eMedicine Specialties > Dermatology > Diseases of the Adnexa

Acne Keloidalis Nuchae: Treatment & Medication

Author: Philip R Letada, MD, Resident Physician, Department of Dermatology, Naval Medical Center San Diego
Coauthor(s): Elizabeth Kline Satter, MD, MPH, Staff Dermatologist and Head of Dermatopathology for Residency Program, Department of Dermatology, Naval Medical Center San Diego
Contributor Information and Disclosures

Updated: Apr 3, 2009

Treatment

Medical Care

Treatment of acne keloidalis nuchae (AKN) is difficult, and numerous modalities have been used with varying degrees of success.

• Education is the key to prevention. Patients need to be made aware that the condition is not caused by unclean clippers but, rather, is exacerbated by short haircuts and close shaving. In addition, patients should be educated to avoid tight-fitting collared shirts and athletic head gear, which may lead to mechanical shearing of the hairs.
• Initiating therapy as quickly as possible after the initial appearance of lesions decreases the chance of long-term cosmetic disfigurement.¹⁵ Daily shampooing with gently foaming benzoyl peroxide washes, chlorhexidine, or mild keratolytic cleansers containing alpha-hydroxy acids or tar is an effective alternative to standard shampoo products. Discontinuance of hair greases and hair pomades should also be advised.¹⁶
• Early, mild papular disease may respond to potent or superpotent topical steroids with or without the use of topical retinoids. This latter combination seems to be somewhat more effective than class 1 or 2 steroids alone. One suggested regimen includes twice-a-day treatment with a combined retinoic acid (Retin-A) and a class 2 or 3 corticosteroid cream or gel.
• When pustules, crust, or drainage is present, use of a topical antibiotic such as clindamycin or erythromycin on a twice-daily basis until the pustules abate may be advantageous. If the patient does not have significant improvement in 4-5 days, a bacterial culture of the involved area should be performed, and, if pathogenic microorganisms are identified, appropriate systemic antibiotics should be initiated. These antibiotics are instituted for both their antibiotic and anti-inflammatory effects. Topical chloramphenicol has been effective and can be prepared by adding 500 mg to 30 g of fluocinonide cream.
• In the rare cases in which large abscesses or draining sinuses are present, a 7- to 10-day tapering course of oral prednisone may be considered in addition to the appropriate systemic antibiotics.
• Isotretinoin may be considered for rapidly progressive disease.
• Intralesional triamcinolone acetonide injection (3-5 mg/mL, up to 40 mg/mL for resistant lesions) of papular lesions is another option. Application of a lidocaine-prilocaine cream mixture under plastic film occlusion 2 hours prior to the injection decreases the pain of injections. Warn patients that the area injected might become hypopigmented and remain so for 6-12 months. Some authors advocate electrodesiccation or liquid nitrogen prior to injection to facilitate the process.¹⁶
• An adjunctive therapy to intralesional steroids is to shave or curette the small papules or nodules prior to injection.
• Intralesional 5-fluorouracil and/or immunotherapy sessions have also been used.
• Cryotherapy has also proven to be successful in some cases.¹⁷ The area is frozen for 20 seconds, allowed to thaw, and is then frozen again 1 minute later. The morbidity (discomfort and drainage) is greater than other modalities, and the treated site often becomes hypopigmented because of destruction of the melanocytes and may remain so for up to 12-18 months.
• Another option is radiation therapy, which causes permanent epilation of the area.
• Once healing has occurred and active disease is controlled, apply a tretinoin-fluorinated steroid mixture to the occipital part of the scalp twice daily to help prevent recurrence.

Surgical Care

• Laser ablation using various lasers (eg, carbon dioxide, 1064-nm Nd:YAG, 810-nm diode) should be considered for lesions refractory to other treatments.¹⁸ One case series showed that 4 monthly laser hair epilation sessions using the diode laser (810 nm) in addition to a topical retinoid and steroid resulted in long-lasting improvement in the appearance and prevention of lesions. Laser hair epilation allows for coagulation necrosis of both viable hair follicles and fragmented hair shafts in the deep dermis.¹⁹
• Excision of small papules via punch biopsy is another therapeutic option. The punch should extend deep into the subcutaneous tissue so that the entire hair follicle is excised. Superficial biopsies tend to have a much higher incidence of recurrence.
  • After the punch biopsy is performed, the wound edges can be injected with 10-40 mg/mL of triamcinolone acetonide to reduce inflammation.
  • The area should be reapproximated using 4-0 suture. Because nylon sutures often irritate the skin, silk sutures can be used to prevent this problem.
  • Instruct patients to clean the postoperative area 3 times a day with a mild cleanser, followed by application of a topical antibiotic ointment.
  • The sutures should be removed in 7-10 days, and the patient should then begin a twice-daily topical retinoic acid/corticosteroid regimen for 4-6 weeks.
  • Injection of 3-5 mg/mL triamcinolone acetonide may also be considered if the area remains indurated. The postoperative surgical site can be injected every 2-4 weeks until the area softens.
• The preferred method of excision for larger linear lesions (1 cm or less in diameter) is a horizontal ellipse with primary closure; however, allowing the lesion to heal by secondary intention is a viable option for lesions that cannot be easily closed primarily.²⁰ The excision should extend below the hair follicles, and the area should be reapproximated with 4-0 silk sutures.
  • Always remember that when closing the area, ensure the patient’s neck is not in a flexed position; otherwise, the patient will spend a week or longer having to look upward.
  • An important caveat with surgical excision is that primary closure often results in recurrences and/or hypertrophic scarring, and data show that allowing lesions to heal by secondary intention results in fewer recurrences. Wound healing is typically achieved within 6-10 weeks, and, in general, the surgical site contracts to an area smaller and flatter than the original site.^21,22
  • Postoperative care is basically the same as with punch grafts.
    • Pain medication may be necessary for the first 48 hours.
    • Have patients return in 24-36 hours (preferably with the person responsible for changing dressings) for removal of the initial dressing. Soak the area with sodium chloride solution to facilitate the removal of the dressing and to clean the postoperative site.
    • Instruct patients to start cleaning the site twice a day (following the regimen above) once the dressing is removed.
    • Instruct patients to return for follow-up in 1 week, or, sooner, if any complications occur.
    • Instruct patients to return for follow-up care for possible initiation of intralesional steroid injections or to begin topical steroid/retinoic acid therapy once the area has healed, usually in 2-3 months. Do not begin intralesional steroids prior to complete would healing because this can result in wound dehiscence.
    • A follicular papule or pustule occasionally develops along the border of the linear scar. Treat all inflammatory lesions with topical clindamycin or chloramphenicol until the infection subsides. The residual papule can then be treated with topical or intralesional steroids or excised via a punch biopsy.
  • Excision followed by grafting is typically not cosmetically acceptable because it results in a large, depressed, non–hair-bearing area.

Medication

The goals of pharmacotherapy are to reduce inflammation and eliminate infection, if present.

Corticosteroids

These agents are used for their anti-inflammatory properties, but they must be used with caution because they have local and systemic side effects.

Topical corticosteroids may be used alone or in combination retinoic acid.

Triamcinolone acetonide (Kenalog, Amcort)

For inflammatory reactions responsive to steroids; decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability.

Prednisone (Deltasone, Meticorten, Orasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Used when patient has acute flare.

Clobetasol propionate (Olux)

Available as a 0.05% foam (Olux).

Fluocinonide (Lidex) or Mometasone furoate (Elocon)

Class 2 steroid (potent). Fluocinonide available as a 0.05% cream, ointment, and gel, and mometasone furoate available as 0.1% ointment.

Retinoids

Although the exact mechanism of action is unknown, retinoids decrease the cohesiveness of abnormal hyperproliferative keratinocytes, modulate keratinocyte differentiation, and have anti-inflammatory properties.

Isotretinoin (Accutane)

Oral agent that treats serious dermatologic conditions. Synthetic 13-cis isomer of the naturally occurring tretinoin (trans -retinoic acid). Both agents are structurally related to vitamin A.
Decreases sebaceous gland size and sebum production. May inhibit sebaceous gland differentiation and abnormal keratinization.
A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.

Tretinoin (Retin-A)

Although exact mechanism of action is unknown, retinoids decrease cohesiveness of abnormal hyperproliferative keratinocytes, modulate keratinocyte differentiation, and have anti-inflammatory properties.
Available as 0.025%, 0.05%, and 0.1% creams. Also available as 0.01% and 0.025% gels.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of this clinical setting.

Erythromycin (E-Mycin, Erythrocin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. Age, weight, and severity of infection determine proper dosage in children. When twice-daily dosing is desired, half total daily dose may be taken q12h. Double the dose for more severe infections.

Mupirocin (Bactroban)

Topical antibiotic; inhibits bacterial growth by inhibiting RNA and protein synthesis.

Doxycycline (Vibramycin)

Broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. Almost completely absorbed, concentrates in bile, and is excreted in urine and feces as a biologically active metabolite in high concentrations.
Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Rifampin (Rifadin, Rimactane)

Inhibits RNA synthesis in bacteria by binding to beta-subunit of DNA-dependent RNA polymerase, which, in turn, blocks RNA transcription.

• Search for CME/CE on This Topic »

• Folliculitis (Dermatology)

• Skin, Hair, and Nails Center
• Teen Health Center
• Acne Overview
• Acne Causes
• Acne Treatment

• Management of Primary Cicatricial Alopecias: Options for Treatment