Hidradenitis Supurativa

01Pathophysiology

Hidradenitis suppurativa (HS) is fundamentally a disease of follicular occlusion, not a primary infectious process. This distinction is critical and repeatedly tested. The disease begins when follicular hyperkeratosis causes plugging of the terminal hair follicle in apocrine gland-bearing skin. The plug traps keratin and debris within the follicle, leading to progressive dilation.

As the occluded follicle expands, it eventually ruptures into the surrounding dermis, releasing its contents (keratin, bacteria, sebaceous material) into the tissue. This triggers a vigorous neutrophilic and granulomatous inflammatory response that is disproportionate to any bacterial load present. The inflammation destroys surrounding tissue and promotes the formation of abscesses. Over time, the body attempts to wall off these areas of chronic inflammation through fibrosis, leading to the characteristic sinus tracts and hypertrophic scarring.

The reason lesions recur in the same anatomical regions (axillae, inguinal folds, perineum, inframammary folds, gluteal clefts) is that these are the sites with the highest density of apocrine glands and terminal hair follicles. Hormonal influence explains the post-pubertal onset and the female predominance, as androgens drive apocrine gland activity.

HS belongs to the follicular occlusion tetrad, which also includes acne conglobata, dissecting cellulitis of the scalp, and pilonidal sinus. All four share the same underlying mechanism of follicular plugging and rupture, but differ in their anatomical distribution.

Secondary bacterial colonization (commonly Staphylococcus aureus, coagulase-negative staphylococci, and anaerobes) worsens the inflammatory cycle but is a consequence, not the cause. This is why antibiotics alone do not cure the disease; they reduce bacterial burden and have anti-inflammatory properties, but the follicular occlusion continues.

02Classification and Clinical Manifestation

Hurley Staging System

The Hurley staging system is the most commonly referenced classification for HS on exams and guides treatment decisions.

Clinical Manifestation by Phase

Associated Comorbidities

03Diagnostic Workup

HS is a clinical diagnosis. There is no single lab test or imaging study that confirms it. The diagnosis rests on three pillars: the morphology of the lesions (nodules, abscesses, sinus tracts, scarring, double-ended comedones), the location of the lesions (apocrine gland-bearing intertriginous skin), and a history of chronicity and recurrence.

The best initial test is a thorough history and physical examination. On exam, you are looking for the hallmarks: recurrent deep-seated nodules in the axillae, groin, or perineum, often bilateral, with evidence of prior scarring or active sinus tract drainage. The presence of double-ended comedones is considered pathognomonic and should immediately point you toward HS.

When the presentation is atypical or the diagnosis is uncertain, a skin punch biopsy is appropriate. Histopathology will reveal follicular occlusion as the initiating event, surrounded by a dense inflammatory infiltrate that may be neutrophilic (acute phase) or granulomatous (chronic phase), with sinus tracts lined by stratified squamous epithelium.

Wound cultures are not used to diagnose HS, but they are ordered when secondary infection is suspected (increasing erythema, fever, rapidly expanding cellulitis) or when antibiotic therapy has failed and you need to tailor coverage. The polymicrobial nature of cultures (staphylococci, streptococci, anaerobes, gram-negative rods) reflects colonization rather than primary causation.

Dermal ultrasound has an emerging role in preoperative planning. It can reveal the true extent of subclinical sinus tracts and fluid collections beneath apparently normal skin, which helps the surgeon define adequate excision margins.

A key exam distinction: you do NOT need imaging to make the diagnosis. A vignette that describes a young obese woman with recurrent bilateral axillary abscesses, draining sinuses, and scarring is giving you HS. Do not be distracted into ordering CT or MRI unless the question is about surgical planning or ruling out a deeper process.

04Management and Treatment

Acute Stabilization

For a patient presenting with an acutely inflamed, fluctuant abscess, the next best step is incision and drainage (I&D). This provides immediate symptomatic relief. However, I&D alone has an extremely high recurrence rate because it does not address the underlying follicular occlusion or the established sinus tract network. I&D is a temporizing measure, not definitive treatment.

For a painful but non-fluctuant nodule, intralesional triamcinolone acetonide (3 to 5 mg/mL) can reduce inflammation rapidly, often within 48 to 72 hours.

Mild Disease (Hurley Stage I)

The first-line therapy is topical clindamycin 1% applied twice daily to affected areas. It works through both antibacterial and anti-inflammatory mechanisms. This is combined with daily use of an antiseptic body wash such as chlorhexidine 4% or benzoyl peroxide wash to reduce bacterial colonization. Treatment is ongoing rather than a fixed course; patients use topical therapy as long as lesions are present and during remission to reduce flare frequency.

Moderate Disease (Hurley Stage II)

When topical therapy is insufficient, systemic antibiotics are added. The two main options are:

1. Doxycycline 100 mg orally twice daily for a 12-week course, chosen primarily for its anti-inflammatory properties rather than antimicrobial action.

2. Clindamycin 300 mg orally twice daily + Rifampin 300 mg orally twice daily for 10 to 12 weeks. This combination is considered more effective than either agent alone and is often preferred for Hurley Stage II disease. An important teaching point: rifampin is a potent CYP450 inducer and will reduce the efficacy of oral contraceptives, warfarin, and many other medications. You must counsel patients accordingly and provide alternative contraception.

For women with evidence of hyperandrogenism or disease flares associated with the menstrual cycle, hormonal therapy with spironolactone (50 to 100 mg daily) or combined oral contraceptives can be added as adjunctive treatment.

Severe / Refractory Disease (Hurley Stage III)

The first-line biologic for severe HS is adalimumab, a TNF-alpha inhibitor and the first FDA-approved biologic therapy for this condition. The dosing schedule is:

• Week 0: 160 mg subcutaneously

• Week 2: 80 mg subcutaneously

• Week 4 onward: 40 mg subcutaneously every week

Before initiating adalimumab, patients must be screened for latent tuberculosis (with a PPD or interferon-gamma release assay) and hepatitis B, as TNF-alpha inhibition can reactivate these infections. Other contraindications include active serious infections, decompensated heart failure, and demyelinating disease.

Secukinumab, an anti-IL-17A monoclonal antibody, has also received approval for moderate to severe HS and represents a second biologic option.

For disease that fails medical therapy, wide local excision of the affected skin and subcutaneous tissue down to healthy tissue is the definitive surgical treatment. Unlike I&D, wide excision removes the entire diseased field, including sinus tracts and fibrotic tissue. The wound may heal by secondary intention or require skin grafting or flap closure. Recurrence rates after wide excision are significantly lower than after limited procedures.

Contraindications and Cautions

• Rifampin in combination with oral contraceptives: reduces contraceptive efficacy.

• Adalimumab in patients with latent TB, hepatitis B, heart failure, or active infection: risk of reactivation and disease exacerbation.

• Avoid isotretinoin: unlike acne vulgaris, isotretinoin has not shown consistent benefit in HS and is not a standard treatment.

• Avoid repeated I&D as sole management: it does not address the underlying disease and can worsen scarring.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common way students get questions about HS wrong is by treating it as a primary infectious disease. When a vignette describes recurrent axillary abscesses, the instinct is to reach for antibiotic escalation, repeated I&D, or wound cultures. But HS is a disease of follicular occlusion with secondary inflammation; if the question asks about the underlying pathophysiology, the answer is follicular hyperkeratosis and rupture, not staphylococcal infection.

A second major trap is the patient who has had "recurrent boils" treated with multiple courses of antibiotics and repeated drainage procedures without improvement. The question is testing whether you can recognize the pattern of chronic relapsing disease in intertriginous areas as HS rather than continuing to manage it as isolated furuncles. The discriminating feature is the chronicity, the bilateral distribution, and the presence of sinus tracts or scarring between active lesions.

Watch for the double-ended comedone. If a vignette mentions this finding, the answer is HS. No other condition produces this sign, and its inclusion in a question stem is a deliberate signpost.

Do not confuse HS with an acute surgical abdomen or necrotizing soft tissue infection. A stable, afebrile patient with chronic draining sinuses and scarring in the groin does not need emergent surgical debridement; they need a dermatology referral and initiation of disease-directed therapy.

Finally, remember the association between HS and Crohn disease. A vignette may present a patient with perianal fistulae and ask about the most likely associated condition. If the patient also has axillary or inguinal nodules with sinus tracts, HS is the connection. Conversely, a patient diagnosed with HS who develops chronic diarrhea should be evaluated for inflammatory bowel disease.

The core competency being tested is the ability to recognize a chronic, relapsing pattern of follicular occlusion in intertriginous skin, distinguish it from simple infectious etiologies, and apply a stepwise management approach that matches treatment intensity to disease severity using the Hurley staging system.