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Hidradenitis Suppurativa: A FrequentlyMissed Diagnosis, Part 2: Treatment Options
C M E1 AMA PRA
Category 1 CreditTMANCC
3.0 Contact Hours
Shirley C. Wang, MD & Clinical Research Coordinator & University Health Network & Toronto, Ontario, Canada
Sheila C. Wang, PhD & Resident & Department of Dermatology, McGill University & Montreal, Quebec, Canada
Afsaneh Alavi, MD, MSc, FRCPC & Assistant Professor & Department of Medicine (Dermatology), University of Toronto &Ontario, Canada
Raed Alhusayen, MD, MSc (Clin Epi), FRCPC & Assistant Professor & Sunnybrook Health Sciences Centre & University ofToronto & Ontario, Canada
Morteza Bashash, PhD & Research Fellow & Dalla Lana Faculty of Public Health & University of Toronto, Ontario, Canada
R. Gary Sibbald, BSc, MD,MEd, FRCPC (MedDerm), MACP, FAAD,MAPWCA & Professor of Public Health andMedicine &University of Toronto & Toronto, Ontario, Canada & Director & International Interprofessional Wound Care Course & Masters ofScience in Community Health (Prevention & Wound Care) & Dalla Lana School of Public Health & University of Toronto & PastPresident, World Union of Wound Healing Societies & Clinical Editor & Advances in Skin &Wound Care & Philadelphia, Pennsylvania
Dr Alavi has disclosed that she was a consultant to AbbVie and Janssen; her institution is a recipient of grant funding from AbbVie; her institution was a recipient of payment for lecturesincluding speakers’ bureau from AbbVie and Janssen; and her spouse/partner (if any), has disclosed that he/she has no financial relationships with, or financial interests in, any commercialcompanies pertaining to this educational activity. Dr Sibbald has disclosed that he is a recipient of grant funding, consulting fee/honorarium, travel support, and participation fees fromAbbVie; and his spouse/partner (if any), has disclosed that he/she has no financial relationships with, or financial interests in, any commercial companies pertaining to this educationalactivity. Dr Alhusayen has disclosed that he is a consultant to Abbott and Janssen; and his spouse/partner (if any), has disclosed that he/she has no financial relationships with, or financialinterests in, any commercial companies pertaining to this educational activity. The remaining coauthors and their spouses/partners (if any), have disclosed that they have no financialrelationships with, or financial interests in, any commercial companies pertaining to this educational activity.
All staff and planners, including spouses/partners (if any), in any position to control the content of this CME activity have disclosed that they have no financial relationships with, or financialinterests in, any commercial companies pertaining to this educational activity.
The authors have disclosed that none of the treatments of hidradenitis suppurativa are approved by the US Food and Drug Administration as discussed in this article.
Lippincott CME Institute has identified and resolved all conflicts of interest concerning this educational activity.
To earn CME credit, you must read the CME article and complete the quiz and evaluation on the enclosed answer form, answering at least 13 of the 18 questions correctly.
This continuing educational activity will expire for physicians on August 31, 2016, and for nurses on August 31, 2017.
If you need CME or CE STAT, take the test online at: http://cme.lww.com for physicians and www.nursingcenter.com for nurses. Complete CE/CME information is on the last page of this article.
Editor’s note: This is the second part of this continuing education topic. ‘‘Hidradenitis Suppurativa: A Frequently Missed Diagnosis, Part 2: A Review of Pathogenesis, Associations, andClinical Features’’ was published in the July 2015 issue.
PURPOSE:
To provide an overview of treatment recommendations for hidradenitis suppurativa (HS).
TARGET AUDIENCE:
This continuing education activity is intended for physicians and nurses with an interest in skin and wound care.
OBJECTIVES:
After participating in this educational activity, the participant should be better able to:
1. Describe current recommendations for treatment of HS.
2. Identify warnings, adverse effects, and implications for patient education.
AUGUST 2015
ADVANCES IN SKIN & WOUND CARE & VOL. 28 NO. 8 372 WWW.WOUNDCAREJOURNAL.COM
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
ABSTRACT
Hidradenitis suppurativa (HS) is a chronic inflammatorydisorder of the intertriginous area. Patients with HS have severalchallenges to their quality of life and activities of everyday living,including malodor, purulent discharge, and discomfort. There isoften a delay in diagnosis and appropriate treatment. The needfor cosmetically acceptable local treatments and dressingapplication makes this disease an important challenge for woundcare specialists. The choice of optimal treatment varies dependingon the disease severity, expert knowledge, the availability of aninterprofessional team, and patient factors.KEYWORDS: hidradenitis suppurativa, inflammatory folliculardisorder, wound care
ADV SKIN WOUND CARE 2015;28:372–80; quiz 381-2.
INTRODUCTIONHidradenitis suppurativa (HS) is a chronic debilitating disease
that significantly affects the quality of life of an active, young
adult population. The large burden of HS and its comorbidities
highlight the need for an interprofessional team approach.
Typically, HS is more common in females mainly involving the
axilla and groin (Figure 1), whereas the perineum and buttocks
are commonly involved in males (Figure 2). Despite multiple
studies, a diversity of expert opinion remains on the optimal stepwise management of HS. The US Food and Drug Admin-
istration (FDA) has not approved any treatments for HS. The
recommendations in this article are based on the scientific
literature, expert knowledge of the authors, published consensus
documents, and patient experience.
GENERAL MEASURESEpidemiological data suggest an association of HS with systemic
diseases, including metabolic syndrome, psychiatric disorders,
and hyperandrogenism.1 The Mayo Clinic (http://mayocl.in/
1hZDzm2) defines metabolic syndrome as a cluster of conditions
that can be remembered by A-increased blood sugar (hemoglo-
bin A1c), B-increased blood pressure, C-abnormal cholesterol,
and D-diet with excess body fat around the waist, all of which
increase an individual’s risk of heart disease, stroke, and diabetes.
The patient’s body weight and lifestyle choices may contribute to
HS. For example, the association of HS and a high body mass
index, along with smoking, warrants weight loss counseling and
smoking cessation. Current adult obesity guidelines include a
lifestyle modification program that ideally involves:
& reduced caloric intake by 500 to 1000 kcal/d,
& 30 minutes of moderate-intensity physical activity 3 to 5 times
per week and an eventual increase to 60 minutes or more on
most days,
& cognitive-behavior therapy.2
Figure 1.
THEAXILLA,GROIN,AND INFRAMMARYAREPREDOMINANTLY
INVOLVED IN FEMALE PATIENTS
Figure 2.
THEGLUTEAL, INGUINAL INVOLVEMENTISPREDOMINATELY
SEEN IN MALE PATIENTS
ADVANCES IN SKIN & WOUND CARE & AUGUST 2015373WWW.WOUNDCAREJOURNAL.COM
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If satisfactory weight-loss progress is not achieved, pharma-
cotherapy and bariatric surgery should be considered. The same
lifestyle modifications should be recommended to patients
with metabolic syndrome, with the additional option of ini-
tiating metformin.3
To help patients with smoking cessation, the clinical approach
begins with an assessment of the patient’s willingness to quit,
and every tobacco user who accepts treatment should be offered
assistance.3 The combination of counseling and smoking cessa-
tion medication is more effective than either option alone. It is
important to note that although lifestyle modifications (such as
weight loss or smoking cessation) have been shown to improve
the symptoms of HS, they do not cure the disease.4,5 Friction from
clothing increases local pain; thus, patients with HS are advised
to avoid wearing tight clothes. In addition, excessive heat and
humidity are known triggers. Avoidance of these climate condi-
tions, such as staying indoors in air conditioning when needed,
may help relieve symptoms. Other potential triggers, although
not causative factors, include the use of deodorants, shaving,
and depilation.
Some expert clinicians recommend warm compresses, topical
antiseptics, and antibacterial soaps to help soothe HS-involved skin.
TOPICAL TREATMENTS AND LOCALWOUND CAREBecause there are no FDA-approved treatments for HS, clinicians
must rely on available evidence to treat patients’ symptoms.
To date, there are very few studies that focus on optimal local
wound care in patients with HS. The choice of local dressing is an
important part of the management. Dressings with high absor-
bency are commonly used. Experts suggest that tubular net
bandages or placing superabsorbent pads or materials in the
seams of clothing are the best ways to keep the wound dressings
in place because of the topography. In general, superabsorbent
dressings are best to treat actively draining lesions or postopera-
tive wounds, with extensive and generous application of simple
white petrolatum, zinc oxide paste, or film-forming liquid acrylate
on the marginal skin to prevent the primary dressing from stick-
ing to the wound. In addition, adhesive tape should be avoided
to minimize trauma to inflamed skin.
Daily gentle cleansing of the affected areas may help to reduce
odor and the occurrence of secondary infection. Consider gentle
antiseptic washes with a lower risk of allergic or irritant contact
dermatitis. Some patients have had success with water-based
chlorhexidine preparations and were instructed to avoid wash-
cloths, harsh sponges/loofahs, or brushes that may cause un-
necessary trauma and skin irritation.
Postoperative wounds were studied by Chen et al6 with a ret-
rospective chart review of HS cases managed surgically between
2005 and 2010. The authors calculated that approximately half of
the patients received negative-pressure wound therapy using the
vacuum-assisted closure system, followed by delayed closure.
The other half received immediate primary closure at the time of
their excision. Wound closure averaged 2.2 months with negative-
pressure wound therapy and 2.7 months in the control group.
The authors also concluded that local excisions may heal with
secondary intention, closed at the time of surgery, delayed with
direct closure, or with skin grafts.
PHARMACOLOGIC TREATMENTSA variety of pharmacologic treatments have been successfully
administered, but as noted, to date, the FDA has not approved
any medical treatment specifically for the treatment of HS.7
AntimicrobialsMany therapeutic algorithms recommend antimicrobials (often
with anti-inflammatory properties) in all severity stages of HS8–10;
however, only a few review articles offer specific recommenda-
tions. Many of the antimicrobial agents that are successful in
HS may be effective because of their antibacterial and anti-
inflammatory properties (eg, tetracyclines, clindamycin). The
majority of published reports recommend initial therapy with
rifampicin combined with clindamycin or a tetracycline.11–14
Matusiak et al15 found that the most commonly prescribed anti-
microbials (eg, tetracycline, doxycycline, minocycline) were in-
effective against cultured isolates.16–18
Topical antimicrobials, including topical clindamycin and
topical resorcinol, have been studied.10,11,16 Topical clindamycin
0.1% was compared with placebo in 27 patients who completed
the study. At the end of the first, second, and third months, the
clindamycin-treated subjects had fewer abscesses, inflammatory
nodules, and pustules (P < .01). Topical resorcinol 15% cream
was a successful treatment when used twice daily in a case study
of 12 patients.17 Resorcinol has topical antiseptic and keratolytic
properties. The most significant effect of this treatment was
noticed in superficial lesions, such as pustules and papules, but
not in deep-seated cysts and sinuses.18
In managing patients with HS, clinicians also must consider that
the use of topical treatments is associated with the risk of allergic
and irritant contact dermatitis to the active agent or components of
the vehicle (Figure 3). The authors also suggest that maintenance
or long-term oral therapy can be provided with the help of
tetracyclines (or erythromycin and related macrolides) due to
their anti-inflammatory properties. Oral dapsone has been used
in mild cases, but the effect appears to be lower in comparison
with the combination of clindamycin and rifampicin.19 In ad-
dition, the HS lesions will not promptly respond to systemic
antimicrobials without surgical debridement and appropriate
ADVANCES IN SKIN & WOUND CARE & VOL. 28 NO. 8 374 WWW.WOUNDCAREJOURNAL.COM
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topical wound care, along with selective intralesional steroid
injections for the associated inflammatory response.
Retinoids. Two oral retinoid drugs, isotretinoin (13-cis-RA
[retinoic acid]) and acitretin have been studied clinically for the
treatment of HS. Zouboulis et al20 studied the effect of these
retinoids utilizing an in vitro sebocyte model. The authors con-
cluded that 13-cis-RA was a potent inhibitor of both cell
proliferation and lipid synthesis in human sebocytes, but that
acitretin decreased only lipogenesis in this model. Blok et al21
reviewed the results of 174 patients enrolled in 7 studies that
evaluated the effect of oral isotretinoin patients with HS. The
combined study report concluded that there was
& significant improvement in 18% of patients,
& moderate improvement in 17% of patients, and
& no response in 64% of patients.
In a more recent study, Puri and Talwar22 compared the effects
of oral acitretin combined with surgical excision to oral acitretin
alone. There was a low 20% recurrence rate in the group of
patients who received both oral acitretin and surgical excision
compared with a 40% recurrence rate in the group that received
oral acitretin alone. In summary, the results from the use of oral
retinoids are disappointing, but may be helpful as adjunct agents
in some difficult-to-control patients.22 Acitretin was viewed as a
more promising agent; however, it is often poorly tolerated,
especially when doses exceed 20 mg daily.23
Corticosteroids. An intralesional injection of a topical cor-
ticosteroid (eg, triamcinolone 8 to 20 mg/mL, with injections of
up to 3 to 6 mL per visit every 3 to 6 weeks) is commonly per-
formed to reduce individual lesion pain and acute erythema/
swelling.7 These injections should be avoided if there is clinical
evidence of infection.
Oral prednisone reduces inflammation, facilitates the heal-
ing of existing HS lesions, and prevents future lesions from
forming. Commonly prescribed prednisone doses for disease
control may vary from 20 to 50 mg. The adverse effects of oral
steroids (weight gain, diabetes, loss of muscle mass, bone frac-
tures, and so on) must be measured against the therapeutic
benefit of using oral steroids compared with other available
treatment options. To the authors’ knowledge, no recent, formal
studies have been conducted on the efficacy of corticosteroids
as part of HS management.
Although the exact role of immune dysregulation in the path-
ogenesis of HS is unknown, it has been demonstrated to have an
impact (see ‘‘Immune Dysregulation’’ in Part 1 of this article
series in the July 2015 issue of Advances in Skin & Wound Care).
Thus, clinicians are increasingly prescribing immunosuppressive
agents as part of the management of HS. Anti-TNfa inhibitors,
anti-IL17/23, and anti-IL1 inhibitors have been used in the man-
agement of HS. Different immunosuppressive medications
including methotrexate have been used in case reports.
Biologics. Evidence that inhibitors of tumor necrosis factor
(TNF) effectively improved HS symptoms in patients who were
primarily being treated for Crohn disease led to the investigation
of anti-TNF agents as an effective treatment for HS. Serum and
skin (lesional, perilesional) TNF- levels are higher in patients with
HS compared with control subjects.24,25 A growing number of stud-
ies have highlighted the efficacy of infliximab and adalimumab,
both anti-TNF agents, in the management of HS.26–28 Bahillo
Monne et al27 found favorable outcomes with adalimumab treat-
ment, with improvement somewhat slower than the responses
with infliximab. Moriarty et al29 described the results of using
infliximab on a 4-week basis in 11 patients with severe HS. The
authors reported that all patients experienced initial disease
improvement assessed by visual analog scale, Dermatology Life
Quality Index (DLQI), and the physician’s clinical assessment.
While on this regimen, the patients experienced secondary in-
fection of HS lesions, respiratory tract infections, tonsillitis, minor
weight gain, and lymphoma. Newer biological treatments that
inhibit interleukin 1 (anakinra) require further study before they
can be recommended for HS patients.
Antiandrogens. A hormonal connection with HS has been
suggested by several studies (see the ‘‘Hormones’’ section in the Part 1
Figure 3.
CONTACT DERMATITIS IS COMMONLY SEEN ASSOCIATED
WITH THE CONTINUOUS DISCHARGE (CONTACT IRRITANT
DERMATITIS) AND TOPOGRAPHY
ADVANCES IN SKIN & WOUND CARE & AUGUST 2015375WWW.WOUNDCAREJOURNAL.COM
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article). The observation of female predominance,30,31 premen-
strual flare-ups, and improvement of HS during pregnancy32
suggest that androgens may be a contributing factor. In some
women with HS, symptoms often correlate with hormonal fluc-
tuations during the menstrual cycle. Previously reported studies
have linked improvement in HS lesions with oral contraceptive
pills and spironolactone.33 Published reports also documented
some male HS patient benefits from finasteride.34,35 More re-
cently, Randhawa et al36 investigated finasteride as an effective
treatment of HS in children and adolescents. The 3 pediatric pa-
tients in this study were treated with oral finasteride in com-
bination with oral contraceptives and/or oral antibiotics. The
authors observed decreased disease flare frequency and severity
with no significant adverse effects. As a result, the authors sug-
gested that finasteride might be a suitable additive therapy for
refractory female HS cases and for judicious use in pediatric
patients with clear communication of the risks and benefits of
the drug.
Metformin. As an antidiabetic agent, metformin provides
some benefit in HS. Arun and Loffeld,37 who presented a case
of a 50-year-old woman with longstanding HS and type 2 diabetes
mellitus, first documented the use of metformin in the treatment
of HS. The patient was taking metformin 500 mg 3 times daily for
more than 5 years until she gained significant control of her
glycemic levels and was subsequently taken off of metformin. The
authors observed that while on metformin the patient’s HS
lesions remained stable and did not require recurrent courses of
antibiotic therapy. However, with the discontinuation of met-
formin, the patient reported a flare-up of her HS lesions. More
recently, Verdolini et al38 reported significant reduction in the
Sartorius score, which was described in Part 1, and the number
of workdays lost among 25 patients with HS who were treated
with metformin. In addition, the DLQI significantly improved in
16 cases. The authors conclude that metformin helps control HS
with very few adverse effects. Based on their results, they suggest
using metformin as an alternative to current treatments, in-
cluding long-term antibiotics.
PAIN MANAGEMENTDespite the painful effects of this chronic, debilitating disease,
few studies have documented treatment for the effective pain
control of HS. Clinicians should accept the patient’s report of
pain. This statement is supported by the findings of a recent study
on the correlation and validity of patient and investigator assess-
ment of disease severity and pain.39 Each of the 20 HS patients
graded a single representative inflammatory nodule in terms of
tenderness and flare, and the investigator graded the level of
erythema. Subsequently, all patients underwent high-resolution
ultrasound scanning of their representative nodule, and the diam-
eter of the nodule was measured to reflect the degree of in-
flammation. The authors found that the patient assessment of
flare activity and pain and the investigator assessment of ery-
thema were strongly associated with morphological changes
identified by ultrasound, suggesting that patients tend to accu-
rately report flare and pain levels and investigators acutely ob-
served the resulting erythema.
Pain control often starts with grading the severity of pain on a
0- to 10-point numerical rating scale, with ‘‘0’’ being no pain and
‘‘10’’ slamming the car door on your finger, and ‘‘5’’ representing a
bee sting. Nociceptive pain (gnawing, aching, tender, throbbing)
often responds to acetaminophen, with a starting dose of 1 g
3 times per day, and the use of alternative agents such as non-
steroidal anti-inflammatory drugs and aspirin. More severe pain is
often treated with opioids, short- and long-acting weaker (codeine),
and subsequently, stronger agents (morphine, hydromorphone).
A fentanyl patch can be used for resistant pain. Neuropathic pain
is often described as burning, stinging, shooting, and stabbing.
Treatment of neuropathic pain may include second-generation
tricyclic agents, such as nortriptyline or desipramine. Scheinfeld40
concluded that when treating HS-related pain that is unresponsive
to topical analgesics, gabapentin and pregabalin should be first-
line therapy because of fewer adverse effects compared with tri-
cyclics or the serotonin and norepinephrine reuptake inhibitors,
duloxetine and venlafaxine. Also, gabapentin and pregabalin can be
combined with acetaminophen, nonsteroidal anti-inflammatory drugs,
and cyclooxygenase 2 inhibitors. In cases of HS accompanied by de-
pression, gabapentin or pregabalin can be combined with duloxe-
tine, which should be tried first and venlafaxine second, if needed.
Scheinfeld40 also reviewed the use of topical agents in the
treatment of HS-related pain. The author summarized that
topical 1% diclofenac should be offered first to a patient who
presents with HS and complains of pain centered on the skin.
Topical ketamine may also be a useful tool for the treatment of
pain. Commercially available topical 5% doxepin may cause
drowsiness, and some clinicians may order lower-dose com-
pounded formulations.
NEW AND TRADITIONAL SURGICALAPPROACHESTraditional surgical approaches to HS management have in-
cluded incision and drainage (I&D), punch debridement, de-
roofing, and excision. It has been suggested that I&D of individual
nodules should generally be avoided because they provide only
short-term relief and tend to recur with no long-term benefit.41
Margesson and Danby42 suggested the practice of punch de-
bridement over I&D, which is a mini unroofing procedure. Punch
debridement involves deeply excising the acutely inflamed folli-
culopilosebaceous unit (FSPU) within an inflammatory nodule
using a 5- to 7-mm circular punch instrument identical to that
used in a punch biopsy. The FSPU is excised with a small amount
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of the surrounding tissue and is followed by aggressive debride-
ment using digital pressure. The curettage or simple scrubbing
is done with gauze wrapped around a cotton-tipped swab. The
goal is to remove the ‘‘bulge’’ of the FSPU that contains the stem
cells hypothesized to be responsible for inducing growth of the
proliferative mass (amorphous material deposited in the dermis)
and the sinus tracts.
Surgical excision of the affected skin tissue in HS with ade-
quate free margins is the criterion-standard treatment for pre-
vention of recurrence7 (Figure 4). The classic deroofing technique
and wide excision are regarded as the preferred surgical methods
for treated HS Hurley Stage I/II and II/III, respectively.43,44
However, the goal of surgery is to completely remove the lesional
tissue, while sparing as much healthy tissue as possible, making
Hurley Stage II/III disease a surgical challenge.45
Skin-Tissue–Sparing Excision withElectrosurgical Peeling ProcedureBlok et al45 proposed a new surgical technique for severe HS
that combines the advantages of both wide excision and the
deroofing technique: skin-tissue–sparing excision with electro-
surgical peeling (STEEP) procedure. The STEEP procedure is
performed under general anesthesia and involves electrosur-
gical incision of the sinus roof with a wire loop tip coupled to an
electrosurgery device.
All lesional tissue, including fibrosis that is identified by
palpation, is removed from the incision on to the deeper skin
layers by successive tangential electrosurgical transections or
peeling. The epithelialized sinus floors and subcutaneous fat
are left intact where possible. Hemostasis is achieved by the
coagulation mode of the electrosurgery device, and wounds are
left open to heal by secondary intention. Generally, patients can
leave the hospital on the day of surgery. Blok et al45 have per-
formed the STEEP procedure on 156 patients with Hurley
Stage II/III disease between 2004 and 2013. Patients have re-
ported low recurrence rates, rapid healing, and an improvement
in DLQI responses. The authors proposed the STEEP procedure
as a promising tissue-saving surgical technique for HS Hurley
Stage II/III as an alternative to laser surgery that can be per-
formed by trained dermatological surgeons.
Split-Thickness Skin GraftAxillary HS has been historically treated with excision of the
affected tissue, and the surgical defect was left to heal by sec-
ondary intention or was grafted with a split-thickness skin graft
(SSG).46 Although an SSG can produce satisfactory results in
patients with mild to moderate disease, in more severe disease it
can predispose to graft contraction, reduced range of movement of
the shoulder, restrictive scarring, prolonged recovery, and an
increased number of subsequent surgical procedures.47–49 More
recently, postexcision HS wounds have been treated with a num-
ber of surgical procedures, including local, regional, and free
flaps (fasciocutaneous V-Y flap, Limberg flap, and musculocu-
taneous flaps). In particular, perforator flaps, including the
thoracodorsal artery perforator (TDAP) flap, have been reported
as advantageous for reconstruction of the soft-tissue defect after
excision.50–52 Wormald et al46 conducted a prospective study
comparing the use of TDAP flap and SSG for the reconstruction
of the axilla following excision of extensive or recurrent axillary
HS, with focus on both operative and patient-related outcomes.
The authors found a significantly longer length of surgery for the
TDAP group, a finding that is supported already in the litera-
ture.53,54 The TDAP cohort had a higher rate of revision surgery,
whereas the SSG group required a significantly greater number
of follow-up appointments in the clinic. The authors summarized
that a TDAP flap may provide a more definitive surgical solution
compared with the SSG technique, requiring fewer clinic appoint-
ments and a shorter period of follow-up and thus is potentially
more cost-effective despite the longer length of surgery.
Genitoperineal HS ResectionFor genitoperineal HS resection in males, partial or total scrotectomy
is almost always required with care to avoid causing injury to the
Figure 4.
SURGICAL APPROACH TO REMOVE CYSTS, TUNNELS,
CICATRIZATION, AND SCAR
ADVANCES IN SKIN & WOUND CARE & AUGUST 2015377WWW.WOUNDCAREJOURNAL.COM
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spermatic cords and testes.55 Perineal disease is resected with care
to avoid injury to the anal sphincter muscles. If both genital-
perineal (anterior) and anal and/or buttock (posterior) disease
resections are recommended, they should be resected in separate
procedures to avoid an arduous and intolerable recovery period.
The anterior tissue of the perineum and genitals is treated first, and
then a referral to a general surgery or plastic surgery practitioner
is suggested for posterior treatment. The complete resection
and reconstruction with skin flaps and grafts provide a viable
treatment for patients with primary genital HS disease. After
surgical debridement of HS, extended soft tissue defects are the
usual result, requiring plastic reconstruction in this site.
CryoinsufflationIf surgical treatment is declined, and systemic therapies should
be avoided in certain patients, a new technique using cryoin-
sufflation (CI) was proposed by Pagliarello et al.56 The authors
presented the case of a female patient in her 30s who pre-
sented with HS Hurley Stage II. She was being treated with oral
contraceptives, topical clindamycin, and monthly intralesional
corticosteroids. However, she decided to become pregnant and
therefore was searching for an alternative treatment, devoid of
teratogenic effects. Effective therapy was necessary because the HS
seriously interfered with sexual intercourse and indirectly with her
planned pregnancy. Surgical treatment was offered and declined.
To control the patient’s HS symptoms and simultaneously dis-
continue her systemic medical therapy, the authors proposed CI, a
modified spray cryotherapy performed by injecting liquid nitrogen
(LN) through an ordinary needle directly into the HS tracts. As
the LN enters infected sinuses, it boils and vaporizes, and quickly
disperses into all communicating pockets because of the large
expansion ratio of liquid to gas. The authors suggested delivering
the LN in a pulsed method to avoid overexpansion and prevent
excessive pain and formation of ‘‘iceballs.’’
The patient received monthly treatment sessions that allowed
focused scarring to replace the sinuses and caused minimal
damage to the skin surface. In total, the authors treated the patient
with 3 monthly treatment sessions, and they reported that no
recurrence was observed after 6 months. Neither hypopigmentation
nor scarring was observed, and the patient was very satisfied
with the results.
In conclusion, the authors proposed CI as a novel, easily con-
ducted, well-tolerated, and inexpensive alternative as monotherapy
or as a useful adjunctive therapy that can be effectively combined
with all other treatments to rapidly achieve symptom relief. Al-
though surgery plays an important role in the management of
HS, the choice of surgery should be individualized based on
patient preference, the Hurley stage, extent of involvement, and
location of the disease.57
THE ROLE OF PHOTODYNAMIC ANDLASER THERAPY
Photodynamic TherapyPhotodynamic therapy (PDT) is effective against acne vulgaris,58
which has led to its use against HS. Earlier studies have reported
the effective treatment of HS by PDT, but they were small case
studies with varying results and variations in the photosensi-
tizers, light sources, and treatment regimens used.59,60 The pro-
posed mechanism of action of PDT in HS involves absorption of
aminolevulinic acid and an increased production of protopor-
phyrin IX in hair follicles compared with other tissues.61 In addi-
tion, the main mechanisms suggested for PDT against acne
vulgaris, including sebum production and reduced follicular
occlusion,44 may also play a role against HS.
Topical PDT is found to be effective when applied to early super-
ficial HS lesions. Researchers, however, have found that the main
limitations of PDT are the low absorption of photosensitizer and
low penetration of the light source.62,63 For this reason, Valladares-
Narganes et al64 proposed a new approach by applying intrale-
sional PDT using a laser diode attached to an optical cable. The
authors suggested that intralesional PDT is less invasive than surgery,
well-tolerated, effective, and less expensive than systemic therapy.
Carbon Dioxide LaserThe use of carbon dioxide laser for HS has been reported in
5 studies.54,65 Lapins et al66 studied carbon dioxide lasers on
24 patients with HS, with 22 of 24 patients having no recurrence after
27 months. Hazen and Hazen67 treated 185 sites in 61 patients
with a carbon dioxide laser and marsupialization technique, with
183 recurrence-free sites during a follow-up period of 1 to 19 years.
Nd:YAG LaserThe long-pulsed 1064-nm Nd:YAG laser is an alternative modality
for the management of HS. The Nd:YAG laser causes a selective
photothemolysis of the follicular units and adjacent inflamma-
tions. Tierney et al68 studied the Nd:YAG laser on 22 patients with
HS Stages II and III and demonstrated a significant decrease in
severity of HS in 3 months (65.3%). Xu et al69 studied a long-
pulsed 1064-Nm Nd:Yag Laser on 19 patients with Hurley
Stage II HS disease. The severity of HS significantly decreased for
both the axillary site (P = .008) and the inguinal site (P = .001).
CONCLUSIONHidradenitis suppurativa is a chronic inflammatory disorder that
commonly involves the intertriginous area. The concerns of malodor,
discharge, and discomfort, along with the need for cosmetically
acceptable local treatments and dressing application, make this
disease an important challenge for wound care specialists. The
ADVANCES IN SKIN & WOUND CARE & VOL. 28 NO. 8 378 WWW.WOUNDCAREJOURNAL.COM
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
lack of randomized clinical trials for most HS therapeutic modalities
complicates optimal treatment selection. The choice of treatment
varies depending on the disease severity, the expert knowledge of
the prescribing healthcare professional, and patient factors (Table).
The associated medical and psychological factors significantly af-
fect patient health and adherence to treatment. It is important to
approach HS as a systemic disease with an interprofessional team.
PRACTICE PEARLS
REFERENCES1. Shlyankevich J, Chen AJ, Kim GE, Kimball AB. Hidradenitis suppurativa is a systemic
disease with substantial comorbidity burden: a chart-verified case-control analysis. J Am
Acad Dermatol 2014;71:1144-50.
2. Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E; Obesity Canada
Clinical Practice Guidelines Expert Panel. 2006 Canadian clinical practice guidelines on
the management and prevention of obesity in adults and children [summary]. CMAJ
2007;176(8):S1-13.
3. Schmelzle J, Rosser WW, Birtwhistle R. Update on pharmacologic and nonpharmacologic
therapies for smoking cessation. Can Fam Phys 2008;54:994-9.
4. Shah N. Hidradenitis suppurativa: a treatment challenge. Am Fam Phys 2005;72:1547-52.
5. Sartorius K, Lapins J, Emtestam L, Jemec GB. Suggestions for uniform outcome variables
when reporting treatment effects in hidradenitis suppurativa. Br J Dermatol 2003;149:211-3.
6. Chen YE, Gerstle T, Verma K, Treiser MD, Kimball AB, Orgill DP. Management of hidradenitis
suppurativa wounds with an internal vacuum-assisted closure device. Plast Reconstr Surg
2014;133:370e-377e.
7. Kerdel FA. Current and emerging nonsurgical treatment options for hidradenitis suppurativa.
Semin Cutan Med Surg 2014;33(3 Suppl):S57-9.
8. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am
Acad Dermatol 2009;60:539-61.
9. Alhusayen R, Shear NH. Pharmacologic interventions for hidradenitis suppurativa: what
does the evidence say? Am J Clin Dermatol 2012;13:283-91.
10. Jemec GB, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment
of hidradenitis suppurativa. J Am Acad Dermatol 1998;39:971-4.
11. Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin
for hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology 2009;219:148-54.
12. van der Zee HH, Boer J, Prens EP, Jemec GB. The effect of combined treatment with oral clindamycin
and oral rifampicin in patients with hidradenitis suppurativa. Dermatology 2009;219:143-7.
13. Bettoli V, Zauli S, Borghi A, et al. Oral clindamycin and rifampicin in the treatment of
hidradenitis suppurativa-acne inversa: a prospective study on 23 patients. J Eur Acad
Dermatol Venereol 2014;2:125-6.14. Mendonca CO, Griffiths CE. Clindamycin and rifampicin combination therapy for hidradenitis
suppurativa. Br J Dermatol 2006;154:977-8.15. Matusiak L/ , Bieniek A, Szepietowski JC. Bacteriology of hidradenitis suppurativaVwhich
antibiotics are the treatment of choice? Acta Derm Venereol 2014;94:699-702.16. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J
Dermatol 1983;22:325-8.17. Boer J, Jemec GB. Resorcinol peels as a possible self-treatment of painful nodules in
hidradenitis suppurativa. Clin Exp Dermatol 2010;35:36-40.18. Cassano N, Alessandrini G, Mastrolonardo M, Vena GA. Peeling agents: toxicological and
allergological aspects. J Eur Acad Dermatol Venereol 1999;13:14-23.19. Yazdanyar S, Boer J, Ingvarsson G, Szepietowski JC, Jemec GB. Dapsone therapy for
hidradenitis suppurativa: a series of 24 patients. Dermatology 2011;222:342-6.20. Zouboulis CC, Korge B, Akamatsu H, et al. Effects of 13-cis-retinoic acid, all-trans-retinoic
acid, and acitretin on the proliferation, lipid synthesis and keratin expression of cultured
human sebocytes in vitro. J Invest Dermatol 1991;96:792-7.21. Blok JL, van Hattem S, Jonkman MF, Horvath B. Systemic therapy with immunosuppressive agents
and retinoids in hidradenitis suppurativa: a systematic review. Br J Dermatol 2013;168:243-52.22. Puri N, Talwar A. A study on the management of hidradenitis suppurativa with retinoids
and surgical excision. Indian J Dermatol 2011;56:650-1.23. dos Santos CH, Netto PO, Kawaguchi KY, Parriera Alves JA, de Alencar Souza VP, Reverdito S.
Association and management of Crohn’s disease plus hidradenitis suppurativa. Inflamm
Bowel Dis 2012;18:E801-2.24. Matusiak L, Bieniek A, Szepietowski JC. Increased serum tumour necrosis factor-alpha
in hidradenitis suppurativa patients: is there a basis for treatment with anti-tumour necrosis
factor-alpha agents? Acta Derm Venereol 2009;89:601-3.25. Martin-Ezquerra G, Masferrer E, Masferrer-Niubo M, et al. Use of biological treatments
in patients with hidradenitis suppurativa. J Eur Acad Dermatol Venereol 2015;29:56-60.
26. Chinniah N, Cains GD. Moderate to severe hidradenitis suppurativa treated with biological
therapies. Australas J Dermatol 2014;55:128-31.27. Bahillo Monne C, Honorato Guerra S, Schoendorff Ortega C, Gargallo Quintero AB. Manage-
ment of hidradenitis suppurativa with biological therapy: report of four cases and review
of the literature. Dermatology 2014;229:279-87.
28. Zhang J, Reeder VJ, Hamzavi IH. Use of biologics in the treatment of hidradenitis suppurativa:
a review of the Henry Ford Hospital experience. Br J Dermatol 2014;171:1600-2.
29. Moriarty B, Jiyad Z, Creamer D. Four-weekly infliximab in treatment of severe hidradenitis
suppurativa. Br J Dermatol 2014;170:986-7.
30. Danby FW, Margesson LJ. Hidradenitis suppurativa. Dermatol Clin 2010;28:779-93.
31. Yazdanyar S, Jemec GB. Hidradenitis suppurativa: a review of cause and treatment. Curr
Opin Infect Dis 2011;24:118-23.
32. Barth JH, Layton AM, Cunliffe WJ. Endocrine factors in pre- and postmenopausal women
with hidradenitis suppurativa. Br J Dermatol 1996;134:1057-9.
33. Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments
based on over 350 hidradenitis patients. Dermatol Online J 2013;19(4):1.
34. Farrell AM, Randall VA, Vafaee T, Dawber RPR. Finasteride as a therapy for hidradenitis
suppurativa. Br J Dermatol 1999;141:1138-9.
35. Joseph MA, Jayaseelan E, Ganapathi B, Stephen J. Hidradenitis suppurativa treated with
finasteride. J Dermatol Treat 2005;16:75-8.
36. Randhawa HK, Hamilton J, Pope E. Finasteride for the treatment of hidradenitis suppurativa
in children and adolescents. JAMA Dermatol 2013;149:732-5.
37. Arun B, Loffeld A. Long-standing hidradenitis suppurativa treated effectively with metformin.
Clin Exp Dermatol 2009;34:920-1.
38. Verdolini R, Clayton N, Smith A, Alwash N, Mannello B. Metformin for the treatment of hidradenitis
suppurativa: a little help along the way. J Eur Acad Dermatol Venereol 2013;27:1101-8.
39. Zarchi K, Yazdanyar N, Yazdanyar S, Wortsman X, Jemec GB. Pain and inflammation in
hidradenitis suppurativa correspond to morphological changes identified by high-frequency
ultrasound. J Eur Acad Dermatol Venereol 2015;29:527-32.
40. ScheinfeldN.Topical treatments of skinpain: ageneral reviewwitha focus onhidradenitis suppurativa
with topical agents. Dermatol Online J 2014;20(7). www.pubfacts.com/detail/25046456/Topical-
treatments-of-skin-pain-a-general-review-with-a-focus-on-hidradenitis-suppurativa-with-topic.
41. Aithal V, Appaih P. Lithium induced hidradenitis suppurativa and acne conglobata. Indian J
Dermatol Venereol Leprol 2004;70:307-9.
42. Margesson LJ, Danby FW. Hidradenitis suppurativa. Best Pract Res Clin Obstet Gynaecol
2014;28:1013-27.
& HS is chronic disorder of the intertriginous area
& Malodor, discharge, and discomfort in HS and lack of stan-
dardization among treatment modalities makes this disease an
important challenge for wound care specialists
& HS is a systemic disease, therefore management of HS should
be done by an interprofessional healthcare team and address
both medical and psychological patient factors
Table.
MANAGEMENT OF HIDRADENITIS SUPPURATIVA
ADVANCES IN SKIN & WOUND CARE & AUGUST 2015379WWW.WOUNDCAREJOURNAL.COM
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
43. van der Zee HH, Prens EP, Boer J. Deroofing: a tissue-saving surgical technique for the treat-
ment of mild to moderate hidradenitis suppurativa lesions. J Am Acad Dermatol 2010;63:475-80.
44. van Hattem S, Spoo JR, Horvath B, Jonkman MF, Leeman FWJ. Surgical treatment of
sinuses by deroofing in hidradenitis suppurativa. Dermatol Surg 2012;38:494-7.
45. Blok JL, Spoo JR, Leeman F, Jonkman M, Horvath B. Skin-tissue–sparing excision with
electrosurgical peeling (STEEP): a surgical treatment option for severe hidradenitis suppurativa
Hurley Stage II/II. J Eur Acad Dermatol Venereol 2014;29:379-82.
46. Wormald JC, Balzano A, Clibbon JJ, Figus A. Surgical treatment of severe hidradenitis
suppurativa of the axilla: thoracodorsal artery perforator (TDAP) flap versus split skin
graft. J Plast Reconstr Aesthetic Surg 2014;67:1118-24.
47. Menderes A, Sunay O, Vayvada H, Yilmaz M. Surgical management of hidradenitis suppurativa.
Int J Med Sci 2010;7:240-7.
48. Buyukasik O, Hasdemir AO, Kahramansoy N, Col C, Erkol H. Surgical approach to extensive
hidradenitis suppurativa. Dermatol Surg 2011;37:835-42.
49. Ellis LZ. Hidradenitis suppurativa: surgical and other management techniques. Dermatol
Surg 2012;38:517-36.
50. Bieniek A, Matusiak L, Okulewicz-Gojlik D, Szepietowski JC. Surgical treatment of hidradenitis
suppurativa: experiences and recommendations. Dermatol Surg 2010;36:1998-2004.
51. Slade DE, Powell BW, Mortimer PS. Hidradenitis suppurativa: pathogenesis and manage-
ment. Br J Plast Surg 2003;56:451-61.
52. Oritz CL, Castillo VL, Pilarte F, Barraguer EL. Experience using the thoracodorsal artery perfo-
rator flap in axillary hidradenitis suppurativa cases. Aesthetic Plast Surg 2010;34:785-92.
53. Busnardo FF, Coltro PS, Olivan MV, Busnardo APV, Ferreira MC. The thoracodorsal artery
perforator flap in the treatment of axillary hidradenitis suppurativa: effect on preservation
of arm abduction. Plast Reconstr Surg 2011;128:949-53.
54. Rambhatla PV, Lim HW, Hamzavi I. A systematic review of treatments for hidradenitis
suppurativa. Arch Dermatol 2012;148:439-46.
55. Chen ML, Odom B, Santucci RA. Surgical management of genitoperineal hidradenitis
suppurativa in men. Urology 2014;83:1412-7.
56. Pagliarello C, Fabrizi G, Feliciani C, Di Nuzzo S. Cryoinsufflation for Hurley Stage II hidrade-
nitis suppurativa: a useful treatment option when systemic therapies should be avoided. JAMA
Dermatol 2014;150:765-6.
57. Kagan RJ, Yakuboff KP, Warner P, Warden GD. Surgical treatment of hidradenitis suppurativa:
a 10-year experience. Surgery 2005;138:734-41.58. Hongcharu W, Taylor CR, Chang Y, Aghassi D, Suthamjariya K, Anderson RR. Topical ALA-
photodynamic therapy for the treatment of acne vulgaris. J Invest Dermatol 2000;115:183-92.59. Rose RF, Stables GI. Topical photodynamic therapy in the treatment of hidradenitis
suppurativa. Photodiagn Photodyn Ther 2008;5:171-5.60. Wollina U KA, Heinig B, Kittner T, Nowak A. Acne inversa (hidradenitis suppurativa): a
review with a focus on pathogenesis and treatment. Indian J Dermatol 2013;4:2-11.61. Divaris DX, Kennedy JC, Pottier RH. Phototoxic damage to sebaceous glands and hair
follicles of mice after systemic administration of 5-aminolevulinic acid correlates with
localized protoporphyrin IX fluorescence. Am J Pathol 1990;136:891-7.62. Passeron T, Khemis A, Ortonne JP. Pulsed dye laser-mediated photodynamic therapy for
acne inversa is not successful: a pilot study on four cases. J Dermatol Treat 2009;20:297-8.63. Strauss RM, Pollock B, Stables GI, Goulden V, Cunliffe WJ. Photodynamic therapy using
aminolevulinic acid does not lead to clinical improvement in hidradenitis suppurativa.
Br J Dermatol 2005;152:803-4.64. Valladares-Narganes LM, Rodrıguez-Prieto MA, Blanco-Suarez M, Rodriguez-Lage C,
Garcia-Doval I. Treatment of hidradenitis suppurativa with intralesional photodynamic
therapy using a laser diode attached to an optical cable: a promising new approach. Br J
Dermatol 2015;172:1136-9.65. Finley EM, Ratz JL. Treatment of hidradenitis suppurativa with carbon dioxide laser excision
and second-intention healing. J Am Acad Dermatol 1996;34:465-9.
66. Lapins J, Sartorius K, Emtestam L. Scanner-assisted carbon dioxide laser surgery: a retro-
spective follow-up study of patients with hidradenitis suppurativa. J Am Acad Dermatol
2002;47:280-5.
67. Hazen PG, Hazen BP. Hidradenitis suppurativa: successful treatment using carbon dioxide
laser excision and marsupialization. Dermatol Surg 2010;36:208-13.
68. Tierney E, Mahmoud BH, Hexsel C, Ozog D, Hamzavi I. Randomized control trial for the
treatment of hidradenitis suppurativa with a neodymium-doped yttrium aluminium garnet
laser. Dermatol Surg 2009;35:1188-98.
69. Xu LY, Wright DR, Mahmoud BH, Ozog DM, Mehregan DA, Hamzavi IH. Histopathologic
study of hidradenitis suppurativa following long-pulsed 1064-nm Nd:YAG laser treatment.
Arch Dermatol. 2011;147(1):21-8.
For more than 127 additional continuing education articles related to skin and wound care topics, go to NursingCenter.com/CE.
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