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12 Anal C ance r
Fig. 12.8 ( a ) Adenocarcinoma of the anal canal . ( b ) H&E section of inguinal lymph node show-
ing metastatic mucinous adenocarcinoma associated with known anal canal adenocarcinoma
• Anal canal adenocarcinoma is a rare malignancy with limited data on outcomes
and consensus on treatment.
• The majority of tumors arise from anal glands or may be associated with fi stula
tracts.
• Outcome is poor with signifi cant potential for distal disease [ 32 , 33 ] .
279
12.14 Case 12
A 32-year-old man was referred with a diagnosis of anal warts by his general practitioner. These lesions had been present for 5 years. He denied anoreceptive intercourse. At EUA he had extensive condyloma acuminatum affecting the perineum
and anal canal. Several areas were removed and sent for histology. Histopathology
reported anal condyloma with an associated squamous cell carcinoma (Fig. 12.9a,
b ). He was treated with chemoradiotherapy, achieving a complete clinical and path-
ological response.
• Condyloma acuminatum and HPV infection of the anal canal/perineum do occur
in the absence of anoreceptive intercourse.
• Risk factors include the number of sexual partners and HPV infection in the
genitals.
• Anal to genital self-inoculation of HPV has been documented. Hand transmis-
sion of HPV to anal canal may be a possibility.
• The two types of HPV that cause most cases of anal and genital warts are HPV-6
and HPV-11. These are low-risk subtypes and are generally not associated with
280
A.M. Hogan et al.
Fig. 12.9 ( a ) Low power view of condyloma acuminatum with squamous cell carcinoma. ( b )
Viral (HPV) cytopathic effect in overlying squamous epithelium: enlarged nuclei and vacuolated
cells (koilocytes)
anal canal cancer. However, patients associated with low-risk types of HPV have
a higher potential to be infected by high-risk types of HPV.
• The presence of anal and genital warts should raise an index of suspicion for an
associated anal canal malignancy.
Because anal cancer is relatively rare, diagnosis can often be missed. A high index
of suspicion in all patients presenting with perianal symptoms is imperative, and extensive investigation must be undertaken until the treating physician is satisfi ed that risk of
neoplasia is acceptably close to zero. Like most disease processes, early detection leads
to far better outcomes, and late presentation or recurrence of anal cancer carries a poor
prognosis. The mainstay of treatment of squamous cell carcinoma of the anal canal is
chemotherapy with mitomycin C and 5-fl uorouracil in combination with local radiotherapy. In the case of residual or recurrent disease, abdominoperineal resection may be
indicated. Physician and patient education are possibly the most important interventions in improving survival from these cancers. Increased awareness among the medical and general communities could lead to earlier detection and resultant improved
outcomes. Delayed diagnosis has signifi cant impact on patient well-being, quality, and
quantity of life. Lack of quality trials investigating optimum management of metastatic
squamous cell carcinoma renders management decision making diffi cult and leads to
variations in care worldwide. It is imperative that all patients with anal cancer be managed by a multidisciplinary team and undergo adequate surveillance following initial
treatment to ensure early detection of recurrent disease.
References
1. Barroso LF. The role of Human Papilloma Virus (HPV) vaccination in the prevention of anal
cancer in individuals with Human Immunodefi ciency Virus-1 (HIV-1) infection. Ther Adv
Vaccines. 2013;1(2):81–92.
2. Palefsky JM, Giuliano AR, Goldstone S, Moreira Jr ED, Aranda C, Jessen H, et al. HPV
vaccine against anal HPV infection and anal intraepithelial neoplasia. N Engl J Med.
2011;365(17):1576–85.
12 Anal C ance r
3. Welton ML, Varma MG. Anal cancer. The ASCRS textbook of colon and rectal surgery.
New York: Springer; 2007. Chap. 35.
4. Bosman FT, Carneiro F, Hruban RH, Theise ND. WHO classifi cation of tumours of the diges-
tive system. 4th ed. Lyon: IARC; 2010.
5. TNM classifi cation of malignant tumours. UICC. 7th ed. Leslie H. Sobin (Editor), Mary K.
Gospodarowicz (Editor), Christian Wittenkind (Editor). Wiley-Blackwell; 2009.
6. Ryan DP, Compton CC, Mayer RJ. Carcinoma of the anal canal. N Engl J Med.
2000;342:792–800.
7. Pintor MP, Northover JM, Nicholls RJ. Squamous cell carcinoma of the anus at one hospital
from 1948 to 1984. Br J Surg. 1989;76:806–10.
8. Boman BM, Moertel CG, O’Connell MJ, et al. Carcinoma of the anal canal: a clinical and
pathologic study of 188 cases. Cancer. 1984;54:114–25.
9. Papillon J, Chassard JL. Respective roles of radiotherapy and surgery in the management of
epidermoid carcinoma of the anal margin. Dis Colon Rectum. 1992;35(5):422–9.
10. Hogan NM, Kerin MJ, Joyce MR. Gastrointestinal complications of pelvic radiotherapy: med-
ical and surgical management strategies. Curr Probl Surg. 2013;50(9):395–407.
11. Caldarella C, Annunziata S, Treglia G, Sadeghi R, Ayati N, Giovanella L. Diagnostic perfor-
mance of positron emission tomography/computed tomography using fl uorine-18 fl uorodeoxyglucose in detecting locoregional nodal involvement in patients with anal canal cancer: a
systematic review and meta-analysis. Scientifi c World Journal. 2014;2014:196068.
12. Palefsky JM, Holly EA, Efi rdc JT, Da Costa M, Jay N, Berry JM, et al. Anal intraepithelial
neoplasia in the highly active antiretroviral therapy era among HIV-positive men who have sex
with men. AIDS. 2005;19:1407–14.
13. Lorenz HP, Wilson W, Leigh B, Crombleholme T, Schecter W, et al. Squamous cell carcinoma
of the anus and HIV infection. Dis Colon Rectum. 1991;34:336–8.
14. Seo Y, Kinsella M, Reynolds HL, Chipman G, Remick SC, Kinsella TJ. Outcomes of chemo-
therapy with 5-fl uorouracil and mitomycin C for anal cancer in immunocompetent versus
immunodefi cient patients. Int J Radiat Oncol Biol Phys. 2009;75:143–9.
15. Place RJ, Gregorcyk SG, Huber PJ, et al. Outcome analysis of HIV-positive patients with anal
squamous cell carcinoma. Dis Colon Rectum. 2001;44:506.
16. Flam M, John M, Pajak TF, et al. Role of mitomycin in combination with fl uorouracil and
radiotherapy, and of salvage chemoradiation in the defi nitive nonsurgical treatment of epidermoid carcinoma of the anal canal: results of a phase III randomized intergroup study. J Clin
Oncol. 1996;14:2527–39.
17. Renehan AG, Saunders MP, Schofi eld PF, et al. Patterns of local disease failure and outcome
after salvage surgery in patients with anal cancer. Br J Surg. 2005;92:605–14.
18. Nilsson PJ, Svensson C, Goldman S, et al. Salvage abdominoperineal resection in anal epider-
moid cancer. Br J Surg. 2002;89:1425–9.
19. Johnson LG, Madeleine MM, Newcomer LM, Schwartz SM, Daling JR. Anal cancer inci-
dence and survival: the surveillance, epidemiology, and end results experience, 1973–2000.
Cancer. 2004;101(2):281–8.
20. Fisher WB, Herbst KD, Sims JE, Critchfi eld CF. Metastatic cloacogenic carcinoma of the
anus: sequential responses to adriamycin and cis-dichlorodiammineplatinum(II). Cancer Treat
Rep. 1978;62(1):91–7.
21. Zimm S, Wampler L. Response of metastatic cloacogenic carcinoma to treatment with semus-
tine. Cancer. 1981;48(12):2575–6.
22. Evans TRJ, Mansi JL, Glees JP. Response of metastatic anal carcinoma to single agent carbo-
platin. Clin Oncol. 1993;5(1):57–8.
23. Golub DV, Civelek AC, Sharma VR. Case report; a regimen of taxol, ifosfamide, and platinum
for recurrent advanced squamous cell cancer of the anal canal. Chemother Res Pract. 2011;
2011:163736. 6 pages.
24. Grifalchi F, Padovani A, Romeo F, Trinca C, Moscetti L, Cortesi E. Response of metastatic
epidermoid anal cancer to single agent irinotecan: a case report. Tumori. 2001;87(1):58–9.
281
282
25. Iddings DM, Fleisig AJ, Chen SL, Faries MB, Morton DL. Practice patterns and outcomes for
anorectal melanoma in the USA, reviewing three decades of treatment: is more extensive surgical resection benefi cial in all patients? Ann Surg Oncol. 2010;17(1):40–4.
26. Kiran RP, Rottoli M, Pokala N, Fazio VW. Long-term outcomes after local excision and radi-
cal surgery for anal melanoma: data from a population database. Dis Colon Rectum.
2010;53(4):402–8.
27. Thomas M, Bienkowski R, Vandermeer TJ. Malignant transformation in perianal fi stulas of
Crohn’s disease: a systematic review of literature. J Gastrointest Surg. 2010;14:66–73.
28. Freeman HJ, Perry T, Webber DL. Mucinous carcinoma in Crohn’s disease originating in a
fi stulous tract. World J Gastrointest Oncol. 2010;2:307–10.
29. Slesser AA, Bhangu A, Bower M, Goldin R, Tekkis PP. A systematic review of anal squamous
cell carcinoma in infl ammatory bowel disease. Surg Oncol. 2013;22(4):230–7.
30. Perez DR, Trakarnsanga A, Shia J, Nash GM, Temple LK, Paty PB, Guillem JG, Garcia-
Aguilar J, Weiser MR. Management and outcome of perianal Paget’s disease: a 6-decade institutional experience. Dis Colon Rectum. 2014;57(6):747–51.
31. Cox NH, Eedy DJ, Morton CA. Therapy Guidelines and Audit Subcommittee, British
Association of Dermatologists Guidelines for management of Bowen’s disease: 2006 update.
Br J Dermatol. 2007;156(1):11–21.
32. Chang GJ, Gonzalez RJ, Skibber JM, et al. A twenty-year experience with adenocarcinoma of
the anal canal. Dis Colon Rectum. 2009;52(8):1375–80.
33. Belkacémi Y, Berger C, Poortmans P, et al. Rare Cancer Network Management of primary anal
canal adenocarcinoma: a large retrospective study from the Rare Cancer Network. Int J Radiat
Oncol Biol Phys. 2003;56(5):1274–83.
A.M. Hogan et al.
Pilonidal Disease
13
Andrea Petrucci , Nancy Morin , and Marylise Boutros
13.1 Definitions and Risk Factors
The term “pilonidal” dates back to the year 1880 when R. M. Hodges coined the
term which basically translates into “hair nest” [ 1 ]. A pilonidal sinus is a chronic
subcutaneous tract in the natal cleft, which spontaneously drains through the skin
openings [ 2 ].
Pilonidal disease is a common problem with an overall incidence of 26 per
100,000 individuals. This disease is most commonly seen in adolescents and young
adults [ 3 ]. Pilonidal disease rarely occurs in individuals older than 40 years of age,
and it is believed to be an acquired condition as opposed to a congenital one [ 4 ].
Patients with a deep natal cleft are prone to acquiring pilonidal disease because it is
a favorable environment for sweating, maceration, bacterial contamination, and
penetration of hairs [ 5 ]. Other predisposing factors include obesity, history of fol-
liculitis or a furuncle on another body region, hirsutism, and family history. In a
retrospective study published in 2009, a positive family history was found to also
predispose patients to a higher recurrence rate after surgery [ 6 ]. It seems as though
the familial predisposition is related to other family members having similar hair
patterns and body habitus rather than an actual genetically transmitted origin of the
disease. In addition, certain occupations such as hairdressers, military personnel,
and sheep shearers were reported to be at increased risk of developing pilonidal
disease [ 3 ].
A. Petrucci , MD, FRCSC • N. Morin , MD, FRCSC, FACS, FASCRS
M. Boutros , MD, FRCSC (
McGill University/Jewish General Hospital , 3755 Cote Sainte-Catherine
Rd., G-304 , Montreal , QC , Canada , H3T 1E2
mboutros@jgh.mcgill.ca; nancy.morin@mcgill.ca; maryliseboutros@gmail.com
e-mail:
© Springer International Publishing Switzerland 2016
M. Zutshi (ed.), Anorectal Disease, DOI 10.1007/978-3-319-23147-1_13
*)
283
284
A. Petrucci et al.
13.2 Pathogenesis of Pilonidal Disease
There is no objectifi ed right answer as to how pilonidal sinuses form; however,
there are two schools of thought about the pathogenesis of this disease. Bascom
believed that the natal cleft was normal and that it was simply the result of a hair
follicle fi lled with keratin that eventually becomes infected, very similar to a furuncle, extending its way into the subcutaneous fat (Fig. 13.1 ). A more common belief
is that of Karydakis, who stated that a loose hair shaft fi nds its way into the gluteal
cleft, burrowing into the skin, causing the formation of a pit which allows for other
hair shafts to insert (Fig. 13.2 ). This loose hair eventually causes an infl ammatory
reaction that can either become chronic or develop into an abscess [ 7 ]. Though the
latter theory is more widely taught and believed, there is no evidence to prove one
theory over the other.
13.3 Clinical Presentation
How does one recognize pilonidal disease? Look for pits. These pits represent primary and secondary openings of the pilonidal sinus. The primary opening(s) is usually located at the base of the natal cleft, roughly 5 cm above the anus, and is the
opening through which hair may be observed to protrude (Fig. 13.3 ). There is a
subcutaneous tract that forms from this primary opening, creating a sinus. The
sinus(es) can vary in length and number. The pit may form tracts that create a
Fig. 13.1 Pathogenesis of
pilonida l disease
Normal
follicle
Stretched
follicle
Infected
follicle
Acute
abscess
Chronic
abscess
Epithelial
tube
13 Pilonidal Disease
Fig. 13.2 Pathogenesis of
lose hair inserting and
burrowing under the skin,
forming a sinus tract
Fig. 13.3 Sinus opening
in the natal cleft (adapted
from Hong and Ryoo [
with permission)
285
7 ],
secondary opening off the midline. These secondary openings are where spontaneous drainage or incision and drainage of an abscess occur. The pilonidal tract along
with its two openings, the primary and secondary sinuses, can be visualized on the
sketch in Fig. 13.2 . Patients can have a single or multiple secondary openings,
depending on the chronicity and complexity of the disease.
Patients can present with either an acute pilonidal abscess, a single chronic
draining sinus, or a complex or recurrent pilonidal sinus [
3 ] which are treated in
different ways as will be discussed later. A pilonidal abscess usually presents as a
tender, fl uctuant mass with overlying cellulitis (Fig. 13.4 ) as opposed to a chronic
draining sinus, which shows no signs of infection. A chronic sinus presents with a
primary pit located in the natal cleft often with possible hair sticking out of it’s
opening (Fig. 13.3 ).
286
Fig. 13.4 Pilonidal
abscess
A. Petrucci et al.
Complex and recurrent pilonidal sinuses are usually the result of persistent
sinuses or multiple abscess drainages that may have more than one opening to the
skin. It is important to keep in mind that other diseases such as anorectal cryptoglandular abscesses, hidradenitis, and fi stulas secondary to complex presentations of
Crohn’s disease can present similarly to pilonidal disease and need to be ruled out
as possible differential diagnoses [ 8 , 9 ]. Although pilonidal disease is not life threat-
ening, it can be debilitating for the patient and poorly impact their quality of life.
Regardless of the presentation of pilonidal disease, the ultimate goal for treatment
is to decrease morbidity for the patient and to allow for quick recovery and return to
daily activities.
13.4 Management of Pilonidal Abscesses
Case 1
A 24-year-old man presents to the emergency room complaining of “pain over their
tailbone.” This is the fi rst time he has ever felt such pain. He recalls falling on his
tailbone during his speed skating practice roughly 2 weeks ago. He also mentions
that he had a fever yesterday with some chills over the last 2 days. He fi rst noticed
13 Pilonidal Disease
Fig. 13.5 Pilonidal
abscess (from Slater [
with permission)
287
9 ]
Gluteal cleft
Midline pits
Anus
Fig. 13.6 Technique for shaving (adapted from Papaconstantinou and Thomas [ 3 ], with
permission)
Two-inch area shaved
around gluteal cleft
(proximity of pits to
anus may limit this)
a “lump” about a week ago but came in today to see you because he felt that it
increased in size and the pain was keeping him up at night. He denies any other
lower gastrointestinal symptoms or abdominal pain.
On exam, he is afebrile and his vital signs are all within normal limits. Abdominal
and digital rectal exam are unremarkable. You notice an infl amed, erythematous
lump at the natal cleft with no spontaneous discharge (Fig. 13.5 ). It is very tender
and fl uctuant.
This is a typical presentation of a pilonidal abscess. Just as in any other clinical
presentation of an abscess, this patient presents with the universal signs of erythema, pain, and cellulitis. In the case of a pilonidal abscess, the technique used to
drain the abscess is important (Fig. 13.6 ).
When a patient presents with a pilonidal abscess, it is usually located lateral to
the midline despite the initial sinuses being located in the midline, along the gluteal
288
Fig. 13.7 Sketch of proper
incision technique for
incision and drainage of a
pilonidal abscess (adapted
from Papaconstantinou and
Thomas [
permission)
3 ], with
A. Petrucci et al.
Incision
Midine
Abscess
At least one cm
Anus
cleft. Studies have shown that the best way to drain the abscess is to make the incision off the midline [ 2 ] because this leads to better healing. A midline wound is
under constant traction and vacuum forces that allow surrounding hair and bacteria
to enter the wound impair wound healing [ 10 ], whereas an off-midline incision may
be less likely to create this traction force. The incision is ideally made about 1 cm
lateral to the midline and deepened all the way down into the cavity, to ensure that
the abscess cavity is opened and pus and any other material, such as hair, can be
evacuated [
3 ] (Fig. 13.7 ).
Once this is completed, the incision is converted to a cruciate or elliptical incision to ensure the skin and subcutaneous tissues overlying the abscess cavity do not
close prematurely and lead to a recurrence of the abscess. The cavity is then copiously irrigated. A randomized control trial assessed the benefi t of performing a
curettage at the time of incision and drainage, and the authors found that there was
a signifi cant difference in healing at 10 weeks after the procedure and lower recurrence rates observed with curettage [
11 ]. This is due to removal of all infl ammatory
debris that may impair healing and removal of all epithelialized surfaces to encourage quicker wound healing. As such, once the cavity is irrigated, a gentle curettage
should be performed, followed by a light packing of the cavity (Fig. 13.8 ).
The act of packing a wound and removing the packing for cleansing at least
once daily promotes healing; however, it can be quite painful and bothersome for
the patient, which may lead to poor posttreatment compliance to wound care. For
this reason some surgeons advocate that the packing be removed the following day
by the patient and the cavity be washed with soap and water, preferably two to
three times a day to accelerate healing [ 2 , 3 ] and to help keep the area clean. If the