- Email: [email protected]
Anal fissure
Surg Clin N Am 82 (2002) 1291–1297
Anal fissure Amanda M. Metcalf, MD Department of Surgery, University of Iowa Hospitals and Clinics, 200 Hawkins Drive 4622 JCP, Iowa City, IA 52242, USA
An anal fissure is a traumatically induced longitudinal split in the squamous epithelium of the distal anal canal. It typically extends from the anal verge cephalad towards the dentate line. It most commonly occurs in the midline posteriorly, but it can also occur in the midline anteriorly. Anterior fissures are more common in women than men, occurring in 10% of women with fissures compared with 1% of men with fissures [1]. In its chronic form it is sometimes called ulcer-in-ano. Symptoms In the majority of patients, the symptoms are so characteristic as to be nearly diagnostic. Patients complain of severe intense pain initiated by the passage of stool. It can be described as knifelike, cutting, or tearing in character. This pain can persist for hours with a tight, throbbing quality. This discomfort can often by ameliorated, at least on a temporary basis, by a hot sitz bath. It is usually accompanied by small volume, bright red rectal bleeding. A minority of patients may also complain of pruritus, swelling, prolapse, and discharge [2]. Often patients will complain of constipation that predates their anal symptoms. Occasionally patients have diarrhea or an alternating pattern of constipation and diarrhea. Etiology and pathogenesis The most widely accepted theory regarding the etiology of anal fissure is that it results from the mechanical forces imposed on the anal canal during the passage of stool. Hard stools are most commonly implicated, but explosive liquid stools can produce the same results. The elliptical arrangement of the
E-mail address: [email protected] (A.M. Metcalf). 0039-6109/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 0 0 3 9 - 6 1 0 9 ( 0 2 ) 0 0 0 5 9 - 2
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external sphincter is felt to provide less support to the anal canal in the anteroposterior axis, thus rendering these locations most susceptible to trauma. Although many acute anal fissures heal spontaneously, some do not. Those that do not, develop secondary changes to the surrounding tissues that signal the long-standing nature of the condition. Over time, the skin distal to the fissure becomes edematous and enlarged, and may form a fibrous skin tag. In this situation, it is often referred to as a sentinel pile. Similarly, the anal papilla cephalad to the fissure can undergo parallel changes and become enlarged. These changes are attributed to chronic low-grade infection. The edges and the base of the fissure tend to become fibrotic over time. With chronicity, one sees the characteristic whitish fibers of the exposed internal sphincter in the base of the fissure. Occasionally invasive infection will occur, and patients will develop an intersphincteric abscess that can either rupture into the anal canal or present as a perianal abscess. Usually, this complication is heralded by the onset of unrelenting pain that is similar in quality to the intermittent pain patients have been experiencing [3]. Many investigations have focused on the question of why some fissures become chronic, whereas others heal readily. Several investigators have demonstrated abnormalities in internal sphincter function in patients with anal fissure. Nothman and Schuster demonstrated that patients with anal fissures had an overshoot in internal sphincter pressure following normal relaxation in response to rectal distension. Farouk et al have demonstrated that patients with anal fissures have fewer spontaneous relaxations of the internal sphincter than controls [4,5]. Anorectal manometry studies have documented increased maximum anal resting pressure (MARP) in patients with chronic anal fissure [4,6–8]. Ultra slow waves, which are pressure variations in baseline pressure occurring less than one or two times per minute, are also found more commonly in patients with fissures than in normal subjects [9]. Ultraslow waves have been associated with increased MARP [6,9,10]. All these abnormalities resolve after lateral internal sphincterotomy [4,6,7,11–13]. There is a growing body of evidence that these findings reflect an underlying abnormality of the internal sphincter that is important in the pathogenesis of anal fissures. Gibbons and Read proposed that the higher incidence of anal fissures seen in young men might be explained by their higher MARP. They suggested that a higher MARP might produce a relative ischemia of the anoderm, secondary to decreased blood flow induced by this increased pressure. Postmortem angiographic studies by Klosterhalfen et al [14] demonstrated that small branches of the inferior rectal artery pass perpendicularly through the muscle fibers of the internal sphincter, and that there was a paucity of blood supply to the posterior midline. They suggested that spasm of the internal sphincter might decrease the blood supply further in this region. Schouten et al [15] used a combination of anal manometry and Doppler laser flowmetry to study the relationship between MARP and anodermal blood flow. They demonstrated that blood flow to the posterior
A.M. Metcalf / Surg Clin N Am 82 (2002) 1291–1297
1293
commissure was decreased compared with flow in other quadrants, and that MARP was inversely related to blood flow. Further, they demonstrated that lateral internal sphincterotomy in patients with chronic fissures produces decreased MARP and increased anodermal blood flow. Diagnosis As stated previously, the patient’s history often strongly suggests the correct diagnosis. The presence of a sentinel pile is also highly suggestive. Gentle retraction of the perianal skin usually allows one to visualize the fissure directly, even in patients with significant spasm. An atypical appearance should prompt consideration of other diagnoses. Lateral location, extension onto the anal verge or above the dentate line, and extension of the base of the ulcer through the internal sphincter are all atypical features. Sexually transmitted diseases, leukemia, tuberculosis, Crohn’s disease, and squamous cell carcinoma should be excluded in such patients by appropriate testing. Endoscopic examination is helpful to exclude higher pathology, but may be impossible to perform adequately at the initial visit secondary to patient discomfort. If this is the case, it should be pursued during later visits. Treatment Medical treatment is most likely to be effective in patients with acute fissures. The higher failure rate of medical therapy for chronic fissures has led to the recent investigation of several pharmacological agents as alternative therapy to surgical therapy. The choice of such agents has been based on a more complete understanding of anorectal physiology. The mainstay of medical treatment remains the avoidance of hard stools. Many specialists believe that this is best achieved with agents that produce a bulky stool. The widespread availability of psyllium or methylcellulose preparations has replaced the use of unprocessed bran to a large extent [16,17]. Warm baths are often recommended in reducing the pain associated with anal fissures. This temporary symptomatic relief may be attributable to the decrease in anal canal pressure produced in patients with fissures in this setting [3]. Pharmacologic agents can also be used to temporarily reduce internal sphincter tone, and therefore MARP. Nitric oxide has been demonstrated to be an important inhibitory neurotransmitter to the internal sphincter [18]. Therefore, the nitric oxide donor trinitrate has been tested, and has gained acceptance in the treatment of anal fissure in both the acute and chronic setting. Treatment involves topical application of 0.2% glyceryl trinitrate (GTN) two to three times daily until the fissure has re-epithelialized. Variable results have been reported in the literature. Some of the variability may be attributable to whether patients had acute or chronic fissures, and the definition of chronic fissure. Generally, healing rates of between 50%
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and 85% have been reported in the treatment of chronic fissures [19–24]. Side effects of therapy tend to be mild and limited to headache, which has been reported in 20% to 40% of patients [19–21,23,25]. Another agent for the treatment of chronic anal fissure that has been proposed but has not achieved widespread popularity is the use of botulinum toxin [26]. Botulinum toxin inhibits release of acetylcholine and thereby causes striated muscle paresis. Injection of various amounts of Botulinum toxin into the sphincter mechanism has been reported to be efficacious in 65% to 87% of patients at two to three months. The optimal dose and precise site of administration have yet to be defined, however [27–30]. An additional pharmacologic agent that has been recently reported in the treatment of chronic anal fissure is diltiazem, a calcium channel blocker. Jonas et al [31] reported on a group of patients with chronic anal fissure who had failed GTN therapy. Topical 2% diltiazem gel was applied to the distal anal canal twice daily. MRAP was significantly lowered during therapy, and 49% were healed after eight weeks of therapy. Similar results were reported by Carapeti et al [32]. Surgical therapy Surgical therapy of anal fissures is reserved for patients who have failed medical therapy, or have developed a fissure-fistula. Many procedures have been devised; most of which involve disruption of the internal sphincter. Currently most authors believe that lateral internal sphincterotomy has replaced other techniques in the treatment of anal fissures associated with high MARP. The majority of studies have demonstrated that unhealed and recurrence rates and alterations in continence are lower with lateral internal sphincterotomy than with these other procedures. Unhealed or recurrence rates are reported in 1% to 6% of patients in large series [10,33–35]. Defects of continence are reported postoperatively. Incontinence to flatus has been reported in 1.5% to 15% of patients, and fecal soilage in 0% to 11% of patients, with most series reporting rates in the lower end of the range. Postoperative complications of prolapsed thrombosed hemorrhoids, hemorrhage, perianal abscess, and fistula-in-ano are each reported in approximately 1% of patients. There is disagreement as to whether the addition of other procedures such as hemorrhoidectomy increases the rate of complications. Some authors have reported increased complication rates [36,37], but others have not [38]. There is some controversy regarding several details of the procedure. The major controversy involves whether it should be performed in an open fashion or a closed fashion. In the closed technique, the groove between the internal sphincter and external sphincter is palpated after placement of an anal retractor. A narrow-bladed scalpel can thus be advanced in the intersphincteric groove to
A.M. Metcalf / Surg Clin N Am 82 (2002) 1291–1297
1295
the level of the dentate line, and then turned towards the lumen. A decrease in tension on the blades of the speculum will be felt. A modification of this technique is to make a small incision in the anal verge just distal to the intersphincteric groove and the internal sphincter dissected from the anoderm to the level of the dentate line and then divided under direct vision. The wound is then closed with absorbable sutures. In the open technique, a linear incision is made extending from the dentate line to the anal verge and the internal sphincter is incised under direct vision. The wound is left open. Proponents of the closed technique suggest that alterations in continence may be less frequent after closed sphincterotomy [39]. Proponents of the open technique suggest that complication rates may be fewer and unhealed and recurrence rates may be lower after open sphincterotomy [34]. A prospective study by Sultan et al [40] suggested that one factor in the development of altered continence postoperatively might be related to the extent of division of the internal sphincter. In their series of patients studied postoperatively with anal endosonography, 90% of female patients were demonstrated to have undergone complete internal sphincterotomy, whereas all male patients had some intact internal sphincter. More recently, Littlejohn and Newstead [41] proposed dividing the internal sphincter to the uppermost aspect of the fissure rather than to the dentate line. This was proposed to decrease the incidence of disturbances in continence postoperatively. In their series of patients, tailored lateral sphincterotomy, as they term their procedure, did appear to have a lower incidence of incontinence than many series, with a recurrence rate/unhealed rate of less than 2%. A special subgroup of patients to consider for alternative surgical therapies are those patients with anal fissure and low MARP. Such patients would be prone to develop alterations in continence if treated with lateral sphincterotomy. For such patients, a V-Y anoplasty as described by Samson et al [42], or an island advancement flap as described by Nyam et al [43] could be considered. Patients with recurrent or persistent anal fissures after lateral internal sphincterotomy may heal with conservative medical management. If unsuccessful, persistence may be secondary to incomplete internal sphincterotomy. Farouk et al [4] investigated 13 such patients with endoluminal ultrasonography, and found that all had either incomplete or no division of the internal sphincter. All were treated with an additional internal sphincterotomy with good results.
Summary Anal fissure is a common condition with a characteristic presentation. Despite increased pharmaceutical options in the medical management of
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anal fissures, surgical therapy is not in danger of becoming obsolete. Lateral internal sphincterotomy remains an attractive option for many patients suffering from this painful condition. References [1] Goligher JC. Surgery of the anus, rectum and colon. 5th edition. Springfield: Bailliere Tindall; 1984. p. 170–191. [2] Gordan PH. Fissure-in-ano. In: Gordon PH, Nivatvongs S, editors. Principles and practice of surgery for the colon, rectum and anus. 2nd edition. St Louis: Quality Medical Publishing; 1999. p. 217–40. [3] Dodi G, Bogoni F, Infantino A, et al. Hot or cold in anal pain? A study in the changes in the internal sphincter pressure profiles. Dis Colon Rectum 1986;29:248–51. [4] Farouk R, Duthie GS, MacGregor AB, et al. Sustained internal sphincter hypertonia in patients with chronic anal fissure. Dis Colon Rectum 1984;37:424–9. [5] Gibbons CP, Read NW. Anal hypertonia in fissures. Cause or effect? Br J Surg 1986; 73:443–5. [6] Keck JO, Staniunas RJ, Coller JA, et al. Computer generated profiles of the anal canal in patients with anal fissure. Dis Colon Rectum 1995;38:72–9. [7] Nothmann BJ, Schuster MM. Internal anal sphincter derangement with anal fissures. Gastroenterology 1974;67:216–20. [8] Xynos E, Tzortzinis A, Chrysos E, et al. Anal manometry in patients with fissure-in-ano before and after internal sphincterotomy. Int J Colorectal Dis 1993;8:125–8. [9] Schouten WR, Blankensteijn JD. Ultraslow wave pressure variations in the anal canal before and after lateral internal sphincterotomy. Int J Colorectal Dis 1992;7:115–8. [10] Vafai M, Mann CV. Closed lateral internal sphincterotomy without removal of sentinel pile for fissure-in-ano. Coloproctology 1981;3:91–3. [11] Abcarian H. Surgical correction of chronic anal fissure: results of lateral internal sphincterotomy vs. fissurectomy-midline sphincterotomy. Dis Colon Rectum 1980;23:31–6. [12] Chowcat NL, Araujo JGC, Boulos PB. Internal sphincterotomy for chronic anal fissure: Long-term effects on anal pressure. Br J Surg 1986;73:915–6. [13] Saad AMA, Omer A. Surgical treatment of chronic fissure-in-ano: a prospective randomized study. East Afr Med J 1992;69:613–5. [14] Klosterhafen B, Vogel P, Rixen H, et al. Topography of the inferior rectal artery. A possible cause of chronic primary anal fissure. Dis Colon Rectum 1989;32:43–52. [15] Schouten WR, Briel JW, Auwerda JJA, et al. Ischemic nature of anal fissure. Br J Surg 1996;83:63–5. [16] Jensen SL. Maintainence therapy with unprocessed bran in the prevention of acute anal fissure recurrence. J R Soc Med 1987;80:296–8. [17] Jensen SL. Treatment of first episodes of acute anal fissure: prospective randomized study of lignocaine ointment verses cortisone ointment or warm sitz baths plus bran. BMJ 1986;292:1167–9. [18] O’Kelly TJ, Brading A, Mortensen N. Nerve mediated relaxation of the human internal anal sphincter: The role of nitric oxide. Gut 1993;34:689–93. [19] Altmore DF, Rinaldi M, Miltito G, et al. Glyceryl trinitrate for chronic anal fissure-healing or headache. Dis Colon Rectum 2000;43:174–81. [20] Bacher H, Mischinger H, Werkgartner G. Local nitroglycerin for treatment of anal fissures: an alternative to lateral sphincterotomy? Dis Colon Rectum 1997;40:840–5. [21] Kennedy ML, Sowter S, Nyugen H, et al. Glyceryl trinitrate ointment for the treatment of chronic anal fissure. Results of a placebo-controlled trial and long term follow-up. Dis Colon Rectum 1999;42:1000–6. [22] Loder PB, Kamm MA, Nicholls RJ, et al. Reversible chemical sphincterotomy by topical application of glyceryl trinitrate. Br J Surg 1994;81:1386–9.
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[23] Lund JN, Scholefeld JH. A randomized, prospective, double-blind, placebo-controlled trial of glyceryl trinitrate ointment in the treatment of anal fissure. Lancet 1997;349:11–4. [24] Oettle GJ. Glyceryl trinitrate vs sphincterotomy for treatment of chronic fissure-in-ano. Dis Colon Rectum 1997;40:1318–20. [25] Lund JN, Scholefield JH. Followup of patients with chronic anal fissure treated with topical glyceryl nitrate. Lancet 1998;352:1681. [26] Brisinda G, Maria G, Bentivoglio AR, et al. A comparison of injections of injections of botulinum toxin and topical nitroglycerine ointment for the treatment of chronic anal fissure. N Engl J Med 1999;341:65–9. [27] Gui D, Cassetta E, Anastasio G, et al. Botulinum toxin for chronic anal fissure. Lancet 1994;344:1127–8. [28] Jankovic J, Brin MF. Therapeutic uses of botulinum toxin. N Engl J Med 1991;324: 1186–94. [29] Jost WH. One hundred cases of anal fissure treated with botulin toxin: early and long term results. Dis Colon Rectum 1997;40:1029–32. [30] Jost WH, Schrank B. Chronic anal fissures treated with botulinum toxin injections: a dosefinding study with Dysport. Colorectal Dis 1999;1:26–8. [31] Jonas M, Speake W, Scholefield JH. Diltiazem heals glyceryl trinitrate-resistant chronic anal fissure: a prospective study. Dis Colon Rectum 2002;45(8):1091–5. [32] Carapeti EA, Kamm MA, Evans BE, et al. Diltiazem and bethanechol decrease anal sphincter pressure and heal anal fissures without side-effects. Gut 1999;45:719–22. [33] Lewis Th, Corman ML, Prager ED, et al. Long term results of open and closed sphincterotomy for anal fissure. Dis Colon Rectum 1988;31:368–71. [34] Oh C, Divino CM, Steinhagen RM. Anal fissure. 20 years experience. Dis Colon Rectum 1995;38:378–82. [35] Pernikoff MJ, Eisenstat TE, Rubin RJ, et al. Reappraisal of partial lateral internal sphincterotomy. Dis Colon Rectum 1994;37:1291–5. [36] Hananel N, Gordon PH. Re-examination of the clinical manifestations and responses to therapy of fissure-in-ano. Dis Colon Rectum 1997;40(2):229–33. [37] Hananel N, Gordon PH. Lateral internal sphincterotomy for fissure-in-ano revisited. Dis Colon Rectum 1997;40:597–602. [38] Leong AFPK, Husain MJ, Seow-Choen F, et al. Performing internal sphincterotomy with other anorectal procedures. Dis Colon Rectum 1994;37:1130–2. [39] Garcia-Aguilar J, Belmonte C, Wong WD, et al. Open vs. closed sphincterotomy for chronic anal fissure: long-term results. Dis Colon Rectum 1996;39:440–3. [40] Sultan AH, Kamm MA, Nicholls RI, et al. Prospective study of the extent of internal anal division during lateral sphincterotomy. Dis Colon Rectum 1994;37:1031–3. [41] Littlejohn DRG, Newstead GL. Tailored lateral sphincterotomy for anal fissure. Dis Colon Rectum 1997;40:1439–42. [42] Samson RB, Stewart WRC. Sliding skin grafts in the treatment of anal fissure. Dis Colon Rectum 1970;13:372–5. [43] Nyam DCNK, Wilson KG, Stewart KJ, et al. Island advancement flaps in the management of anal fissures. Br J Surg 1995;82:526–8.
Anal fissure Amanda M. Metcalf, MD Department of Surgery, University of Iowa Hospitals and Clinics, 200 Hawkins Drive 4622 JCP, Iowa City, IA 52242, USA
An anal fissure is a traumatically induced longitudinal split in the squamous epithelium of the distal anal canal. It typically extends from the anal verge cephalad towards the dentate line. It most commonly occurs in the midline posteriorly, but it can also occur in the midline anteriorly. Anterior fissures are more common in women than men, occurring in 10% of women with fissures compared with 1% of men with fissures [1]. In its chronic form it is sometimes called ulcer-in-ano. Symptoms In the majority of patients, the symptoms are so characteristic as to be nearly diagnostic. Patients complain of severe intense pain initiated by the passage of stool. It can be described as knifelike, cutting, or tearing in character. This pain can persist for hours with a tight, throbbing quality. This discomfort can often by ameliorated, at least on a temporary basis, by a hot sitz bath. It is usually accompanied by small volume, bright red rectal bleeding. A minority of patients may also complain of pruritus, swelling, prolapse, and discharge [2]. Often patients will complain of constipation that predates their anal symptoms. Occasionally patients have diarrhea or an alternating pattern of constipation and diarrhea. Etiology and pathogenesis The most widely accepted theory regarding the etiology of anal fissure is that it results from the mechanical forces imposed on the anal canal during the passage of stool. Hard stools are most commonly implicated, but explosive liquid stools can produce the same results. The elliptical arrangement of the
E-mail address: [email protected] (A.M. Metcalf). 0039-6109/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 0 0 3 9 - 6 1 0 9 ( 0 2 ) 0 0 0 5 9 - 2
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A.M. Metcalf / Surg Clin N Am 82 (2002) 1291–1297
external sphincter is felt to provide less support to the anal canal in the anteroposterior axis, thus rendering these locations most susceptible to trauma. Although many acute anal fissures heal spontaneously, some do not. Those that do not, develop secondary changes to the surrounding tissues that signal the long-standing nature of the condition. Over time, the skin distal to the fissure becomes edematous and enlarged, and may form a fibrous skin tag. In this situation, it is often referred to as a sentinel pile. Similarly, the anal papilla cephalad to the fissure can undergo parallel changes and become enlarged. These changes are attributed to chronic low-grade infection. The edges and the base of the fissure tend to become fibrotic over time. With chronicity, one sees the characteristic whitish fibers of the exposed internal sphincter in the base of the fissure. Occasionally invasive infection will occur, and patients will develop an intersphincteric abscess that can either rupture into the anal canal or present as a perianal abscess. Usually, this complication is heralded by the onset of unrelenting pain that is similar in quality to the intermittent pain patients have been experiencing [3]. Many investigations have focused on the question of why some fissures become chronic, whereas others heal readily. Several investigators have demonstrated abnormalities in internal sphincter function in patients with anal fissure. Nothman and Schuster demonstrated that patients with anal fissures had an overshoot in internal sphincter pressure following normal relaxation in response to rectal distension. Farouk et al have demonstrated that patients with anal fissures have fewer spontaneous relaxations of the internal sphincter than controls [4,5]. Anorectal manometry studies have documented increased maximum anal resting pressure (MARP) in patients with chronic anal fissure [4,6–8]. Ultra slow waves, which are pressure variations in baseline pressure occurring less than one or two times per minute, are also found more commonly in patients with fissures than in normal subjects [9]. Ultraslow waves have been associated with increased MARP [6,9,10]. All these abnormalities resolve after lateral internal sphincterotomy [4,6,7,11–13]. There is a growing body of evidence that these findings reflect an underlying abnormality of the internal sphincter that is important in the pathogenesis of anal fissures. Gibbons and Read proposed that the higher incidence of anal fissures seen in young men might be explained by their higher MARP. They suggested that a higher MARP might produce a relative ischemia of the anoderm, secondary to decreased blood flow induced by this increased pressure. Postmortem angiographic studies by Klosterhalfen et al [14] demonstrated that small branches of the inferior rectal artery pass perpendicularly through the muscle fibers of the internal sphincter, and that there was a paucity of blood supply to the posterior midline. They suggested that spasm of the internal sphincter might decrease the blood supply further in this region. Schouten et al [15] used a combination of anal manometry and Doppler laser flowmetry to study the relationship between MARP and anodermal blood flow. They demonstrated that blood flow to the posterior
A.M. Metcalf / Surg Clin N Am 82 (2002) 1291–1297
1293
commissure was decreased compared with flow in other quadrants, and that MARP was inversely related to blood flow. Further, they demonstrated that lateral internal sphincterotomy in patients with chronic fissures produces decreased MARP and increased anodermal blood flow. Diagnosis As stated previously, the patient’s history often strongly suggests the correct diagnosis. The presence of a sentinel pile is also highly suggestive. Gentle retraction of the perianal skin usually allows one to visualize the fissure directly, even in patients with significant spasm. An atypical appearance should prompt consideration of other diagnoses. Lateral location, extension onto the anal verge or above the dentate line, and extension of the base of the ulcer through the internal sphincter are all atypical features. Sexually transmitted diseases, leukemia, tuberculosis, Crohn’s disease, and squamous cell carcinoma should be excluded in such patients by appropriate testing. Endoscopic examination is helpful to exclude higher pathology, but may be impossible to perform adequately at the initial visit secondary to patient discomfort. If this is the case, it should be pursued during later visits. Treatment Medical treatment is most likely to be effective in patients with acute fissures. The higher failure rate of medical therapy for chronic fissures has led to the recent investigation of several pharmacological agents as alternative therapy to surgical therapy. The choice of such agents has been based on a more complete understanding of anorectal physiology. The mainstay of medical treatment remains the avoidance of hard stools. Many specialists believe that this is best achieved with agents that produce a bulky stool. The widespread availability of psyllium or methylcellulose preparations has replaced the use of unprocessed bran to a large extent [16,17]. Warm baths are often recommended in reducing the pain associated with anal fissures. This temporary symptomatic relief may be attributable to the decrease in anal canal pressure produced in patients with fissures in this setting [3]. Pharmacologic agents can also be used to temporarily reduce internal sphincter tone, and therefore MARP. Nitric oxide has been demonstrated to be an important inhibitory neurotransmitter to the internal sphincter [18]. Therefore, the nitric oxide donor trinitrate has been tested, and has gained acceptance in the treatment of anal fissure in both the acute and chronic setting. Treatment involves topical application of 0.2% glyceryl trinitrate (GTN) two to three times daily until the fissure has re-epithelialized. Variable results have been reported in the literature. Some of the variability may be attributable to whether patients had acute or chronic fissures, and the definition of chronic fissure. Generally, healing rates of between 50%
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and 85% have been reported in the treatment of chronic fissures [19–24]. Side effects of therapy tend to be mild and limited to headache, which has been reported in 20% to 40% of patients [19–21,23,25]. Another agent for the treatment of chronic anal fissure that has been proposed but has not achieved widespread popularity is the use of botulinum toxin [26]. Botulinum toxin inhibits release of acetylcholine and thereby causes striated muscle paresis. Injection of various amounts of Botulinum toxin into the sphincter mechanism has been reported to be efficacious in 65% to 87% of patients at two to three months. The optimal dose and precise site of administration have yet to be defined, however [27–30]. An additional pharmacologic agent that has been recently reported in the treatment of chronic anal fissure is diltiazem, a calcium channel blocker. Jonas et al [31] reported on a group of patients with chronic anal fissure who had failed GTN therapy. Topical 2% diltiazem gel was applied to the distal anal canal twice daily. MRAP was significantly lowered during therapy, and 49% were healed after eight weeks of therapy. Similar results were reported by Carapeti et al [32]. Surgical therapy Surgical therapy of anal fissures is reserved for patients who have failed medical therapy, or have developed a fissure-fistula. Many procedures have been devised; most of which involve disruption of the internal sphincter. Currently most authors believe that lateral internal sphincterotomy has replaced other techniques in the treatment of anal fissures associated with high MARP. The majority of studies have demonstrated that unhealed and recurrence rates and alterations in continence are lower with lateral internal sphincterotomy than with these other procedures. Unhealed or recurrence rates are reported in 1% to 6% of patients in large series [10,33–35]. Defects of continence are reported postoperatively. Incontinence to flatus has been reported in 1.5% to 15% of patients, and fecal soilage in 0% to 11% of patients, with most series reporting rates in the lower end of the range. Postoperative complications of prolapsed thrombosed hemorrhoids, hemorrhage, perianal abscess, and fistula-in-ano are each reported in approximately 1% of patients. There is disagreement as to whether the addition of other procedures such as hemorrhoidectomy increases the rate of complications. Some authors have reported increased complication rates [36,37], but others have not [38]. There is some controversy regarding several details of the procedure. The major controversy involves whether it should be performed in an open fashion or a closed fashion. In the closed technique, the groove between the internal sphincter and external sphincter is palpated after placement of an anal retractor. A narrow-bladed scalpel can thus be advanced in the intersphincteric groove to
A.M. Metcalf / Surg Clin N Am 82 (2002) 1291–1297
1295
the level of the dentate line, and then turned towards the lumen. A decrease in tension on the blades of the speculum will be felt. A modification of this technique is to make a small incision in the anal verge just distal to the intersphincteric groove and the internal sphincter dissected from the anoderm to the level of the dentate line and then divided under direct vision. The wound is then closed with absorbable sutures. In the open technique, a linear incision is made extending from the dentate line to the anal verge and the internal sphincter is incised under direct vision. The wound is left open. Proponents of the closed technique suggest that alterations in continence may be less frequent after closed sphincterotomy [39]. Proponents of the open technique suggest that complication rates may be fewer and unhealed and recurrence rates may be lower after open sphincterotomy [34]. A prospective study by Sultan et al [40] suggested that one factor in the development of altered continence postoperatively might be related to the extent of division of the internal sphincter. In their series of patients studied postoperatively with anal endosonography, 90% of female patients were demonstrated to have undergone complete internal sphincterotomy, whereas all male patients had some intact internal sphincter. More recently, Littlejohn and Newstead [41] proposed dividing the internal sphincter to the uppermost aspect of the fissure rather than to the dentate line. This was proposed to decrease the incidence of disturbances in continence postoperatively. In their series of patients, tailored lateral sphincterotomy, as they term their procedure, did appear to have a lower incidence of incontinence than many series, with a recurrence rate/unhealed rate of less than 2%. A special subgroup of patients to consider for alternative surgical therapies are those patients with anal fissure and low MARP. Such patients would be prone to develop alterations in continence if treated with lateral sphincterotomy. For such patients, a V-Y anoplasty as described by Samson et al [42], or an island advancement flap as described by Nyam et al [43] could be considered. Patients with recurrent or persistent anal fissures after lateral internal sphincterotomy may heal with conservative medical management. If unsuccessful, persistence may be secondary to incomplete internal sphincterotomy. Farouk et al [4] investigated 13 such patients with endoluminal ultrasonography, and found that all had either incomplete or no division of the internal sphincter. All were treated with an additional internal sphincterotomy with good results.
Summary Anal fissure is a common condition with a characteristic presentation. Despite increased pharmaceutical options in the medical management of
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