Last reviewed: November 2017
Last updated: November  2017

Introduction

Condition
Description

Dry, pruritic skin, typically with erythema, scaling, or vesicles; lichenification in skin flexures when there is chronic inflammation. [1] com.bmj.content.model.overview.Caption@70f60d0c [Figure caption and citation for the preceding image starts]: Acute atopic dermatitis on the face of an infant Personal collection of Dr A. Hebert [Citation ends]. In infants the extensor surfaces, cheeks, and forehead are preferentially affected. [2] Patients often have a history of other atopic diseases such as asthma or allergic rhinitis. [2] [3]

Atopic dermatitis is a chronic, relapsing disease, and educating patients and their families is necessary so that they develop an understanding of basic skin care and how to avoid trigger factors. [4] [5] [6] First-line treatment is with emollients and topical corticosteroids. Other options that may be used in patients unresponsive to first-line therapy include topical calcineurin inhibitors, phototherapy, or immunosuppressive agents. [ Cochrane Clinical Answers logo ]

Irritant contact dermatitis (ICD) is caused by direct toxicity and can occur in any person without prior sensitization. Allergic contact dermatitis (ACD) is a delayed hypersensitivity reaction, which requires prior sensitization.

Both result in localized burning, stinging, itching, blistering, erythema, and swelling after contact with an allergen or irritant. com.bmj.content.model.overview.Caption@cdbe847 [Figure caption and citation for the preceding image starts]: Allergic contact dermatitis to nickel in watchband Personal collection of Dr Snehal Desai [Citation ends]. Eruption is often clearly delineated with sharp borders. Hyperpigmentation, fissuring, and scaling may also occur. [7]

After an allergen or irritant is identified, the main goals of treatment are avoidance of future exposure and resolution of existing dermatitis. ICD is treated with exposure reduction and moisturizers. [8] ACD is treated with exposure elimination, and topical corticosteroids or topical calcineurin inhibitors. Severe ACD may require treatment with oral corticosteroids.

Poison ivy, oak, and sumac dermatitis is the prototypical allergic contact dermatitis of the northern US. It is caused by skin contact with soluble oleoresins (urushiols) from the poison ivy, oak, and sumac plants ( Toxicodendron species), resulting in severe acute dermatitis. [9] [10] [11] [12] Contact can result in a severe, itchy dermatitis, which often persists for 10 to 15 days.

The main goal of treatment is to prevent exposure to poison ivy, oak, and sumac plants by patient education and by wearing protective clothing. [13] [14] [10]

Immediate washing of the skin after inadvertent contact may prevent development of the allergic response. First-line treatment is corticosteroids: topically for mild to moderate cases, and orally for severe reactions.

Recurrent crops of 1- to 2-mm vesicles, with pruritus on the palms, soles, and lateral aspects of the fingers. com.bmj.content.model.overview.Caption@23e63fb7 [Figure caption and citation for the preceding image starts]: Dyshidrotic eczema Photograph courtesy of Dr Spencer Holmes, MD [Citation ends]. Pompholyx is more acute, severe eruptions of large bullae on the hands and feet. [15] The common exacerbating factor is irritation, as seen in frequent hand washing, hyperhidrosis, and stress. However, the underlying etiology is unknown.

The foremost objective in treatment is identification and avoidance of exacerbating factors. All patients should be instructed on strategies to maintain effective skin barrier mechanisms, such as frequent use of emollients and avoidance of irritants. [16] In patients unresponsive to lifestyle measures, topical corticosteroids [17] [18] or immunomodulators are used. [19] [20] For severe cases of eruptive bullae on the palms and soles (pompholyx), oral corticosteroids are helpful. Recalcitrant cases of dyshidrotic conditions are treated with a wide variety of therapeutic options, including phototherapy, oral immunosuppressants, or nickel-directed therapy.

Erythematous and greasy scaly patches on the scalp, glabella, nasolabial fold, posterior auricular skin, and anterior chest. [21] com.bmj.content.model.overview.Caption@af7241a [Figure caption and citation for the preceding image starts]: Seborrheic dermatitis, glabella, with scaling and mild erythema Personal collection of Dr Robert A. Schwartz [Citation ends]. It is a chronic condition that includes dandruff (pityriasis capitis) in adults and cradle cap in infants. It can present as a central facial rash, similar to that associated with systemic lupus erythematosus (SLE).

Variable course that seldom completely subsides. An infant form (cradle cap) usually resolves within the first few months of life. Symptom control is the mainstay of treatment. Topical agents such as corticosteroids, coal tar, calcineurin inhibitors, and antifungals are used for treatment. [22] [23] [24] Shampoos and scalp preparations are appropriate treatments when seborrheic dermatitis is confined to the scalp. [25] Cradle cap in infants can usually be managed using emollients such as topical olive oil. Systemic antifungals should be reserved for severe cases and avoided in infants and children.

Primarily an irritant contact dermatitis, diaper rash is inflammation of the skin in the area of the body covered by a diaper. It is most common in the first 1 to 2 years of life, but can occur in any person who routinely wears diapers. Recalcitrant diaper rash may signal secondary infection or underlying systemic or dermatologic disorders, and requires further evaluation.

Initial treatment involves re-enforcing good diapering practices, such as frequent diaper changes, use of superabsorbent disposable diapers, cleansing the diaper area of potential irritants by using commercial cleansing wipes or using water on cotton cloth, periods of diaper-free time, and application of barrier cream, ointment, or paste. [26]

Circumscribed lichenified erythematous, often hyperpigmented, cutaneous plaques occurring most commonly on the scalp, neck, forearms, ankles, and genitalia as a result of chronic scratching and rubbing. com.bmj.content.model.overview.Caption@4aa9c625 [Figure caption and citation for the preceding image starts]: Secondary lichen simplex chronicus in the setting of atopic dermatitis Personal collection of Dr Swick [Citation ends]. One or multiple LSC patches or plaques can arise on skin affected by an underlying dermatosis such as atopic dermatitis, allergic contact dermatitis, stasis dermatitis, superficial fungal (tinea and candidiasis) and dermatophyte infections, lichen sclerosis, viral warts, scabies, lice, arthropod bite, or cutaneous neoplasia. [27] [28]

LSC can be a difficult condition to treat, causing frustration in both the patient and physician. [27]

The main goals of treatment are to remove any triggering and exacerbating environmental factors, repair the barrier function of the skin, identify and treat any underlying dermatologic or systemic condition that could be driving the condition in secondary LSC, and disrupt the itch-scratch cycle characteristic of LSC through reduction in the degree of skin inflammation and control of nocturnal pruritus. [28] Treatment of LSC should be individualized and may include topical corticosteroid, emollients, and lifestyle modification. Nocturnal pruritus may be treated with an older-generation sedating antihistamine.

Sunburn is an acute inflammatory reaction of the skin induced by overexposure to UV radiation. Skin findings include erythema and edema, with or without vesiculation, followed by desquamation. Symptoms include pain and/or pruritus. Acute sunburn is a self-limited condition and typically requires only supportive care. No current treatments can reverse UV-induced skin damage. [29] [30] Primary prevention via sun avoidance, physical protection, and the appropriate use of sunscreen is key to managing the condition, as cellular damage caused by UV radiation is irreversible and may, with time, accelerate photoaging and increase the risk of skin cancer.

The most common symptom in dermatology is itching, which may occur with or without visible skin lesions. A thorough history and complete physical examination are central to the evaluation of pruritus. During medical examination it is important to identify a possible cause/disease responsible for itching as well as determining the intensity and timeframe of the pruritus.

The etiology can often be a dermatitis but may also include infections and urticaria. Of the inflammatory dermatoses, atopic dermatitis is the most common diagnosis for patients seen in pediatric dermatologists' clinics. [31] Seborrheic dermatitis occurs in 2 age groups: infants (beginning before age 2 months) and adolescents. In adolescents, sebaceous secretions are altered by the normal skin flora, which induces dermatitis in the affected areas. [32] The most common agents causing allergic contact dermatitis in children are species of Toxicodendron (poison ivy, poison oak, or poison sumac) and the metal nickel. [33] [34]

The dermatologic manifestations of HIV are protean and often multiple in patients with HIV infection.

Some skin diseases are fairly specific to HIV. HIV-specific dermatoses include HIV-related lipodystrophy, eosinophilic folliculitis, oral hairy leukoplakia, papular pruritic eruption of HIV, and HIV photodermatitis.

Other skin diseases may appear in non-HIV-infected populations but have altered presentation with HIV, presenting more commonly or in a more severe form in HIV-infected people. Seborrheic dermatitis is occurring with strikingly increased prevalence. [35] [36] Prevalence increases with increased immunosuppression. Atopic dermatitis has a high prevalence in adult as well as pediatric patient populations with HIV. [37]

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This overview has been compiled using the information in existing sub-topics.

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