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190 S.L. Dykes and R.D. Madoff
66. Dorfman G, Levitt M, Platell C. Treatment of chronic anal fis­sure with topical glyceryl trinitrate. Dis Colon Rectum 1999;42:1007–1010.
67. Graziano A, Svidler Lopez L, Lencinas S, Masciangioli G, Gualdrini U, Bisisio O. Long-term results of topical nitroglyc­erin in the treatment of chronic anal fissures are disappointing. Tech Coloproctol 2001;5:143–147.
68. Chrysos E, Xynos E, Tzovaras G, Zoras OJ, Tsiaoussis J, Vassilakis SJ. Effect of nifedipine on rectoanal motility. Dis Colon Rectum 1996;39:212–216.
69. Carapeti EA, Kamm MA, Phillips RK. Topical diltiazem and bethanechol decrease anal sphincter pressure and heal anal fis­sures without side effects. Dis Colon Rectum 2000;43: 1359–1362.
70. Knight JS, Birks M, Farouk R. Topical diltiazem ointment in the treatment of chronic anal fissure. Br J Surg 2001;88: 553–556.
71. Agaoglu N, Cengiz S, Arslan MK, Turkyilmaz S. Oral nifedip­ine in the treatment of chronic anal fissure. Dig Surg 2003;20: 452–456.
72. Ansaloni L, Bernabe A, Ghetti R, Riccardi R, Tranchino RM, Gardini G. Oral lacidipine in the treatment of anal fissure. Tech Coloproctol 2002;6:79–82.
73. Antropoli C, Perrotti P, Rubino M, et al. Nifedipine for local use in conservative treatment of anal fissures: preliminary results of a multicenter study. Dis Colon Rectum 1999;42(8): 1011–1015.
74. Perrotti P, Bove A, Antropoli C, et al. Topical nifedipine with lidocaine ointment vs. active control for treatment of chronic anal fissure: results of a prospective, randomized, double-blind study. Dis Colon Rectum 2002;45:1468–1475.
75. Jonas M, Neal KR, Abercrombie JF, Scholefield JH. A ran­domized trial of oral vs. topical diltiazem for chronic anal fis­sures. Dis Colon Rectum 2001;44:1074–1078.
76. Kocher HM, Steward M, Leather AJ, Cullen PT. Randomized clinical trial assessing the side-effects of glyceryl trinitrate and diltiazem hydrochloride in the treatment of chronic anal fis­sure. Br J Surg 2002;89:413–417.
77. Bielecki K, Kolodziejczak M. A prospective randomized trial of diltiazem and glyceryltrinitrate ointment in the treatment of chronic anal fissure. Colorectal Dis 2003;5:256–257.
78. Ezri T, Susmallian S. Topical nifedipine vs. topical glyceryl trinitrate for treatment of chronic anal fissure. Dis Colon Rectum 2003;46:805–808.
79. Pitt J, Dawson PM, Hallan RI, Boulos PB. A double-blind ran­domized placebo-controlled trial of oral indoramin to treat chronic anal fissure. Colorectal Dis 2001;3:165–168.
80. Pitt J, Craggs MM, Henry MM, Boulos PB. Alpha-1 adreno­ceptor blockade: potential new treatment for anal fissures. Dis Colon Rectum 2000;43:800–803.
81. Carapeti EA, Kamm MA, Evans BK, Phillips RK. Topical dil­tiazem and bethanechol decrease anal sphincter pressure with­out side effects. Gut 1999;45(5):719–722.
82. Jones OM, Brading AF, McC Mortnensen NJ. Phosphodies­terase inhibitors cause relaxation of the internal anal sphincter in vitro. Dis Colon Rectum 2002;45:530–536.
83. Jones OM, Moore JA, Brading AF, Mortensen NJ. Botulinum toxin injection inhibits myogenic tone and sympathetic nerve function in the porcine internal anal sphincter. Colorectal Dis 2003;5:552–557.
84. Maria G, Cassetta E, Gui D, Brisinda G, Bentivoglio AR, Albanese A. A comparison of botulinum toxin and saline for the treatment of chronic anal fissure [see comments]. N Engl J Med 1998;338(4):217–220.
85. Colak T, Ipek T, Kanik A, Aydin S. A randomized trial of bot­ulinum toxin vs lidocain pomade for chronic anal fissure. Acta Gastroenterol Belg 2002;65:187–190.
86. Siproudhis L, Sebille V, Pigot F, Hemery P, Juguet F, Bellissant E. Lack of efficacy of botulinum toxin in chronic anal fissure. Aliment Pharmacol Ther 2003;18:515–524.
87. Brisinda G, Maria G, Sganga G, Bentivoglio AR, Albanese A, Castagneto M. Effectiveness of higher doses of botulinum toxin to induce healing in patients with chronic anal fissures. Surgery 2002;131:179–184.
88. Madalinski MH, Slawek J, Zbytek B, et al. Topical nitrates and the higher doses of botulinum toxin for chronic anal fissure. Hepatogastroenterology 2001;48:977–979.
89. Lindsey I, Jones OM, Cunningham C, George BD, Mortensen NJ. Botulinum toxin as second-line therapy for chronic anal fissure failing 0.2 percent glyceryl trinitrate. Dis Colon Rectum 2003;46:361–366.
90. Brisinda G, Maria G, Bentivoglio AR, Cassetta E, Gui D, Albanese A. A comparison of injections of botulinum toxin and topical nitroglycerin ointment for the treatment of chronic anal fissure [see comments]. N Engl J Med 1999;341(2): 65–69 [published erratum appears in N Engl J Med 1999; 341(8):624].
91. Mentes BB, Irkorucu O, Akin M, Leventoglu S, Tatlicioglu E. Comparison of botulinum toxin injection and lateral internal sphincterotomy for the treatment of chronic anal fissure. Dis Colon Rectum 2003;46:232–237.
92. Minguez M, Herreros B, Espi A, et al. Long-term follow-up (42 months) of chronic anal fissure after healing with botu­linum toxin. Gastroenterology 2002;123:112–117.
93. Tilney HS, Heriot AG, Cripps NP. Complication of botulinum toxin injections for anal fissure. Dis Colon Rectum 2001; 44:1721–1724.
94. Jost WH, Schanne S, Mlitz H, Schimrigk K. Perianal thrombo­sis following injection therapy into the external anal sphincter using botulin toxin. Dis Colon Rectum 1995;38:781.
95. Jost WH. Ten years’ experience with botulin toxin in anal fis­sure. Int J Colorectal Dis 2002;17:298–302.
96. Corby H, Donnelly VS, O’Herlihy C, O’Connell PR. Anal canal pressures are low in women with postpartum anal fissure. Br J Surg 1997;84(1):86–88.
97. Nyam DC, Wilson RG, Stewart KJ, Farouk R, Bartolo DC. Island advancement flaps in the management of anal fissures. Br J Surg 1995;82:326–328.
98. Platell C, Mackay J, Collopy B, Fink R, Ryan P, Woods R. Anal pathology in patients with Crohn’s disease. Aust N Z J Surg 1996;66(1):5–9.
99. Sangwan YP, Schoetz DJ Jr, Murray JJ, Roberts PL, Coller JA. Perianal Crohn’s disease. Results of local surgical treatment. Dis Colon Rectum 1996;39(5):529–535.
100. Fleshner PR, Schoetz DJ Jr, Roberts PL, Murray JJ, Coller JA, Veidenheimer MC. Anal fissure in Crohn’s disease: a plea for aggressive management. Dis Colon Rectum 1995;38(11): 1137–1143.
101. Sweeney JL, Ritchie JK, Nicholls RJ. Anal fissure in Crohn’s disease. Br J Surg 1988;75(1):56–57.
12. Benign Anorectal: Anal Fissure 191
102. Wolkomir AF, Luchtefeld MA. Surgery for symptomatic hem­orrhoids and anal fissures in Crohn’s disease. Dis Colon Rectum 1993;36(6):545–547.
103. Allan A, Keighley MR. Management of perianal Crohn’s dis­ease. World J Surg 1988;12(2):198–202.
104. Viamonte M, Dailey TH, Gottesman L. Ulcerative disease of the anorectum in the HIV+ patient. Dis Colon Rectum 1993; 36(9):801–805.
105. Weiss EG, Wexner SD. Surgery for anal lesions in HIV­infected patients. Ann Med 1995;27(4):467–475.
106. Barrett WL, Callahan TD, Orkin BA. Perianal manifestations of human immunodeficiency virus infection: experience with 260 patients. Dis Colon Rectum 1998;41(5):606–611; discus­sion 611–602.
107. Keighley MR, Greca F, Nevah E, Hares M, Alexander­Williams J. Treatment of anal fissure by lateral subcutaneous sphincterotomy should be under general anaesthesia. Br J Surg 1981;68(6):400–401.
108. Ravikumar TS, Sridhar S, Rao RN. Subcutaneous lateral inter­nal sphincterotomy for chronic fissure-in-ano. Dis Colon Rectum 1982;25(8):798–801.
109. Gingold BS. Simple in-office sphincterotomy with partial fis­surectomy for chronic anal fissure. Surg Gynecol Obstet 1987;165(1):46–48.
110. Zinkin L. Left lateral internal sphincterotomy for anal fissure: as an office procedure. N J Med 1988;85(1):43–45.
111. Prohm P, Bonner C. Is manometry essential for surgery of chronic fissure-in-ano? Dis Colon Rectum 1995;38(7): 735–738.
112. Wiley M, Day P, Rieger N, Stephens J, Moore J. Open vs. closed lateral internal sphincterotomy for idiopathic fissure-in­ano: a prospective, randomized, controlled trial. Dis Colon Rectum 2004;47(6):847–852.
113. Parellada C. Randomized, prospective trial comparing 0.2 per­cent isosorbide dinitrate ointment with sphincterotomy in treat­ment of chronic anal fissure: a two-year follow-up. Dis Colon Rectum 2004;47(4):437–443.
114. Lund JN, Scholefield JH. A randomised, prospective, double­blind, placebo-controlled trial of glyceryl trinitrate ointment in treatment of anal fissure [see comments]. Lancet 1997; 349(9044):11–14 [published erratum appears in Lancet 1997; 349(9052):656].
115. Kennedy ML, Sowter S, Nguyen H, Lubowski DZ. 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(8):1000–1006.
116. Chaudhuri S, Pal AK, Acharya A, et al. Treatment of chronic anal fissure with topical glyceryl trinitrate: a double-blind, placebo­controlled trial. Indian J Gastroenterol 2001;20(3):101–102.
13
Benign Anorectal: Abscess and Fistula
Carol-Ann Vasilevsky and Philip H. Gordon
Anorectal abscesses and fistula-in-ano represent different stages along the continuum of a common pathogenic spec­trum. The abscess represents the acute inflammatory event whereas the fistula is representative of the chronic process.
Abscess
Anatomy
Successful eradication of anorectal suppuration and fistula­in-ano requires an in-depth understanding of anorectal anatomy. Essential is an understanding of the existence of potential anorectal spaces space is located in the area of the anal verge. It becomes continuous with the ischioanal fat laterally while it extends into the lower portion of the anal canal medially. It is con­tinuous with the intersphincteric space. The ischioanal space extends from the levator ani to the perineum. Anteriorly it is bounded by the transverse perineal muscles; the lower border of the gluteus maximus and the sacro­tuberous ligament form its posterior border. The medial bor­der is formed by the levator ani and external sphincter muscles; the obturator internus muscle forms the lateral bor­der. The intersphincteric space lies between the internal and external sphincters and is continuous inferiorly with the perianal space and superiorly with the rectal wall. The supralevator space is bounded superiorly by peritoneum, lat­erally by the pelvic wall, medially by the rectal wall, and inferiorly by the levator ani muscle. The deep postanal space is located between the tip of the coccyx posteriorly and lies below the levator ani and above the anococcygeal ligament (Figure 13-1B).
At the level of the dentate line, the ducts of the anal glands empty into the anal crypts. Some 80% of the anal glands are submucosal in extent, 8% extend to the inter­nal sphincter, 8% to the conjoined longitudinal muscle, 2% to the intersphincteric space, and 1% penetrate the internal sphincter.
2
1
(Figure 13-1A). The perianal
Pathophysiology
Etiology
Ninety percent of all anorectal abscesses result from nonspe­cific cryptoglandular infection whereas the remainder result from the causes as listed in Table 13-1. According to the cryp­toglandular theory championed by Parks, from obstruction of the anal glands and ducts. Obstruction of a duct may result in stasis, infection, and formation of an abscess. Persistence of anal gland epithelium in part of the tract between the crypt and the blocked part of the duct results in the formation of a fistula. Predisposing factors include diar­rhea and trauma in the form of a hard stool. Associated fac­tors may be anal fissures, infection of a hematoma, or Crohn’s disease.
3
abscesses result
Classification
Abscesses are classified according to their location in the aforementioned potential anorectal spaces: perianal, ischioanal, intersphincteric, and supralevator (Figure 13-2). Perianal abscesses are the most common type whereas supra­levator abscesses are the rarest. Pus can also spread circum­ferentially through the intersphincteric, supralevator, or ischioanal spaces, the latter via the deep postanal space, resulting in a horseshoe abscess.
Evaluation and Treatment
Symptoms
Pain, swelling, and fever are the hallmarks associated with an abscess. The patient with a supralevator abscess may com­plain of gluteal pain. Severe rectal pain accompanied by urinary symptoms such as dysuria, retention, or inability to void may be suggestive of an intersphincteric or supralevator abscess.
4
Rectal bleeding has been reported.
192
13. Benign Anorectal: Abscess and Fistula 193
TABLE 13-1. Etiology of anorectal abscess
Nonspecific
Cryptoglandular
Specific
Inflammatory bowel disease
Crohn’s disease Ulcerative colitis Infection Tuberculosis Actinomycosis Lymphogranuloma venereum
Trauma
Impalement Foreign body Surgery
Episiotomy Hemorrhoidectomy Prostatectomy
Malignancy
Carcinoma Leukemia Lymphoma Radiation
FIGURE 13-1. Anorectal spaces. A Coronal section. B Sagittal sec­tion. (From Vasilevsky CA. Anorectal abscess and fistula-in-ano. In: Beck D, ed. Handbook of Colorectal Surgery. 2nd ed. Copyright 2003 by Taylor & Francis Group LLC (B). Reproduced with per­mission of Taylor & Francis Group LLC (B) in the format Textbook via Copyright Clearance Center.)
Physical Examination
Inspection will reveal erythema, swelling, and possible fluc­tuation. It is crucial to recognize that no visible external man­ifestations will be present with the intersphincteric or supralevator abscesses despite the patient’s complaint of excruciating pain. possible because of extreme tenderness, palpation, if possible, will demonstrate tenderness and a mass. With a supralevator abscess, a tender mass may be palpated on rectal or vaginal examination. ate in the acute setting.
1
Although digital examination may not be
4
Anoscopy and sigmoidoscopy are inappropri-
Treatment
General Principles
Essentially, the treatment of an anorectal abscess involves incision and drainage. Watchful waiting under the cover of antibiotics is ineffective and may allow the suppurative process to progress resulting in the creation of a more com­plicated abscess and thus possible injury to the sphincter mechanism. Rarely, delay in diagnosis and management of anorectal abscesses may result in life-threatening necrotizing infection and death.
FIGURE 13-2. Classification of anorectal abscess. (Reprinted from Vasilevsky CA. Fistula-in-ano and abscess. In: Beck DE, Wexner SD, eds. Fundamentals of Anorectal Surgery. London: WB Saunders, copyright 1998, with permission from Elsevier.)
5
194 C.-A. Vasilevsky and P.H. Gordon
Operative Management
Incision and Drainage
Perianal abscesses can be effectively drained under local anesthesia. mined, the area is infiltrated with 0.5% lidocaine with 1:200,000 epinephrine. A cruciate or elliptical incision is made and the edges are trimmed to prevent coaptation which may result in poor drainage or recurrence (Figure 13-3). No packing is required.
Most ischioanal abscesses can be incised and drained in a similar manner with the site of incision shifted close to the anal side of the abscess, minimizing the complexity of a sub­sequent fistula. Large ischioanal or horseshoe abscesses often require drainage with the patient under a regional or general anesthetic and in the prone jackknife or left lateral (Sim’s) position. The location of infection is often in the deep
4,6
After the most tender point has been deter-
postanal space. Access to this space may be achieved by a midline incision between the coccyx and anus, spreading the superficial external sphincter to enter the space. An opening is made in the posterior midline and the lower half of the internal sphincter is divided to drain the anal gland in which
4
the infection originated.
Counter-incisions are made over
each ischioanal fossa to allow drainage of the anterior exten-
5,7
sions of the abscess (Hanley procedure)
(Figure 13-4).
Because the diagnosis of an intersphincteric abscess is entertained when the patient presents with pain out of propor­tion to the physical findings, an examination under anesthesia is mandatory to completely assess the cause of the pain. Once the diagnosis is established, either by palpation of a protrusion into the anal canal or by needle aspiration in the intersphinc­teric plane, treatment consists of dividing the internal sphinc­ter along the length of the abscess cavity. The wound is then marsupialized to allow adequate drainage and quicker healing.
Before the treatment of a supralevator abscess, it is essen­tial to determine its origin because it may arise from an upward extension of an intersphincteric or an ischioanal abscess, or downward extension of a pelvic abscess.
1,4
The treatment in each case will be different. If the origin is an intersphincteric abscess, it should be drained through the rec­tum by dividing the internal sphincter and not through the ischioanal fossa, because this will result in the creation of a suprasphincteric fistula. However, if it arises from an ischioanal abscess, it should be drained through the perineal skin and not through the rectum; otherwise, an extrasphinc­teric fistula will occur (Figure 13-5). If the abscess is of pelvic origin, it may be drained through the rectum, ischioanal fossa, or abdominal wall via percutaneous drainage depending on the direction to which it is pointing.
FIGURE 13-3. Drainage of abscess. A Injection of local anesthesia. B Cruciate incision. C Excision of skin. D Drainage cavity.
Catheter Drainage
An alternative method of treatment for selected patients is catheter drainage. Patients suitable for this technique should not have severe sepsis or any serious systemic illness.
8
The patient is placed in the prone jackknife position or left lateral
FIGURE 13-4. Drainage of horseshoe abscess.
13. Benign Anorectal: Abscess and Fistula 195
FIGURE 13-5. Drainage of a supralevator abscess.
(Sim’s) position. The skin is prepared with a proviodine­iodine solution and the fluctuant point of the abscess is selected. Local anesthesia consisting of 0.5% lidocaine with 1:200,000 epinephrine is injected in a 1-cm area of skin and a stab incision is made to drain the pus. The lidocaine should be injected into the skin around, rather than immediately over, the point of maximal fluctuation because the acid environ­ment may otherwise preclude adequate anesthesia (Figure 13-6A). A 10- to 16-French soft latex mushroom catheter is inserted over a probe into the abscess cavity. When released, the shape of the catheter tip will hold the catheter in place, obviating the need for sutures. The external portion of the catheter is shortened to leave 2–3 cm outside the skin with the tip in the depth of the abscess cavity (Figure 13-6B). This reduces the chances of the catheter falling out of or into the abscess cavity. A small bandage is placed over the catheter.
Several portions of this technique deserve further com­ment. First, the stab incision should be placed as close as pos­sible to the anus, minimizing the amount of tissue that must be opened if a fistula is found after resolution of inflammation
FIGURE 13-6. Catheter drainage of an abscess. A Stab incision. B Catheter in abscess cavity.
trace the suppurative process because of the presence of pus. Primary fistulotomy eliminates the source of infection and decreases the rate of recurrence, obviating the need for sub­sequent surgery with the potential to decrease disability and morbidity. Fucini
11
reported no recurrences in 51 of 58 primary
(Figure 13-6A). Second, the size and length of the catheter should correspond to the size of the abscess cavity (Figure 13-7A). A catheter that is too small or too short may fall into the wound (Figure 13-7B). Third, the length of time that the catheter should be left in place requires clinical judgment. Factors involved in this decision should include the size of the original abscess cavity, the amount of granulation tissue around the catheter, and the character and amount of drainage. If there is doubt, it is better to leave the catheter in place for a longer period of time.
Primary Fistulotomy
A point of controversy is whether primary fistulotomy should be performed at the time of initial abscess drainage. Proponents
5,9–11
believe that in the acute phase one can better
FIGURE 13-7. Catheter in an abscess cavity. A Correct size and length of catheter. B Catheter too short.
196 C.-A. Vasilevsky and P.H. Gordon
fistulotomies when internal openings could be identified. No major incontinence was reported, but impaired control of flatus was seen in 17%. In eight patients in whom only incision and drainage were performed because of failure to identify an inter­nal opening, recurrences were reported in 87%.
Opponents
6,12
are reluctant to perform primary fistulotomy
11
in the presence of acute inflammation because the search for an internal opening may lead to creation of false passages resulting in neglect of the main source of infection. Failure to identify an internal opening has been reported to occur in as high as 66% of patients.
10
In addition, 34%–50% of patients who present with an abscess for the first time will not develop a fistula.
6,12
Thus, primary fistulotomy in these patients would be unnecessary and may result in needless disturbances of continence. Of those patients whose abscesses are drained, 11% may develop a fistula whereas 37% may develop a recur­rent abscess. ischioanal abscesses.
6
This is most often observed in conjunction with
6
The search for an internal opening con­verts the operative procedure from one that can be performed under local anesthesia to one that requires regional or general anesthesia. A prospective, randomized trial of drainage alone versus drainage and fistulotomy for acute perianal abscesses with proven internal openings revealed that incision and drainage alone demonstrated no statistical significance in recurrence compared with concurrent fistulotomy although there was a tendency to recurrence in the former group. Another prospective study advocated a conservative approach in the treatment of anorectal abscess, reserving fistulotomy as a second-stage procedure if necessary.
14
If the internal opening of a low transsphincteric fistula is readily apparent at the time of abscess drainage, primary fis­tulotomy is feasible with the following exceptions: 1) patients with Crohn’s disease, 2) patients with acquired immunodefi­ciency syndrome (AIDS), 3) elderly patients, 4) patients with high transsphincteric fistulas, and 5) women with anterior fis­tulas and episiotomy scars.
The decision to perform a primary fistulotomy should be individualized but should only be attempted by a surgeon with a sound knowledge of the regional anatomy. Insistence upon finding a fistula may encourage creation of a false passage and unnecessary division of sphincter muscle.
11
As will be seen in the discussions of the use of fibrin glue ranal plug in the treatment of fistula-in-ano further on in this chapter, many of the former proponents of primary fistulotomy have abandoned this approach and have instead elected to await the appearance of a fistula after drainage only to treat it with fib­rin glue ranal plug so as to avoid cutting any sphincter muscle.
Antibiotics
There is little if any role for antibiotics in the primary man­agement of anorectal abscesses except as an adjunct in patients with valvular heart disease or prosthetic valves, extensive soft tissue cellulitis, prosthetic devices, diabetes, immunosuppression, or systemic sepsis.
Postoperative care
Patients are instructed to continue with a regular diet and to take a bulk-forming agent, non-codeine-containing analgesic, and sitz baths. Patients are generally seen in follow-up in 2–4 weeks or for intersphincteric or supralevator abscesses, 2 weeks postoperatively. Those patients in whom catheter drainage has been performed are seen within 7–10 days after the procedure. If the cavity has closed around the catheter and drainage has ceased, the catheter is removed. If the cavity has not healed, the catheter is left in place or replaced with a smaller one. In all cases, patients are observed until complete healing has occurred.
Complications
Recurrence
After incision and drainage, ischioanal and intersphincteric abscesses are associated with the development of recurrent abscesses or fistulas in as many as 89% of patients. Recurrence is more likely to occur in patients with a history of abscess drainage to infection have been destroyed.
Reasons for recurrence of anorectal infections include missed infection in adjacent anatomic spaces, the presence of an undiagnosed fistula or abscess at initial abscess drainage,
13
and failure to completely drain the abscess.
If a patient waits too long for follow-up after catheter drainage, the skin may seal and a second incision may be required to retrieve the catheter or redrain a recurrent abscess.
Failure to detect a primary opening at the time of primary fistulotomy and abscess drainage may result in persistence of the infection.
Extra-anal Causes
Extra-anal disease should be considered once the usual causes of recurrence have been ruled out. Hidradenitis suppurativa and downward extension of a pilonidal abscess should be con­sidered.
1
A prospective review of recurrent anorectal abscesses by Chrabot et al. of patients with recurrent abscesses. In addition, the possibil­ity of Crohn’s disease should be suspected.
Incontinence
Incontinence may result after incision and drainage of an abscess either from iatrogenic damage to the sphincter or inappropriate wound care. Continence may be compromised if the superficial external sphincter is inadvertently divided during drainage of a perianal or deep postanal abscess in a patient with preoperative borderline continence. Drainage of a supralevator abscess may lead to incontinence if the pub­orectalis is inappropriately divided. drained abscess may impair continence by preventing the development of granulation tissue and promoting the forma­tion of excess scar tissue.
6,14,15
perhaps because the natural barriers
5
16
reported hidradenitis in one-third
17
Prolonged packing of a
18
6,14,15
13. Benign Anorectal: Abscess and Fistula 197
Although advocated to decrease recurrence rates, primary fistulotomy may result in unnecessary division of sphincter muscle in acutely inflamed tissue. Schouten and van Vroonhoven
14
reported a 39% rate of continence disturbances
in a prospective, randomized trial.
Special Considerations
Necrotizing Anorectal Infection
Rarely, anorectal abscesses may result in necrotizing infec­tion and death. Factors thought to be responsible include delay in diagnosis and management, virulence of the organ­ism involved, bacteremia and metastatic infections, or under­lying disorders such as diabetes, blood dyscrasias, heart disease, chronic renal failure, hemorrhoids, and previous abscess or fistula.
Symptoms and Signs
Spreading soft tissue infection of the perineum can be classi­fied into two groups.19The first group includes anorectal sep­sis in which the infection extends superficially around the perineum resulting in necrosis of skin, subcutaneous tissue, fascia, or muscle. Perianal crepitation, erythematous, indurated skin, blistering, or gangrene may be present (Figure 13-8). A black spot may appear early and indicates a wide­spread necrotizing infection. sepsis in which the preperitoneal or retroperitoneal spaces have become involved. include abdominal wall induration, tenderness, or a vague mass. It is important to realize that systemic symptoms such as fever, tachycardia, and vascular volume depletion may pre­cede the appearance of overt signs of infection.
Treatment
Treatment consists of vigorous intravenous fluid hydration, restoration of electrolyte balance, and insertion of a Foley cathe­ter. Accompanying coagulopathy, respiratory insufficiency, and
FIGURE 13-8. Necrotizing anorectal infection.
5
20
The second group includes
19
Subtle signs may be present which
21
renal failure must be aggressively treated. Invasive monitor-
22
ing and ventilatory support may be necessary.
Pus or necrotic tissue from the infected region must be cultured for aerobes and anaerobes. A Gram stain can be used to distin­guish between the presence of clostridial and nonclostridial organisms.
23
Empiric broad-spectrum antibiotic therapy should be instituted regardless of Gram stain and culture results. The chosen antibiotic regimen should be effective against staphylococci and streptococci, Gram-negative col­iforms, Pseudomonas, Bacteroides, and Clostridium. For Gram-positive rods seen on Gram stain, antibiotics adminis­tered should include sodium penicillin G in doses of 24–30 million units per day and an aminoglycoside. Tetanus toxoid should also be administered.
22
Surgical treatment consists of wide radical debridement until healthy tissue is encountered. The goals of surgical debridement are to remove all nonviable tissue, halt the pro­gression of infection, and alleviate the systemic toxicity.
21
is crucial to realize that the preoperative skin changes may be minimal compared with the operative findings which may include edema, liquefactive necrosis of subcutaneous tissues, watery pus formation, and extensive necrosis of underlying
22
fascia.
Reexamination under anesthesia is usually necessary
because this is the only manner by which adequate wound
22
examination can be conducted.
The need for colostomy is a debatable issue and has been recommended if the sphincter muscle is grossly infected, if there is colonic or rectal perfo­ration, if the rectal wound is large, if the patient is immuno­compromised, or if incontinence is present. some authors
23
believe that colostomy is seldom necessary,
19,21
Whereas
fecal diversion may also be accomplished with the use of a “medical colostomy” consisting of enteral or parenteral nutri­tion. Controversy also exists with regard to the need for uri­nary diversion by suprapubic catheterization. It has been suggested that this may be indicated in the presence of known stricture and urinary extravasation with phlegmon.
24
Although antibiotics and adequate surgical drainage are thought to be sufficient, the use of hyperbaric oxygen (HBO) has been advocated as an adjunct to treatment, particularly in patients with diffuse spreading infections who do not have chronic obstructive pulmonary disease.
25
It is postulated that HBO has a direct antibacterial effect on anaerobic bacteria by diminishing the effect of endotoxins and optimizing leukocyte phagocytic function. by facilitating fibroblast proliferation.
20
HBO may also promote wound healing
25
HBO is delivered as 100% oxygen through an oronasal mask or endotracheal tube at 3 atm for one or two cycles each lasting 2 hours. If HBO is to be used as an adjunctive therapy, appropriate surgical inter­vention with wide debridement cannot be compromised because ischemic tissue cannot be salvaged by HBO.
21
Despite aggressive surgical and multidisciplinary manage­ment of anorectal sepsis, mortality rates ranging from 8% to 67% have been reported.
19,21
This high mortality rate is attrib­utable in part to the aggressive nature of the infection and to the underlying comorbid diseases that are present in these
It
198 C.-A. Vasilevsky and P.H. Gordon
patients.21Mortality rates are 2–3 times higher in diabetics, in elderly patients, and in patients in whom treatment is delayed.
Anal Infection and Hematologic Diseases
Acute anorectal suppuration poses an interesting and often life-threatening problem in patients with acute hematologic diseases. In patients with acute leukemia, mortality rates of 45%–78% have been reported.
26
There is a definite relation­ship between the number of circulating granulocytes and the incidence of perianal infection in patients with hematologic diseases. In one study, patients with neutrophil counts below 500 per cubic millimeter had an incidence of anorectal infec­tions of 11% whereas those with counts greater than 500 per cubic millimeter had an incidence of 0.4%.
27
Glenn et al. reported that 63% of anorectal infectious episodes occurred when fewer than 500 neutrophils were present per cubic mil­limeter. The risk of developing anorectal infection in this patient population has been found to be related to the severity and duration of the neutropenia.
26
The most important prog­nostic indicator was the number of days of neutropenia during the infectious episode.
28
The most common presenting symptoms include fever which precedes pain, and urinary retention. Point tenderness and poorly demarcated induration constitute the earliest
26
signs, appear late in the course of infection.
whereas external swelling and fluctuation often
28
Controversy surrounds the treatment of acute anorectal infections in patients with hematologic malignancies. Surgery has generally been avoided because what may seem to be sim­ple incision and drainage may produce scant or no pus and may instead cause hemorrhage, poor wound healing, or expanding soft tissue infection.
28
Any patient with perianal pain is assumed to have a peri­anal complication and is started on precautionary measures which consist of no digital rectal examinations, suppositories, or enemas.
29
Sitz baths, stool softeners, bulk agents, and anal­gesia are advised. On aspiration of most abscesses in this group, the most common organisms have been found to be Escherichia coli and group D streptococcus.
28
Consequently, infections are successfully controlled with a third-generation cephalosporin combined with anaerobic coverage or an extended spectrum penicillin in combination with an amino­glycoside and an anti-anaerobic antibiotic. This combination has been associated with an 88% success rate.
28
Barnes et al.26recommend an aggressive surgical approach. Through this approach, 13 of 15 patients who were severely neutropenic with neutrophil counts of fewer than 100 per cubic millimeter recovered with incision and drainage. It must be noted that these patients were found to have extensive soft tissue infection. Because appropriate antibiotic coverage has been found to control infection successfully, surgery has gen­erally been recommended only if there is obvious fluctuation, progression of soft tissue infection, or persistent sepsis after a trial of antibiotic therapy.
28
With severe neutropenia of fewer than 500 neutrophils per
21
cubic millimeter, low-dose radiation therapy of 300–400 rads for a period of 1–3 days has been suggested. Spontaneous drainage or subsidence of induration has been found to occur in 3–5 days. failed to confirm the utility of this approach.
29
A randomized, controlled study, however, has
30
Anorectal Sepsis in the Patient Positive for the Human Immunodeficiency Virus
Patients who are human immunodeficiency virus (HIV) posi­tive and present with abscesses require drainage either by incision and drainage or use of catheter drainage. Because these patients are immunosuppressed, adjunctive antibiotics should be used. Efforts should be directed at keeping wounds
28
small because these patients are at risk of poor wound heal-
31
ing.
An increased incidence of perianal sepsis32may be observed in HIV-positive patients. Serious septic complica­tions or uncommon presentations of anorectal sepsis were found in 13% of patients who initially presented with anorec­tal suppuration in one study. sis was associated with in situ neoplasia.
31
In another study, perianal sep-
33
Fistula-in-ano
Familiarity of the surgeon with the anatomy of the anorectal area and with the pathogenesis and classification of fistulas is essential for their adequate management.
Pathophysiology
Etiology
A fistula is defined as an abnormal communication between any two epithelium-lined surfaces. A fistula-in-ano is an abnormal tract or cavity communicating with the rectum or anal canal by an identifiable internal opening. Most fistulas are thought to arise as a result of cryptoglandular infection.
Classification
The most helpful yet complicated classification of fistula-in­ano is that described by Parks et al. (Table 13-2). It has been suggested that its use is particularly applicable to the treat­ment of recurrent fistulas.
Intersphincteric Fistula-in-ano
This fistula is the result of a perianal abscess. The tract passes within the intersphincteric space (Figure 13-9A). This is the most common type of fistula and accounts for approximately 70% of fistulas. tract to the rectal wall may occur; in addition, the tract may also pass into the lower rectum. The infectious process may pass into the intersphincteric plane and terminate as a blind tract. There is no downward extension to the anal margin, and
34
10
A high blind tract passing from the fistula
13. Benign Anorectal: Abscess and Fistula 199
TABLE 13-2. Classification of fistula-in-ano
Intersphincteric
Simple low tract High blind tract High tract with rectal opening Rectal opening without perineal opening Extrarectal extension Secondary to pelvic disease
Transsphincteric
Uncomplicated High blind tract
Suprasphincteric
Uncomplicated High blind tract
Extrasphincteric
Secondary to anal fistula Secondary to trauma Secondary to anorectal disease Secondary to pelvic inflammation
thus no external opening is present. Infection may also spread in the intersphincteric plane to reach the pelvic cavity to lie above the levator ani muscles. Lastly, an intersphincteric fis­tula may originate in the pelvis as a pelvic abscess but mani­fest itself in the perianal area.
fistula is the rectovaginal fistula. This is discussed further in Chapter 14.
Suprasphincteric Fistula-in-ano
This fistula results from a supralevator abscess and accounts for approximately 5% of fistulas in some series. passes above the puborectalis after arising as an intersphinc­teric abscess. The tract curves downward lateral to the exter­nal sphincter in the ischioanal space to the perianal skin (Figure 13-9C). A high blind tract may also occur in this vari­ety and result in a horseshoe extension.
34
The tract
Extrasphincteric Fistula-in-ano
This constitutes the rarest type of fistula and accounts for 2% of fistulas. tors and through them to the perianal skin via the ischioanal space (Figure 13-9D). This fistula may result from foreign body penetration of the rectum with drainage through the lev­ators, from penetrating injury to the perineum, or from Crohn’s disease or carcinoma or its treatment. However, the most common cause may be iatrogenic secondary to vigorous probing during fistula surgery.
34
The tract passes from the rectum above the leva-
4
Transsphincteric Fistula-in-ano
In its usual variety, this fistula results from an ischioanal abscess and constitutes approximately 23% of fistulas seen. The tract passes from the internal opening through the internal and external sphincters to the ischioanal fossa (Figure 13-9B). A high blind tract may also occur in this situation in which the upper arm of the tract may pass toward the apex of the ischioanal fossa or may extend through the levator ani muscles and thereby into the pelvis. One form of transsphincteric
FIGURE 13-9. Classification of fistula-in-ano. A Intersphincteric. B Transsphincteric. C Suprasphincteric. D Extrasphincteric.
Evaluation and Treatment
Symptoms
34
A patient with a fistula-in-ano will often recount a history of an abscess that has been drained either surgically or sponta­neously. Patients may complain of drainage, pain with defeca­tion, bleeding caused by the presence of granulation tissue at the internal opening, swelling, or decrease in pain with drainage. Additional bowel symptoms may be present when the fistula is secondary to proctocolitis, Crohn’s disease, actin­omycosis, or anorectal carcinoma. HIV, carcinoma, and lymphoma should be entertained.
Physical Examination
The external or secondary opening may be seen as an eleva­tion of granulation tissue discharging pus. This may be elicited on digital rectal examination. In most cases, the inter­nal or primary opening is not apparent. The number of exter­nal openings and their location may be helpful in identifying the primary opening. According to Goodsall’s rule (Figure 13-10), an opening seen posterior to a line drawn transversely across the perineum will originate from an internal opening in the posterior midline. An anterior external opening will orig­inate in the nearest crypt. Generally, the greater the distance from the anal margin, the greater the probability of a compli­cated upward extension. Cirocco and Reilly Goodsall’s rule was accurate in describing the course of anal fistulas with a posterior external opening. It was inaccurate in patients with anterior external openings because 71% of these fistulas tracked to a midline anterior primary opening. This
35
Systemic diseases such as
36
35
found that