Hidradenitis Suppurativa (HS) is a chronic, painful, debilitating disease that is poorly understood and with ill-defined treatment. It affects approximately 4% of the US population, and frequently brings patients to the ER with pain and inflammation (1). Due to the unclear nature and treatment, this condition is dealt with in many ways, some with poor outcomes, leading to increased morbidity and necessitating more radical treatments downstream.
The disease is diagnosed by the confluence of three criteria (2):
The underlying cause is debated but currently thought to be occlusion of the terminal follicular acro-infundibulum, which causes follicular duct expansion, wall rupture, antigen release and resulting inflammation (2). Bacterial infection was long thought to be part of the disorder, leading to wide use of antibiotics for treatment (3,4).
However approximately half of HS lesions are sterile upon culture (S. aureus and S. epidermidis being the most common isolates in non-sterile cultures), indicating that other inflammatory processes are at work as well (4).
Due to the unclear underlying etiology of HS, it has been difficult to target therapy for this disease process. Numerous treatment modalities have been offered with varying success: antibiotics, immunosuppresants, anti-inflammatory medications, isotretinoins, surgical unroofing, classic I & D, and surgical excision (5).
Current treatment recommendations vary based on stage of the disease utilizing the Hurley Staging System (6):
Stage I: One or more abscesses with no sinus tract or scarring.
Stage II: One or more widely separated recurrent abscesses, with a tract and scarring.
Stage III: Multiple interconnected tracts and abscesses through the entire affected area.
After extensive research, a number of treatment modalities have proven themselves to be more efficacious, although none appear perfect. Some are easily implemented in the ER, while others are better tolerated in the hands of a specialist. A treatment algorithm based on the Hurley Staging System is offered below.
Notably, classic incision and drainage is not a preferred treatment. It may lead to short-term relief of symptoms but does not have any positive effects on the long-term progression of the disease. It should be reserved for use in patients with tense abscesses creating unbearable pain (13). If done, the wound should be packed, and patients should be given oral antibiotics with the first dose in the ER.
HS is a complicated, chronic disease, burdening patients with great pain and disability. Much work remains to elucidate the exact underlying mechanisms and the most appropriate therapy. However employment of uniform therapy tailored to severity stage appears to decrease symptoms, recurrence, and will ideally decrease the need for more radical interventions.
-- Peter Acker MD MPH
References:
The disease is diagnosed by the confluence of three criteria (2):
- Typical lesions: multiple deep seated nodules and fibrosis
- Typical locations (areas with apocrine glands): groin, axilla, perineal, peri-anal and infra-mammary regions
- Chronicity and relapse
The underlying cause is debated but currently thought to be occlusion of the terminal follicular acro-infundibulum, which causes follicular duct expansion, wall rupture, antigen release and resulting inflammation (2). Bacterial infection was long thought to be part of the disorder, leading to wide use of antibiotics for treatment (3,4).
However approximately half of HS lesions are sterile upon culture (S. aureus and S. epidermidis being the most common isolates in non-sterile cultures), indicating that other inflammatory processes are at work as well (4).
Due to the unclear underlying etiology of HS, it has been difficult to target therapy for this disease process. Numerous treatment modalities have been offered with varying success: antibiotics, immunosuppresants, anti-inflammatory medications, isotretinoins, surgical unroofing, classic I & D, and surgical excision (5).
Current treatment recommendations vary based on stage of the disease utilizing the Hurley Staging System (6):
Stage I: One or more abscesses with no sinus tract or scarring.
Stage II: One or more widely separated recurrent abscesses, with a tract and scarring.
Stage III: Multiple interconnected tracts and abscesses through the entire affected area.
After extensive research, a number of treatment modalities have proven themselves to be more efficacious, although none appear perfect. Some are easily implemented in the ER, while others are better tolerated in the hands of a specialist. A treatment algorithm based on the Hurley Staging System is offered below.
| Hurley Stage | ER Treatments |
| General (all stages) | -Minimize trauma, wear loose fitting clothes -Quit smoking (7) -Avoid anti-perspirants -Avoid high pH soaps -Do not shave affected areas |
| Stage I | Topical ABX8,9 -Clindamycin 1% BID X 12 weeks Topical ABX failures → Oral antibiotics X 7-10 days9,10 -Tetracycline 250-500 mg QID -Doxycycline 100 mg BID -Clindamycin 300 mg BID -Augmentin 500 mg-1 g TID Dermatology referral -Intra-lesional steroid injections -Anti-androgen initiation |
| Stage II | Oral ABX (same as Stage I) Severe cases: -Rifampin + Clindamycin combination therapy -Clindamycin 300 mg BID + Rifampin 300 mg BID X 3 months11,12 Referral to surgery for unroofing |
| Stage III | Employ same treatment principles from Stage I & II Surgical referral |
Notably, classic incision and drainage is not a preferred treatment. It may lead to short-term relief of symptoms but does not have any positive effects on the long-term progression of the disease. It should be reserved for use in patients with tense abscesses creating unbearable pain (13). If done, the wound should be packed, and patients should be given oral antibiotics with the first dose in the ER.
HS is a complicated, chronic disease, burdening patients with great pain and disability. Much work remains to elucidate the exact underlying mechanisms and the most appropriate therapy. However employment of uniform therapy tailored to severity stage appears to decrease symptoms, recurrence, and will ideally decrease the need for more radical interventions.
-- Peter Acker MD MPH
References:
1. Harrison BJ, Mudge M, Hughes LE. Recurrence after surgical treatment of hidradenitis suppurativa. Br Med J (Clin Res Ed) 1987; 294:487.
2. Gordon SW. Hidradenitis suppurativa: a closer look. J Natl Med Assoc 1978; 70:339.
3. Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Dermatol 1999; 140:90.
4. Jemec GBE, Faber M, Gutschik E, Wendelboe P. The bacteriology of hidradenitis suppurativa. Dermatology 1996; 193:203–6.
5. Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977–978.
6. Hurley H. Axillary hyperhidrosis, apocrine bromhidrosis, hidradenitis suppurativa, and familial benign pemphigus. In: Roenigk RH, Roenigk HH Jr, eds. Dermatologic surgery: principles and practice. New York, NY: Marcel Dekker; 1989:729-739.
7. Sartorius K, Emtestam L, Jemec GB, Lapins J. Objective scoring of hidradenitis suppurativa reflecting the role of tobacco smoking and obesity. Br J Dermatol 2009; 161:831.
8. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol 1983; 22:325.
9. Jemec GB, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol 1998; 39:971.
10. Kaur MR, Lewis HM. Hidradenitis suppurativa treated with dapsone: A case series of five patients. J Dermatolog Treat 2006; 17:211.
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.
12. Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977–978.
13. Lapins, J, Emtestam, L. Surgery. In: Hidradenitis Suppurativa, Jemec, GB, Revuz, J, Leyden, J (Eds), Springer, New York 2006. p.160.
2. Gordon SW. Hidradenitis suppurativa: a closer look. J Natl Med Assoc 1978; 70:339.
3. Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Dermatol 1999; 140:90.
4. Jemec GBE, Faber M, Gutschik E, Wendelboe P. The bacteriology of hidradenitis suppurativa. Dermatology 1996; 193:203–6.
5. Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977–978.
6. Hurley H. Axillary hyperhidrosis, apocrine bromhidrosis, hidradenitis suppurativa, and familial benign pemphigus. In: Roenigk RH, Roenigk HH Jr, eds. Dermatologic surgery: principles and practice. New York, NY: Marcel Dekker; 1989:729-739.
7. Sartorius K, Emtestam L, Jemec GB, Lapins J. Objective scoring of hidradenitis suppurativa reflecting the role of tobacco smoking and obesity. Br J Dermatol 2009; 161:831.
8. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol 1983; 22:325.
9. Jemec GB, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol 1998; 39:971.
10. Kaur MR, Lewis HM. Hidradenitis suppurativa treated with dapsone: A case series of five patients. J Dermatolog Treat 2006; 17:211.
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.
12. Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977–978.
13. Lapins, J, Emtestam, L. Surgery. In: Hidradenitis Suppurativa, Jemec, GB, Revuz, J, Leyden, J (Eds), Springer, New York 2006. p.160.
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