomy have been reported by Patti et al. [68] and Witte et al. [69], demonstrating healing in 10/10 and 19/21 patients, respectively.

The commercial availability of BTX and the ability to perform injection in the office setting has made its use commonplace. Complications of BTX injection include local discomfort at the site of injection, hematoma or hemorrhoidal thrombosis, local infection, and disturbances in continence of varying severity and duration. Recurrences rates have been reported to be as many as 41.5 % [62]. Contraindications to the use of BTX include known hypersensitivity, pregnancy, myasthenia gravis, Lambert-Eaton syndrome, and amyotrophic lateral sclerosis. Injection of BTX in patients using aminoglycosides should also be avoided due to potential enhancement of the effect of BTX [70]. In 1999, the US Food and Drug Administration issued a warning regarding overdosing with resultant respiratory failure and death [71].


5.4.5 Other Sphincter Relaxing Agents


Other pharmacologic agents have been shown to demonstrate potential in the management of anal fissures by reducing IAS pressure. Pitt et al. found that oral administration of indoramin (an alpha-1 adrenergic antagonist) reduced anal pressure in both patients with chronic anal fissure as well as in healthy controls [72]. However, in a placebo-controlled trial, the same authors found that, despite a 29.8 % reduction in MRAP, healing occurred in only 7 % of the treatment group compared with 22 % in the placebo group [73].

Bethanechol, a cholinergic agonist, has also been shown to lower anal sphincter pressure when applied topically [74]. Carpeti et al. reported healing of fissures in 60 % of patients treated with topical 0.1 % bethanechol gel with no side effects [48]. In a non-randomized trial comparing the efficacy of DTZ with bethanechol in the treatment of fissures, Araujo et al. found similar healing rates (53 % vs. 50 %, p = 0.8) after 8 weeks [75].

Jones et al. [76] have demonstrated that there are several functionally important phosphodiesterases in the IAS and rectal circular smooth muscle. Both adenosine 3′,5′-cyclic monophosphate and guanosine 3′,5′-cyclic monophosphate appear to be important in the myogenic tone of the IAS. Sildenafil, a phosphodiesterase inhibitor and nitric oxide donor, has been shown to decrease internal anal sphincter tone in vitro [77]. Torrabadella et al. reported that sildenafil significantly reduced anal sphincter pressure in a series of 19 patients with chronic anal fissures [78]. Tadalafil, another phosphodiesterase inhibitor, has also been shown to improve symptoms related to anal fissures [79].

More recently, topical application of 0.28 % captopril (an ACE inhibitor) has also been shown to result in reductions in MRAP in healthy volunteers [80]. Further studies are needed to clarify its clinical efficacy in treating anal fissures.


5.4.6 Surgical Management


While initial management of acute anal fissures is typically via conservative measures, failure of these means to resolve fissure-related symptoms after a period of 6–12 weeks warrants discussion with the patient regarding surgical management. Surgical treatment of anal fissures is targeted towards the goals of medical treatment, namely, addressing IAS hypertonia and enhancing mucosal blood flow to improve healing. Options include anal dilation, LIAS, and advancement flaps.


5.5 Case 2



5.5.1 Chronic Fissure


A 32-year-old male has been treated for the past several months for a refractory anal fissure. Prior to the onset of symptoms, his diet consisted mainly of fast food and soda, and he suffered from chronic constipation. He has increased his fiber and fluid intake and has been treated with prolonged courses of both topical 2.5 % hydrocortisone and 5 % diltiazem with no improvement in pain or bleeding. On examination he has a chronic-appearing anterior midline fissure with raised mucosal edges, visible IAS fibers at the base of the fissure, and a small sentinel skin tag at the apex of the fissure.

After discussing the options of undergoing BTX injection or LIAS, he opts for the latter. A closed LIAS and excision of the tag is performed in the operating room under monitored anesthesia care with injection of local anesthetic. At the time of surgery, a prominent IAS “band” is noted on palpation of the intersphincteric groove; this disappears after performing the sphincterotomy. At 6-week follow-up, he reports no pain or bleeding with bowel movements and has no alterations in continence. On examination, the fissure has healed, and anoscopy is unremarkable. He is instructed to maintain a high-fiber diet.


5.5.2 Anal Dilation


Anal dilation , or sphincter stretch, was first described in the early 1800s [1] and for a long period was the most widely practiced means of treating anal fissure. Its use in the current era is limited and it is mentioned herein mainly for historical completeness. The procedure involves a slow, controlled dilation of the anal canal, using up to four fingers. Healing rates range from 40 to 70 %, and recurrence rates range from 2 to 55 % [4]. However, the major limiting complication is damage to the anal sphincter with resultant alterations in continence, which includes incontinence to flatus or fecal soiling in up to 40 % of patients and true fecal incontinence in as many as 16 % [4]. A Cochrane Database review of operative procedures for anal fissures in 2011 suggested abandonment of manual dilation due to the significant risk of nonhealing and incontinence [81].


5.5.3 Lateral Internal Anal Sphincterotomy


Lateral internal anal sphincterotomy (LIAS ) is recommended as the surgical treatment of choice for anal fissures refractory to medical management [82]. The procedure involves dividing the distal portion of the internal anal sphincter to reduce MRAP and facilitate healing. As initially described by Eisenhammer [83], internal anal sphincterotomy for chronic anal fissure was performed at the site of the fissure itself, typically though the posterior midline. However, this was later found to be associated with development of a scarred groove, or “keyhole deformity,” in as many as 28 % of patients, leading to trapping of fecal matter and subsequent soiling [84]. As a result, the procedure was modified and is currently performed in a lateral location.

LIAS can be performed using either an open or a closed technique. The open technique utilizes an incision made over the intersphincteric groove with isolation and division of the distal internal anal sphincter under direct visualization (Fig. 5.3). The closed technique is performed by insertion of a beaver blade or #11 blade into the intersphincteric groove parallel to the muscles, then rotating the blade medially 90°, and withdrawing the blade, thus dividing the distal internal anal sphincter in a lateral to medial direction (Fig. 5.4). Alternatively, the blade can be inserted into the submucosal space instead of the intersphincteric space and rotated laterally, dividing the muscle in a medial to lateral direction.

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Fig. 5.3
Open lateral internal anal sphincterotomy. (a) Lateral incision to expose IAS. (b) Division of IAS under direct visualization. (c) Closure of incision


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Fig. 5.4
Closed lateral internal anal sphincterotomy. (a) Identficaton of intersphincteric groove in lateral position. (b) Insertion of scalpel into intersphincteric groove parallel to direction of sphincters. (c) Medial rotation (90 degrees) and withdrawal of scalpel, dividing the distal IAS

Reported rates of fissure healing after LIAS are generally in the range of 90–100 % [8599]. The major drawback to the procedure is the potential for altered continence postoperatively. These disturbances are typically mild and may involve fecal seepage/soiling, impaired control of flatus, or stress incontinence to liquid stool. While most of these disturbances are transient, some can persist long-term effect. The general mindset of many practicing clinicians is that altered continence after LIAS occurs infrequently, though careful review of the literature reveals that it may be seen in more than 35 % of patients postoperatively [90]. Part of the problem with determining the true incidence lies in the variability of what investigators define as “altered continence” as well as inconsistencies in follow-up.

A recent meta-analysis that included 22 studies reported continence disturbances in 14 % of patients undergoing LIAS, with weighted analysis revealing incontinence to flatus in 9 %, soilage/seepage in 6 %, accidental defecation in 0.91 %, and incontinence to liquid stool in 0.67 % [100]. Levin et al. found that in patients who developed delayed incontinence after surgery for anal fissure, the onset of incontinence was 8 years younger than patients with incontinence who had not undergone prior fissure surgery and 15 years sooner than in patients with incontinence related to post-obstetric trauma [101]. In a study designed specifically to define the risk of postoperative incontinence after LIAS, Hyman followed 34 patients prospectively and found that only three had post-op deterioration in continence scores and only one reported deterioration in quality of life [102].

Certain factors, such as prior obstetric injury or previous anorectal surgery, may predispose a patient to continence disturbances after LIAS. Kement et al. reported an 11.7 % incontinence rate after LIAS and found that prior vaginal delivery was associated with a higher incidence of “severe” incontinence [103]. This highlights the importance of taking a detailed history when considering LIAS.

A number of studies have compared the open and closed techniques to attempt to identify differences in rates of healing and postoperative incontinence. In a retrospective review reported by Garcia-Aguilar et al., patients undergoing open LIAS experienced a higher incidence of postoperative difficulties with soiling and incontinence to both flatus and stool compared with those undergoing closed LIAS [90]. Gupta et al. also reported more complications with the open technique [104]. Patel et al. found that open LIAS compared with closed LIAS was associated with a higher incidence of wound infections (10.3 % vs. 4.2 %), temporary incontinence to flatus (8.3 % vs. 3.4 %), and temporary incontinence to stool (3.4 % vs. 0 %) [105]. In contrast, other studies have shown no difference in the incidence of incontinence rates comparing the open and closed techniques [88, 94]. Yurko et al. compared 387 patients undergoing open LIAS, closed LIAS, and fissurectomy and found no differences in time to healing, incontinence, or recurrence [106]. A Cochrane Database review found no difference between open and closed LIAS in terms of persistence and postoperative incontinence [107].

Variations in LIAS technique have also been described. Lasheen et al. have described a “segmental internal sphincterotomy,” in which the IAS is divided with two separate incisions (one proximally and the other distally) in different radial planes within the anal canal; in their series of 50 patients, all fissures had healed at a mean follow-up of 18.5 months, with no reported incontinence [108]. Kang et al. described making circumferential incisions instead of radial incisions for open LIAS and found that this reduced time to wound healing significantly [109]. Bilateral LIAS has also been reported and was found to be more likely to result in healing than unilateral LIAS, with no difference in incontinence rates [81].


5.5.4 Advancement Flap


In patients that have low-pressure fissures or hypertonic fissures with risk factors for postoperative incontinence, another option is to perform an anodermal advancement flap (AAF), which is often performed in conjunction with a fissurectomy. Leong et al. reported the results of a prospective controlled trial in which 40 patients were randomized to undergo either LIAS or AAF; they found no difference between the two groups in terms of healing rates and reported no postoperative incontinence in either group [110]. Chambers et al. reported a series of 54 consecutive patients undergoing V-Y AAF and reported healing in all but one patient at 6-month follow-up and suggested that AAF be considered as first-line treatment for chronic fissures [111].

Patel et al. compared the results of 50 patients undergoing AAF to a matched cohort of patients undergoing LIAS and found that, while there was no difference in incontinence rates or healing, AAF was associated with a higher incidence of resolution of symptoms [112]. Hancke et al. also compared AAF to LIAS and found no difference in terms of healing rates, though the incidence of both short-term and long-term mild incontinence was higher in patients undergoing LIAS (short term, 20.0 % vs. 0 %, p < 0.05; long term, 47.6 % vs. 5.8 %, p < 0.05) [113].

Madgy et al. compared conventional LIAS, V-Y AAF, and a “tailored” LIAS combined with a V-Y AAF and reported healing rates of 84, 48, and 94 %, respectively. The combined LIAS/AAF group had the lowest recurrence rate (2 %), and the incontinence rate was lower in the combined LIAS/AAF group compared with conventional LIAS alone (2 % vs. 14 %) [114]. Theodoropoulos et al. also compared a “tailored” LIAS, which was extended to the apex of the fissure, combined with a V-Y AAF to conventional LIAS alone and reported faster healing, less postoperative soiling, and decreased postoperative use of analgesics in the combined LIAS/AAF group [115]. Patti et al. studied the effect of combined BTX injection along with fissurectomy and AAF in 22 patients; they reported a 100 % initial healing rate, with recurrences in 8 % at a mean 24-month follow-up. No changes in continence from baseline were reported [116].


5.5.5 Comparison of Treatment Modalities



5.5.5.1 Topical Nitrates vs. Calcium Channel Blockers


There have been a number of randomized controlled trials comparing the efficacy of topical nitrates in the treatment of anal fissures to CCBs (Table 5.1) [117132]. The majority of studies have found that CCBs are either equally or more effective than topical nitrates in healing anal fissures, with a preferable side effect profile. Most importantly, the incidence of headache, which is often the limiting factor preventing continued therapy with nitrates, is significantly reduced with the use of topical CCBs.


Table 5.1
Trials comparing topical nitrates and calcium channel blockers





















































































































Year

Author

N

Treatment

Healing (%)

Side effects (%)

2000

Carapeti [48]

15

GTN

60
 

15

DTZ

67a

2002

Kocher [117]

29

GTN

86.2

72.4

31

DTZ

77.4a

41.9b

2003

Bielecki [118]

21

GTN

85.7

33.3

22

DTZ

86.3a

0b

2003

Ezri [119]

26

GTN

58

40

26

NFD

89b

5b

2007

Shrivastava [120]

30

GTN

73

67

31

DTZ

80b

0b

30

Placebo

33

0

2009

Sanei [121]

51

GTN

54.9
 

51

DTZ

66.7a

2009

Jawaid [122]

40

GTN

82.5

72.5

40

DTZ

77.5a

32.5b

2012

Ala [123]

25

GTN

60

100

36

DTZ

91.66b

0b


CCB calcium channel blocker, GTN glyceryl trinitrate, DTZ diltiazem, NFD nifedipine

aNot statistically significant

bStatistically significant

A recent systematic review published by Sajid et al. included seven randomized trials comparing DTZ and GTN and confirmed that they are equally effective in terms of fissure healing, but DTZ is associated with a significantly lower incidence of headache and recurrence [124]. These results are similar to those previously published in a Cochrane review [125] and an earlier meta-analysis [126]. Unfortunately, trials with long-term follow-up comparing the two modalities are lacking.


5.5.5.2 Topical Nitrates vs. Botulinum Toxin


Table 5.2 summarizes the trials comparing the efficacy of topical nitrates compared with BTX in the management of anal fissures [127132]. The majority of reported trials either favors BTX or shows no statistical difference between the two modalities. Fruehauf et al. reported superior healing rates with NTG over BTX, though patients were assessed only after 2 weeks of therapy [129]. Asim et al. studied the effect of GTN treatment after BTX injection and found that it did not improve healing rates [132].
May 30, 2017 | Posted by in GASTROENTEROLOGY | Comments Off on Anal Fissure

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