++
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 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
++
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
++
++
++
++
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.
++
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
+++
Education and reassurance
++
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.
+++
Improve skin condition
++
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
++
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
+++
Topical corticosteroid therapy
++
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
++
++
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:
++
++
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
+++
OTHER TYPES OF ATOPIC DERMATITIS
++
+++
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.
++
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
++
+++
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
++
+++
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
++
++
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)
++
++
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 painful heels are a common problem, especially in adult women. It is a manifestation of very dry skin.
++
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.
++
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.
++
++
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.
++
++
++
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.
++
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.
++
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
++
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.
++
Treatment principles for seborrhoeic dermatitis
Keratolytics such as salicylic acid may be used to lift the scale.
Antiyeast treatments reduce the skin’s load of Malassezia sp., e.g. ketoconazole, miconazole and ciclopirox.
Topical corticosteroids target inflammation and pruritus and often used in combination.
+++
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’.
++
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
++
++
++
For persistent scalp erythema:
++
+++
Face, flexures and trunk
++
desonide 0.05% lotion, bd for up to 7 days
or
hydrocortisone 1% ointment, bd for up to 7 days
++
++
Most children are clear by 18 months (rare after 2 years).
+++
Adult seborrhoeic dermatitis
++
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
++
++
++
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:
++
++
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:
++
++
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 (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
++
++
++
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
++
About 5% can develop a painful arthropathy (fingers, toes or a large joint) or a spondyloarthropathy (sacroiliitis).7
++
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).
++
++
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
+++
Chronic stable plaque psoriasis
++
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.
+++
Palmoplantar psoriasis
++
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
+++
Flexural (inverse) and genital psoriasis
++
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 onycholysis or subungual hyperkeratosis:
++
++
Dithranol topical therapy is rarely used, can stain clothes and burn unaffected skin
Narrowband ultraviolet B phytotherapy (UV-B)
Methotrexate
Cyclosporin
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 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:
++
++
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 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.
++
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)
++
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.
+++
Histiocytosis X (Letterer–Siwe syndrome)
++
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.
++
Basic care (instructions to parents/carers):
++
Keep the area dry. Change wet or soiled nappies frequently and as soon as you notice them. Use highly absorbent disposable nappies.
After removing nappy, gently remove any urine or moisture with a soap substitute or warm water.
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.
Expose the bare skin to fresh air wherever possible.
Use a soap substitute and bath oil for bathing.
Avoid powder and plastic pants.
++
++
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.
++
++
++
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 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.
++
++
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
++
+++
Support and counselling
++
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
++
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.
Decrease bacteria in the sebum with systemic antibiotics—tetracyclines or erythromycin—or with a topical antibiotic such as clindamycin.
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):
++
++
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.
++
Common mistakes with acne
Not treating comedomes with a comedolytic
Monotherapy (e.g. antibiotics only)
Not using recommended combinations
Not using isotretinoin for cystic acne
++
Rosacea is a common persistent eruption of unknown aetiology. It is typically chronic and persistent with a fluctuant course.
++
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)
++
++
++
++
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):
++
++
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.
++
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).
++
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
++
++
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.
++
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.
++
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).
++
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 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).
++
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
++
++
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
++
In Australia tinea capitis is usually due to M. canis acquired from cats and dogs.
++
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)
++
++
Take hair plucking and scale for culture. Treat Trichophyton tonsurans with terbinafine and Microsporum canis with griseofulvin.
++
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).
++
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 unguium (toenails and fingernails)
++
+++
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:
++
reddish brown, slightly scaly patches on upper trunk
hypopigmented area that will not tan, especially in suntanned skin
++
The term ‘versicolor’ means variable colours.
++
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).
++
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
++
++
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.