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13 Pruritus Ani
235
lacking. Smith and colleagues [12] evaluated the
psychological proles of 25 patients with pruritus
ani by administering the Minnesota Multiphasic
Personality Inventory. The authors found no statistically signicant deviations from the clinical
scales provided for non-pruritic patients, but it
was noted that the pruritus patients demonstrated
some possible tendencies toward “a relatively
high degree of inhibition of aggression and denial
of feeling of social and emotional alienation”. In
another study 17 patients suffering from pruritus
ani were compared to 23 patients who did not by
administering a personality test [46]. The mean
hypomania and depression scale scores were
greater and smaller respectively in the idiopathic
pruritus ani group. Nevertheless, the percentage
of abnormal psychological proles was not signicantly different between the two groups.
Drugs
Fig. 13.8 Erythematous, hyperkeratotic plaque sharply
demarcated from the surrounding skin caused by anal
squamous cell carcinoma
chronic renal failure, iron-deciency anemia,
hyperthyroidism, and cholestatic disease. These
conditions are more often associated with generalized pruritus rather than pruritus ani specically.
Uremic pruritus, or pruritus due to chronic renal
failure, is a common symptom affecting up to 90%
of dialysis patients. At present time, the only known
cure is kidney transplantation [44]. Cholestatic pruritus is a common symptom among patients with
hepatic dysfunction, which may be alleviated with
medications such as cholestyramine. In these cases,
pruritus is rarely the sole symptom, and denitive
treatment should be directed towards the underlying disease process [45].
Psychological
The role of psychological factors in the etiology
of pruritus ani has been poorly studied and overall
Several oral medications have been implicated
in eliciting pruritus ani, by both contact irritation
and increased leakage of fecal material from the
anal opening. Quinidine, quinine, and colchicine can initiate the acute onset of pruritus, even
though the patient may have been taking these
medications in consistent dosages for years.
Pruritus is usually controlled when the medication is temporarily stopped, which may be related
to a threshold phenomenon. Mineral oil (taken
orally) has also been detected as an offending
agent; in this instance, pruritus is believed to be
secondary to the pasty stool the patient develops
and the associated perianal seepage. Ingestion
of tetracycline also may cause pruritus by irritating the gut, which leads to a loose stool. In
addition, tetracycline facilitates the occurrence
of secondary perianal candidal infections. The
intravenous administration of hydrocortisone
phosphate has also been shown to produce pruritus ani. The application of certain topical ointments, creams or cleansing agents may also elicit
pruritus. Preparations containing either ester or
amide based local anesthetics (“caines”) can produce an allergic reaction in susceptible patients.
Many over-the-counter hygiene products, such as
236
B. R. Davis
scented soaps, deodorants, colored toilet tissues
and laundry detergents contain chemicals that
may cause increased skin sensitivity and irritation. These chemicals include formaldehyde,
alcohol, perfumes and astringents, which elicit
symptomatology by depriving the skin of its
natural acidity. Patients must be assisted in their
selection of appropriate nonirritating, atraumatic
perianal cleansing products.
Patient Evaluation
History
A detailed history and physical examination are
critical to the evaluation of any patient presenting
with perianal pruritus. The history should focus
on the following points: onset and duration of
pruritus; toileting behaviors and post-defecation
cleansing habits; anal hygiene; mucous leakage or perianal moisture; travel history; dietary
history specic to pruritogenic foods and beverages; and any accompanying symptoms. All
medications should be identied, as many can
contribute to pruritus; special attention should
be given to antibiotics, colchicine, quinidine and
topical medicines containing corticosteroids,
estrogens or “caine” drugs. The history should
also elicit any symptoms of inammatory bowel
disease or acholic stools. Prior anorectal surgery
may suggest deformed anorectal anatomy, which
in turn can lead to poor continence. The physician should also document whether the patient
has allergies or any generalized dermatoses
such as psoriasis or seborrhea. A sexual history
should include the patient’s sexual orientation
and specic practices, especially the practice of
anal receptive intercourse. The immune status of
the patient is also important, not only because
of primary immunodecient states or contracted
states such as acquired immunodeciency syndrome, but also in transplantation patients who
are receiving immunosuppressive medications.
A careful gynecologic and obstetric history
should be obtained from female patients and
should include contraceptive practices and any
history of inammatory or ulcerative lesions. A
history of difcult vaginal deliveries and/or perineal trauma should increase the suspicion for
anatomic and/or functional sphincter compromise; manometry and rectal ultrasound can be
helpful in selected cases.
Physical Examination
The goal of the physical examination is to identify any secondary causes of pruritus. Physical
examination should include close inspection of
perianal skin and anoderm, genitalia, inguinal
lymph nodes, and digital rectal examination.
Anoscopy should also be performed to evaluate the anal canal for evidence of disease, and
if malignancy is suspected, biopsies and further
endoscopic evaluation should be pursued.
Developed at the Washington Hospital
Center, the Washington criteria (Table 13.2) are
often used to stage the appearance of perianal
skin according to severity of disease [47]. Stage
I disease consists of erythematous and inamed
skin; stage II disease consists of lichenied
changes in addition to perianal erythema; and
stage III disease reveals coarse ridges and ulcerations. In a small minority of patients, perianal
skin may appear normal (Washington stage 0).
Any suspicious lesions should be biopsied in
the ofce with a simple (3–4mm) punch biopsy,
including both normal-appearing perianal skin
and the lesion in question. If Bowen’s disease
(carcinoma in situ) or condyloma acuminata are
suspected, application of 3–5% acetic acid can
help guide the biopsy. Infectious causes of pruritus can be evaluated with aerobic, anaerobic,
and fungal swabs. If there has been any exposure to children harboring pinworm (Enterobius
vermicularis), a scotch tape test can easily be
performed, ideally done in the early morning
Table 13.2 Washington hospital staging criteria
Stage 0 Normal-appearing perianal skin
Stage I Erythematous and inamed perianal skin
Stage II White, lichenied perianal skin
Stage
III
Lichenied skin with coarse ridges and
ulceration
13 Pruritus Ani
237
on consecutive days. All children suffering from
pruritic symptoms should be evaluated with the
cellophane “scotch tape” test.
Treatment
Once the diagnosis of pruritus ani has been
reached, patient education and treatment modalities should proceed simultaneously. Treatment
may include: Conservative dietary changes to
identify offending agents or their symptomatic
thresholds; Appropriate medical therapy for
infections, dermatoses or systemic disorders;
Surgical intervention for the few anatomic deformities which contribute to pruritus; Supportive
therapy for the majority of patients with pruritus who have no identiable etiology and subsequently fall into the category of idiopathic
pruritus ani. Success in this group begins with
proper perianal hygiene, bowel augmentation,
and the discontinuation of any offending agents.
Most patients achieve symptomatic relief and
reversal of morphologic features with these
conservative measures. Patient suffering from
idiopathic pruritus ani frequently present with
chronic symptoms and resultant social anxiety, thus patient reassurance and counseling are
invaluable adjuncts to medical therapy.
The goal of perianal hygiene is to restore clean
dry perianal skin. Optimal anal hygiene includes
avoidance of over wiping, alcohol-based wipes,
perfumes, dyes, and witch hazel products. The
patient should also initially discontinue the use of
any topical steroid agents because of their harmful
thinning of the perianal skin. Trauma incurred by
scratching must be stopped, and for patients with
severe symptoms, wearing white cotton gloves at
bedtime may be necessary. Patients should only
use plain, white, unscented, toilet paper for wiping the anal area. In severe cases patients should
be encouraged to take a bath after a bowel movement or take a shower. While uncommon in North
American the use of a bidet following a bowel
movements may be a more convenient option for
some patients [48]. Otherwise, simple cleansing
with disposable moist towels, such as baby wipes,
is sufcient. Afterwards, the skin should be pat
dried with unscented toilet paper or a soft towel,
as vigorous wiping results in further trauma to the
area. Clean and dry skin should be maintained
throughout the day. Moist areas can be kept dry with
cornstarch, talcum powder, or a simple cotton ball.
The skin can also be protected with a zinc oxide–
based barrier ointment, such as Calmoseptine
(Calmoseptine, Inc., Huntington Beach, CA). For
severe cases application of Berwick’s dye and benzoin can create a barrier for up to a week so long as
only water is used as a cleanser [49].
If chronic diarrhea or mucous leakage impedes
proper perianal hygiene, bowel-augmenting
medications such as ber supplement may be
prescribed. The psyllium regimens should be tailored to achieve soft, well-formed stools, while
minimizing fecal soiling. Tap water enemas may
also be a helpful adjunct if incomplete evacuation
remains a problem.
As stated earlier there are at least six common foods believed to precipitate pruritus ani
although the evidence is generally lacking and is
mostly anecdotal. Patients should be counseled
against excessive consumption of these so-called
pruritogenic foods (coffee, colas, chocolate, tea,
tomatoes and beer). Gradual reintroduction of the
offending foods can then help the patient identify
both the food group and the threshold for tolerance. Other factors that contribute to the disease
process are listed in Table13.3, and should also
be eliminated once identied. These potential
triggers include specic medications, pruritogenic foods, topical agents, and lifestyle changes.
Topical steroids may serve as an effective adjunct to the aforementioned measures.
Evidence for the use of topical steroids is conicting, but in the setting of refractory disease, a
short course of betamethasone or 1% hydrocortisone cream may alleviate pruritic symptoms.
A small randomized controlled trial comparing
1% hydrocortisone cream versus placebo noted
a 68% reduction in symptoms and 75% improvement in quality of life after a 2-week course [50].
The use of topical steroids should be limited to
several weeks, as chronic use may result in atrophic changes to the perianal skin.
238
B. R. Davis
Table 13.3 Factors contributing to pruritic symptoms
Medications Tetracycline
Foods Coffee
Lifestyle Poor hygiene
Topical
agents
Colchicine
Quinidine
Erythromycin
Stool softeners
Colas
Citrus fruits
Chocolate
Tea
Energy drinks
Beer
Spicy foods
Chronic diarrhea
Excessive wiping
Perianal sweat (obesity, athletic activity)
Tight-tting garments
Moist environments
Nocturnal scratching
Lotions
Scented creams
Perfumes
Detergents
Recent Advances
The majority of patients suffering from idiopathic
pruritus ani respond favorably to conservative
measures. There exist a subset of patients, however, who remain refractory to treatment despite
strict adherence to hygienic and dietary modications. After 4weeks of conservative therapy,
and secondary causes are again excluded, one
of several second-line interventions may be pursued. These include topical capsaicin, topical
tacrolimus, and methylene blue injection. Several
studies have been performed in recent years to
support the use of these second-line agents.
Capsaicin is a product of Capsicum chili peppers, and is postulated to increase the resting
threshold for depolarization inlocal C-type nerve
bers. Topical capsaicin (0.006%) can be applied
in a thin layer over the perianal skin, up to three
times daily for 4weeks. This is diluted from the
usual concentration of capsaicin at 0.025%, which
reduces the local burning sensation. Patients
undergoing topical capsaicin therapy should be
advised against specic side-effects, including
burning sensation and urticaria upon application.
A randomized, placebo-controlled trial comparing active capsaicin versus menthol ointment noted symptomatic relief in 70% in the
capsaicin arm. After a mean follow-up period
of 10.9 months, 94% of original responders
remained symptom-free but continued to use
topical capsaicin on a near-daily basis. The study
also noted that capsaicin treatment was associated with higher burning sensation scores upon
application [51]. A systematic review of six
randomized controlled trials comparing topically applied capsaicin in treating pruritus in any
medical condition concluded that there was no
convincing evidence for the use of capsaicin in
pruritus [52].
Tacrolimus, an immunosuppressive agent, is
commonly utilized in the treatment of eczema.
Ucak etal. aimed to compare topical tacrolimus
with Vaseline placebo, in patients suffering from
refractory pruritus ani. Notably, these patients
also suffered from atopic dermatitis. Topical
tacrolimus ointment (0.03%), applied twice
daily, resulted in a signicant decrease in symptoms after a 4-week period [53]. The study is not
without its limitations, namely its small size and
lack of long-term follow-up.
Several studies have investigated intradermal methylene blue as a treatment modality
for refractory pruritus ani. Methylene blue is
believed to be directly toxic to the sensory nerves
supplying the perianal skin. A 15 mL solution
of 1% methylene blue can be injected using a
22-gauge needle, mixed with local anesthetics if desired. The injection should be localized
to the affected perianal area, up to the level of
the dentate line. A repeat injection may be performed at 4 weeks for partial response. A prospective study by Mentes etal. noted complete
relief of symptoms with methylene blue therapy
in 24 of 30 patients after 1month. Twenty-three
of 30 patients remained symptom-free after a
12 months of follow-up [54]. A more recent
prospective study demonstrated similar results:
symptomatic improvement in 96% and complete
resolution in 57% of patients after a single treatment [55]. The positive effect of methylene blue
to control the symptoms of pruritus may only
be short term with 8 out of 10 patients report-
13 Pruritus Ani
239
ing recurrence of their symptoms at a median
follow up of 47months [56]. Patients should be
informed about the side-effects of methylene
blue prior to injection, including numbness and
discoloration at the injection site. Skin necrosis
and anaphylaxis are rare, but have been reported.
Summary
Pruritus ani is a common ailment, affecting up
to 5% of the population on a daily basis. The
diagnosis heavily relies on a focused history and
physical examination. Any secondary causes of
pruritus ani should be elucidated if present, and
treatment should be guided towards any identied potential etiology. Simple procedures, such
as punch biopsies or anal swabs, may be performed in the ofce setting to aid in unclear situations. The majority of cases can be managed with
adequate perianal hygiene, topical agents, and
the elimination of any offending agents. Patient
education and reassurance are critical adjuncts to
the healing process.
References
1. Oueidat D, Bou Assi T, Jurjus A.Pruritus ani: more
than a decade of personal experience in Lebanon. J
Med Liban. 2014;62(4):203–6.
2. Siddiqi S, Vijay V, Ward M, Mahendran R,
Warren S. Pruritus ani. Ann R Coll Surg Engl.
2008;90(6):457–63.
3. Hanno R, Murphy P.Pruritus ani. Classication and
management. Dermatol Clin. 1987;5(4):811–6.
4. Murrray DH. Pruritus ani the probable cause
and outline of treatment. J Am Med Assoc.
1911;LVII(24):1913–4.
5. Ringkamp M, Schepers RJ, Shimada SG, Johanek
LM, Hartke TV, Borzan J, etal. A role for nociceptive,
myelinated nerve bers in itch sensation. J Neurosci.
2011;31(42):14841–9.
6. Twycross R, Greaves MW, Handwerker H, Jones EA,
Libretto SE, Szepietowski JC, etal. Itch: scratching
more than the surface. QJM. 2003;96(1):7–26.
7. Kuehn HG, Gebbensleben O, Hilger Y, Rohde
H. Relationship between anal symptoms and anal
ndings. Int J Med Sci. 2009;6(2):77–84.
8. Abramowitz L, Benabderrahmane M, Pospait D,
Philip J, Laouenan C.The prevalence of proctological
symptoms amongst patients who see general practitioners in France. Eur J Gen Pract. 2014;20(4):301–6.
9. Caplan RM.The irritant role of feces in the genesis of
perianal itch. Gastroenterology. 1966;50(1):19–23.
10. Allan A, Ambrose NS, Silverman S, Keighley
MR. Physiological study of pruritus ani. Br J Surg.
1987;74(7):576–9.
11. Farouk R, Duthie GS, Pryde A, Bartolo DC.Abnormal
transient internal sphincter relaxation in idiopathic
pruritus ani: physiological evidence from ambulatory
monitoring. Br J Surg. 1994;81(4):603–6.
12. Smith LE, Henrichs D, McCullah RD. Prospective
studies on the etiology and treatment of pruritus ani.
Dis Colon Rectum. 1982;25(4):358–63.
13. Marks MM.The inuence of the intestinal ph. on anal
pruritus. South Med J. 1968;61(9):1005–6.
14. Friend WG. The cause and treatment of idiopathic
pruritus ani. Dis Colon Rectum. 1977;20(1):40–2.
15. Kahlke V, Jongen J, Peleikis HG, Herbst RA.Perianal
streptococcal dermatitis in adults: its association with
pruritic anorectal diseases is mainly caused by group
B Streptococci. Color Dis. 2013;15(5):602–7.
16. Baral J.Pruritus ani and Staphylococcus aureus. J Am
Acad Dermatol. 1983;9(6):962.
17. Bowyer A, McColl I. Erythrasma and pruritus ani.
Acta Derm Venereol. 1971;51(6):444–7.
18. Watts PJ, Greenberg HL, Khachemoune A. Unusual
primary syphilis: presentation of a likely case with a
review of the stages of acquired syphilis, its differential diagnoses, management, and current recommendations. Int J Dermatol. 2016;55:714–28.
19. Birkmann A, Zimmermann H.HSV antivirals—current and future treatment options. Curr Opin Virol.
2016;18:9–13.
20. Long KC, Menon R, Bastawrous A, Billingham
R. Screening, surveillance, and treatment of anal
intraepithelial neoplasia. Clin Colon Rectal Surg.
2016;29(1):57–64.
21. Zuccati G, Lotti T, Mastrolorenzo A, Rapaccini
A, Tiradritti L. Pruritus ani. Dermatol Ther.
2005;18(4):355–62.
22. Gray M, Beeckman D, Bliss DZ, Fader M, Logan S,
Junkin J, etal. Incontinence-associated dermatitis: a
comprehensive review and update. J Wound Ostomy
Continence Nurs. 2012;39(1):61–74.
23. Nasseri YY, Osborne MC. Pruritus ani: diagnosis and
treatment. Gastroenterol Clin N Am. 2013;42(4):801–13.
24. Stermer E, Sukhotnic I, Shaoul R. Pruritus ani:
an approach to an itching condition. J Pediatr
Gastroenterol Nutr. 2009;48(5):513–6.
25. Jillson OF.Pruritus ani: disputing the passage. Cutis.
1984;33(6):537, 41, 44 passim.
26. St Georgiev V.Chemotherapy of enterobiasis (oxyuriasis). Expert Opin Pharmacother. 2001;2(2):267–75.
27. Rezaee E, Goldust M, Alipour H.Treatment of scabies: comparison of lindane 1% vs permethrin 5.
Skinmed. 2015;13(4):283–6.
28. Do-Pham G, Monsel G, Chosidow O.Lice. Semin
Cutan Med Surg. 2014;33(3):116–8.
29. Daniel GL, Longo WE, Vernava AM 3rd. Pruritus
ani. Causes and concerns. Dis Colon Rectum.
1994;37(7):670–4.
240
B. R. Davis
30. Murie JA, Sim AJ, Mackenzie I. The importance of
pain, pruritus and soiling as symptoms of haemorrhoids and their response to haemorrhoidectomy or
rubber band ligation. Br J Surg. 1981;68(4):247–9.
31. Bowyer A, McColl I.A study of 200 patients with
pruritus ani. Proc R Soc Med. 1970;63(Suppl):96–8.
32. Nosbaum A, Vocanson M, Rozieres A, Hennino A,
Nicolas JF. Allergic and irritant contact dermatitis.
Eur J Dermatol. 2009;19(4):325–32.
33. Nahm DH, Lee ES, Park HJ, Kim HA, Choi GS, Jeon
SY.Treatment of atopic dermatitis with a combination
of allergen-specic immunotherapy and a histamineimmunoglobulin complex. Int Arch Allergy Immunol.
2008;146(3):235–40.
34. Carli P, Cattaneo A, De Magnis A, Biggeri A, Taddei
G, Giannotti B.Squamous cell carcinoma arising in
vulval lichen sclerosus: a longitudinal cohort study.
Eur J Cancer Prev. 1995;4(6):491–5.
35. Neill SM, Tatnall FM, Cox NH. Guidelines for the
management of lichen sclerosus. Br J Dermatol.
2002;147(4):640–9.
36. Assmann T, Becker-Wegerich P, Grewe M, Megahed
M, Ruzicka T.Tacrolimus ointment for the treatment
of vulvar lichen sclerosus. J Am Acad Dermatol.
2003;48(6):935–7.
37. Wang G, Li C, Gao T, Liu Y.Clinical analysis of 48
cases of inverse psoriasis: a hospital-based study. Eur
J Dermat. 2005;15(3):176–8.
38. Kalb RE, Bagel J, Korman NJ, Lebwohl MG, Young
M, Horn EJ, etal. Treatment of intertriginous psoriasis: from the Medical Board of the National Psoriasis
Foundation. J Am Acad Dermatol. 2009;60(1):120–4.
39. Lian P, Gu WL, Zhang Z, Cai GX, Wang MH, Xu Y,
et al. Retrospective analysis of perianal Paget's disease with underlying anorectal carcinoma. World J
Gastroenterol. 2010;16(23):2943–8.
40. Perez DR, Trakarnsanga A, Shia J, Nash GM, Temple
LK, Paty PB, etal. Management and outcome of perianal Paget’s disease: a 6-decade institutional experience. Dis Colon Rectum. 2014;57(6):747–51.
41. Lo OS, Li GK, Law WL.Management of perianal
extramammary Paget’s disease involving the dentate line without abdominoperineal resection. Tech
Coloproctol. 2016;20:419–22.
42. Zhan W, Liao X, Tian T, Zhang RY, Li P, Wu XP, etal.
Perianal multiple Bowen’s disease: a case report. Int J
Clin Exp Pathol. 2015;8(11):15039–41.
43. Bath-Hextall FJ, Matin RN, Wilkinson D, LeonardiBee J.Interventions for cutaneous Bowen’s disease.
Cochrane Database Syst Rev. 2013;6:Cd007281.
44. Kfoury LW, Jurdi MA.Uremic pruritus. J Nephrol.
2012;25(5):644–52.
45. Gossard AA. Care of the cholestatic patient. Clin
Liver Dis. 2013;17(2):331–44.
46. Laurent A, Boucharlat J, Bosson JL, Derry A,
Imbert R. Psychological assessment of patients
with idiopathic pruritus ani. Psychother Psychosom.
1997;66(3):163–6.
47. Billingham RP, Isler JT, Kimmins MH, Nelson JM,
Schweitzer J, Murphy MM.The diagnosis and management of common anorectal disorders. Curr Probl
Surg. 2004;41(7):586–645.
48. Sauer T.The role of the bidet in pruritus ani. Aust Fam
Physician. 2010;39(10):715.
49. Tomi N, Weiser R, Strohal R, Mittlboeck M.A liquidlm forming acrylate cream for the treatment of anal
pruritus. Br J Nurs. 2012;21(2):98. 100–2.
50. Al-Ghnaniem R, Short K, Pullen A, Fuller LC,
Rennie JA, Leather AJ. 1% hydrocortisone ointment
is an effective treatment of pruritus ani: a pilot randomized controlled crossover trial. Int J Color Dis.
2007;22(12):1463–7.
51. Lysy J, Sistiery-Ittah M, Israelit Y, Shmueli A,
Strauss-Liviatan N, Mindrul V, et al. Topical capsaicin—a novel and effective treatment for idiopathic
intractable pruritus ani: a randomised, placebo controlled, crossover study. Gut. 2003;52(9):1323–6.
52. Gooding SM, Canter PH, Coelho HF, Boddy K, Ernst
E.Systematic review of topical capsaicin in the treatment of pruritus. Int J Dermatol. 2010;49(8):858–65.
53. Ucak H, Demir B, Cicek D, Dertlioglu SB, Akkurt
ZM, Ucmak D, et al. Efcacy of topical tacrolimus for the treatment of persistent pruritus ani in
patients with atopic dermatitis. J Dermatolog Treat.
2013;24(6):454–7.
54. Mentes BB, Akin M, Leventoglu S, Gultekin FA,
Oguz M.Intradermal methylene blue injection for the
treatment of intractable idiopathic pruritus ani: results
of 30 cases. Tech Coloproctol. 2004;8(1):11–4.
55. Sutherland AD, Faragher IG, Frizelle FA.Intradermal
injection of methylene blue for the treatment of
refractory pruritus ani. Color Dis. 2009;11(3):282–7.
56. Samalavicius NE, Poskus T, Gupta RK, Lunevicius
R. Long-term results of single intradermal 1%
methylene blue injection for intractable idiopathic
pruritus ani: a prospective study. Tech Coloproctol.
2012;16(4):295–9.
Anal Fissure andAnal Stenosis
DanielL.Feingold andStevenA.Lee-Kong
14
Anal Fissure
Introduction
Patients suffering from anal ssure, typically an
oval or tear-shaped, posterior midline ulceration
distal to the dentate line, are commonly referred
to surgeons for diagnosis and treatment. The
severity of presenting symptoms ranges from
minor, annoying pain or bleeding to severe,
consuming, incapacitating pain. The duration
of symptoms upon presentation varies, as well,
and ssures persisting beyond about 6–8weeks
are arbitrarily categorized as chronic. Given the
spectrum of presentation related to ssuring as
well as the risk of functional decit related to
operative sphincterotomy, the clinician must consider the unique presentation of each patient and
individualize the care plan. The management of
pediatric patients with ssures was discussed in
Chap. 4.
Pathogenesis
The majority of ssures are ascribed to a traumatic tear or split in the anoderm caused most
D. L. Feingold (*) · S. A. Lee-Kong
Department of Surgery, Columbia University,
New York, NY, USA
e-mail: df347@columbia.edu
commonly by straining at a hard bowel movement or, alternatively, the irritation of diarrhea. Doppler and angiographic investigations
have demonstrated that the posterior anal commissure has relatively poor blood supply and
wounds developing in this location may be difcult to heal due to the aggravation of repeated
evacuations and the relative tissue ischemia.
Hypothetically, an acute ssure and its associated
pain cause spasm and hypertonicity of the internal anal sphincter muscle, which further reduces
blood ow and impedes the ability to heal the
ulcerated wound. Persistence of the ssure leads
to more pain that leads to more spasm in what has
been coined the “ssure cycle”. Most therapies
for anal ssure target sphincter hypertonicity to
break the ssure cycle, improve blood ow and
promote healing.
Presentation
The typical patient with a ssure is a young adult
who experiences pain during defecation that can
last for hours afterwards. While some patients
may recall the instigating acute event that resulted
in the ssure, many patients cannot pinpoint what
exactly caused the ssure to develop. The pain,
described as sharp, burning or throbbing, can be
severe and patients often appreciate themselves
the hypertonicity associated with their ssure.
More symptomatic patients commonly complain
© Springer International Publishing AG, part of Springer Nature 2019
D. E. Beck et al. (eds.), Fundamentals of Anorectal Surgery,
https://doi.org/10.1007/978-3-319-65966-4_14
241
242
that passing a bowel movement feels like getting cut by shards of glass. While most patients
will experience bleeding or blood upon wiping
as part of their constellation of symptoms, a subset of patients, more commonly women, report
bleeding as their main complaint, rather than
pain. Some patients experience repeated bouts of
healing with symptom resolution followed by reopening of their ssure (cycling) and present to
the surgeon seeking denitive care. By the time
patients present to the surgeon, many have inevitably tried any of a number of over-the-counter
remedies that have failed to control their symptoms or have tried, unsuccessfully, established
ssure therapies recommended by prior physicians. Considering prior failed treatments is helpful when deciding the next course of action.
Differential diagnosis for patients presenting
with anal ssure might include abscess, external
hemorrhoid thrombosis, anal cancer, pruritis ani
and a variety of anogential infections. Given the
typical history and symptomology of a ssure
and the alternative diagnoses in the differential,
the astute clinician is able to diagnose a ssure
based on history alone in the majority of patients
and commonly relies on the physical exam only
to conrm the diagnosis.
In terms of diagnosing an anal ssure, gently spreading the buttocks with the patient in the
left lateral or prone position will usually reveal
the presence and location of the ssure. Signs
of ssure chronicity include a sentinel pile or
skin tag, raised or heaped-up edges and observing the concentrically oriented white bers of
the internal sphincter muscle at the base of the
ssure (Fig. 14.1). There is commonly a lack
of granulation tissue at the base of the wound.
Given the pain and tenderness associated with
ssuring and the usually readily apparent ssure
upon simple inspection, it is not required, recommended or helpful to perform a digital or anoscopic examination during the presenting ofce
encounter. Patients will often lament how the
doctor they saw previously regarding their anal
pain performed an overly-aggressive, traumatic
anal exam. Similarly, anorectal physiology testing is not routinely performed at this juncture.
D. L. Feingold and S. A. Lee-Kong
Fig. 14.1 Intra-operative photo demonstrating the classic
ssure triad: a chronic ssure, an indurated, brotic skin
tag and a hypertrophied papilla. Courtesy of Dr. Daniel
L.Feingold
Importantly, patients presenting with severe anal
pain who do not have a demonstrable ssure
should consider examination under anesthesia to
condently establish their diagnosis and to effect
treatment. Patients who are too tender to tolerate
a limited external examination in the ofce may
have a highly symptomatic anal ssure or may
possibly have a more insidious process like an
inter-sphincteric abscess or cancer.
While ssures develop around the circumference of the anus, approximately 80–90% of
patients will have a single, posterior midline
ssure. Up to about 25% of ssures in women
and 8% of ssures in men are located anterior
midline. Post-partum ssures are also commonly
anterior midline. Off-midline or multiple ssures
are considered atypical and should alert the clinician to the possibility of an occult underlying
etiology (Table 14.1). An asymptomatic ssure
should raise the suspicion of Crohn’s disease.
Atypical ssures and persistent or recurrent ssures after sphincterotomy are commonly considered for biopsy to evaluate for an underlying
occult etiology.
14 Anal Fissure andAnal Stenosis
243
Table 14.1 Underlying etiologies for anal ssure
•Psoriasis
•Post-radiation
•Trauma or ano-receptive practices
•Non-healing post-operative wounds
•Crohn’s disease
•Anal cancer
•Tuberculosis
•Syphilis
•HIV infection
Medical Therapy
Patients with acute ssures with a constellation
of symptoms not severe enough to warrant moving directly to operative treatment are usually
treated with a combination of ber supplementation with adequate water intake, stool softeners and hot baths. Smoking cessation should be
addressed, as well. The majority of patients with
acute ssures will heal with this management,
while only about 10% of patients with chronic
ssures will heal with medical therapy. Patients
presenting with chronic ssures or more severe
pain have traditionally been offered partial lateral
internal sphincterotomy (PLIS), a highly successful treatment that is associated with varying
degrees of incontinence. In an effort to minimize
the potential morbidity of treatment, a number of
non-operative, pharmacy-based alternatives have
been studied and are routinely offered to patients
in an effort to avoid PLIS.
A variety of peri-anal topical or injection
therapies, used in conjunction with the medical
therapy outlined above, relax the internal anal
sphincter, improve blood ow and can facilitate
ssure healing. The literature reports a wide
range of healing rates related to the variety of
available compounds that is difcult to reconcile.
These therapies are generally not FDA-approved
for the treatment of anal ssure and their use in
this setting is considered “off-label”. Intra-anal
application is painful, does not improve efcacy
over topical therapy and should be dissuaded.
Thrice daily application of topical therapy may
improve efcacy as compared with twice a day
dosing. Patients with anal ssure refractory to a
particular medical therapy may benet from try-
ing a different compound. Ofce-based silver
nitrate cauterization, oral low-dose diazepam,
topical analgesics or metronidazole ointment, in
conjunction with medical therapy, may be helpful
in certain patients.
Nitric oxide donors like glyceryl trinitrate 0.2% ointment (also known as nitroglycerin) applied twice or thrice daily for 8 weeks
can promote healing. The variable potency of
compounded products can reduce efcacy. A
commercially available, FDA-approved 0.4%
formulation may be easier for patients to acquire,
rather than relying on a compounding pharmacy, and may be a more reliable product [1].
This therapy causes nitrate-induced headaches in
most patients, which are frequently disabling and
lead to non-compliance and treatment failure.
Pre-treating with over-the-counter non-steroidals
or switching to a different topical agent may be
advantageous. Topical calcium-channel blockers
(diltiazem 2% or nifedipine 0.2%) used twice or
thrice daily for 8weeks is generally considered as
effective as nitroglycerin but causes fewer headaches and may have fewer recurrences. These
agents, in some patients, cause pruritis severe
enough to interfere with therapy.
Chemical sphincterotomy (chemodenervation)
by botulinum neurotoxin A injection addresses
anal hypertonicity by inhibiting acetylcholine
release at neuromuscular junctions. Muscle
relaxation occurs within days and may last for
2–4months. Injection of 10–100units at various
locations in and around the anal ssure has been
described and may account for the highly variable reported success rates of this intervention.
As with topical anal ssure therapies, botulinum
injection has a high risk of recurrence after initial
healing. Botulinum therapy may be contra-indicated in pregnancy or in patients with neuromuscular disorders. Patients should be counselled
regarding the potential incontinence after botulinum toxin injection, which is uncommon and is
almost always transient. Fissurectomy at the time
of botulinum toxin injection freshens the wound
and may facilitate healing [2].
An updated Cochrane review of non-surgical
therapy for anal ssure including 77 randomized,
controlled trials with 5031 patients found nitro-
244
D. L. Feingold and S. A. Lee-Kong
glycerin to be marginally but statistically signicantly better than placebo in healing ssures
(48.9% versus 35.5%) [3]. Across these studies,
the ssure recurrence rate after initially healing
with nitroglycerin-based therapy was approximately 50%. The efcacy of calcium-channel
blocker therapy or botulinum therapy was equivalent to the efcacy of using nitroglycerin but
these agents were associated with fewer adverse
events. Other meta-analyses have reported similar disappointing clinical outcomes for medical
therapy.
Operative Therapy
Given the high failure and recurrence rates associated with medical therapy in the setting of
chronic anal ssure and the persistent symptoms
of recalcitrant ssures, many patients undergo
surgery to facilitate healing. The standard operative treatment for patients with refractory anal
ssure persisting despite medical therapy is partial lateral internal sphincterotomy (PLIS) [4].
This operation, highly effective at reducing anal
manometric pressures, heals ssures with success
rates typically quoted as 90–95% or higher and
restores pre-ssure quality of life. Most patients
are highly satised after undergoing PLIS and
experience pain relief within a few days and heal
their ssure after a few weeks. Recurrent ssure
after PLIS occurs in up to 10% of patients and
is commonly treated with medical therapy rather
than re-operation. Post-PLIS complications are
relatively uncommon and may include incontinence, prolonged pain, delayed wound healing,
bleeding, abscess, infection, stula or persistent
or recurrent ssure.
The most signicant long-term complication
of PLIS is derangement of anal function, which
is variably reported to occur, to some degree, in
as many as 30% patients or more. It is generally accepted that the incidence of incontinence
is under-reported among patients and their surgeons whether due to embarrassment or a degree
of denial on the part of patients or inadequate
post-procedure follow-up or reporting bias on
the part of surgeons. The most common dysfunc-
tion after PLIS is typically for controlling atus
or liquid stool and major incontinence of stool
is rare, especially with appropriate patient selection. Prior to performing PLIS, it is important to
consider the details of a patient’s unique history
with regards to prior sphincter damage, previous
anal surgery or vaginal delivery, frequency of
diarrhea and baseline continence and to appropriately counsel patients regarding alternatives,
risks and benets of PLIS.
The concern over potential PLIS-related anal
dysfunction is greater when you consider that the
muscle disruption from PLIS is permanent. Even
when function is preserved in the short-term after
PLIS, patients may be at greater risk for future
incontinence given the age-related decrease in
resting tone as well as possible sphincter damage from future obstetric trauma or anal surgery.
Muscle-sparing alternatives to PLIS can be considered in patients who want to reduce the risk of
post-operative dysfunction [5].
PLIS Operative Techniques
Open PLIS: An appropriately sized HillFerguson of Sawyer retractor accentuates the
bow-stringing of the internal anal sphincter
muscle (Fig.14.2). The muscle is palpated and
the caudal extent of the muscle is appreciated
at the inter-sphincteric groove. A short, radial
incision over the internal muscle and the medial
aspect of inter-sphincteric grove is made in the
lateral position. The distal most aspect of the
internal anal sphincter muscle is visualized and
a curved clamp is passed under the targeted
muscle. The anatomy is conrmed by observing the white, concentric muscle bers of the
internal anal sphincter and demonstrating that
these bers do not fasciculate when stimulated
by cautery. The appropriate length of muscle is
divided with electro-cautery and pressure is held
for hemostasis and to release any residual muscle bers. Transecting a portion of the internal
anal sphincter in the mid-portion of the muscle
instead of at the most distal aspect of the muscle
may reduce the success rate of PLIS and may
result in stula formation. This technical failure can be avoided by conrming the location of
the inter-sphincteric groove and visualizing the