Surg Clin N Am 82 (2002) 1187–1197

Hidradenitis suppurativa
Karen M. Mitchell, MD, David E. Beck, MD*
Department of Colon and Rectal Surgery, Ochsner Clinic Foundation,
1514 Jefferson Highway, New Orleans, LA 70121, USA

Hidradenitis suppurativa (HS) is a chronic, recurrent inflammatory pro-

cess involving the apocrine glands of the axilla, groin, perineal, and perianal
regions [1,2]. The disease can become quite painful and debilitating, result-
ing in chronically draining wounds and sinus tracts. Although the pre-
cise etiology remains unclear, evidence suggests that the primary process
involves occlusion of either the apocrine or follicular ducts, followed by
secondary infection of the apocrine system, with extension into the
surrounding subcutaneous tissues as sinus tracts. Medical management may
temporize the symptoms of this disease, but most patients with chronic
wounds will require some form of surgical therapy, ranging from simple
incision and drainage, unroofing of sinus tracts and local excision, to wide
excision with grafting or advancement flap coverage [1].

Pathogenesis
This disease was first documented in 1839 by Velpeau, who described a
patient with an inflammatory process affecting the skin of the axillary, mam-
mary, and perianal regions [3]. It was not until 1854, however, that it was
suggested by Verneuil that the disease originated in the sweat glands [4].
In 1922, Schiefferdecker further classified sweat glands as apocrine or
eccrine, and localized this disorder to the apocrine glands [5]. The histology
was defined in 1939 by Brunsting, who suggested that the inciting event was
luminal obstruction of the apocrine glands [6].
Apocrine glands are compound sweat glands located in the dermis of
the axilla, inguinal, perineal, and perianal regions of the body. Each gland
is composed of a coiled secretory unit that drains via a long excretory duct
into a hair follicle. Glandular secretion is an odorless, milky fluid produced

* Corresponding author.
E-mail address: dbeckmd@aol.com (D.E. Beck).

0039-6109/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 0 3 9 - 6 1 0 9 ( 0 2 ) 0 0 0 6 0 - 9
1188 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197

in response to pain, anger, or sexual arousal, which subsequently becomes

malodorous after interaction with bacteria on the skin surface [7].
It has been proposed that the primary event leading to hidradenitis sup-
purativa is either apocrine or follicular duct occlusion by keratin, which
leads to ductal dilatation and stasis in the gland. Bacteria can then enter the
apocrine system through the hair follicles, resulting in superinfection [2].
The glands may then rupture, extending the infectious process into the adja-
cent subcutaneous tissue [8]. Eventually, the chronic inflammatory process
results in significant fibrosis and scarring of the involved skin, forming char-
acteristic ‘‘pit-like’’ scars. The damaged pilosebaceous units eventually coa-
lesce to form a network of chronically draining subcutaneous abscesses and
sinuses [9].

Bacteriology
The bacterial flora involved in hidradenitis is inconsistent and unpredict-
able. Wounds in patients with positive cultures have grown bacteria such as
Staphylococcus epidermidis, Escherichia coli, Klebsiella, Proteus, alpha Strep-
tococcus, anaerobic bacteria, and diptheroids [8]. Thornton and Abcarian,
however, found that half of their patients treated for perianal and perineal
disease had negative cultures [10]. Highet and colleagues associated Strepto-
coccus milleri infection with perineal hidradenitis, isolating this bacterium in
21 of 32 patients with perineal disease [8]. Others have suggested an associ-
ation of this disease with Chlamydia trachomatis or Bilophila wadsworthia
infection [11,12].

Etiology
The underlying reason for apocrine or follicular occlusion remains uncer-
tain, though several predisposing factors have been suggested. Histologic
studies have not demonstrated a difference in glandular structure to account
for susceptibility to the disease [7]. Although the use of antiperspirants may
prevent discharge of apocrine gland secretions and predispose the develop-
ment of hidradenitis, Morgan and Leicester found no significant differences
in shaving practices, deodorant usage, and application of chemical depila-
tory agents between affected patients and age-matched controls [7]. Most
authors agree that obesity predisposes patients to hidradenitis, likely secon-
dary to increased shearing forces on the involved skin. Wiltz et al reviewed a
series of patients with hidradenitis at the Lahey Clinic and found that 70%
of these patients were smokers, although no causal relationship could be
demonstrated [13].
Because hidradenitis is virtually nonexistent before puberty and the
development of secondary sexual characteristics and apocrine gland func-
tion, hormones likely play a role in its development. Androgen excess, due
 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197 1189

to either overproduction by the adrenals or the gonads, may augment

keratinization and predispose to follicular occlusion [14]. Pregnancy, the
latter half of the menstrual cycle, and oral contraceptives can also increase dis-
ease activity [15]. Apocrine sweat contains dihydroepiandrosterone sulfate,
which stimulates sebaceous secretion [16]. The disease has also been re-
ported in patients with endocrinopathies such as Cushing’s disease, diabetes
mellitus, and acromegaly [17–19].
Fitzsimmons and associates suggested a possible familial predisposition
for the development of hidradenitis [20–22]. Jemec reported that 18 of 70
patients with hidradenitis (26%) had a positive family history of the disease,
compared with 2% of control patients [23]. Von Der Werth proposed an
autosomal dominant pattern of inheritance in the familial form [24].

Incidence
The incidence of hidradenitis in the general population is unknown,
mainly secondary to under reporting and misdiagnosis. However, it has
been estimated that 1 in 300 adults is affected, usually presenting after pu-
berty and before the age of forty [22]. Hidradenitis may be more common
in females and blacks [25,26], but perianal disease appears to be twice as
common in males as in females [9,13].

Clinical presentation
Any region of the body harboring apocrine glands may be involved, but
the axillary and inguinal-perineal regions are most commonly affected [14].
Initially, patients will experience pain and present with indurated, deep sub-
cutaneous nodules that organize as abscesses and may start spontaneously
draining malodorous discharge. The wound usually does not heal com-
pletely, and recurrences are common. With each recurrence, the subcutane-
ous cavities tend to grow larger. The final result is an indurated, fibrotic
meshwork of subcutaneous cavities and sinus tracts, the extent of which can
be highly variable (Fig. 1) [2,26]. Some patients are affected in limited re-
gions with mild disease, and others are affected by extensive involvement
at multiple sites [14]. Cycles of remission and relapse are typical, each epi-
sode producing distressing pain and embarrassing, foul-smelling discharge.
The disease becomes quite debilitating.

Diagnosis
Differentiating hidradenitis from other cutaneous infections such as
furuncles, carbuncles, lymphogranuloma venereum, erysipelas, epidermoid or
dermoid cysts, and tuberculosis can be difficult [13,27]. Perianal hidradenitis
1190 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197

Fig. 1. Hidradenitis suppurativa. (From Waters GS, Nelson H. Perianal hidradenitis sup-
purativa. In: Beck DE, Wexner SD, editors. Fundamentals of anorectal surgery. 2nd edition.
London: W.B. Saunders, Ltd., 1998. p. 233–6; with permission.)

must be distinguished from other perianal pathology that can mimic its pre-
sentation. Cryptoglandular fistulae, for example, arise from the dentate line
and involve the intersphincteric plane, whereas the tracts from hidradenitis
do not involve the sphincter mechanism. Also, because only the distal two
thirds of the anal canal contains apocrine glands, the dentate line should not
appear abnormal in patients with hidradenitis [28].
Pilonidal disease may be difficult to distinguish from hidradenitis if
the tracts involve the presacral region. There have been several published
reports of concurrent HS and Crohn’s disease, and differentiating between
the two can be challenging. Some authors believe the two diseases may
in fact be related [28–30]. If Crohn’s is suspected, endoscopy with biopsy
is indicated, as the treatment for each differs markedly. Wide excision in
a patient with undiagnosed Crohn’s disease could result in a devastating
chronic wound.
The follicular occlusion triad consists of acne conglobata, perifolliculitis
capitis, and hidradenitis suppurativa [31]. Acne conglobata is a severe man-
ifestation of acne involving the chest, back, and buttocks, and comedones
and small purulent nodules are the dominant features. Perifolliculitis capitis
is a similar condition involving inflammatory and purulent nodules on the
scalp, which can cause focal alopecia. Hidradenitis suppurativa completes
the triad.
 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197 1191

Squamous cell carcinoma is a rarely reported complication developing in

the chronic wounds in patients with HS, with fewer than thirty cases
described to date [32–34]. All published cases were reviewed by Perez-Diaz,
who found that the average age at diagnosis was 47 years, and that most
cases arose in the perineal, gluteal, and perianal regions. HS was present for
an average of 20 years before the development of cancer. Treatment ranged
from wide excision to abdominoperineal resection with chemotherapy and
radiation [32]. The infrequent but real incidence of squamous cell carcinoma
developing in these patients underscores the importance of close wound sur-
veillance, and biopsy of any suspicious lesions should be performed. Also,
any resected specimens should be carefully marked and sent for pathological
evaluation.

Treatment
Hidradenitis suppurativa presents as a spectrum of disease, ranging from
mild, localized disease to extensive skin involvement in multiple affected
areas. Treatment should be prioritized, with the most severe sites addressed
first.

Medical therapy
Conservative measures may be initiated first, aiming toward relief of pain
and other distressing symptoms. Warm baths, hydrotherapy, and topical
cleansing agents meant to maintain hygiene and reduce bacterial load are
attempted first [26]. Patients are instructed to wear loose-fitting clothing and
lose weight if they are obese.
Both topical and systemic antibiotics are usually empirically begun, using
antistaphylococcal agents for axillary disease and more broad spectrum cov-
erage for perineal disease. Therapy can then be tailored based on culture
results. The only topical antibiotic that has been shown to be effective in
a randomized, controlled trial is topical clindamycin [35]. Systemic tetracy-
cline has been shown to be as effective as topical clindamycin [23], but there
is no evidence that chronic suppressive antibiotic therapy alters the natural
history of HS [14,28].
With the thought that hidradenitis may be in part under hormonal con-
trol, some practitioners have attempted treatment with hormonal therapy.
Androgen levels, thought to play a role in disease activity, can be reduced
with steroid administration by suppressing the hypothalamic-pituitary axis
[36]. Leuprolide, a synthetic gonadoropin-releasing hormone, has also been
used to inhibit the axis, and has shown some promise in reducing disease
activity in some patients [37]. European trials have demonstrated success
using the antiandrogen cyproterone acetate, but this drug is not approved
for use in the United States [38,39].
1192 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197

Isotretinoin (Accutane), a derivative of vitamin A, has long been success-

fully used in the treatment of acne by reducing epithelial differentiation and
sebaceous secretions, but variable results have been reported when used in
patients with HS [40,41]. There currently are no established dosing guide-
lines for use in this subset of patients. Known complications of therapy
include teratogenicity, alteration of lipid profiles, hepatic dysfunction, and
pseudotumor cerebri.
Oral cyclosporine has demonstrated some benefit in patients with HS, but
further investigations are necessary before it can be recommended as treat-
ment, especially when one considers the serious toxicity that can be associ-
ated with long-term use [42].

Surgical therapy
Controversy still exists regarding the optimal surgical therapy for pa-
tients suffering from HS. Factors that influence the extent of surgery include
the site affected, the extent of disease, and whether the patient presents in
the acute or chronic state of the disease.

Local Incision and drainage

Verneuil, when he originally described this disease in 1854, suggested
treatment with simple incision and drainage of all fluctuant areas [4].
Although this form of therapy may control the acute symptoms and result
in little initial morbidity, recurrence of the disease is common [26,43,44].

Unroofing of sinus tracts and marsupialization

Unroofing involves probing and exploring all sinus tracts and fistulae,
completely removing the roof of all tracts, curetting the tract, and leaving
the floor intact to aid in closure by secondary intention [9,45]. The technique
is somewhat tedious and time-consuming but leaves islands of epidermis
from which regeneration occurs rapidly. Marsupializing the wounds may
further facilitate healing. Postoperatively, patients undergo sitz baths and
whirlpool therapy and are instructed in meticulous wound care. Although
high recurrence rates may limit its usefulness [26,43], unroofing is especially
valuable in patients with extensive perineal disease [45]. Culp [28] reported a
series of 30 patients perineal and perianal hydradenitis treated by exteriori-
zation or unroofing. He found that the extent of excision directly influenced
the risk of recurrence. Patients should understand that by leaving the disease
in situ, they harbor not only an increased chance of disease recurrence but
also a chance of developing squamous cell carcinoma.

Limited local excision

If the extent of skin involvement is limited, a viable surgical option is
local excision with primary closure. Local excision is associated with a higher
 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197 1193

incidence of local recurrence when compared with more radical operations,

but the morbidity is markedly lower [46]. For reasons that are unclear, local
excision of perianal HS is associated with a substantially lower risk of local
recurrence than perineal lesions [23,34,46–54]. Factors that may increase the
incidence of recurrence include obesity, insufficient excision, significant skin
maceration, and chronic skin infection [14].

Wide excision
Once the disease process has become chronic and extensive, most authors
recommend excision of the affected area of apocrine gland-bearing skin 1 cm
to 2 cm beyond visible evidence of disease in order to minimize the chance of
recurrence [49]. Before proceeding with more radical excision, however,
patients must be fully informed about the extent of the wounds to expect
postoperatively. Wound care assistance must be arranged in advance.
Under regional or general anesthesia, the patient is positioned in either
the prone jackknife or lithotomy position, depending on the area of involve-
ment. The affected area should be resected in its entirety down to normal
fascia, or at least into 0.5 cm of subcutaneous fat, to ensure adequate
removal of all apocrine glands [49]. In patients suffering from extensive peri-
neal disease, staged excision is recommended.
Delineating the apocrine gland-bearing skin with iodine-starch test can
direct an adequate excision. Eccrine secretion is blocked with intravenous
atropine. Oxytocin is then administered in order to stimulate contraction
of the myoepithelial cells around the apocrine glands. Topical iodine is
applied to the skin, followed by starch powder in castor oil. Black dots mark
the areas where apocrine secretion (sweat) came in contact with the iodine-
starch mixture [7]. All visibly involved areas are then excised. An alternative
method of mapping involves injection of 3 cc to 5 cc of methylviolet solution
into the sinus tracts to define their extent. All colored areas are then com-
pletely excised [50].
Once the wide excision has been performed, the wound can be managed
in one of several ways, including primary closure, split-thickness skin graft
coverage, advancement flap coverage, or healing by secondary intention.
Recurrence is related to adequacy of resection and the severity of the
disease, not the selected method of wound closure [50]. If possible, primary
closure is desirable, and is usually feasible for small and moderate-sized
wounds. Larger defects may necessitate skin grafting or flap coverage.
Skin grafting can either be performed immediately or in a delayed man-
ner, once granulation tissue has started forming. Early wound coverage,
rapid healing, and reduction of postoperative pain are attractive features
of split-thickness grafting. The drawbacks, however, include prolonged
operative time, potential donor site complications, the need for immobiliza-
tion, the possibility of graft loss, and the need for frequent dressing changes.
Grafting perineal wounds immediately is not recommended, because the
1194 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197

bacterial contamination in this region would result in a prohibitively high

incidence of infection and graft loss [51,52]. Skin grafting in the anal canal
may lead to anal stenosis and is not recommended.
Flap coverage from either the posterior thigh, gluteus muscle, or lumbo-
sacral region can be useful following perineal excisions. Flap coverage offers
more rapid healing of wounds, with resultant earlier return to normal activ-
ity. Disadvantages, however, include prolonged operative time, blood loss,
pain, potential flap loss secondary to infection, and recurrence of disease
below the flap [53]. Whether wounds are closed primarily or with skin grafts
or flaps, perioperative antibiotics should be used.
Most practitioners would agree that perineal wounds are best managed
by allowing them to granulate [45]. The benefits of allowing granulation
include earlier ambulation and discharge and avoidance of donor site pain
and morbidity [10,13]. Healing by secondary intention can take months,
however, and wound care can become a burden.
Harrison and associates reviewed the course of 82 patients treated with
wide excision, and found the following recurrence rates: perianal disease,
0%; axillary disease, 3%; and inguinoperineal disease, 37% [14]. The higher
rate of recurrence after excision of inguinoperineal HS is likely related to the
wider distribution of apocrine glands in this area, making complete removal
more challenging.
Routine colostomy in patients undergoing surgical treatment of perineal
disease is usually not necessary, as long as aggressive wound care is insti-
tuted. Patients who might benefit from fecal diversion are those in whom
proper wound care is not feasible, and those patients suffering from concom-
itant Crohn’s disease and HS [49].

Summary
Hidradenitis suppurativa is a chronic, debilitating disease of apocrine
gland-bearing skin. Its management must be individualized according to the
site and extent of the disease. Initial conservative measures with antibiotics,
local wound care, and limited incision and drainage can alleviate the acute
symptoms, but more radical surgery will likely eventually be necessary in
order to control and prevent recurrent disease. Options include unroofing
and marsupialization, local excision, or more extensive operative excision
with primary or secondary closure, skin grafting, or flap coverage of defects.
Wide excision will offer the most definitive therapy, with the trade-off being
a higher morbidity. Split-thickness skin grafts in the anal canal may contract
and result in anal stenosis and should be avoided. Perianal disease is often
best managed with local excision alone, with primary closure for small
defects, and either unroofing or healing by secondary intention for larger
wounds.
 K.M. Mitchell, D.E. Beck / Surg Clin N Am 82 (2002) 1187–1197 1195

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