Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1185_Библиотеки_им_академика_М_И_Перельмана
.pdf
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
Соседние файлы в папке Библиотека им академика М.И. Перельмана
