Infantile Dermatology Lecture 3 PDF

Lecture 3 – Infantile Dermatology Diaper Dermatitis Diaper dermatitis is extremely common in children of diaper wearing age. Diaper dermatitis encompasses several distinct diseases, which can all look similar. In general, diaper dermatitis encompasses any erythematous eruption involving the skin...

Lecture 3 – Infantile Dermatology Diaper Dermatitis Diaper dermatitis is extremely common in children of diaper wearing age. Diaper dermatitis encompasses several distinct diseases, which can all look similar. In general, diaper dermatitis encompasses any erythematous eruption involving the skin that is covered by the diaper. Each disease will be discussed separately, but it is common for a given child to have more than one disease contributing to diaper dermatitis. Irritation is the most common cause of diaper dermatitis. Chronic moisture from urine can lead to damage of the epidermis, and the alkaline stool can also be quite irritating. Stool with a high content of bilirubin (such as in an infant with jaundice) is especially irritating. Once initial irritation develops, the skin is much more susceptible to further irritation. This is called irritant contact dermatitis. In this setting, there is typically sparing of the skin in the folds, as these areas are relatively protected from the irritants (Figure 3.1). Candidiasis is also very common and commonly coexists with irritant diaper dermatitis. Candida tends to thrive in moist, warm environments, and the diaper area presents a near ideal set of conditions for Candida growth. Candida should be especially suspected when pustules on a red base, called satellite pustules, are noted at the edges of the diaper dermatitis (Figure 3.2). Seborrheic dermatitis is another common cause of diaper dermatitis. There is no particular morphologic finding in the diaper area that is strongly suggestive of seborrheic dermatitis. Seborrheic dermatitis tends to involve the skin folds, and in isolated seborrheic diaper dermatitis, there should not be satellite pustules. Infants with seborrheic diaper dermatitis will also often have seborrheic dermatitis of the scalp (cradle cap), so one should look for cradle cap in infants with diaper dermatitis as a clue to the diagnosis (Figure 3.3). Psoriasis is an uncommon cause of diaper dermatitis. Although no particular findings are diagnostic of psoriatic diaper dermatitis, a silvery scale is sometimes appreciated (Figure 3.4). Histiocytosis is a very rare cause of diaper dermatitis. The rash is usually severe, often with significant petechiae. These infants are usually quite sick and often have hepatosplenomegaly. Atopic dermatitis typically spares the diaper area. Unless histiocytosis is suspected, diaper dermatitis is rarely biopsied. In difficult to manage cases, a biopsy may help to differentiate between irritation, candidiasis, and seborrheic dermatitis, and a swab culture can evaluate for Candida. Frequent diaper changes to minimize moisture and use of disposable diapers which pull moisture away from the skin are important steps in treatment. Other initial treatments include the use of barrier pastes that contain zinc oxide (up to 40%). The paste forms a protective barrier blocking the irritants from contacting the skin. Plain Vaseline or Aquaphor can also be effective barriers. When plain barriers are not effective, anti-candida topical agents, such as nystatin cream, are often used if candidiasis is suspected. If candidiasis is not suspected or if nystatin is not effective, then a mild anti-inflammatory topical steroid, such as hydrocortisone 1% cream, is often used. Experienced physicians will often use combination creams with various mixtures of anti-candida agents and anti-inflammatory agents (a 1:1 mixture of hydrocortisone cream and nystatin cream or a 1:1:1 mixture of nystatin, hydrocortisone 1%, and 40% zinc oxide paste). Early Atopic Dermatitis The current prevalence of atopic dermatitis (AD) in toddlers and school aged children is between 15 and 20%. The prevalence has been increasing for the last 50 years. The vast majority of cases start in the first 5 years of life. There is a strong familial component, with the atopic triad tending to run in families: atopic dermatitis, asthma, and seasonal allergies. Given individuals may be affected with one, two, or all three disorders, but a family history of any of these disorders increases the chances that a given child will develop atopic dermatitis. The term eczema is commonly used interchangeably with atopic dermatitis. This should be avoided, as eczema refers to any rash that is itchy, red and flaky. While atopic dermatitis fits this description, so do many other diagnoses (dry skin, allergic or irritant contact dermatitis, etc.). In infants, AD typically involves the face and the extensor surfaces of the extremities, although anywhere may be involved. The distribution changes as children age (see Lecture 5). Acute lesions tend to be bright red, scaly, and often have weeping of serous fluid (Figure 3.5). While much is known of the pathophysiology of atopic dermatitis, the pathogenesis of the disease is not fully understood. Recent data has shown that patients with atopic dermatitis may have a mutation in a protein called filaggrin. Filaggrins are filament-associated proteins which bind to keratin fibers in epithelial cells. They are responsible for maintaining an intact epidermal barrier. These findings provide evidence that in a subset of people, the presence of a non-intact epithelium may be the fundamental predisposing factor not only for the development of eczema but also for initial sensitization and progression of allergic disease. It is known that there is significant immunologic dysregulation in the skin in patients with atopic dermatitis. In acute lesions, there is predominantly a Th-2 phenotype, while in chronic lesions the cytokine profile becomes Th-1 dominant. The predominant cells involved are lymphocytes and keratinocytes. Systemically, patients often have elevated IgE levels and blood eosinophilia. Another interesting hypothesis involves hygiene. Epidemiologically, it is clear that the higher the level of community hygiene (and thus the lower the level of exposure to infectious agents and antigens in general), the higher the prevalence of AD. It is hypothesized that the developing immune system is “primed” to react against many different agents, and when there is insufficient exposure to relevant agents, the “primed” immune system begins to direct its efforts against minor antigens endogenous to the skin or those, such as dust mite, to which the skin is exposed. Finally, many patients with atopic dermatitis have heavy Staphylococcal colonization of the skin, nose, umbilicus, etc. Many of these Staph strains produce toxins with super-antigen function, and the immune activation by these toxins may significantly exacerbate atopic dermatitis. Treatment is multifaceted. In all cases, aggressive moisturization is extremely important. In mild cases, this may be sufficient. Given our enhanced understanding of atopic dermatitis, most efforts are directed at trying to repair the non-intact skin barrier. This includes the regular, aggressive use of ceramide-based moisturizers and also occlusive moisturizers like plain petroleum jelly applied immediately after bathing. After moisturization, topical steroids are the next step in treatment. The strength of steroid used depends on the age of the patient, severity of disease, and location of disease. Steroids ideally should be used intermittently. If topical steroids must be used continuously, then patients should be transitioned to topical immunomodulators (TIMS), such as tacrolimus or pimecrolimus. These are agents that specifically inhibit activation of T-lymphocytes, as opposed to steroids which are non-specifically immunosuppressive and anti-inflammatory. In general, steroids are significantly more effective, but TIMS have fewer long-term side effects. Systemic steroids can be used in short bursts for flares of disease. Sedating antihistamines are helpful at bedtime, as the sedative effect improves sleep and decreases nocturnal scratching. Finally, bacterial infection and colonization should be aggressively monitored for and treated. Many children have atopic dermatitis that is significantly exacerbated by dietary allergens, especially egg, milk, peanut, soy and wheat. History is a very poor tool for diagnosing food sensitivity, so consideration should be given to referring children to allergists for evaluation of dietary allergy if their disease is severe and/or resistant to treatment. Infantile Acne Neonatal acne occurs in up to 50% of infants during the first months of life, sometimes persisting up to a year of age. Neonatal acne typically presents as inflammatory papules on the face that develop into pustules (Figure 3.6). Other typical areas of acne involvement (chest and back) may also be involved. It is differentiated from sebaceous hyperplasia and milia as these conditions lack inflammation. Erythema toxicum typically has a much larger area of redness surrounding the pustule/papule. Infantile acne is thought to be related to two factors: 1. The androgenic hormonal milieu of the pre-partum mother extending to the neonate, simulating hormonal conditions found at puberty, and thus stimulating sebaceous activity. 2. Pityrosporum overgrowth and hypersensitivity. Pityrosporum are a group of yeast that normally inhabitant the skin. They thrive on sebum. Overgrowth of this yeast, and a subsequent inflammatory response, may be a factor in the etiology of infantile acne. Spontaneous resolution will occur. If treatment is desired, the anti-yeast agent ketoconazole cream can be tried. Benzoyl peroxide has also been reported effective. Whether children with infantile acne are at risk for severe acne as adolescents is unknown. Cradle Cap (Seborrheic Dermatitis of the scalp) Cradle cap is very common in infants and neonates. Cradle cap typically presents as erythema and thick, yellowish, greasy scales of the scalp (Figure 3.7). It may involve the diaper area (as noted above) or extend from the scalp onto the forehead. It may rarely involve the retro-auricular folds, neck, axilla, or chest. If a case is particularly severe or recalcitrant to therapy, or if petechiae are present, histiocytosis should be considered. Cradle cap is also thought to be related to overgrowth of Pityrosporum, and a subsequent inflammatory response to the yeast. Treatment can be directed at removing the Pityrosporum with good hygiene (shampooing with regular baby shampoo at least every other day) or with anti-yeast agents (ketoconazole cream). If these steps are not sufficient, then mild anti-inflammatory topical steroids can be used for up to one week at a time (hydrocortisone cream 1% or 2.5%).