Skin disorders

Published on 21/03/2015 by admin

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Last modified 22/04/2025

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Skin disorders

Features of skin disorders in children include:

The newborn

The skin at birth is covered with vernix caseosa. This chalky-white greasy coat, mainly composed of water, proteins and lipids, protects the skin in utero from the amniotic fluid. Shedding of vernix towards the end of gestation coincides with maturation of the transepidermal barrier. In the preterm infant, the skin is thin, poorly keratinised and lacks subcutaneous fat. Transepidermal water loss is markedly increased when compared with a term infant. The preterm infant is also unable to sweat until a few weeks old, whereas the term infant can sweat from birth.

Common naevi and rashes in the newborn period are described under the examination of the newborn infant (see Ch. 9). Some less common skin conditions presenting in the newborn period are described in this chapter.

Bullous impetigo

This is an uncommon but potentially serious blistering form of impetigo, the most superficial form of bacterial infection, seen particularly in the newborn (Fig. 24.1). It is most often caused by Staphylococcus aureus. Treatment is with systemic antibiotics, e.g. penicillinase-resistant penicillin (see also Ch. 14).

Melanocytic naevi (moles)

Congenital moles occur in up to 3% of neonates and any that are present are usually small. Congenital pigmented naevi involving extensive areas of skin (i.e. naevi >9 cm in diameter) are rare but disfiguring (Fig. 24.2) and carry a 4–6% lifetime risk of subsequent malignant melanoma. They require prompt referral to a paediatric dermatologist and plastic surgeon to assess the feasibility of removal.

Melanocytic naevi become increasingly common as children get older and the presence of large numbers in an adult may be indicative of childhood sun exposure. Prolonged exposure to sunlight should be avoided and sunscreen preparations with a sun protection factor exceeding 20 should be applied liberally to exposed skin in bright weather and reapplied every few hours.

Malignant melanoma is rare before puberty, except in giant naevi. However, in adults, the incidence of malignant melanoma has increased dramatically over the past 30 years. Risk factors for melanoma include a positive family history, having a large number of melanocytic naevi, fair skin, repeated episodes of sunburn and living in a hot climate with chronic skin exposure to the sun.

Albinism

This is due to a defect in biosynthesis and distribution of melanin. The albinism may be oculocutaneous, ocular or partial, depending on the distribution of depigmentation in the skin and eye (Fig. 24.3). The lack of pigment in the iris, retina, eyelids and eyebrows results in failure to develop a fixation reflex. There is pendular nystagmus and photophobia, which causes constant frowning. Correction of refractive errors and tinted lenses may be helpful. In a few children, the fitting of tinted contact lenses from early infancy allows the development of normal fixation. The disorder is an important cause of severe visual impairment. The pale skin is prone to sunburn and skin cancer. In sunlight, a hat should be worn and high factor barrier cream applied to the skin.

Epidermolysis bullosa

This is a rare group of genetic conditions with many types, characterised by blistering of the skin and mucous membranes. Autosomal dominant variants tend to be milder; autosomal recessive variants may be severe and even fatal. Blisters occur spontaneously or follow minor trauma (Fig. 24.4). They need to be differentiated from scalds. Management is directed to avoiding injury from even minor skin trauma and treating secondary infection. In the severe forms, the fingers and toes may become fused, and contractures of the limbs develop from repeated blistering and healing. Mucous membrane involvement may result in oral ulceration and stenosis from oesophageal erosions. Management, including maintenance of adequate nutrition, should be by a multidisciplinary team including a paediatric dermatologist, paediatrician, plastic surgeon and dietician.

Collodion baby

This is a rare manifestation of the inherited ichthyoses, a group of conditions in which the skin is dry and scaly. Infants are born with a taut parchment-like or collodion-like membrane (Fig. 24.5). Emollients are usually applied to moisturise and soften the skin. The membrane becomes fissured and separates within a few weeks, usually leaving either ichthyotic or less commonly, normal skin.

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Figure 24.5 Collodion baby.

Rashes of infancy

Napkin rashes

Napkin rashes are common, although irritant reactions are much less of a problem with the widespread use of disposable nappies, as they are more absorbent. Some causes are listed in Box 24.1. Irritant dermatitis, the most common napkin rash, may occur if nappies are not changed frequently enough or if the infant has diarrhoea. However, irritant dermatitis can occur even when the napkin area is cleaned regularly. The rash is due to the irritant effect of urine on the skin of susceptible infants. Urea-splitting organisms in faeces increase the alkalinity and likelihood of a rash.

The irritant eruption affects the convex surfaces of the buttocks, perineal region, lower abdomen and top of thighs. Characteristically, the flexures are spared, which differentiates it from other causes of napkin rash. The rash is erythematous and may have a scalded appearance. More severe forms are associated with erosions and ulcer formation. Mild cases respond to the use of a protective emollient, whereas more severe cases may require mild topical corticosteroids. While leaving the child without a napkin will accelerate resolution, it is rarely practical at home.

Candida infection may cause and often complicates napkin rashes. The rash is erythematous, includes the skin flexures and there may be satellite lesions (Fig. 24.6). Treatment is with a topical antifungal agent.

Infantile seborrhoeic dermatitis

This eruption of unknown cause presents in the first 2 months of life. It starts on the scalp as an erythematous scaly eruption. The scales form a thick yellow adherent layer, commonly called cradle cap (Fig. 24.7a). The scaly rash may spread to the face, behind the ears and then extend to the flexures and napkin area (Fig. 24.7b). In contrast to atopic eczema, it is not itchy and the child is unperturbed by it. However, it is associated with an increased risk of subsequently developing atopic eczema. Mild cases will resolve with emollients. The scales on the scalp can be cleared with an ointment containing low-concentration sulphur and salicylic acid applied to the scalp daily for a few hours and then washed off. Widespread body eruption will clear with a mild topical corticosteroid, either alone or mixed with an antibacterial and antifungal agent if appropriate.

Atopic eczema (atopic dermatitis)

The prevalence of atopic eczema in children in the UK is about 20%. A genetic deficiency of skin barrier function is important in the pathogenesis of atopic eczema. Onset of atopic eczema is usually in the first year of life. It is, however, uncommon in the first 2 months, unlike infantile seborrhoeic dermatitis, which is relatively common at this age. There is often a family history of atopic disorders: eczema, asthma, allergic rhinitis (hay fever). Around one-third of children with atopic eczema will develop asthma. Exclusive breast-feeding may delay the onset of eczema in predisposed children but does not appear to have a significant impact on the prevalence of eczema during later childhood. Atopic eczema is mainly a disease of childhood, being most severe and troublesome in the first year of life and resolving in 50% by 12 years of age, and in 75% by 16 years.

Clinical features

Rashes may itch in many conditions (Box 24.2), but in atopic eczema, itching (pruritus) is the main symptom at all ages and this results in scratching and exacerbation of the rash (Fig. 24.8). The excoriated areas become erythematous, weeping and crusted. Distribution of the eruption tends to change with age, as indicated in Figure 24.9.

Atopic skin is usually dry, and prolonged scratching and rubbing of the skin may lead to lichenification, in which there is accentuation of the normal skin markings (Fig. 24.10).

Complications

Causes of exacerbations of eczema are listed in Box 24.3. However, flare-ups are common, often for no obvious reason. Eczematous skin can readily become infected, usually with Staphylococcus or Streptococcus (Fig. 24.11). Inflammation increases the avidity of skin for Staph. aureus and reduces the expression of antimicrobial peptides, which are needed to control microbial infections. Staph. aureus thrives on atopic skin and releases superantigens which seem to maintain and worsen eczema. Herpes simplex virus infection, although less frequent, is potentially very serious as it can spread rapidly on atopic skin, causing an extensive vesicular reaction, eczema herpeticum (see Ch. 14). Regional lymphadenopathy is common and often marked in active eczema; it usually resolves when the skin improves.

Management

A number of treatment modalities are available.

Topical corticosteroids

These are an effective treatment for eczema, but must be used with care. Mildly potent corticosteroids, such as 1% hydrocortisone ointment, can be applied to the eczematous areas twice daily. Moderately potent topical steroids play a pivotal role in the management of acute exacerbations, but their use must be kept to a minimum. They should be applied thinly and their use on the face should be generally avoided. Excessive use of topical steroids may cause thinning of the skin as well as systemic side-effects. However, fear of these side-effects should not deter their use in controlling exacerbations.

Dietary elimination

Food allergy may be present if the child reacted with immediate symptoms to a food, or in infants and young children with moderate or severe atopic eczema, particularly if associated with gut dysmotility (colic, vomiting, altered bowel habit) or failure to thrive. It may even occur in young infants with severe eczema who are exclusively breast-fed at the time. The most common food allergies are to egg, cow’s milk and peanut. However, any food may be implicated in an eczema flare-up. Dietary elimination for 4–6 weeks is required to detect a response. A trial of an extensively hydrolysed protein formula or amino acid formula in place of cow’s milk formula is also recommended for bottle-fed infants under 6 months old with severe atopic eczema that has not been controlled by optimal treatment with emollients and mild topical corticosteroids. Dietary elimination should be carried out with the advice of a dietician to ensure complete avoidance of specific food constituents and that the diet remains nutritionally adequate. A food challenge is required to be fully objective. Children can usually tolerate the offending foods by the age of 3–4 years with the important exception of peanut allergy, which usually persists.

Infections and infestations

Bullous impetigo has been considered earlier in this chapter and acute bacterial and viral infections of the skin are considered in Chapter 14.

Viral infections

Viral warts

These are caused by the human papillomavirus, of which there are well over 100 types. Warts are common in children, usually on the fingers and soles (verrucae). Most disappear spontaneously over a few months or years and treatment is only indicated if the lesions are painful or are a cosmetic problem. They can be difficult to treat, but daily application of a proprietary salicylic acid and lactic acid paint or glutaraldehyde (10%) lotion can be used. Cryotherapy with liquid nitrogen is effective treatment but can be painful and often needs repeated application, and its use should be reserved for older children.

Molluscum contagiosum

This is caused by a poxvirus. The lesions are small, skin-coloured, pearly papules with central umbilication (Fig. 24.12). They may be single but are usually multiple. Lesions are often widespread but tend to disappear spontaneously within a year. If necessary, a topical antibacterial can be applied to prevent or treat secondary bacterial infection, and cryotherapy (2–3 s only) can be used in older children, away from the face, to hasten the disappearance of more chronic lesions.

Fungal infections

Ringworm

Dermatophyte fungi invade dead keratinous structures, such as the horny layer of skin, nails and hair. The term ‘ringworm’ is used because of the often ringed (annular) appearance of skin lesions. A severe inflammatory pustular ringworm patch is called a kerion (Fig. 24.13).

Tinea capitis (scalp ringworm), sometimes acquired from dogs and cats, causes scaling and patchy alopecia with broken hairs. Examination under filtered ultraviolet (Wood’s) light may show bright greenish/yellow fluorescence of the infected hairs with some fungal species.

Rapid diagnosis can be made by microscopic examination of skin scrapings for fungal hyphae. Definitive identification of the fungus is by culture. Treatment of mild infections is with topical antifungal preparations, but more severe infections require systemic antifungal treatment for several weeks. Any animal source of infection also needs to be treated.

Parasitic infestations

Scabies

Scabies is caused by an infestation with the eight-legged mite Sarcoptes scabiei, which burrows down the epidermis along the stratum corneum. Severe itching occurs 2–6 weeks after infestation and is worse in warm conditions and at night.

In older children, burrows, papules and vesicles involve the skin between the fingers and toes, axillae, flexor aspects of the wrists, belt line and around the nipples, penis and buttocks. In infants and young children, the distribution often includes the palms (Fig. 24.14), soles and trunk. The presence of lesions on the soles can be helpful in making the diagnosis. The head, neck and face can be involved in babies but is uncommon.

Diagnosis is made on clinical grounds with the history of itching and characteristic lesions. Although burrows are considered pathognomonic, they may be hard to identify because of secondary infection due to scratching. Itching in other family members is a helpful clinical indicator. Confirmation can be made by microscopic examination of skin scrapings from the lesions to identify mite, eggs and mite faeces.

Pediculosis

Pediculosis capitis (head lice infestation) is the most common form of lice infestation in children. It is widespread and troublesome among primary school children. Presentation may be itching of the scalp and nape or from identifying live lice on the scalp or nits (empty egg cases) on hairs (Fig. 24.15). Louse eggs are cemented to hair close to the scalp and the nits (small whitish oval capsules) remain attached to the hair shaft as the hair grows. There may be secondary bacterial infection, often over the nape of the neck, leading to a misdiagnosis of impetigo. Sub-occipital lymphadenopathy is common. Once infestation is confirmed by finding live lice, treatment is by applying a solution of 0.5% malathion to the hair and leaving it on overnight. The hair is then shampooed and the lice and nits removed with a fine-tooth comb. Treatment should be repeated a week later. Permethrin (1%) as a cream rinse would be an alternative application; it is left on for 10 min only. Flammability of alcohol-based lotions should be noted. Wet combing to remove live lice (bug-busting) every 3–4 days for at least 2 weeks is a useful and safe physical treatment, particularly when parents treat with enthusiasm.

Other childhood skin disorders

Psoriasis

This familial disorder rarely presents before the age of 2 years. The guttate type (Fig. 24.16) is common in children and often follows a streptococcal or viral sore throat or ear infection. Lesions are small, raindrop-like, round or oval erythematous scaly patches on the trunk and upper limbs, and an attack usually resolves over 3–4 months. However, most get a recurrence of psoriasis within the next 3–5 years. Chronic psoriasis with plaques or annular lesions is less common. Fine pitting of the nails may be seen in chronic disease but is unusual in children. Treatment for guttate psoriasis is with bland ointments. Coal tar preparations are useful for plaque psoriasis and scalp involvement. Dithranol preparations are very effective in resistant plaque psoriasis. Calcipotriol, a vitamin D analogue, which does not stain the skin, can also be useful for plaque psoriasis in those over 6 years old. Occasionally, children with chronic psoriasis develop psoriatic arthritis. Chronic psoriasis may have a considerable effect on quality of life. The Psoriasis Association can be helpful in offering support and advice.

Alopecia areata

This is a common form of hair loss in children and, understandably, a cause of much family distress. Hairless, single or multiple non-inflamed smooth areas of skin, usually over the scalp, are present (Fig. 24.17); remnants of broken-off hairs, visible as ‘exclamation mark’ hairs may be seen at the edge of active patches of hair fall. The more extensive the hair loss, the poorer the prognosis, but regrowth often occurs within 6–12 months in localised hair loss. Prognosis should be more guarded in children with atopic disorders.

Granuloma annulare

Lesions are typically ringed (annular) with a raised flesh-coloured non-scaling edge (unlike ringworm) (Fig. 24.18). They may occur anywhere but usually over bony prominences, especially over hands and feet. Lesions may be single or multiple, are usually 1–3 cm in diameter, and tend to disappear spontaneously but may take years to do so. There is also a subcutaneous form.

Acne vulgaris

Acne may begin 1–2 years before the onset of puberty following androgenic stimulation of the sebaceous glands and an increased sebum excretion rate. Obstruction to the flow of sebum in the sebaceous follicle initiates the process of acne. There are a variety of lesions, initially open comedones (blackheads) or closed comedones (whiteheads) progressing to papules, pustules, nodules and cysts. Lesions occur mainly on the face, back, chest and shoulders. The more severe cystic and nodular lesions often produce scarring. Menstruation and emotional stress may be associated with exacerbations. The condition usually resolves in the late teens, although it may persist.

Topical treatment is directed at encouraging the skin to peel using a keratolytic agent, such as benzoyl peroxide, applied once or twice daily after washing. Sunshine, in moderation, topical antibiotics or topical retinoids may be helpful. For more severe acne, oral antibiotic therapy with tetracyclines (only when over 12 years old, because they may discolour the teeth in younger children) or erythromycin is indicated. The oral retinoid isotretinoin is reserved for severe acne in teenagers unresponsive to other treatments.

Rashes and systemic disease

Skin rashes may be a sign of systemic disease. Examples are:

• Facial rash in systemic lupus erythematosus (SLE) or dermatomyositis

• Purpura over the buttocks, lower limbs and elbows in Henoch–Schönlein purpura

• Erythema nodosum (Fig. 24.19, Box 24.4) and erythema multiforme (Fig. 24.20, Box 24.5); both can be associated with a systemic disorder, but often no cause is identified

• Stevens–Johnson syndrome, a severe bullous form of erythema multiforme also involving the mucous membranes (Fig. 24.21). The eye involvement may include conjunctivitis, corneal ulceration and uveitis, and ophthalmological assessment is required. It may be caused by drug sensitivity or infection, with morbidity and sometimes even mortality from infection, toxaemia or renal damage

• Urticaria.

Urticaria

Urticaria (hives), characterised by flesh-coloured weals, is described in Chapter 15 and the management of anaphylaxis in Chapter 6.

Papular urticaria is a delayed hypersensitivity reaction most commonly seen on the legs, following a bite from a flea, bedbug, or animal or bird mite. Irritation, vesicles, papules and weals appear and secondary infection due to scratching is common. It may last for weeks or months and may be recurrent.

Hereditary angioedema is a rare autosomal dominant disorder caused by a deficiency or dysfunction of C1-esterase inhibitor. There is no urticaria, but subcutaneous swellings occur, often accompanied by abdominal pain. The trigger is usually trauma. Angioedema may cause respiratory obstruction. Specific treatment of a severe acute attack is with a purified preparation of the inhibitor, but replacement therapy with fresh frozen plasma can be used as a short-term measure.

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