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8.8.1.5 Excision and Rotation Flap
These techniques are recommended when there is extensive tissue loss, such as occurs
after multiple operations or after an extensive primary procedure. To eliminate the intergluteal fold and the conventional vertical wound (that tends to open), a Z-plasty (
Fig. 8.7)
can be performed, in which skin flaps are mobilized, rotated, and alternated. The branches
of the Z-plasty are cut at a 30–60 degrees angle, with respect to the longitudinal axis of
the wound.
45,46
The risk for infection is 9.3%, for dehiscence is 5.5%, and for recurrence
is 2.4%.
41
Incision
MidlineMidline
Midline
Resection site
Pits
Anus
Anus
Wound
Sutured
wounds
A
bscess
(A) (B)
FIG. 8.6 Bascom I technique, modified by Nelson and Billingham.
FIG. 8.7 Z-plasty technique.
108 ANORECTAL DISORDERS
Pradeep Sharma performed the multiple Z-plasty technique under local anesthesia on
115 patients and reported the advantages of a minimal lateral dissection resulting in a scar
with less lateral extension and a low recurrence rate (2%).
47
Other authors suggest a rhomboid excision to cover the wound with a Limberg flap.
The technique consists of en bloc extirpation of the pilonidal sinus through a rhombusshaped incision at a 60 degrees angle and an obliquely displaced rhombus-shaped sliding
flap (
Fig. 8.8). Sutures are not located at the midline with this procedure thus preventing
tension and facilitating healing.
48,49
Milito et al. reported the risks for infection as 2.6%, for
dehiscence as 3.4%, and for recurrence as 1.5%.
50
Some years ago, a modification of the Limberg technique was proposed, in which
the inferior edge of the wound remains outsid e of the midline (which is the location of
the largest number of recurrences with the original method) through modification of
the flap.
51
Dufourmentel developed a modification of the Limberg technique that involves rotating a full-thickness flap to the plane of the right gluteal fascia. The cure rate is close to
100% and it is ideal for the treatment of recurrences.
52
V-Y flaps have also been utilized, mobilizing the skin, the subcutaneous tissue, and the
fascial layer toward the defect (
Fig. 8.9).
53
Infection has been reported to occur in 1.9% of
FIG. 8.8 Limberg technique with flattening of the natal cleft by the flap.
FIG. 8.9 Reconstruction with V-Y flap at the midline.
Chapter 8 • Pilonidal Disease 109
the patients, dehiscence in 3.8%, and recurrence in 2.7%.41Sinus resection should be lateral, given that wounds should not be left at the midline. Suction drains have not been
shown to be useful.
41,46
The Bascom II procedure has been proposed for the treatment of unhealed wounds
from a previous surgery. It consists of flattening the intergluteal fold. Skin from the
affected area is resected at the side of the midline in the form of an ellipse. The defect
is closed through a full-thickness rotation flap proceeding from the contralateral
buttock.
24,43,44
8.8.1.6 Cryosurgical Ablation
Treatment with cryoablation consists of opening the sinus and its branches, curetting the
cavity, and applying electrocoagulation to the bleeding sites, leaving a smaller wound than
that of a wide resection. Liquid nit rogen is applied to the open wound for approximately
5min.
54
8.8.1.7 Sclerosing Therapy
Hegge described the injection of phenol as a conservative treatment of pilonidal disease.
55
It is a simple treatment whose efficacy has been shown to be similar to that of surgical
techniques, with the advantages of not requiring hospitalization, a shorter disability
period, lower cost, and being a less painful procedure. After the cavity is curetted, sterile
gauze is introduced into it, and phenol 80% is instilled. The phenol-soaked gauze is
removed at 24h.
56
Sclerosing therapy has been reported to have a 60% cure rate and a
healing time of 6.2 weeks.
24
Crystallized phenol has also been used with a cure rate of
95% after a mean follow-up period of 24 months.
57
8.8.1.8 Conservative Management
John Armstrong and Peter Barcia analyzed the results of conservative treatment at a military hospital.
58
The method consisted of hair control through shaving the intergluteal
fold, improved personal hygiene, and abscess drainage through a small lateral incision.
24,58
Of 101 cases examined over 17 years, only 23 required surger y.
8.8.1.9 Laser Depilation
The usefulness of laser depilation in the postoperative management of pilonidal disease
has been demonstrated, helping prevent the complication of folliculitis and recurrence. It
is not a curative method per se.
59
In the systematic review by Pronk et al.,6014 studies were
selected that included a total of 963 patients. Seven of the studies were retrospective
cohort stud ies, three were prospective cohort studies, two were randomized controlled
trials, and two were case-control studies. Mean follow-up duration was 37months.
The recurrence rate was 9.3% (34 of 366) in patients that had laser depilation, 23.4%
(36 of 154) in those that had razor shaving/cream depilation, and 19.7% (85 of 431) in
patients that had no hair removal after surgery for pilonidal disease.
110 ANORECTAL DISORDERS
8.8.1.10 Biologic Sealant
In another conservative procedure, biologic sealant is used under the same precepts as in
anal fistula; however, there are few studies on its use at present. After curetting the cavity
and its tracts, 1–2 mL of fibrin glue are applied. The wounds are not covered, nor is antimicrobial management given. Currently there is no conclusive evidence in relation to the
benefits associated with fibrin glue as monotherapy or as a complement to surgery in persons with pilonidal disease. An analysis by Lund et al. identified four studies, each of
which was small with the risk of bias, thus producing low-quality results. Future studies
should include a larger number of participants.
61
8.8.1.11 Cutting Seton
A vertical incision is made at the midline that includes all the affe cted tissue in a longitudinal direction. The cavity of the sinus is then drained and curett ed. An artificial tunnel
is created just above the sacral fascia and the seton is place d inside it. The seton is initially tightened at 24 or 48 h after t he surgery and then every 4 or 5 days. There is a report
on eigh t cases managed with a cutting seton in wh ich it was removed at 2 weeks. Total
healing occurred at 4 weeks and there was no recurrence with in a 22-month follow-up
period.
62
8.9 Postoperative Care
Postoperative management is of great importance in the suc cess of the surgery. Hospital
stay depends on the technique employed. The patient is examined in the office to monitor
wound care and rule out complications that delay healing.
In the postoperative period followi ng techniques that do not employ primary clo sure,
the indications for t he patient are normal diet and early ambulation. Ana lgesics are prescribed, but topical or systemic a ntimicrobials should not be used. The patient must be
instructed in the daily changing of gauzes, so that they are dry and sterile. Gauzes coated
in antiinflam matory agents a nd substances to promote scarring can prolong healing
time. Afte r t he performance of ope n techniques, irrigation, cleansing, and shaving of
the contiguous skin are essential every 1–4 weeks, until healing is complete. In cases
of delayed cicatrization, especially in the area most caudal to the wound, compacted
gauzes should be placed to expan d the intergluteal fold, thus preventing friction,
absorbing humidity, and favoring healing. Packing the wound with gauzes prevents
bleeding.
After closed procedures, signs of infection or dehiscence and the presence of seroma or
hematoma must be monitored for. The patient should maintain relative rest, limiting the
degree of activities for several weeks to prevent increased woun d tension. Periodic shaving
of the skin adjacent to the wound is important. When the wound extends close to the anus,
it is preferable to delay bowel movements through dietary modifications and drugs.
Regardless of the surgical technique employed, the patient should be followed-up for
several months, due to the possibility of recurrence—the most unwelcome complication.
Chapter 8 • Pilonidal Disease 111
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bone marrow aplasia. Treatment by large excision and closing by local flaps. Ann Chir Plast Esthet.
1999;44:552–555.
28. Mateo S, Moreno TJJ, Blazquez C, Echevarria JI. Osteomielitis sacra complicada con meningitis aguda
secundaria a un fistula pilonidal. Rev Quir Esp. 1984;11:212–215.
29. Jukic I, Grandic L, Tonkic A, Tonkic M, Rosenzweig D, Kuscevic D. Sepsis-induced disseminated intra-
vascular coagulation: a rare complication of sacrococcygeal pilonidal sinus disease. Mt Sinai J Med.
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30. Montes G, Herrera PJJ. Enfermedad pilonidal. Clin Gastroenterol M"ex. 2010;2:125–140.
31. Boulanger G, Abet E, Brau-Weber AG, et al. Is histological analysis of pilonidal sinus useful? Retrospec-
tive analysis of 731 resections. J Visc Surg. 2017. pii: S1878-7886(17)30140-6.
32. Mavros MN, Mitsikostas PK, Alexiou VG, Peppas G, Falagas ME. Antimicrobials as an adjunct to
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33. Hamsa SB, Asaad SH. Effect of surgical wound care methods of the lay open technique on the outcome
of chronic sacrococcygeal pilonidal sinus management. Wound Med. 2017;16:1–6.
34. Ga rg P, Garg M, Gupta V, Mehta SK, Lakhtaria P. Laying open (deroofing) and curettage under local
anesthesia for pilonidal disease: an outpatient procedure. World J Gastrointest Surg. 2015;7:
214–218.
35. Wienert V. Knowledge-based therapy of the pilonidal sinus. Eur Surg. 2004;36:166–167.
36. Bobkiewicz A, Borejsza-Wysocki M, Biczysko M, Ratajczak A, Malingere S, Drews M. Portable VAC
therapy improve the results of the treatment of the pilonidal sinus—randomized prospective study.
Pol Przegl Chir. 2013;85:371–376.
37. McGuinness JG, Winter DC, O’Connell PR. Vacuum-assisted closure of a complex pilonidal sinus.
Dis Colon Rectum. 2003;46:274–276.
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an optimal procedure for recurrent pilonidal disease. An
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Ital Chir. 2015;86:575–579.
39. Rouch JD, Keeley JA, Scott A, Sydorak R, DeUgarte D, Lee SL. Short- and long-term results of unroofing
and marsupialization for adolescent pilonidal disease. JAMA Surg. 2016;151:877–879.
40. Mentes O, Bagci M, Bilgin T, Coskun I, Ozgul O, Ozdemir M. Management of pilonidal sinus disease
with oblique excision and primary closure: results of 493 patients. Dis Colon Rectum. 2006;49:
104–108.
41. Petersen S, Koch R, Stelzner S, Wendlandt TP, Ludwing K. Primary closure techniques in chronic pilo-
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42. Ehrl D, Choplain C, Heidekrueger P, et al. Treatment options for pilonidal disease. Am Surg.
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43. Senapati A, Cripps NPJ, Thompson MR. Bascom’s operation in the day-surgical management of symp-
tomatic pilonidal sinus. Br J Surg. 2000;87:1067–1070.
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Surg. 2002;137:1146–1150.
Chapter 8 • Pilonidal Disease 113
45. Fazeli MS, Adel MG, Lebaschi AH. Comparison of outcomes in Z-plasty and delayed healing by
secondary intention of the wound after excision of the sacral pilonidal sinus: results of a randomized,
clinical trial. Dis Colon Rectum. 2006;49:1831–1836.
46. Rao J, Deora H, Mandia R. A retrospective study of 40 cases of pilonidal sinus with excision of tract
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47. Sharma PP. Multiple Z-plasty in pilonidal sinus—a new technique under local anesthesia. World J Surg.
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48. Singh PK, Gohil RK, Saxen N. Limberg flap procedure for sacrococcygeal pilonidal sinus: a prospective
study. Int Surg J. 2017;4:2238–2242.
49. Daphan C, Tekelioglu MH, Sayilgan C. Limberg flap repair for pilonidal sinus disease. Dis Colon Rec-
tum. 2004;47:233–237.
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all? Adv Clin Exp Med. 2017;26:63–67.
53.
€
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flap and Limberg transposition flap for recurrent sacrococcygeal pilonidal sinus disease. Asian J Surg.
2017;40:197–202.
54. Gage AA, Dutta P. Cryosurgery for pilonidal disease. Am J Surg. 1977;133:249–254.
55. Hegge HG, Vos GA, Patka P, Hoitsma HF. Treatment of complicated or infected pilonidal sinus disease
by local application of phenol. Surgery. 1987;102:52–54.
56. Bayhan Z, Zeren S, D€uzg€un SA. Crystallized phenol treatment in postoperative recurrent pilonidal dis-
ease. J Clin Exp Investig. 2016;7:19–22.
57. Yuksel ME. Pilonidal sinus disease can be treated with crystallized phenol using a simple three-step
technique. Acta Dermatovenerol Alp Panonica Adriat. 2017;26:15–17.
58. Armstrong JH, Barcia PJ. Pilonidal sinus disease. The conservative approach. Arch Surg.
1994;129:
914
–918.
59. Conroy FJ, Kandamany N, Mahaffey PJ. Laser depilation and hygiene: preventing recurrent pilonidal
sinus disease. J Plast Reconstr Aesthet Surg. 2008;61:1069–1072.
60. Pronk AA, Eppink L, Smakman N, Furnee EJB. The effect of hair removal after surgery for sacrococ-
cygeal pilonidal sinus disease: a systematic review of the literature. Tech Coloporctol. 2018;22:7–14.
61. Lund J, Tou S, Doleman B, Williams JP. Fibrin glue for pilonidal sinus disease. Cochrane Database Syst
Rev. 2017;1:CD011923.
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Further Reading
63.
Oncel M, Kurt N, Kement M, Colak E, Eser M, Uzun H. Excision and marsupialization versus sinus
excision for the treatment of limited chronic pilonidal disease: a prospective, randomized trial. Tech
Coloproctol. 2002;6:165–169.
114 ANORECTAL DISORDERS
9
Pruritus Ani
Elizabeth Barba Orozco
DI G E S T I V E S Y S T E M R E S E A R C H UN I T , UN IV E R S I T Y H O S P I T A L V A L L D ’H E B R O N, B A R C E L O N A ,
SP A I N
9.1 Introduction
Pruritus ani is the Latin term for “itchy anus” and results from irritation of the skin of the
perianal region and anus. Anal itching causes intolerable discomfort that often is accompanied by burning. The main symptom of pruritus ani is the strong impulse to scratch the
perianal area. The incidence ranges from 1% to 5% in the general population.
1
Most
patients are distributed in the 30–70years age range,
1
but there is an increased prevalence
in ages 30–50years.
2
Men are more commonly affected than women with 4:1.
3, 4
Although
it is considered as a symptom more than a diagnosis, this condition has a significant
impact on quality of life.
9.2 Etiology
The pathophysiology of pruritus ani is related to pruriceptors of sensory C-fibers in the
skin; other mediator pruriceptives involved are bradykinin and kallikrein. Histamine
has been widely used to study the neuronal mechanism of itch; however, antihistamines
are ineffective in treating pruritis suggesting that it is mediated through nonhistaminergic
mechanisms.
5
Compounds like serotonin, prostigmine, neuropeptides, and endogenous
opioids have also been incriminated in the physiopathological mechanism of itch. The
events that trigger anal itching and perpetuate a feedback loop are shown in
Fig. 9.1.
An itch classification scheme has been proposed by Twycross,
6
defining four
categories:
•
Pruriceptive itch: prurit originating in the skin, as in parasitism by pinworms or
scabies;
•
Neuropathic itch: as a consequence of disease located at any point along the afferent
pathway, brain tumors;
•
Neurogenic itch: as a consequence of neurochemical activity as the action of opioid
neuropeptides in cholestatic liver disease;
•
Psychogenic itch: associated with parasitephobia.
Pruritus ani is classified as primary or idiopathic when no cause can be found, but almost
25%–75% of cases have a co-existing pathology.
7
The majority are secondary causes,
Anorectal Disorders.
https://doi.org/10.1016/B978-0-12-815346-8.00009-6
© 2019 Elsevier Inc. All rights reserved.
115
associated with conditions like local irritation; anorectal diseases, predominantly hemorrhoids and fissures; premalignant or malignant lesions; infection; inflammation; or systemic diseases.
9.3 Primary or Idiopathic Pruritus
Pruritus ani is considered primary or i diopathic if no one demonstrable cause can be
found. Washington Hospital Center has a useful classification system for pruritus ani
based on the skin condition. In stage 0 the skin appears normal, in stage 1 t he skin i s
red and inflamed, in stage 2 it is lichenified, and in stage 3 the patient presents with
lichenified skin with erosions and ulcerations secondary to scratching. It is necessary
to exclude the use of some triggers, like cream, perfumes, and other kind of irritant products; evaluate fecal soilage; and identify inadequate, poor, or extensiv e anal hygiene. No
controlled trials have been done to evaluate speci fic foods or diet as a direct cause of
pruritus ani, but it is necessary exclude the involvement of some specific foods like
tomatoes, beer, cola, tea, peanuts, milk, chocolat e, and some kind of medicines, for
example, tetracy cline and colchicine.
7, 8
Fecal soilage due to an exaggerated recto anal
inhibitory reflexes and earlier incontinence are always prese nt in patients with pruritus
ani an d provide some evidence for the role o f soiling as a cause of idiopathic o r primary
prurit us ani (
Table 9.1).
9,10
Specific measures should be initiated once any underlying cause has been excluded:
use a high fiber diet and softener to treat constipation and if diarrhea is present this should
also be treated.
FIG. 9.1 Event association in the pruritus ani evolution.
116 ANORECTAL DISORDERS
9.4 Treatment
9.4.1 Elimination Step
This consists of avoiding irritants like creams, soaps, detergents, and wipes; using cotton
underwear; following an elimination diet; and avoiding the food identified as a trigger for
pruritus ani. Once general control is achieved the patient should keep the anal region dry,
avoid vigorous rubbing, and use a bidet or shower head to keep the anorectal and perineum region clean if soiling is an issue.
9.4.2 Topical Therapy
If general measures are not enough to alleviate pruritus topical treatments are recommended. Anal emollients like 10%–20% zinc oxide ointment or petrolatum ointment
can be applied several times a day.
4,11
In patients who do not respond to topical emollients, a short course of mild to medium potency steroids should be initiated for a shorter
duration under strict monitoring, such as 1% hydrocortisone cream two to three times a
day for a short period of time is effective in relieving the symp toms of pruritus.
12
However,
it should not be used for more than 2 weeks due to the potential risk of prolonged use causing skin atrophy and sometimes worsening of pruritus ani.
13,14
Topical capsaicin (0.006%) has been used to treat pruritus ani. It is a natural alkaloid
extracted from red chili pepper. The mechanism of capsaicin in patients with pain and
pruritus ani is not completely understood. There is a phenotypic change in the polymodal
sensory fibers that normally express capsaicin/heat receptor ( VR1) , although pharmacological action appears to be depletion in the synthesis, storage, and release of substance P,
which is a neuropeptide than triggers the sensation of itching and burning pain.
15
In a
Table 9.1 Etiology of Pruritus Ani
Hygiene conditions Poor or excessive hygiene
Fecal soiling Encopresis, fecal incontinence, chronic diarrhea, internal relaxation of the anal
sphincter, recto anal inhibitory reflex increased
Anorectal diseases Hemorrhoids, anal fissure, fistula, rectal prolapse
Dermatologic diseases Psoriasis, lichen plane, pemphigus, contact dermatitis, atopic dermatitis, hidradenitis
suppurativa, vitiligo, Paget diseases
Systemic diseases Diabetes mellitus, hyperbilirrubinemia, leukemia, thyroid diseases, iron deficiency,
chronic renal failure
Infections Parasites (pinworms), fungal infections (Candida sp.), bacterial infections
(Streptococcus, Staphylococcus aureus)
Local irritants Excessive hair, perfume, anal creams, wipes, dyed toilet paper
Diet Coffee, decaffeinated coffee, tea, cola, alcohol, chocolate, tomatoes, beer, wine,
spicy foods
Psychological conditions Anxiety, parasite-phobia, psychosis
Primary pruritus No demonstrable cause
Chapter 9 • Pruritus Ani 117
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