INTRODUCTION — Acne keloidalis nuchae (AKN) is a common, chronic, inflammatory scalp disorder characterized by the development of papules, pustules, and keloidal scarring on the posterior scalp or posterior upper neck (picture 1A-G). AKN can cause pruritus, pain, and cosmetic disfigurement.
Treatment of AKN generally consists of interventions intended to reduce inflammation and scarring as well as avoidance of potential exacerbating factors (algorithm 1). Early treatment is preferred, given the potential for disfiguring scarring.
The management of AKN will be reviewed here. The pathogenesis, clinical manifestations, and diagnosis of AKN are reviewed separately.
TREATMENT PRINCIPLES — Treatment data on AKN are limited, and there are no consensus guidelines regarding therapy . Decisions for treatment are usually guided by clinician experience and modified based upon the clinical presentation and patient preferences. The lack of consensus is evident in the widely variable treatment suggestions made by a panel of dermatologists in a review of AKN .
Our approach to the treatment of AKN based upon the limited available evidence and clinical experience is reviewed here (algorithm 1). Other approaches to treatment may be reasonable.
General approach — Early treatment is important to minimize risk for severe scarring. Our management of AKN consists of measures directed at improving the clinical manifestations and symptoms of AKN.
Our initial interventions typically include (algorithm 1):
●Counseling of patients to avoid potential exacerbating factors (see 'Avoidance of exacerbating factors' below)
●Interventions to improve active inflammation (see 'Treatment of inflammation' below)
●Interventions to minimize the appearance of scars (see 'Treatment of keloidal scarring' below)
Interventions for scarring may be addressed concurrently or following the control of active inflammation.
Secondary infection — Occasionally, infection occurs as a complication of AKN. Findings suggestive of infection include extensive erythema, suppuration, pain, drainage, odor, or systemic symptoms such as fever. In this setting, obtaining a culture with susceptibility testing and initiating antibiotic therapy to treat the infection are appropriate. We typically delay treatment with topical corticosteroids and intralesional corticosteroids, both common treatments for AKN, until resolution of infection.
AVOIDANCE OF EXACERBATING FACTORS — Although the cause of AKN is not definitively known, a variety of factors have been proposed as exacerbating factors (see "Acne keloidalis nuchae: Pathogenesis, clinical manifestations, and diagnosis", section on 'Pathogenesis'). In an attempt to minimize exacerbations, we encourage patients to [3-7]:
●Avoid picking, rubbing, or scratching the affected area
●Discontinue close shaving, trimming, or razor or clipper edging of the posterior hairline
●Avoid irritation from tight-fitting hats, helmets, or high-collared shirts
However, the efficacy of such measures on AKN has not been studied.
Patients often express concern that AKN resulted from contact with infected barber tools. Therefore, we also educate patients that AKN is not an infectious condition.
TREATMENT OF INFLAMMATION — Topical or systemic medications with anti-inflammatory properties represent the primary method of improving inflammatory manifestations of AKN (inflammatory papules and pustules). The severity of inflammation influences treatment selection. (See 'Mild to moderate inflammation' below and 'Moderate to severe inflammation' below.)
Mild to moderate inflammation — Patients who present with small, inflammatory papules or pustules can often achieve improvement in symptoms with topical therapy (algorithm 1). Topical corticosteroid therapy is often combined with topical antibacterial therapy and topical retinoid therapy in an attempt to augment the response to treatment. In our experience, inclusion of a topical antibacterial agent can be particularly helpful in patients with pustules. (See 'Topical corticosteroids' below and 'Topical antibacterial agents' below and 'Topical retinoids' below.)
Intralesional injection of corticosteroids, as often used for moderate to severe inflammation in AKN, is an alternative approach for local corticosteroid therapy that some patients may prefer. (See 'Moderate to severe inflammation' below.)
Topical corticosteroids — The anti-inflammatory effects of topical corticosteroids appear useful for AKN:
●Administration – The best regimen for topical corticosteroid therapy for AKN is unclear. A high-potency (group 1 or 2 (table 1)) topical corticosteroid can be applied once or twice daily to the affected area. We usually have patients apply a topical corticosteroid once daily and an adjunctive therapy once daily. (See 'Topical antibacterial agents' below and 'Topical retinoids' below.)
A typical regimen consists of application of the topical corticosteroid in two-week cycles that alternate with two-week, treatment-free intervals in an attempt to minimize risk for topical corticosteroid-related adverse effects . (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)
Topical corticosteroids are available in a variety of vehicles (eg, ointments, foams, gels, creams, solutions), which can be selected based upon patient preference. In our experience, many patients prefer ointments or lotions, as these formulations tend to be more soothing and cosmetically acceptable.
We re-evaluate patients every four to six weeks to assess the response to treatment and to observe for adverse effects. We expect a response to topical corticosteroid therapy (noticeable reduction in severity of papules and pustules) within the first six to eight weeks of treatment, followed by continued improvement with continued therapy.
Once sufficient improvement is achieved, we discontinue the topical corticosteroid, with the plan to restart therapy if symptoms recur. If little improvement is evident after six to eight weeks of treatment, we transition to other therapies. (See 'Moderate to severe inflammation' below and 'Refractory inflammation' below.)
●Efficacy – Despite the frequent use of topical corticosteroids for AKN, there are few data on efficacy. Some support stems from an open-label study in which 20 African American adults with mild to moderate AKN (defined as fewer than 50 papules or pustules) were treated with topical clobetasol propionate 0.05% foam (applied twice daily for two weeks alternating with no therapy for two weeks) over an eight-week period . At the end of treatment, mean papule and pustule counts were significantly reduced compared with baseline. Patients who continued to have active disease after this period were treated with betamethasone valerate 0.12% foam (a less potent topical corticosteroid) for an additional four weeks. However, a significant difference in response was not noted between 8 and 12 weeks.
●Adverse effects – Potential adverse effects of topical corticosteroids include cutaneous atrophy and hypopigmentation at the treatment site. Therefore, patients should be cautioned to apply the corticosteroid only to the affected areas of the scalp and to avoid applying the corticosteroid for extended periods without medical supervision. Additional adverse effects of topical corticosteroids are reviewed separately. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)
Topical antibacterial agents — Although AKN is not a primary infectious condition, clinical experience suggests that topical antibacterial agents are sometimes useful for improving AKN (algorithm 1).
Topical antibacterial agents may help to minimize disease exacerbations via the treatment and prevention of secondary infection. The anti-inflammatory effects of antibacterials may also be of benefit:
●Administration – We typically prescribe topical clindamycin-benzoyl peroxide combination gel, applied to the affected area once daily. Alternative topical products include clindamycin, erythromycin, benzoyl peroxide, or erythromycin-benzoyl peroxide combination gel.
Gel, solution, foam, or pledget formulations of topical antibacterial agents may be additionally useful for their drying effects on pustules.
In our experience, significant improvement in pustules and inflamed papules often occurs within four to six weeks.
●Efficacy – Use of topical antibacterial agents is based upon clinical experience that suggests benefit. The comparative efficacy of different topical antimicrobial agents for AKN is unknown.
●Adverse effects – Potential adverse effects of topical antibacterial agents include allergic or irritant reactions. If gels, solutions, or pledget formulations are too irritating, lotion formulations are an alternative. Patients using benzoyl peroxide should be informed of the potential for the product to bleach fabrics.
Topical retinoids — It is theorized that topical retinoids may help to improve AKN by normalizing follicular keratinocyte maturation and desquamation, thereby decreasing follicular blockage (algorithm 1). Topical retinoids also have anti-inflammatory properties [9,10]:
●Administration – Topical retinoids available for use in the United States include tretinoin, adapalene, tazarotene, and trifarotene. We typically use tretinoin 0.025% cream applied once every other day and increase to daily application as tolerated.
Topical tretinoin is generally applied at night, as some forms of tretinoin are subject to photodegradation, particularly in the presence of benzoyl peroxide [11,12]. Other topical retinoids and some specialized formulations of tretinoin are more light stable than standard tretinoin, making application at night less critical. (See "Acne vulgaris: Overview of management", section on 'Topical retinoids'.)
The strength of tretinoin can be increased as well, depending on response. In our experience, at least two to three months of treatment is necessary to assess efficacy. If beneficial, topical retinoid therapy can be continued indefinitely.
●Efficacy – Use of topical retinoids for AKN is based upon clinical experience that suggests benefit. The relative efficacy of different topical retinoids for AKN is unclear.
●Adverse effects – Irritation is a common side effect of topical retinoids, particularly at the start of therapy. Starting with every-other-day application may help to reduce skin irritation.
Use of topical retinoids during pregnancy is discouraged. In particular, tazarotene is contraindicated in pregnancy. The adverse effects of topical retinoids are reviewed in greater detail separately. (See "Acne vulgaris: Overview of management", section on 'Topical retinoids'.)
Moderate to severe inflammation — When patients present with numerous inflammatory lesions; extensive pustulation or suppuration; or larger, inflammatory lesions, we alter the approach to therapy (algorithm 1). Oral antibiotics given in conjunction with topical or intralesional corticosteroids and topical retinoids may be useful for improving AKN in this population.
The possibility of active secondary infection warranting a different approach to treatment should also be considered in these patients. (See 'Secondary infection' above.)
Oral antibiotics — Tetracycline derivatives are the antibiotics most frequently prescribed for AKN because of their gram-positive coverage and anti-inflammatory effects:
●Administration – We typically treat adults with AKN with oral doxycycline (100 mg twice daily) for several weeks to several months depending on the response to treatment. Minocycline (75 to 100 mg twice daily) is an alternative, but there is increased risk of adverse events. (See "Minocycline (systemic): Drug information".)
We re-evaluate patients after six to eight weeks of treatment and expect to see at least a partial response at this period. We continue therapy until resolution of clinical signs of inflammation provided there is progressive improvement.
Once inflammation is controlled for approximately two months, we taper the doxycycline as tolerated to the lowest dose that maintains the response to treatment. The goal is to eventually discontinue oral antibiotic therapy and maintain improvement with the topical therapies used for milder inflammation. In our experience, subantimicrobial dosing of doxycycline (40 mg per day) is sometimes useful for maintaining disease control in patients who flare upon discontinuation of oral antibiotic therapy. (See 'Mild to moderate inflammation' above.)
If flares occur during or after tapering, we instruct patients to restart doxycycline 100 mg twice daily. We reattempt tapering after control of inflammation for at least two months and encourage long-term, consistent use of topical antibacterial and topical retinoid therapy.
●Efficacy – The efficacy of oral antibiotics for AKN has not been assessed in clinical trials. Use of these agents is based upon clinical experience that suggests benefit for improving inflammation.
●Adverse effects – Doxycycline and minocycline are generally well tolerated. Common side effects of tetracycline derivatives include photosensitivity and gastrointestinal distress. In addition, minocycline has been associated with vertigo, skin pigmentation, serum sickness, drug reaction with eosinophilia and systemic symptoms (DRESS), hepatic abnormalities, and a lupus-like syndrome. (See "Doxycycline: Drug information" and "Minocycline (systemic): Drug information".)
Topical or intralesional corticosteroids — Treatment of moderate to severe inflammation with topical corticosteroids is similar to treatment of mild to moderate inflammation. (See 'Topical corticosteroids' above.)
Intralesional corticosteroid injections may be useful for treating persistent, inflammatory papules that cannot be resolved with topical or systemic therapy:
●Administration – We typically inject triamcinolone acetonide (2.5 to 5 mg/mL) into inflamed papules and re-evaluate in four weeks. Limiting the total dose of triamcinolone acetonide to less than 40 mg per month is advised to reduce risk for systemic adverse effects. In our experience, clinical improvement in papules is usually evident within two to four weeks. (See "Intralesional corticosteroid injection" and "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)
●Efficacy – Use of intralesional corticosteroids is based upon clinical experience that suggests benefit.
●Adverse effects – Cutaneous atrophy and hypopigmentation are among the most common side effects of this therapy. (See "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)
Refractory inflammation — Some patients with AKN experience continued disease activity or progression despite standard initial therapies. As an initial step, patients with mild to moderate inflammation who fail to improve with topical therapy may transition to oral antibiotic and intralesional corticosteroid therapies used for moderate to severe inflammation (algorithm 1). (See 'Moderate to severe inflammation' above.)
Next-line options for patients who are refractory to standard therapy for moderate to severe inflammation include surgery, laser hair reduction, ablative laser resurfacing, and oral isotretinoin. However, efficacy data for these approaches are limited. Selection among these approaches is based upon clinical findings, treatment availability, and patient preferences. As an example, surgery or erbium:yttrium aluminum garnet (Er:YAG) laser resurfacing may be preferred for patients in whom active inflammation is accompanied by plaque-like, keloidal scarring. (See 'Treatment of keloidal scarring' below.)
Surgery — Because AKN is typically localized, surgical excision can be used to remove the affected skin. Recurrence is possible, particularly if the excision is insufficiently deep to remove hair follicles. Surgery for AKN is discussed below. (See 'Surgery' below.)
Laser therapy — Studies evaluating the long-pulsed, long-wave hair removal lasers, such as the 1064 nm neodymium:yttrium aluminum garnet (Nd:YAG) and 755 nm alexandrite laser, suggest benefit for AKN [13-16]. The advantage of these lasers may be the ability to penetrate deeply enough to target the entire dermal depth of the average follicular length of 2 to 4 mm . Papular and pustular lesions may respond better than keloidal plaques to this treatment.
Examples of studies supporting efficacy of these lasers are listed below. Benefit of the 810 nm diode laser, another hair removal laser, is documented in case reports :
●An uncontrolled study in which 16 patients with AKN were given five laser treatments with a long-pulsed 1064 nm Nd:YAG laser at four-week intervals (fluence 35 to 45 J/cm2, pulse duration 10 to 30 msec) suggests benefit of laser hair removal for AKN . Improvement was detected in all patients, and the mean papule count, plaque count, and plaque size decreased after treatment. Softening of keloidal plaques was also observed. The best results occurred in patients with early, papular lesions compared with later-stage disease with keloidal plaques. Recurrence of active AKN (characterized by a few papular lesions) developed in 2 of 10 patients who were re-evaluated after one year; however, these patients responded well to additional laser treatment.
●In a prospective, uncontrolled study in which 17 patients with AKN received six treatments with a 755 nm alexandrite laser (starting fluence 12 J/cm2, spot size 18 mm, 3 ms pulse duration), treatment was associated with reductions in mean papule count, mean pustule count, keloidal plaque size, and keloidal plaque pliability . Papulopustular lesions exhibited a greater degree of improvement than keloidal lesions. No recurrences occurred within treated areas during a three-month, follow-up period.
Benefit of non-hair removal lasers has also been proposed. A trial that randomly assigned 30 male patients with AKN to six treatment sessions with either an ablative 2940 nm Er:YAG laser or a long-pulsed 1064 nm Nd:YAG laser found reductions in mean papule counts, plaque size, and plaque consistency in both groups and a decrease in plaque count in the Er:YAG group .
Reduced hair density in the treatment site is an expected side effect of laser treatment. Other potential side effects of laser therapy include dyspigmentation, blistering, and scarring.
Oral isotretinoin — Case reports suggest that oral isotretinoin may help some patients with severe, treatment-resistant inflammation. However, limited efficacy data and multiple side effects of isotretinoin (teratogenicity, hyperlipidemia, xerosis, visual changes, etc) prevent a recommendation for routine use for AKN. Given the limited data, the best regimen for isotretinoin therapy is unclear.
One case report describes a male patient with both keratosis follicularis spinulosa decalvans (KFSD) and AKN who experienced improvement in AKN during treatment with 20 mg of oral isotretinoin daily (0.25 mg/kg per day) . The AKN on the vertex demonstrated rapid improvement in inflammation within weeks; however, the reduction in inflammation on the nuchal area was less dramatic. Improvement was maintained for at least one year with a reduced dose of isotretinoin (20 mg every two to three days). (See "Keratosis pilaris atrophicans", section on 'Keratosis follicularis spinulosa decalvans'.)
In a second case report, six months of oral isotretinoin (initial dose 0.6 mg/kg per day for three months, then 0.3 mg/kg per day for three months) was associated with resolution of papules in a patient with AKN . A recurrence after the end of treatment responded to a second course of isotretinoin (0.1 mg/kg per day).
Isotretinoin is teratogenic and should not be given to pregnant patients. In the United States, participation in the iPLEDGE program, a computer-based risk management program designed to reduce fetal exposure to isotretinoin, is required for prescribing the drug. The multiple adverse effects of isotretinoin are reviewed separately. (See "Oral isotretinoin therapy for acne vulgaris", section on 'Adverse effects'.)
TREATMENT OF KELOIDAL SCARRING — The major therapeutic options for the treatment of keloidal scarring in AKN are intralesional corticosteroid injections and surgery (algorithm 1).
Papules and small plaques — Our preferred first-line treatment for small, keloidal scars is intralesional corticosteroid injection. (See "Intralesional corticosteroid injection".)
Intralesional corticosteroids — Use of intralesional corticosteroid injection for keloidal lesions in AKN is based upon the efficacy demonstrated for keloids and clinical experience that supports benefit for AKN. Treatment may support softening and shrinking of keloidal papules or plaques of AKN. (See "Keloids and hypertrophic scars".)
We typically use triamcinolone acetonide in concentrations of 5 to 40 mg/mL depending on the size of the scarred area. Keloidal papules may improve with doses as low as 5 mg/mL, whereas large, thick plaques may require higher doses to achieve noticeable improvement. Limiting the total dose to 40 mg or less per month is advised to minimize risk for systemic adverse effects of corticosteroid treatment. (See "Intralesional corticosteroid injection" and "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)
Injections can be repeated every four to six weeks, and the dose can be progressively titrated upward based upon the response. At least a partial clinical response (at least some softening of the lesions) is expected within one to three treatments.
Intralesional injections can be uncomfortable. When necessary, application of a topical analgesic (eg, topical lidocaine) prior to treatment can help to reduce discomfort. Alternatively, the corticosteroid may be diluted in lidocaine. Spraying the site with liquid nitrogen prior to injection may also help to reduce pain of injection and may ease injection into the tissue. However, hypopigmentation is a risk of liquid nitrogen, particularly in individuals with moderately to highly pigmented skin. We typically do not use liquid nitrogen for analgesia. (See "Intralesional corticosteroid injection", section on 'Reducing injection pain'.)
Larger plaques — Patients with extensive scarring or scars that fail to improve adequately with intralesional corticosteroid therapy may benefit from surgical therapy to remove the affected area.
Surgery — Surgical therapies are indicated for the treatment of extensive scarring seen in plaque- or tumor-stage AKN. Once large plaques have developed, surgical options are the only effective recourse. Surgery can also be used to remove the site of disease in patients with active disease that is poorly responsive to medical therapy (see 'Refractory inflammation' above):
●Procedures – AKN has been successfully treated with scalpel excision, electrosurgical excision, and laser excision. Regardless of the surgical technique selected, the following measures may optimize results:
•Deep excision – The depth of excision must extend below the base of the hair follicles to reduce risk of recurrence [21-23]. Some authors suggest excising to the level of the deep subcutaneous tissue or muscular fascia, given the propensity for hair follicles to extend into the subcutaneous fat .
•Horizontal excision – Orienting the excision horizontally with intent to incorporate the posterior hairline may yield the best cosmetic results . Some authors have proposed performance of a bat-shaped excision as a method of promoting a natural-appearing hairline after healing .
Options for closure of excision wounds include primary closure and healing by secondary intention:
•Primary wound closure – Primary wound closure provides immediate closure of the wound and simplifies wound care for the patient. However, high tension on the closure may result in spreading of the scar, hypertrophic scarring, or restricted head movement. Therefore, the preoperative evaluation should include an assessment of the excision size and surrounding skin laxity to determine if the wound can be comfortably closed. If the affected area is too large to excise in a single procedure, staged excision with primary closure or secondary intention healing are options .
•Secondary intention healing – Secondary intention healing eliminates concern for excessive wound tension that may occur with primary wound closure but requires an average of 6 to 12 weeks for the wound to close. Scars often contract to a smaller size than the initial excised area, yielding improved cosmesis after healing . Some authors have proposed debridement of granulation tissue as a potential method of promoting wound contraction to minimize scarring .
One review found data to suggest that fewer recurrences occur with secondary intention healing than with primary closure; however, further study would be necessary to confirm this finding . The authors postulated that the secondary intention healing process might effectively eliminate hair-bearing tissue or that the inflammatory response or process of prolonged healing might have other beneficial effects on AKN .
Split-thickness skin grafting has also been described but is considered less than optimal, since the scar is usually depressed and texturally different (shiny and smooth) compared with the surrounding skin . In addition, the color of the grafted skin usually does not match the surrounding skin.
●Efficacy – Although surgery is considered an effective treatment for AKN, few studies have evaluated its efficacy. One of the largest studies evaluating surgical intervention for AKN involved 25 male patients with AKN refractory to medical therapy . The patients had extensive, coalescent, keloidal plaques on the nuchal scalp. Twenty patients underwent complete excision with primary closure of the surgical defect. The remainder had lesions too large for this procedure and had either a two-stage excision with primary closure (four patients) or excision with secondary intention healing (one patient).
One year after the procedure, the surgeon and the patients both rated cosmetic results as good to excellent. Complications included mild recurrence of small papules and pustules in 15 patients (managed with topical corticosteroids) and hypertrophic scars in four patients who had excision of large lesions and primary wound closure in a single procedure. In this particular study, the four patients who underwent electrosurgical excision seemed to have a greater requirement for pain medication than patients whose excisions were performed with a scalpel. However, good tolerance of electrosurgery has also been reported .
Successful treatment with carbon dioxide (CO2) laser excision followed by secondary intention healing was described in a series that included six patients treated with this modality . No patients experienced recurrences during follow-up periods of 3 to 47 months. Two patients developed slight hypertrophic scarring that responded well to intralesional injection of corticosteroids.
●Postsurgical interventions – Intralesional corticosteroid injections are useful for softening and flattening hypertrophic scars and can be used if such scars develop after surgery . Some authors suggest use of intralesional corticosteroid injections beginning at the time of suture removal from sutured wounds, as is often done after the excision of true keloids . However, the effect of prophylactic intralesional corticosteroid injections on patient outcomes has not been specifically evaluated for AKN. Of note, intralesional corticosteroid injections may inhibit wound contraction and should not be performed in wounds that will heal by secondary intention. (See "Keloids and hypertrophic scars", section on 'Surgical excision plus postoperative adjuvant therapy'.)
●Ultraviolet light – Ultraviolet light can induce antifibrotic effects in skin by inducing matrix metalloproteinase production as well as anti-inflammatory effects .
The findings of a small, split-scalp, randomized trial of patients with papular lesions of AKN suggest that targeted ultraviolet B (UVB) phototherapy may be a useful therapy . Patients were randomly assigned to targeted UVB treatment three times per week to the affected area on either the right or left side of the scalp for eight weeks. The UVB device emitted 290 to 320 nm light, with peaks at 303 and 313 nm. After eight weeks, both sides of the scalp were treated. After the initial eight-week period, the mean lesion count on the treated sides decreased significantly, while the counts on the untreated side did not change. Further improvement was demonstrated in sites that received an additional eight weeks of UVB treatment.
UVB therapy was well tolerated; side effects were mild, including a transient burning sensation, erythema, and hyperpigmentation. However, the need for multiple clinical visits can make phototherapy inconvenient for some patients.
●Radiotherapy – Radiotherapy led to resolution of active disease in a patient with treatment-refractory AKN . The disease did not recur during a follow-up period of 20 months.
SUMMARY AND RECOMMENDATIONS
●Disease overview – Acne keloidalis nuchae (AKN) is a chronic, inflammatory scalp condition characterized by inflamed papules, pustules, and keloid-like scarring on the posterior scalp and nape of the neck (picture 1A-G). (See "Acne keloidalis nuchae: Pathogenesis, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)
●General approach – Data on treatments for AKN are limited. Treatment goals include reducing inflammation, improving keloidal lesions, and minimizing exposure to potential exacerbating factors (algorithm 1). Early treatment is important to minimize risk for severe scarring. (See 'Treatment principles' above.)
●Treatment of inflammation – The approach to improving inflammatory lesions is dependent upon the clinical presentation (algorithm 1):
•Small, inflammatory papules or pustules (mild to moderate inflammation) – For patients with small, inflammatory papules or pustules, we suggest combination therapy with a high-potency topical corticosteroid, topical antibacterial agent, and topical retinoid, rather than monotherapy with any of these agents (Grade 2C). In our experience, combination therapy is more effective than monotherapy. Examples of options for topical antibacterial agents include topical clindamycin-benzoyl peroxide, clindamycin, erythromycin-benzoyl peroxide, and erythromycin. (See 'Mild to moderate inflammation' above and 'Topical corticosteroids' above and 'Topical antibacterial agents' above and 'Topical retinoids' above.)
•Numerous inflammatory lesions; extensive pustulation or suppuration; or larger, inflammatory lesions (moderate to severe inflammation) – For patients with moderate to severe inflammation (picture 1D-E), we suggest combination therapy with oral doxycycline, a high-potency topical corticosteroid, and a topical retinoid for treatment, rather than monotherapy with any of these agents (Grade 2C). (See 'Moderate to severe inflammation' above and 'Oral antibiotics' above.)
Intralesional injection of corticosteroids may be helpful for patients with insufficient responses to topical corticosteroids. For patients with persistent, inflammatory papules after six to eight weeks of topical corticosteroid treatment, we suggest intralesional corticosteroid injections (Grade 2C). (See 'Topical or intralesional corticosteroids' above.)
●Treatment of keloidal lesions – The approach to improving keloidal lesions is dependent upon the clinical presentation:
•Keloidal papules or small plaques – For keloidal papules (dome-shaped, firm papules (picture 1F)) or small plaques in patients who desire improvement of these lesions, we suggest intralesional corticosteroid injection as initial treatment (Grade 2C). (See 'Papules and small plaques' above.)
•Larger, keloidal plaques or keloidal lesions refractory to intralesional corticosteroid injections – For patients with larger plaques or keloidal scars that do not improve sufficiently with intralesional corticosteroid injection, we suggest surgical excision (Grade 2C). (See 'Larger plaques' above.)
●Secondary infection – Secondary infection may complicate AKN. If findings suggestive of secondary infection are present (eg, extensive erythema, suppuration, pain, drainage, odor, or systemic symptoms such as fever), cultures and antibiotic susceptibility testing should be performed, and antibiotic therapy should be prescribed as appropriate. (See 'Secondary infection' above.)
●Refractory disease – Treatment options for patients who experience continued disease activity or progression despite standard initial therapies for inflammation include surgery, laser therapy, and oral isotretinoin (algorithm 1). (See 'Refractory inflammation' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟