Chapter 121: Common skin problems

Skin disorders are common. They account for 10.8% of all problems¹ encountered in general practice, the most common being dermatitis/eczema, malignant skin neoplasms, solar keratoses, lacerations, warts and acne.

This chapter focuses on the common dermatoses.

Dermatitis is a nonspecific inflammatory response of the skin, presenting as an erythematous rash, that is usually itchy, and sometimes scaly.² The terms dermatitis and eczema are often used interchangeably, with eczema referring to the process that causes dermatitis.

Dermatitis can be divided into exogenous causes (allergic contact, primary irritant contact, photo-allergic and phototoxic) and endogenous, which implies all forms of dermatitis not directly related to external causative factors. Endogenous types are atopic, nummular (discoid), vesicular hand/foot (pompholyx), pityriasis alba, lichen simplex chronicus and seborrhoeic.

Dermatitis can occur as the result of dry skin, which impairs the barrier function of the skin, making it more susceptible to irritation by soap and other contact irritants, the weather, temperature and non-specific triggers.

The meaning of atopy

The term ‘atopic’ refers to a hereditary background or tendency to develop one or more of a group of conditions, such as allergic rhinitis, asthma, eczema, skin sensitivities and urticaria. It is not synonymous with allergy.

An estimated 10% of the population are atopics, with allergic rhinitis being the most common manifestation.³

Atopic dermatitis

Features of classic atopic dermatitis:^2,4

• itch

• usually a family history of atopy

• about 3% of infants are affected, signs appearing between 3 months and 2 years

• often known trigger factors (see TABLE 121.1) are evident

• consider environmental allergens (e.g. dust mite, grasses, pollen, animal dander) especially if concurrent allergic rhinitis and prominent facial or periorbital involvement (usually older than 2 years)

• food allergies are rarely the main cause of the condition

• lichenification may occur with chronic atopic dermatitis

• flexures are usually involved (see FIG. 121.1)

• dryness is usually a feature

Distribution

The typical distribution of atopic dermatitis changes as the patient grows older. In infants the rash appears typically on the cheeks of the face, the folds of the neck and scalp and extensor surfaces of the limbs. It may then spread to the flexures of limbs and groins (see FIG. 91.10 in CHAPTER 91). The change from infancy through to adulthood is presented in FIGURE 121.2.

During childhood a drier and thicker rash tends to develop in the cubital and popliteal fossae and on the hands and feet, which may be dry, itchy, fissured and painful. The face often clears. Refer to CHAPTER 91.

Prognosis

It is generally correct that children tend to ‘grow out of’ the problem as the function of their oil and sweat glands matures. Most children go into remission or substantially improve by the time they enter primary school. A minority still have atopic dermatitis in their teenage years and then into adulthood.²

Management

Explanation, reassurance and support are very important. It is common for patients and parents to look for a ‘cure’ (particularly food allergies) and to have misplaced fear of the safety of topical corticosteroids. Emphasise that it is a chronic, relapsing condition, address allergy concerns and provide education and reassurance of the safety of topical corticosteroids.⁵ Counselling is indicated where family stress and psychological factors are contributing to the problem.

• Avoid soap and perfumed products.

• Older children should have short, tepid showers.

• Avoid rubbing and scratching—keep fingernails short, consider mittens or splints at night if severe.

• Avoid overheating, particularly at night.

• Avoid sudden changes of temperature, especially those that cause sweating.

• Wear light, soft, loose clothes, preferably made of cotton. Cotton clothing should be worn next to the skin.

• Avoid wool next to the skin.

• Avoid dusty conditions and sand, especially sandpits.

• Consider dust mite strategies:

  • – dust mite covers (premium grade) for bedding

  • – wash linen in hot water >55°C

  • – consider replacing fabric on chairs and changing carpet.

• Frequent use of emollients is essential to improve skin barrier function and prevent flares.

• Use a bland bath oil in the bath and a soap substitute (e.g. aqueous cream, soap-free bars, soap-free wash).

• If itch is severe, make an oatmeal bath (put half a cup of oats in a sock or stocking and add this to the bathwater).

• Apply an emollient soon after bathing.

• Apply emollients at least twice/day (choose from):

  • – aqueous cream

  • – sorbolene, alone or with 10% glycerine (can sting)

  • – emulsifying ointment

  • – paraffin creams—good in infants

  • – moisturising lotions in summer

Medication²

Topical corticosteroids are the mainstay of therapy. The current approach is to apply them liberally until the inflamed skin is perfectly clear. Most dermatitis should clear within 7–14 days with use of the appropriate strength steroid but may require longer in severe cases. Emollients are the key to preventing flares, although periodic flares are common. When the condition flares, resume the topical corticosteroid promptly until the skin clears again.

Topical corticosteroids are available in ointments, creams and lotions. Ointments are usually the preferred option as they are more effective for dry skin and sting less. The appropriate strength corticosteroid depends on the site and the severity of the rash, see CHAPTER 119.

A general rule for recommended strength of topical corticosteroid for site:

• Face, axillae and groin—mild

• Trunk and limbs—moderately potent, potent if severe

• Hands and feet—potent

For face, axillae and groin:

• 1% hydrocortisone ointment, daily until skin is clear

• if inadequate response, methylprednisolone aceponate 0.1% ointment or fatty ointment, daily for 7–14 days

For trunk and limbs:

• triamcinolone acetonide 0.02% ointment, daily until skin is clear

• if more severe or in the flexures, use:

  • methylprednisolone aceponate 0.1% ointment or fatty ointment, daily

  • or

  • mometasone furoate 0.1% ointment, daily

For hands, feet, lichenified wrists and ankles:

• betamethasone dipropionate 0.05% ointment, daily until skin is clear

• or

• betamethasone valerate 0.1% ointment, daily

• or

• mometasone furoate 0.1% ointment, daily

A non-steroidal alternative is pimecrolimus 1% (Elidel) cream once to twice daily as a maintenance preparation for sensitive areas e.g. face, eyelids, axillae, groin.

Oral antihistamines generally have no role in the treatment of atopic dermatitis, however, a sedating antihistamine at night is appropriate if itch prevents sleep.

Atopic skin is particularly susceptible to secondary bacterial and viral infection. Skin and nasal staphylococcal carriage is also more common and may require eradication measures. Secondary infection often reduces the effectiveness of topical treatments and is a common cause of treatment failure.

Consider taking skin or nasal swabs if:

• crusting or pustules present

• dermatitis fails to respond to appropriate topical therapy.

Mupirocin 2% ointment is appropriate for localised bacterial infection, while a short course (5–10 days) of oral antibiotics is appropriate for widespread infection. For recurrent infection, consider bleach baths (sodium hypochlorite 6% solution 60 mL per bath, twice weekly).

Eczema with secondary HSV infection (eczema herpeticum) requires prompt antiviral therapy and specialist referral.

• Expert advice usually required

• Consider occlusive dressings

• Consider wet dressings

• Consider hospitalisation

• UV band therapy as back-up

• Systemic immunosuppressants may be used for recalcitrant cases

• Oral corticosteroids are generally not recommended unless advised by a specialist

Nummular (discoid) eczema

• Chronic, red, coin-shaped plaques

• Crusted, scaling and intensely itchy

• Secondary infection common due to excoriation

• Mainly on the legs, also buttocks and trunk

• Often symmetrical (no central clearing)

• Common in middle-aged patients

• May be related to stress

• Tends to persist for months, seek expert advice

Treatment as for moderate to severe atopic dermatitis, using a potent topical corticosteroid.

Pityriasis alba

• These are white, scaly, poorly demarcated patches on the face of children and adolescents

• Very common mild condition

• More common around the mouth and on cheeks

• Can occur on the neck and upper limbs, occasionally on trunk

• It is a subacute form of atopic dermatitis

• Full repigmentation occurs eventually

Treatment

• Reassurance

• Avoid skin irritants

• Simple emollients

• May prescribe hydrocortisone 1% ointment bd for 5–7 days (rarely necessary)

Lichen simplex chronicus

• Circumscribed thick plaques of lichenification

• Caused by repeated rubbing and scratching of previously normal skin

• Due to chronic itch of unknown cause

• At sites within reach of fingers (e.g. neck, forearms, thighs, vulva, heels, fingers)

• May arise from habit

Treatment

• Explanation

• Refrain from scratching

• Potent topical corticosteroid ointment (with or without occlusion) to break the itch–scratch cycle

Dyshidrotic dermatitis (pompholyx)

• Typically in patients aged 20–40 years

• Itching vesicles usually on fingers (see FIG. 121.3)

• May be larger vesicles on palms and soles

• Commonly affects sides of digits and palms

• Initial phase may be exudative as vesicles burst

• Lasts a few weeks

• Tends to recur

• Associated with atopic dermatitis, although cause is unclear

• Can be precipitated by tinea of the feet

• Possibly related to stress

• Often triggered by high humidity

Treatment

• Salt water soaks if exudative (1/2 teaspoon in 1 cup of water)

• Consider infection if exudative and treat

• Potent corticosteroids as for atopic dermatitis

• Use a cream for exudative phase, then ointment as skin dries

• Consider occlusion (e.g. damp cotton gloves)

• Oral corticosteroids (3 weeks) may be necessary

Asteatotic dermatitis

This is the common, very itchy dermatitis that occurs in the elderly, especially in the winter, with a dry ‘crazy paving’ pattern, especially on the legs (see CHAPTER 120).

‘Asteatotic’ means without moisture.

Cracked (fissured) hands/fingers

This common cause of disability is usually due to dermatitis of the hands, irritant contact dermatitis or very dry skin. It is usually part of the atopic dermatitis problem and it is important to consider allergic contact dermatitis.

Management (hand dermatitis)

Hand protection:

• avoid domestic or occupational duties that involve contact with irritants and detergents

• wear protective work gloves; cotton-lined PVC gloves

• avoid perfumed toilet soaps—use a substitute (e.g. Cetaphil lotion)

• apply emollients frequently (e.g. emulsifying ointment, glycerine-rich creams), especially after finishing work duties

• potent topical corticosteroid as for atopic dermatitis

• oral corticosteroids may be required for severe flare

• expert referral for severe cases for patch testing

Cracked heels

Cracked painful heels are a common problem, especially in adult women. It is a manifestation of very dry skin.

Treatment

• Soak the feet for 15 minutes in warm water containing an oil such as Alpha Keri or Derma Oil.

• Pat dry, then apply an emollient foot cream (e.g. Nutraplus—10% urea).

• Can use tissue glue (with care) to hold edges together.

• Consider surgical closure, especially if bleeding.

Contact dermatitis

Acute contact (exogenous) dermatitis can be either irritant or allergic and it is estimated that at least 70% of patients have an irritant cause. It is difficult to separate these types on clinical or histological grounds. The presence of irritant dermatitis increases the risk of developing a contact allergy.

Features:

• itchy, inflamed skin

• red and swollen

• papulovesicular

• may be dry and fissured

Irritant contact dermatitis

This is caused by primary irritants such as acids, alkalis, detergents, soaps, oils, solvents. A reaction may result from either a once-only exposure to a very irritant chemical or, more commonly, repeated exposure to weaker irritants. This is irritation, not allergy.

Allergic contact dermatitis

Caused by allergens that provoke an allergic reaction in some individuals only—most people can handle the chemicals without undue effect. It is immunologically mediated. This allergic group also includes photo-contact allergens. Approximately 4.5% of the population is allergic to nickel, which is found in jewellery, studs on jeans, keys and coins (see FIG. 121.4). Contact dermatitis is due to delayed hypersensitivity, sometimes with a long time of days to years. It is common in industrial or occupational situations, where it usually affects the hands and forearms.

Common allergens:

• ingredients/fragrances in cosmetics (e.g. perfumes, preservatives)

• topical antibiotics (e.g. neomycin)

• topical anaesthetics (e.g. benzocaine)

• topical antihistamines

• plants: Rhus, Grevillea, Primula, poison ivy

• metal salts (e.g. nickel sulphate, chromate)

• dyes (especially clothing dyes)

• perfumes, cosmetics

• hairdressing chemicals

• rubber/latex

• epoxy resins and glues/acrylates

• glutaraldehyde (e.g. sterilising agents)

• toluene sulfonamide compound resins: nail polish

• coral

Note: The skin of mangoes cross-reacts with Rhus and Grevillea.

Clinical features⁴

• Site and shape suggest contact

• Dermatitis ranges from faint erythema to ‘water melon’ face oedema

• Worse in peri-orbital region, genitalia and hairy skin; least in glabrous skin (e.g. palms and soles)

• Think of Rhus, Grevillea or poison ivy allergy if linear blisters on forearms and/or puffy eyes

• Improvement when off work or on holiday

Note: Can be delayed onset.

Diagnosis

• Take a thorough history; consider occupation, family history, vacation or travel history and clothes

• Review all topical applications (e.g. medicines, cosmetics) for allergic or irritant potential

• Usage test—apply products used by the patient to the cubital fossa and note development of rash

• Refer to a dermatologist for patch testing

Management

• Determine cause with vigour and remove it

• Topical corticosteroid treatment as for atopic dermatitis

• Oral prednisolone for severe cases² (start with 25–50 mg daily for adults for 5–7 days then gradually reduce over 2 weeks)

Seborrhoeic dermatitis

Seborrhoeic dermatitis is a very common skin inflammation that usually affects areas abundant in sebaceous glands or intertriginous areas. It is therefore common in hair-bearing areas of the body, especially the scalp and eyebrows. It can also affect the scalp, face, neck, axillae and groins, eyelids (blepharitis), external auditory meatus and nasolabial folds. The presternal area is often involved (see FIG. 121.5).

There are two distinct clinical forms: seborrhoeic dermatitis of infancy, and the adult form.

Studies have indicated that it may be caused by a reaction to the yeast Malassezia sp. It may be associated with HIV infection and Parkinson disease.

A feature of seborrhoeic dermatitis is that, unlike atopic dermatitis, it is not itchy. Seborrhoeic scale is greasy and yellowish unlike the silvery scale of psoriasis.

Seborrhoeic dermatitis of infancy

Infantile seborrhoeic dermatitis is different from adult seborrhoeic dermatitis. In infancy, it is often known as ‘cradle cap’ if it affects the scalp, or nappy rash/diaper dermatitis if it involves the napkin area.

It can be difficult to differentiate the rash from that of atopic dermatitis but seborrhoeic dermatitis tends to appear very early (before atopic dermatitis), from 3–12 weeks, when androgen activity is most prevalent. Both atopic dermatitis and seborrhoeic dermatitis can present with red, scaly patches.

The different features are summarised in TABLE 121.2 and the distribution is presented in FIGURE 121.6.

In cradle cap, a flaky, scurf-like dandruff appears first, and then a yellowish, greasy, scaly crust forms. This scurf is usually associated with reddening of the skin. It may resolve spontaneously within a few months (see Cradle cap, CHAPTER 91).

The dermatitis can become infected, especially in the napkin area, and this may be difficult to treat. If untreated, it often spreads to many areas of the body. It is said that cradle cap and nappy rash ‘may meet in the middle’.

Treatment

Simple basic methods are:

• keep areas dry and clean

• keep skin exposed to air as much as possible

• use soap substitute (e.g. Cetaphil lotion)

• rub scales of cradle cap gently with baby oil or white soft paraffin then wash away loose scales

Medication²

Infants:

• 1–2% sulphur and 1–2% salicylic acid in aqueous cream or same cream with 2% liquor picis carbonis added:

  • – apply overnight to scalp, wash off next day with soap substitute

  • – use 3 times a week until it clears

• Egozite cradle cap lotion (6% salicylic acid)

For persistent scalp erythema:

• desonide 0.05% lotion, daily after bath

• desonide 0.05% lotion, bd for up to 7 days

• or

• hydrocortisone 1% ointment, bd for up to 7 days

• Mix equal parts 1% hydrocortisone with nystatin or miconazole + zinc oxide

Prognosis

Most children are clear by 18 months (rare after 2 years).

Adult seborrhoeic dermatitis

Clinical features

• Any age from teenage onwards

• The head is a common area: scalp and ears, face, eyebrows, eyelids (blepharitis), nasolabial folds (see FIG. 121.7)

• Other areas: centre of chest, centre of back, scapular area, intertriginous areas, especially perianal (see FIG. 121.8)

• Pale pink, ill-defined erythematous rash characterised by loose, flaky scale

• Scale may be yellow and greasy

• Dandruff a feature of scalp area

• Worse with stress and fatigue

• It is a chronic, recurring condition

Treatment²

First line treatment is an anti-yeast shampoo applied often (twice per week to daily). Shampoos often require rotation as response diminishes.

Anti-yeast shampoo options:

• ketoconazole

• ciclopirox olamine

• zinc pyrithione

• selenium sulfide

If inadequate, add a topical corticosteroid lotion for 7 nights. Options include:

• betamethasone dipropionate 0.05%

• methylprednisolone aceponate 0.1%

• mometasone furoate 0.1%

If inadequate response and especially if thick scale, add coal tar (LPC) at night, once or twice weekly and wash off the next morning with anti-yeast shampoo. Recommended topical tar preparations:

• coal tar prepared 1% emulsion or gel

• LPC 3–6% + salicylic acid 3% in aqueous cream

If all above therapies fail, use corticosteroid shampoo, clobetasol propionate 0.05%, twice weekly (use anti-yeast shampoo on the other 5 days).

• Wash regularly using bland soap

• Combination antifungal cream and topical corticosteroid is first line:

  • hydrocortisone 1% + clotrimazole 1% once or twice daily

  • or

  • hydrocortisone 1% + miconazole 2% cream, once or twice daily for up to 2 weeks

• If inadequate, use separate topical corticosteroids and antifungal creams:

  • desonide 0.05% lotion daily for up to 2 weeks

  • or

  • methylprednisolone aceponate 0.1% cream daily for up to 2 weeks

  • in combination with

  • ketoconazole 2% or bifonazole 2% creams daily for up to 2 weeks

  • or

  • clotrimazole 1%, econazole 1% or miconazole 2% creams twice daily for up to 2 weeks

If treatment fails, a tar cream can be used such as LPC 1–2% (for face, flexures and groin) and LPC 3–6% (for trunk and limbs) in aqueous or sorbolene cream, once daily for up to 2 weeks.

Note: Oral antifungals are not recommended at all.

Psoriasis

Psoriasis (see FIG. 121.9) is a chronic, immune-mediated skin disorder of unknown aetiology which affects 2–4% of the population. It appears most often between the ages of 10 and 30 years, although its onset can occur any time from infancy to old age. It has a familial predisposition although its mode of inheritance is debatable. If one parent is affected there is a 25% chance of developing it; this rises to 65% if both parents are affected.³

Psoriasis is now regarded as a disorder involving activation of helper T cells in the skin. Cytokines are then released and cause skin cells to multiply faster, leading to thickening of the skin and overscaling. The new ‘biological agents’ intervene in this process.

Capillary dilatation explains the redness.

Be aware of association with cardiovascular disease, particularly heart disease, depressive illness, diabetes, arthritis, inflammatory bowel disease and lymphoma.⁶

Factors that may worsen or precipitate psoriasis

• Infection, especially group A Streptococcus

• Trauma or other physical stress

• Emotional stress

• Sunburn

• Puberty/menopause

• Drugs:

  • – antimalarials (e.g. chloroquine)

  • – beta blockers

  • – lithium

  • – NSAIDs

  • – oral contraceptives

The typical patient

• Older teenager or young adult

• Possible family history

• Onset may follow stress, illness or injury

• Rash may appear on areas of minor trauma—the Koebner phenomenon

• Rash improves on exposure to sun but worse with sunburn

• Worse in winter

• Itching not a feature but is present sometimes

Arthropathy

About 5% can develop a painful arthropathy (fingers, toes or a large joint) or a spondyloarthropathy (sacroiliitis).⁷

The rash

The appearance depends on the site affected. The commonest form is plaque psoriasis, which begins with red lesions that enlarge and develop silvery scaling. The commonest sites are the extensor surfaces of the elbows and knees; then the scalp, sacral areas, genitals and nails are affected (see FIG. 121.10).

Diagnosis

Psoriasis is a clinical diagnosis but biopsy may be needed for confirmation. No laboratory test (including blood testing) is available.

Principles of management

While realising there is no cure for psoriasis, the aim of treatment is to relieve discomfort, slow down the rapid skin cell division and work in consultation with a specialist to achieve these aims.⁷

• Provide education, reassurance and support.

• Promote general measures such as rest, and holidays, preferably in the sun.

• Promote healthy lifestyle, including balanced diet, exercise, reduced alcohol and smoking cessation.

• Advise prevention, including avoidance of skin damage and stress if possible.

• Avoid irritants and use a soap substitute.

• Recommend regular use of emollients.

• Tailor treatment (including referral) according to the degree of severity and extent of the disease.

• Shared care with a consultant is advisable.

Topical treatment options²

Topical agents useful for treatment of psoriasis in primary care:

• Tar preparations

  • – anti-inflammatory, anti-pruritic

  • – often used in combination with keratolytics (e.g. salicylic acid) to soften and lift scale

  • – stinging can be avoided by using with topical corticosteroid or when symptoms mild

  • – colour and odour limit concordance, apply at night

  • – common preparation is liquor picis carbonis (LPC)

• Topical corticosteroids

  • – most common treatment for psoriasis

  • – anti-inflammatory, reduces rate of skin turnover

  • – useful for flares; add tar or calcipotriol if ineffective or step down to tar alone once controlled

• Calcipotriol

  • – vitamin D derivative, regulates proliferation and differentiation of keratinocytes

  • – takes up to 6 weeks to take effect

  • – stinging is common, reduced when used in combination with topical corticosteroid

Therapy can be monotherapy or combined therapy, e.g. tar and corticosteroids or corticosteroids and calcipotriol. Rotational therapy is often required as patients become less sensitive to one therapy over time, especially topical corticosteroids. Adding another treatment can extend disease control.

Recommended topical regimens

For trunk and limb psoriasis, apply:

• coal tar prepared 1% emulsion or gel, once or twice daily, for 1 month

• or

• LPC 6% + salicylic acid 3% cream or ointment, twice daily for 1 month

• if insufficient or flare, add

• moderately potent to potent topical corticosteroid ointment, daily until skin is clear (usually 2 to 6 weeks)

• or if inadequate response

• calcipotriol + betamethasone dipropionate

• 50 + 500 mcg/g ointment, daily until skin is clear (usually about 6 weeks)

Once psoriasis controlled, reduce the potency of steroid and withdraw if possible. Continue tar as maintenance therapy.

Treat as for trunk or limb psoriasis, however higher dose of salicylic acid is required if hyperkeratotic, i.e. LPC 6% + salicylic acid 6%. Also consider earlier use of calcipotriol, given common resistance to topical therapy.

• potent corticosteroid lotion or shampoo (as for seborrhoeic dermatitis), daily until skin is clear (usually 2 to 6 weeks)

• then

• coal-tar shampoo (over the counter) for maintenance

• or if thickened scale, add

• LPC 6% + salicylic acid 3% in aqueous cream, twice daily

• if inadequate response

• calcipotriol + betamethasone dipropionate 50 + 500 mcg/g gel, once daily until skin is clear (expect some response within 2 weeks)

• methylprednisolone aceponate 0.1% ointment or fatty ointment, daily for several weeks (usually 2 to 6 weeks) or 1% hydrocortisone for children

• once controlled

• LPC 2% + salicylic acid 2% in aqueous cream at night

Note that fissuring (e.g. inframammary, natal cleft) is a feature. There is little or no scale.

• methylprednisolone aceponate 0.1% ointment or fatty ointment, once daily for several weeks (up to 2 weeks in children)

• once controlled

• LPC 2% in emulsifying ointment at night

If patient motivated:

• calcipotriol + betamethasone dipropionate 50 + 500 mcg/g ointment, in proximal nail fold and under nail, at night for up to 3 months

If onycholysis or subungual hyperkeratosis:

• betamethasone dipropionate 0.05% lotion topically, twice daily under nail for up to 3 months

Expert treatments

• Dithranol topical therapy is rarely used, can stain clothes and burn unaffected skin

• Narrowband ultraviolet B phytotherapy (UV-B)

  • – treatment 2–3 times a week for a few months

  • – often used in combination with other therapies

• Methotrexate

  • – dramatic results in severe cases

• Cyclosporin

  • – symptoms quickly return when treatment stops and not recommended long term

• Acitretin is a vitamin A derivative and effective in severe intractable psoriasis (never use in females of child-bearing age)

• Biological agents

  • – directed at the T cell dysfunction (i.e. immune response modifiers), e.g. efalizumab, infliximab, ustekinumab, alefacept

Nappy rash²

Nappy rash (or diaper dermatitis) is an inflammatory contact dermatitis occurring in the napkin area and can be a common presentation of mild or moderate underlying skin disease. It is found in children up to 2 years old and has a peak incidence from 9–12 months.⁸

Most children will develop nappy rash at some stage of infancy with an estimated 50% having it to a significant extent. The commonest type is irritant dermatitis, but consider also:

• Candida albicans (invariably present although often not obvious)

• seborrhoeic dermatitis

• atopic dermatitis

• psoriasis

Irritant dermatitis

This is a type of contact dermatitis with the erythema and scaling conforming to the napkin area. The flexures are usually spared. It is related to the activity of faecal proteases and lipases and probably not to the activity of ammonia (from urea) as previously promoted. The problem can vary from mild erythema to a severe blistering eruption with ulceration. Ultrabsorbent disposable nappies appear to be better than cloth nappies.⁹ Diarrhoea is a causative factor of irritant dermatitis. If the eruption extends further than the points of contact with the nappy, an underlying skin disease such as seborrhoeic or atopic dermatitis must be suspected. Psoriasis always involves the skin folds.

Seborrhoeic dermatitis

This affects mainly the flexures of the natal cleft and groin. It is important to look for evidence of seborrhoeic dermatitis elsewhere, such as cradle cap and lesions on the face and axillae.

Atopic dermatitis

Atopic dermatitis can involve the napkin area. Pruritus is a feature and the child may be observed scratching the area. There may be evidence of atopic dermatitis elsewhere, such as on the face.

Candidiasis (monilia nappy rash)

Superinfection of intertrigo or napkin dermatitis will result in a diffuse, red, raw, shiny rash that will involve the flexures and extend beyond the napkin area as ‘satellite lesions’. Candida tends to invade the skin folds and the foreskin of male babies.

Causes of nappy rash

The main predisposing factor in all types is dampness due to urine and faeces. It is far less common since the use of disposable nappies. Persistent cases often become colonised with Candida albicans. Other causes or aggravating factors are:

• a tendency of the baby to eczema

• a tendency of the baby to seborrhoeic dermatitis

• infection, especially Candida (thrush)

• rough-textured nappies

• chemicals in some baby wipes

• plastic pants (aggravates wetness)

• excessive washing of the skin with soap

• too much powder over the nappy area (avoid talcum powders)

Uncommon causes

This presents as a non-scaling eruption, primarily on the napkin area, but can extend to the flexures, trunk and limbs. The edge of the rash is sharply demarcated. The typical psoriatic scale is absent. It tends to occur in the first weeks of life. There is usually a family history.

Bacterial infections to consider include staphylococcal folliculitis, impetigo and perianal streptococcal dermatitis. Culture of the lesion will reveal the cause.

If there is Staphylococcus superinfection, bullae and pus-filled blisters will be present.

There is a similar rash to seborrhoeic dermatitis but the lesions are purpuric. In this serious syndrome the child is very ill and usually lymphadenopathy and hepatosplenomegaly may be found.

May be more common than realised.

Management

Basic care (instructions to parents/carers):

1. Keep the area dry. Change wet or soiled nappies frequently and as soon as you notice them. Use highly absorbent disposable nappies.

2. After removing nappy, gently remove any urine or moisture with a soap substitute or warm water.

3. Wash gently with warm water, pat dry (do not rub) and then apply a barrier preparation to help protect the area. Vaseline or zinc cream applied lightly will do.

4. Expose the bare skin to fresh air wherever possible.

5. Use a soap substitute and bath oil for bathing.

6. Avoid powder and plastic pants.

Medical treatment

Some principles follow:

• The cornerstone of treatment is prevention.

• Barrier preparations should be used to protect the skin, e.g. zinc oxide (best) or white soft paraffin or a mixture of zinc oxide and castor oil or Vaseline.

• A mild topical corticosteroid is the treatment of choice.

• It is useful to add an antifungal agent.

• If infection is suspected, confirm by swab or skin scraping.

• Consider a combined steroid and antifungal agent e.g. Hydrozole.

• When nappy rash is severe, apply a stronger topical steroid for up to 7 days, e.g. methylprednisolone aceponate 0.1% ointment or fatty ointment, once daily.

Treatment:

Common facial skin disorders include acne, rosacea, peri-oral dermatitis and seborrhoeic dermatitis. These conditions must be distinguished from lupus erythematosus (discoid LE is more common).

Acne

Acne is inflammation of the pilosebaceous (oil) glands of the skin (see FIG. 121.11). At first there is excessive sebum production due to the action of androgen. These glands become blocked (blackheads and whiteheads) due to increased keratinisation of the sebaceous duct. A secondary bacterial infection due to Propionibacterium acnes in the sebum produces lipases with the resultant free fatty acids, thus provoking inflammation characterised by red papules, pustules, nodules and cysts.

Acne usually peaks early in puberty and resolves in males during the early twenties.² Females are more likely to suffer ongoing acne. Consider PCOS as a causative condition.

History

In women, enquire about hirsutism and menstrual irregularity. Consider the patient’s occupation (e.g chef, exposure to grease and oil exposure). Enquire about use of skin preparations—therapeutic or cosmetic, exposure to oils and drug intake.

Drugs that aggravate acne:¹⁰

• corticosteroids

• chloral hydrate

• iodides or bromides

• lithium

• anti-epileptics (e.g. phenytoin)

• quinine

• hormonal contraceptives (consider switching to an anti-androgenic combined oral contraceptive)

Management

Adolescents hate acne; they find it embarrassing and require the sympathetic care and support not only of their doctor but also of their family. It should not be dismissed as a minor problem.

People with acne should understand its pathogenesis and be given leaflets with appropriate explanations. Myths must be dispelled.

• It is not a dietary or infectious disorder.

• It is not caused by oily hair or hair touching the forehead.

• Blackheads are not dirt, and will not dissolve in hot, soapy water.

Reassure the patient that acne usually becomes less of a problem after the age of 25 years, although 15% of women and 5% of men continue to have acne as adults.

• Diet is not considered to be a causative factor but a healthy diet is encouraged.

• Special soaps and overscrubbing are unhelpful. Use a normal soap and wash gently.

• Avoid oily or creamy cosmetics and all moisturisers. Use cosmetics sparingly.

• Avoid picking and squeezing blackheads.

• Exercise, hair washing and shampoos are not of proven value.

• Ultraviolet light such as sunlight may help improve acne but avoid overexposure to the sun.

Principles of treatment²

1. Comedolysis: unblock the pores (follicular ducts) with keratolytics such as salicylic acid (5–10%) or benzoyl peroxide (2.5%, 5% or 10%) which also has antibacterial properties. Topical retinoids are the most effective comedolytics, e.g. tretinoin 0.025% cream or adapalene 0.1% cream or gel.

2. Decrease bacteria in the sebum with systemic antibiotics—tetracyclines or erythromycin—or with a topical antibiotic such as clindamycin.

3. Decrease sebaceous gland activity with oestrogens, spironolactone, cyproterone acetate, or isotretinoin.

Note: Oral isotretinoin is teratogenic.

Avoid concomitant use of oral and topical antibiotics.

Recommended treatment regimens

Suitable for mild to moderate acne.

• Basic starting regimen is a topical retinoid in combination with benzoyl peroxide:

  • – use tretinoin 0.025% cream or adapalene 0.1% cream or gel, apply each night

  • – if slow response after 6 weeks, add benzoyl peroxide 2.5% or 5% gel or cream once daily (in the morning)

  • – maintain for 3 months and review.

• Alternative or add-on regimens, if persistent: clindamycin HCl 600 mg in 60 mL of 70% isopropyl alcohol (e.g. ClindaTech). Apply with fingertips twice daily.

Use for inflammatory acne: (moderate to severe papulopustular) ± trunk involvement

• doxycycline or minocycline, 50 to 100 mg per day

• erythromycin 250 to 500 mg twice daily is an alternative, especially for pregnant women

• give a minimum 12 week trial; 6 months is standard

• avoid using antibiotics alone

Severe cystic or recalcitrant acne (specialist care):

• spironolactone

• isotretinoin (Roaccutane): outstanding agent

Females not responding to first-line treatment:

• combined oral contraceptive pill with anti-androgenic effect (e.g. ethinyloestradiol/cyproterone acetate: Diane-35 ED)

• oral spirinolactone may be used in combination with an oral contraceptive pill as an anti-androgen (single use should be avoided due to risk of menstrual irregularity and contraindication in pregnancy)

Note: Response to any acne treatment occurs in about 8 weeks or longer.

Rosacea

Rosacea is a common persistent eruption of unknown aetiology. It is typically chronic and persistent with a fluctuant course.

Clinical features³

• Mainly 30–50 years

• Usually females of Celtic origin: ‘the curse of the Celts’

• On forehead, cheeks, nose and chin (see FIG. 121.12 and FIG. 121.13)

• ‘Flushing and blushing’ (often precedes the rash)

• Fluctuates from day to day

• Peri-orbital and peri-oral areas spared

• Vascular changes—erythema and telangiectasia

• Inflammation—papules and pustules (sterile)

Complications

• Blepharitis

• Conjunctivitis, rarely keratitis and corneal ulcer

• Associated rhinophyma in some cases

Management²

• Avoid factors that cause facial flushings (e.g. excessive sun exposure, heat, wind, alcohol, excessive exercise, hot baths, spicy foods, hot drinks—tea and coffee)

• Sun protection

• Use a gentle soap-free cleanser

• Apply green-tinted foundation to mask redness

• Avoid topical corticosteroids which can cause rebound vascular changes on cessation

For mild erythema and inflammatory lesions:

• metronidazole 0.75% gel or cream, bd

• or

• azelaic acid 15% gel, once daily

Apply for 6 to 12 weeks for maximal response. Long-term treatment is usually required to prolong remission. If topical therapy is unsuccessful, add or replace with oral therapy.

For erythrotelangiectatic skin, applying a topical vasoconstrictor improves its cosmetic appearance, but the effect is temporary (about 12 hours):

• brimonidine tartrate 5 mg/g gel, once daily in the morning

Antibiotics are used for their anti-inflammatory effect:

• Doxycycline 50 to 100 mg daily for a total of 8–10 weeks.

• If inadequate after 4 weeks, consider minocycline 50 to 100 mg daily for up to 8 weeks. Repeat for recurrences.

• Erythromycin 250 to 500 mg twice daily is an alternative for pregnant women or if doxycycline or minocycline are not tolerated.

• Low dose doxycyline or minocycline, 50 mg daily, is appropriate for longer use if symptoms recur within a month.

Telangectasia, erythema and rhinophymas respond to laser therapy.

Rhinophyma

This is due to hypertrophy of the nasal sebaceous glands and is associated with older men with rosacea. Treatment options include laser ablation, shave excision or isotretinoin (see CHAPTER 59).

Peri-oral dermatitis

Clinical features

• Papular and pustular, acne-like dermatitis of lower face

• Usually young women 20–50 years

• May be seen in children and adolescents

• ‘Muzzle area’ distribution around mouth and on chin, sparing adjacent peri-oral area (see FIG. 121.14 and FIG. 123.15)

• Peri-orbital skin involvement is common in men

• Rash may be unilateral

• Frequently begins at the nasolabial folds

• Multiple small red macules and papules

• On a background of erythema and scaling

• Burning and irritation

• May be associated seborrhoeic dermatitis on scalp and head

• May be related to pregnancy and oral contraception

• Related to the use of creamy cosmetic products

• May be related to repeated topical corticosteroid use (may be a rebound on ceasing it)

• Peri-oral dermatitis belongs to the rosacea spectrum of disease

Treatment

• Discontinue any topical corticosteroid therapy (tends to flare initially) and all ‘creamy’ preparations including cleansers, moisturisers and make-up.

• Simple treatments include cleansing with a gentle soap substitute, cold compress for irritation and use of a light emollient

• Treatment is with oral antibiotics for their anti-inflammatory properties, as for rosacea.

• Topical treatments are not as effective and may irritate: metronidazole 0.75% gel or clindamycin 1% lotion twice daily.

Tinea (ringworm infections) is caused mainly by three major classes of dermatophytic organisms that have the ability to invade and proliferate in keratin of the skin, nails and hair.

It is most useful to perform skin scrapings and microscopy to look for encroaching septate hyphae. Confirm the diagnosis by fungal culture. Tinea cruris is presented in CHAPTER 120.

Tinea pedis (athlete’s foot)

Tinea pedis is usually caused by Trichophyton rubrum and is the commonest type of fungal infection in humans. Candida intertrigo and interdigital maceration (alone without secondary tinea) in particular and also erythrasma, eczema and psoriasis, are important differential diagnoses.

Symptoms

The commonest symptoms are itchiness and foot odour. Sweat and water make the top layer of skin white and soggy. There is scaling, maceration and fissuring of the skin between the fourth and fifth toes and also third and fourth toes.

Advice to patients

• Keep your feet as clean and dry as possible.

• Carefully dry your feet after bathing and showering.

• After drying your feet, use an antifungal powder, especially between the toes.

• Remove flaky skin from beneath the toes each day with dry tissue paper or gauze.

• Wear light socks made of natural absorbent fibres, such as cotton and wool, to allow better circulation of air and to reduce sweating. Avoid synthetic socks.

• Change your shoes and socks daily. Spray shoes with an antifungal agent.

• If possible, wear open sandals or shoes with porous soles and uppers.

• Go barefoot whenever possible.

• Use thongs in public showers such as at swimming pools (rather than bare feet).

Treatment

Several topical antifungals can be used. Preferable to use terbinafine 1% once or twice daily for 1–2 weeks and review. If severe and spreading, prescribe oral griseofulvin (see Tinea corporis) or terbinafine for up to 6 weeks after confirming the diagnosis by fungal culture.

Castellani paint may be helpful for macerated areas.

Tinea corporis¹¹

Tinea corporis (ringworm infection of the body) is usually caused by Trichophyton rubrum (60%) or Microsporum canis.¹² Strongly related to exposure to cats and dogs, while the guinea pig is a potent source of facial tinea (can present as pustular folliculitis).

Clinical features

• Spreading circular erythematous lesions (see FIG. 121.16)

• Slight scaling or vesicles at the advancing edge

• Central areas usually normal

• Mild itch

• May involve hair, feet and nails

Treatment

• First choice is terbinafine 1% cream or gel, once or twice daily for 1–2 weeks

• Other options include clotrimazole 1%, miconazole 2% cream, bifonazole 1% cream, ketoconazole 2% cream, applied bd for 2–4 weeks

• Oral terbinafine 250 mg or griseofulvin 500 mg daily, for up to 6 weeks if no response or widespread

Tinea capitis²

In Australia tinea capitis is usually due to M. canis acquired from cats and dogs.

Clinical features

• Usually in children (rare after puberty)

• Patches of partial alopecia

• Scaly patches

• Small broken-off hair shafts

• Hairs fluoresce yellow-green with Wood’s light (not invariably, e.g. with Trichophyton tonsurans infection)

Treatment

• terbinafine (o): adults 250 mg daily for 4 weeks; children 62.5–125 mg

• or

• griseofulvin (o): adults 500 mg daily; children 10 mg/kg/day (max. 500 mg) 6–8 week course

Take hair plucking and scale for culture. Treat Trichophyton tonsurans with terbinafine and Microsporum canis with griseofulvin.

Kerion

Kerion of the scalp and beard area may present like an abscess—tender and fluctuant. Usually occurs on the scalp, face or limbs. A fungal cause is possible if the hairs are plucked out easily and without pain (if painful and stuck, bacterial infection is likely).

Tinea incognito

This is the term used for unrecognised tinea infection due to modification with corticosteroid treatment. The lesions are enlarging and persistent, especially on the groins, hands and face.

The sequence is initial symptomatic relief of itching, stopping the ointment or cream and then relapse.

Tinea cruris

Refer to CHAPTER 120.

Tinea unguium (toenails and fingernails)

Refer to CHAPTER 127.

Pityriasis versicolor (tinea versicolor)¹²

Pityriasis versicolor is a superficial yeast infection of the skin (usually on the trunk) caused by Malassezia sp.). The old name, tinea versicolor, is inappropriate because the problem is not a dermatophyte infection. It occurs worldwide but is more common in tropical and subtropical climates.

There are two distinct presentations:

1. reddish brown, slightly scaly patches on upper trunk

2. hypopigmented area that will not tan, especially in suntanned skin

The term ‘versicolor’ means variable colours.

Clinical features

• Mainly young and middle-aged adults

• Brown on pale skin or white on tanned skin (see FIG. 121.17)

• Trunk distribution (see FIG. 121.18)

• Patches may coalesce

• May involve neck, upper arms, face and groin

• Slight scaling when scratched indicates active infection

• Scales removed by scraping show characteristic short stunted hyphae with spores on microscopy

• Often recurrent, especially in summer

Differential diagnosis

Seborrhoeic dermatitis of trunk (more erythematous), pityriasis rosea, vitiligo, pityriasis alba (affects face).

Treatment²

• econazole 1% solution to wet skin, leave overnight, for 3 nights

• or

• ketoconazole shampoo, once daily for 3–5 minutes and wash off, for 5 days

• or

• selenium sulphide 2.5% shampoo, once daily, leave on for at least 10 minutes or overnight, for 7–10 days

• or (for persistent or recurrent problems) fluconazole 400 mg orally, as a single dose

• or

• (for prophylaxis) itraconazole 200 mg (o) twice daily for 1 day per month for 6 months²

Note:

• Griseofulvin and terbinafine are inappropriate because the rash is not a fungal infection.

• Warn patients that the white patches will take a long time to disappear and that cure does not equate to disappearance. Pigment will return once there is sufficient sun to repigment the white patches.

Disorders associated with scaling and roughness of the skin include:

• atopic dermatitis—all types (e.g. pityriasis alba, nummular eczema, asteatotic dermatitis)

• ageing skin

• psoriasis

• ichthyotic disorders

• keratosis pilaris

Itching may be a feature of dry skin (but is not inevitable).

Aggravating factors:

• low humidity (e.g. heaters, air-conditioners)

• frequent immersion in water

• heat/hot water

• toilet soaps

• swimming in chlorinated pools

Management

• Avoid a dry home environment if possible.

• Reduce bathing.

• Bathe or shower in tepid water.

• Use a soap substitute (e.g. Dove or Neutrogena/Cetaphil lotion).

• Pat dry—avoid vigorous towelling.

• Rub in baby oil after bathing (better than adding oil to the bath).

• Avoid wool next to the skin (wear cotton).

• Use emollients/moisturisers (e.g. Alpha-Keri lotion, QV skin lotion, Nutraplus).

Sunburn

Sunburn is normally caused by UV-B radiation, which penetrates the epidermis and superficial dermis, releasing substances such as leucotrienes and histamines, which cause redness and pain. Severe sunburn may develop on relatively dull days because thin clouds filter UV-B poorly. Beware of solariums and the midday sun. Clinical presentations:

Differential diagnosis

• General photosensitivity: consider drugs (e.g. thiazide diuretics, tetracyclines, sulphonamides, phenothiazines, griseofulvin, NSAIDs, isotretinoin)

• Acute systemic lupus erythematosus may present as unexpectedly severe sunburn

• Photocontact dermatitis

Treatment

Oral aspirin or ibuprofen ease pain. Oil in water baths or bicarbonate of soda paste may help, and wet applications such as oily calamine lotions or simply cool compresses may give relief. Topical corticosteroids may be applied to unblistered erythematous skin, twice daily for the first 2 or 3 days. Use a moisturiser that contains aloe vera to soothe skin.

Prevention

Avoid direct exposure to summer sunlight during peak UV periods (10 am to 3 pm). Use natural shade—beware of reflected light from sand or water and light cloud. Use a sunscreen with a minimum of SPF 30. Wear broad-brimmed hats and protective clothing.

Photo-ageing/wrinkles

Prevention

• Stop smoking.

• Avoid cold, dry and windy conditions.

• Avoid exposure to the sun.

• Use an SPF 30 or more sunscreen during the day.

• Avoid soaps with perfume and alcohol.

• Wash with a ‘neutral’ mild soap (e.g. Neutrogena, max. twice daily) and pat dry.

• Apply a simple moisturiser immediately after the bath.

Treatment (options)

• Optimal nutrition—diet rich in fruit and vegetables

• Alpha hydroxy acid preparations (e.g. Elucent cream)

• Tretinoin (Retin-A) cream: apply once daily at bedtime (on dry skin); test for skin irritation by gradual exposure (e.g. 5 minutes at first, wash off, then 15 minutes until it can be left on overnight)

• Topical olive oil

• Lac-Hydrin (US): 12% solution may be effective alternative; other lactic acid preparations may be useful

• Botulinum toxin injections

Primary hyperhidrosis (excessive sweating)¹³

This problem is usually idiopathic and prolonged.

Clinical features

• Male = female incidence

• Affects axilla, groin, soles and palms

• Onset usually around puberty

• Tends to improve after age 25 years

• Family history

• ± Bromhidrosis (malodorous perspiration)

• Usually independent of climate

• Exacerbated by stress and heat; stops during sleep

Causes (secondary/pathological)

• Fever/sepsis

• Thyrotoxicosis

• Acromegaly

• Diabetes mellitus

• Phaeochromocytoma

• Drugs: alcohol/narcotics/antidepressants

• Some neurological conditions (e.g. Parkinson)

• Malignancies especially lymphomas

Treatment^2,13

• Avoid known aggravating factors

• First use:

  • an aluminium chlorohydrate-containing antiperspirant deodorant (spray or roll on each morning) in axilla (suitable for palms and soles)

  • or

  • aluminium chloride hexahydrate 20% solution or spray (Driclor)—apply to affected areas at night when the area is dry (best for palms and soles, although irritation is a problem).

• Iontophoresis (in specialist centres) to hands and feet.

• Injection of botulinum toxin into dermis of affected area. Proven effectiveness for axillae and palms with up to 6 months of anhydrosis.

• Oral anticholinergics (e.g. oxybutynin, propantheline) may give some benefit but are often poorly tolerated.

• Surgical sympathectomy is an option for severe, recalcitrant cases.

Body odour/bromhidrosis

Cause: poor hygiene, excessive sweating, active skin bacteria, metabolic disorders e.g. trimethylaminuria (rare)—causes fishy odour

Main focus: axillae and groin

Precautions: consider uraemia, vaginitis

Treatment

• Scrub body, especially groins and axillae, with deodorant soap at least morning and night

• Try an antibacterial surgical scrub

• Keep clothes clean, launder regularly

• Choose suitable clothes—natural fibres (e.g. cotton), not synthetics

• Use an antiperspirant deodorant

• Alternative soap—pine soap

• Diet: avoid garlic, fish, asparagus, onions, curry

• Reduce caffeine (coffee, tea and cola drinks), which stimulates sweat activity

• Consider a sugar-free diet

• Remove axillary hair

• Consider injections of botulinum toxin for excessive perspiration

Foot odour (smelly and sweaty feet)

Includes pitted keratolysis secondary to hyperhidrosis (common in teenagers).

Treatment (with options)

• Education and reassurance

• Wear cotton or woollen socks

• Aluminium chloride hexahydrate 20% solution (Driclor) or Neat Feet—apply nocte for 1 week, then 1–2 times weekly as necessary

• Shoe liners (e.g. ‘Odor eaters’), charcoal inner soles

• Apply undiluted Burow’s solution after a shower or bath

• Formalin 1–5% soaks every second night

• Iontophoresis

• The teabag treatment (if desperate):

  • – prepare 600 mL of strong hot tea (from two teabags left in water for 15 minutes)

  • – pour the hot tea into a basin with 2 L of cool water

  • – soak the feet in this for 20–30 minutes daily for 10 days, then as often as required

Two conditions commonly seen in teenagers are pitted keratolysis and juvenile plantar dermatosis.

Pitted keratolysis

This common malodorous condition known as ‘stinky feet’ or ‘sneakers feet’, usually seen in 10–14-year-olds, is related to sweaty feet. It is caused by an overgrowth of bacteria that digest keratin on the feet (Corynebacterium sp. most common). It has a ‘honeycomb’ pitted appearance with maceration between the toes, resembling tinea. For mild cases no specific treatment is needed other than attending to hyperhidrosis. Otherwise, treatment includes keeping the feet dry and using clindamycin 1% lotion bd for 10 days, to remove the responsible organism. Try oral roxithromycin if topical therapy fails. Consider changing to all-leather shoes with charcoal liners. Use a drying agent to decrease sweating.

Juvenile plantar dermatosis

‘Sweaty sock dermatitis’ is a painful condition of weight-bearing areas of the feet. The affected skin is red, shiny, smooth and often cracked. It is rare in adults. The treatment is to avoid friction as much as possible with a barrier cream and suitable footwear, preferably with leather or open shoes and cotton socks. A simple emollient such as urea cream gives relief. Cracks can be treated with medicinal glues.

Prickly heat (miliaria/heat rash)

• Avoid sweating as much as possible.

• Keep the skin dry and cool (e.g. fan, air-conditioner).

• Dress in loose-fitting cotton clothing.

• Attend to bedding—cotton sheets, no plastic underlay.

• Reduce activity.

• Avoid frequent bathing and overuse of soap.

• Dilute topical steroid cream bd.

Treatment

• lotion: salicylic acid 2%, menthol 1%, chlorhexidine 0.5% in alcohol or calamine lotion

• or

• Egozite (infants), Isophyl (adults)

If severe: hydrocortisone 1% + clotrimazole 1% cream (brief spells only).

Prevention

• Ego Prickly Heat powder

Chilblains (perniosis)

These are localised inflammatory reactions, caused by prolonged exposure to cold, usually on toes and fingers (see FIG. 121.19) but also on heels, nose, ears and thighs (horse riding).

Precautions

• Think Raynaud phenomenon.

• Protect from trauma and secondary infection.

• Do not rub or massage injured tissues.

• Do not apply heat or ice.

• Wear warm gloves and socks.

Differences between chilblains and Raynaud phenomenon:

• chilblains are intermittent without a pattern

• itchy at the onset

• patchy appearance (can be more generalised)

• Raynaud has two or three phases including a ‘dead white’ phase with line of demarcation

• it is significant if it extends to the MCP joints

Treatment

• Elevate affected part

• Warm gradually to room temperature

• Potent topical corticosteroid (see TABLE 119.9 in CHAPTER 119) twice daily

• If severe and recurrent, apply glyceryl trinitrate vasodilator spray or 0.2% ointment or patch sparingly once daily (use plastic gloves and wash hands for ointment), although weak supportive evidence

• Drink rum at night

• Nifedipine CR 30 mg (o) once daily (if very severe)

• UVB therapy weekly for 4–6 weeks prior to cold weather

Frostbite

Treatment depends on severity.

Precautions

• Watch for secondary infection, tetanus, gangrene.

Treatment

• Elevate affected limb

• Rewarm in water just above body temperature 40°C (104°F) or use body heat (e.g. in axillae)

• Avoid thawing or refreezing

• Surgical debridement

• Don’t debride early (wait until dead tissue dried)

• Don’t drink alcohol or smoke

• For blistering, apply warm water compresses for 15 minutes every 2 hours

• Analgesics

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Atopic dermatitis (eczema)

• Body odour

• Contact dermatitis

• Dry skin

• House dust mite management

• Nappy rash

• Pityriasis rosea

• Psoriasis

• Ringworm (tinea)

• Rosacea and perioral dermatitis

• Seborrhoea in infants

• Sunburn

• Sweaty and smelly feet

• Tinea pedis

DermNet NZ: the dermatology resource <www.dermnetnz.org>

Therapeutic Guidelines: eTG Complete <www.tg.org.au>