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Tinea pedis and onychomycosis Hyperhidrosis and pitted keratolysis Plantar warts Palmoplantar pustulosis Pompholyx and dermatitis Allergic contact dermatitis Juvenile plantar dermatosis Heel fissures Perniosis Palmoplantar keratoderma

The author

Pedal dermatoses
Background
DERMATOLOGICAL problems represent a significant proportion of consultations in general practice, and a large number of these relate to dermatoses of the feet. The unique nature of glabrous skin, the cultural need for footwear in Westernised societies, and the fact that the feet are always under significant physical pressure and exposed to constant minor trauma, creates a unique set of cutaneous afflictions. This article discusses several problems likely to be encountered by the family physician. The focus is on specific and practical management of infective and acquired conditions, with relatively accessible therapies that I have found useful. Other texts are available for a more comprehensive discussion of detailed clinical features and all available treatments, and other diseases of the pedal skin. To make this article more practical and useful, specific topical and systemic treatments are suggested. These are examples only and alternatives may be as effective. I do not specifically endorse any product mentioned.
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DR KENG-EE THAI, consultant dermatologist, North Shore Associates in Dermatology, Gordon; The Brien Walder department of dermatology, The Prince of Wales Hospital, Randwick; and the department of dermatology, Royal North Shore Hospital, St Leonards, NSW.

HOW TO TREAT Pedal dermatoses

Tinea pedis and onychomycosis

TINEA occurs when a mould (or dermatophyte) infects dead, keratinised structures. It is likely to be the most common condition found on feet. Regardless of the species, the most common source of dermatophytes are communal bathing areas and change rooms. Once adherent (within two hours of contact) to the skin, the hot, sweaty environment provided by the wearing of socks and covered shoes provides the ideal environment for germination and penetration. Men and those who wear closed shoes are more commonly affected than women and those who go shoeless. Tinea pedis leads to a breakdown in skin integrity and allows the entry of bacteria, predisposing to cellulitis and lymphangitis. Patients who experience recurrent cellulitis should be examined for tinea; effective treatment of the fungus should prevent bacterial reinfection. Clinical features vary with the dermatophyte species and the degree of host immune response. Zoophilic fungi tend to elicit more inflammation compared with geophilic and anthropophilic strains. Interdigital tinea (intertriginous dermatitis) is most common and presents with macerated, wet, red or scaly toe webs (figure 1). This form can also be secondarily infected with Pseudomonas, which gives a greenish tinge to the maceration (figure 2). Dry moccasin-type tinea involves fine scale and erythema of the entire plantar surface (figure 3). Inflammatory tinea can have scale, erythema and pustules (figure 4). Classic ringworm can occur on the sides of the sole or dorsum of the foot. Thus any red scaly eruption on the feet could potentially be tinea pedis and should have skin scrapings for fungal microscopy and culture. General preventive measFigure 1: Interdigital tinea. Note the white maceration of the skin. Figure 2: Severe interdigital tinea with Pseudomonas co-infection. Note the greenish pigmentation typical of Pseudomonas. forms of other types may be treated topically, while moccasin-type, extensive and very inflammatory tinea often require combination with oral agents. Oral terbinafine 250mg daily for 2-3 weeks is useful, as is itraconazole or ketoconazole 200mg daily. Rarely, significant inflammation may require oral corticosteroid support. Onychomycosis is also very common in Western nations, with up to a 10% prevalence. Many patients have dystrophic toenails but may elect not to treat if they are asymptomatic and do not serve as a reservoir for auto-inoculation with dermatophyte elsewhere. Topical treatments typically fail; oral terbinafine is the gold standard. For dermatophyte infections, terbinafine 250mg a day for three months is said to give mycological cure rates of up to 80%. Liver function should be tested at least once during the course of treatment, and patients should be made aware of uncommon but concerning adverse events, including loss of taste, loss of appetite, severe drug rashes and hepatic impairment. In practice I prefer a pulsed regimen of once-daily dosing for one week, alternating with a week off, to be continued until the diseased nail grows out completely and is replaced with normal nail plate. Enough of the medication is deposited in the nail plate in the week on to provide continued efficacy in the week off. This regimen allows prolonged treatment with greater economy and lower adverseeffect risk. Alternatives include itraconazole 400mg daily for one week a month for 3-4 months. Itraconazole is also the drug of choice for nondermatophyte infections. Griseofulvin should be avoided, with a 30% cure rate even after 18 months of treatment.

Figure 3: Dry moccasin-type tinea pedis. Note the erythema and fine scales.

Figure 4: Tinea pedis. Note inflammatory bulla formation.

ures are instituted to deny the organism further residence and prevent re-infection. Rubber thongs/flipflops should be worn in public showers. The skin and interdigital web spaces require deliberate drying. Note that much of the irritation and itch of interdigital tinea occurs simply due to the irritant dermatitis from moisture and occlusion. Open or ventilated footwear should be encouraged and, if suitable, patients should walk barefoot at home. Patients with diabetes and those with peripheral neuropathy or vasculopathy who require constant protective footwear should attempt to find shoes or sandals that have some open panels to allow ventilation. Some shoe-free time may be appropriate when resting. Patients can dry with tis-

sues after bathing, with further desiccation of the web spaces facilitated by prying the toes apart and blowdrying with a hair dryer. Some clinicians advocate using antiseptic soap bars to clean the feet in the shower. Antifungal powders sprinkled into the shoes may prevent re-infection but will not treat active disease. Old moist shoes should be replaced. If there is obvious onychomycosis, this could be a source of fungus, and treatment should be pursued. Topical terbinafine is the treatment of choice; it has higher efficacy and treats tinea faster than topical azoles. Regardless of the agent used, my preference is to use sprays, lotions and tinctures applied twice daily, rather than creams. Liquids

tend to dry on, and so do not perpetuate the wet macerated skin that encourages further tinea growth. Terbinafine spray should be applied twice daily and allowed to dry on before shoes and socks are donned. Other azole alternatives may include miconazole (Daktarin) lotion, tincture or spray powder or another equivalent. If there is significant inflammation and itch within the toe web, topical mometasone lotion (Elocon) can be applied and rubbed in at night to reduce the inflammation. While the application of this topical steroid is counter-intuitive, it is reasonable to reduce itch and improve the condition of the skin, thus allowing faster healing of the skin barrier. Interdigital tinea and mild

Hyperhidrosis and pitted keratolysis

EXCESSIVE sweatiness of the feet is common, forming the pedal component of palmoplantar hyperhidrosis and can accompany axillary hyperhidrosis. Sweaty feet are uncomfortable, potentially embarrassing and predispose to tinea and pitted keratolysis. Most cases of plantar hyperhidrosis are idiopathic; localised pathological causes include: Local central or peripheral nervous system injury. Syringomyelia. Neuritis. Myelitis. Tabes dorsalis. Vascular disease. Cold injury. Arteriovenous malformation. Erythrocyanosis. As with any socially debilitating condition, there are many interest groups and internet forums. Patients need guidance to avoid the use of inappropriate, expensive and ineffective treatments. Aluminium chloride hexahydrate 20% lotion (Drichlor) is first-line therapy. Occlusion of the epidermal eccrine duct is the likely mechanism of action. This alcohol-based lotion should be applied on a nightly basis for 2-3 weeks according to tolerance, after which the frequency of application can be weaned to a weekly maintenance application. Patients should be relaxed, having had a cool shower, and the feet airdried with a hair-dryer on the cool setting. The lotion needs to be applied to completely dry skin, as any moisture will react with the Drichlor to produce hydrochloric acid and lead to irritation. A midpotency topical corticosteroid may be applied if this occurs. Iontophoresis is a method of transferring salt ions in solution into the skin using an electrical curwww.australiandoctor.com.au

rent. The feet are placed in individual small baths and an electric current applied between them, with the rest of the body completing the circuit. The treatment solution may be tap water, saline or a solution of glycopyrrolate. The mechanism of action is unclear. Most major capital cities in Australia have a specialised practice or clinic providing this service, and there are also several commercially available systems for home use (eg, Drionic units). The need for specialised equipment and the inconsistency of response limits the utility of iontophoresis. Patients

should be referred to a dermatologist for further advice. Botulinum toxin is highly effective in blocking acetylcholine signalling between autonomic nerves and eccrine sweat glands. Intradermal injections are most useful for axillary and palmar hyperhidrosis but less useful for plantar disease. Treatment is painful, and palmar injection is best done under a regional nerve block. Patients should be referred to a dermatologist for further advice. Endoscopic thoracic sympathectomy is performed by vascular surcontd page 28

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geons for palmar and axillary hyperhidrosis. This denervation procedure can be effective but is associated with significant adverse effects such as: Compensatory hyperhidrosis (elsewhere on the body). Horners syndrome. Pneumothorax. Intraoperative cardiac arrest. Lumbar sympathectomy can be performed for plantar hyperhidrosis but is often associated with ejaculatory failure, impotence and anorgasmia. These procedures are generally not recommended. Having hot, sweaty occluded

Figure 5: Pitted keratolysis. Note the white oedematous plaques and the pitted nature of the skin.

feet predisposes to pitted keratolysis. This condition is characterised by white, oedematous, boggy plantar skin with minute punched-out pits within, and is caused by overgrowth of corynebacteria (figure 5). Treatment requires reversal of the local conditions and any hyperhidrosis. An antibacterial in the form of topical clindamycin lotion (Clindatech) may be applied twice daily. The clinidamycin treats the corynebacteria while the alcoholic base helps dry out the oedematous skin. Indeed, this condition may be treated with almost any topical antibiotic and even azole antifun-

gals, but the most important elements of treatment are reversal of the predisposing sweatiness and drying out the feet. A second-line treatment is 2% formalin solution soaks. Patients are advised to acquire a flat-bottomed container that will fit one or both feet. Enough formalin solution is placed in the container to just immerse the sole of the foot. Patients soak the feet for 20 minutes each time, several times a week, according to tolerance and dryness. Once a dry, glazed appearance is achieved, the soaks should stop, as further treatment may well cause irritation or allergic contact dermatitis.

Plantar warts
PLANTAR warts are difficult to treat the multitude of wart treatments available reflect their recalcitrant nature. Paediatric cases typically resolve over time, but expeditious treatment may well be requested for various reasons. Adult warts do not resolve spontaneously. Plantar warts are either discrete singular (figure 6) or multiple (figure 7), or cover a large area as a mosaic wart. Viral warts produce a cordon sanitaire, a barrier that prevents their immune recognition. Thus all wart treatments not only destroy warty tissue but also inflame the wart, allowing access by immunemediated cells to facilitate immune recognition and destruction. Multiple concurrent treatments are often used to facilitate a synergistic effect; simple treatments may well be just as effective as complex and expensive ones. The clinician has to balance the local inflammation and trauma with the rapidity of resolution. Patients have often already made their own diagnosis and started treatment with over-the-counter preparations. These may be effective, but persistence and regular paring are needed for any benefit; many patients tend to lose patience. Singular plantar warts are often easily treated with a combination of keratolytics and cryotherapy. A single application of Uptons paste can be applied to the wart under waterproof tape for one week. Care is taken to protect the surrounding normal skin with tape first, before applying the paste only to the wart, and the whole area then further covered with more tape. The patient then attends for the clinician to pare away the macerated tissue and apply cryotherapy to the base of the wart. The wart needs to be kept frozen for 20-30 seconds, enough to result in a small haemorrhagic bulla overnight. Patients are warned that the blister is requisite for effective treatment. A Figure 6: Singular plantar wart on the sole. Figure 7: Multiple plantar warts, coalescing into a large aggregate on an HIV-positive man.

small stellate scar can result occasionally. If needed, the cryotherapy can be repeated at four-weekly intervals, but without the Uptons paste. Alternatively, an extemporaneous preparation of formalin 20% paint may be applied nightly after paring. This process takes several weeks, but the fixation effect hardens the wart-infected

tissue (and kills virus), thus facilitating effective paring. Prescribe 30mL of formaldehyde 20%, salicylic acid 20%, acetone 25% in flexible collodion, applied with a small paintbrush nightly after blade paring or vigorous pumicing. Persistence is the key, although patients can take breaks from treatment to allow healing of the

pared area and observation for residual wart tissue. Mosaic warts are too broad for cryotherapy and are best treated with formaldehyde paint or soaks and pumicing. Other physical alternatives used by dermatologists include: Topical diphenylcyclopropenone (DCP, DPCP)

immunotherapy. Bleomycin injections under local anaesthesia. Curettage and cautery. Ablative or vascular laser therapy. Photodynamic therapy. Patients for whom conventional keratolytics, paring and cryotherapy fail should be considered for the alternative treatments.

Palmoplantar pustulosis
PALMOPLANTAR pustulosis is a relatively common relapsingremitting condition that presents with broad plaques of erythema, scale and vesicopustules (figure 8). Before committing to this diagnosis it is vital that fungal skin scrapings, bacterial skin swab and/or biopsy be performed to rule out tinea or infected eczema. Despite the suggestive clinical features of palmoplantar pustulosis and its response to anti-psoriatic treatments, its classification as a form of pustular psoriasis has been questioned. Note that there are associations with smoking, diabetes and thyroid disease. Mild forms may respond to topical treatments, which should be trialled for at least six weeks. A potent topical steroid may be applied under socks twice a day, such as betamethasone dipropionate ointment in an optimised vehicle (Diprosone OV ointment), or calcipotriol with betamethasone (Daivobet) ointment can be used. Overnight, a tar preparation such as liquor picis carbonis (LPC) 10% with salicylic acid 10% in yellow paraffin may be used, also under sock occlusion. This combination can occasionally irritate fissured or eroded areas; the tar ointment can be withheld for a short period. Failure to respond to topical treatments should trigger a dermatological review to consider alternatives such as psoralen with ultraviolet A, oral acitretin, methotrexate, cyclosporin or the biological agents. Other third-line therapies described include oral corticosteroids hydroxyurea, colchicine, clofazimine and Grenz ray radiotherapy. Figure 8: Palmoplantar pustulosis. Note the broad sheets of scaly erythema studded with vesicopustules, with a discrete border.

Pompholyx and dermatitis

POMPHOLYX (dyshidrotic eczema/dermatitis) presents as an acute eruption of intensely pruritic vesicopapules located on the glabrous skin of the palms and soles and often on the sides of the fingers and toes. There can be associated oedema, weeping and secondary infection. Although pathologically classified as a form of acute dermatitis, the relationship to endogenous eczema is not always present. Pompholyx is often related to acutely stressful events and can have a relapsingremitting course. Although more common on the hands, the feet are often concurrently affected. As always, inflammatory tinea should be ruled out. Management for the feet is similar to that for the hands. Mild forms may be treatable with a potent topical steroid (Diprosone OV) once or twice daily under

Pompholyx is often related to acutely stressful events and can have a relapsing remitting course.

socks. Wet dressing may be used if there is more inflammation or weeping. Infection should be treated concurrently with oral antibiotics. Oral corticosteroids are quite often required to manage severe cases: prednisone at 0.51.0mg/kg daily tapered over two weeks. Treatment can be slowly withdrawn over time, but a relapsingremitting nature is common. Refrac-

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tory cases require systemic immunosuppression. Chronic, endogenous, hyperkeratotic foot eczema (figure 9) is less common than hand eczema. It can occur de novo or, less commonly, can result from recurrent bouts of pompholyx. This can look very similar to palmoplantar pustulosis or tinea, especially if bacterial infection sets in. Skin scrapings and bacterial swabs need to be performed before

starting treatment. After initiation of general measures, topical treatment is identical to that for palmoplantar pustulosis. The tar preparation at night may be withheld if there is excessive irritation. Fissures may be sealed with Tinc Benz Co 3% in petrolatum. With recalcitrant foot eczema, a biopsy should be performed for definitive diagnosis, and oral immunosupression may be required.

Allergic contract dermatitis on the feet results from a delayed hypersensitivity to one of the components of shoes or socks.

Allergic contact dermatitis

ALLERGIC contact dermatitis on the feet results from a delayed hypersensitivity reaction to one of the components of shoes or socks. It should be suspected if the pattern of rash is somewhat geometric with a sharp cutoff, corresponds to a part of the footwear exposed, or occurs after specific exposure to particular shoes or socks. The allergens are varied and can include rubber products (figure 10), glues, fabric dyes, chromate in leathers or nickel from buckles or studs. However, the rash may not always be bilateral and can involve the whole foot if tight-fitting footwear distributes the allergen broadly. Epicutaneous patch testing (not prick testing or RAST) is required to make the diagnosis; the patient should be referred to a dermatologist with a special interest in patch testing. Localised eczema is treated with general measures and potent topical steroids. Beyond that, the mainstays of therapy are identifying and avoiding the relevant allergen. Depending on the allergen, various avoidance strategies are available but usually involve simply seeking an alternative style of footwear that does not have that allergen. Avoidance of dyes in socks and fabric shoes is straightforward. Vegetable-dyed (chromate-free) leather shoes are available for people with chromate sensitivity. Cork insoles may be substituted for rubber insoles, and bespoke full-leather shoes are available to avoid rubber allergens. Clear nail polish can be used to coat buckles and studs to prevent contact with nickel.

Figure 9: Chronic foot eczema as part of generalised eczema. Note the associated hyperpigmentation in Asian skin.

Figure 10: Allergic contact dermatitis to the rubber strap of thongs/flip-flops.

Juvenile plantar dermatosis

JUVENILE plantar dermatosis is a specific condition that occurs in schoolaged children, typically settling by puberty. The load-bearing areas are affected great toe, forefoot and heel sparing the instep and interdigital areas. The skin has a dry glazed appearance, often with fissuring and scaling. The putative aetiology is thought to be the wearing of synthetic material and sneakers. Repeated sweating and drying washes away the essential lipids, leading to the clinical appearance. Ruling out other diseases and regular reassurance of eventual spontaneous resolution is needed, as no treatment is reliably effective. Changing to socks made of natural fibres and use of less occlusive footwear may be tried. Topical steroids are used if there is inflammation. Keratolytic moisturisers are the mainstay of therapy, although it is said that any improvement is relatively short lived. Patients may rotate through various over-thecounter heel balms, urea 10% creams (eg, Calmurid cream), salicylic acid 8% in emulsifying ointment, etc. Deeper fissures may be sealed with a twice-daily application of Tinc Benz Co 3% in yellow paraffin, before application of the moisturiser.

Heel fissures
CRACKS and fissures of the plantar skin, especially the heel, become more common with age. Progressive hyperkeratosis and asteatosis of older skin is exacerbated by exposure through the use of open footwear. With the regular deformation and expansion of the plantar skin through walking, this thick, dry, inflexible, unyielding stratum corneum cracks and leads to painful fissures. The fissures can be sealed with twice-daily applications of Tinc Benz Co 3% in petrolatum. The ointment is applied to the fissure with a finger or cotton bud. This relieves the tenderness as well as preventing irritation by the subsequent application of moisturisers and keratolytics. Moisturisation is the mainstay to prevent further desiccation, and the wearing of occlusive footwear is synergistic (maintains the hydration and supports the heel). Patients should therefore be encouraged to use commercial heel balms (eg, Eulactol Heel Balm, Neutrogena Norwegian Formula Foot Cream, etc) 2-3 times daily, under socks and shoes during the day and socks overnight. Further softening can be achieved by extemporaneous preparations of keratolytics such as salicylic acid 10% or urea 20% in emulsifying ointment. Gross hyperkeratosis may be debrided by pumicing or shaving with an appropriate device before application of the moisturiser. Patients with deep or recalcitrant cracks may require further support by regular strapping with athletic tape or referral to an orthotist for heel cups or supports.

Perniosis
CHILBLAINS (perniosis) causes painful, itchy, erythematous inflammatory nodules on the extremities. Apart from the toes, these nodules can also be found on the heels, legs, thighs, fingers, nose and ears. Individual lesions can also ulcerate and blister. Perniosis is due to an abnormal vascular response to cold moist conditions, and so tends to occur during autumn and winter. Associated conditions include: Anorexia. Connective tissue diseases. Myelodysplastic disease. Peripheral vascular disease (diabetes, smoking, hyperlipidaemia). Cyroproteins in children. These should be sought clinically and investigated for with: Full blood examination. Autoimmune screening, including cryoglobulins and cold agglutinins. Diabetes screen. Peripheral vascular imaging. Fasting lipids. Chilblain lupus erythematosus is a different disease but may present in a similar fashion. Most cases are recurrent but self-limiting. Keeping the extremities warm is the key, so thick socks and closed shoes are important as prophylaxis. Potent topical steroids are useful (eg, Diprosone ointment twice daily). A peripheral vasodilator in the form of calciumchannel blockers (eg, nifedipine 20-60mg daily, diltiazem 60-120mg tds) should be used for several weeks as both treatment and prophylaxis. Topical minoxidil 5% lotion tds may also be used for patients intolerant of the oral agents.

Palmoplantar keratoderma
THE term palmoplantar keratoderma is a clinical description for when both the palmar and plantar surfaces are affected by gross hyperkeratosis. The differential diagnostic list is extensive and involves inherited, acquired and malignant causes. Inherited causes typically arise early in life and are accompanied by other diagnostic features as part of a syndrome. Thus these rarely present later in general practice without a pre-existing diagnosis (figure 11, see page 30). Acquired palmoplantar keratoderma also can present with other signs that aid in the diagnosis, but not always. The more common causes include: Psoriasis. Eczema variant. Lichen planus (figure 12, see page 30). SLE. Pityriasis rubra pilaris. Reiters-type spondyloarthropathy.
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Dermatophyte infection. Viral warts. Scabies. Syphilis. HIV. Drug reactions. Rare causes include myxodematous or lymphoedematous keratodermas, mycosis fungiodes and as a paraneoplastic syndrome. Diagnosis can be challenging, so a thorough history and examination is required to discover other

diagnostic features. A biopsy may be needed to differentiate similar rashes. A scraping for fungal culture is mandatory, and microscopic examination for scabies if suspicious. Further investigations may be performed for associations if relevant. Treatment of any form of palmoplantar keratoderma is challenging and would be directed to aetiology. Regardless of the cause, reducing
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the hyperkeratosis may be of benefit, not only for symptomatic relief but also to facilitate the penetration of other therapeutic applications. Topical keratolytics in the form of salicylic acid 5-10%, urea 10-20%, propylene glycol 10-40% or lactic acid 5% in aqueous or other cream base can be applied twice daily under occlusion. Potent topical steroids are of use with inflammatory diseases. Topical psoralen and ultraviolet A therapy can be effective for psoriasis and eczema. Oral retinoids are used for many inherited forms of this disease, as well as for psoriasis, lichen planus and pityriasis rubra pilaris.

Figure 11: Palmoplantar keratoderma due to WeberCockayne-type epidermolysis bullosa simplex. An example of a genetic syndrome with an associated plantar keratoderma.

Figure 12: Hypertrophic lichen planus leading to plantar keratoderma. Note the associated plaque on the leg, which aids in the diagnosis.

Conclusion
THE specialised skin of the feet results in atypical presentations of typical diseases as well as dermatoses unique to that area. Fungal infection is the most common diagnosis and must be ruled out with any scaly erythematous eruption on the feet. Biopsies are often needed to clinch a diagnosis before launching into treatment. General non-drug measures of caring for the feet are as important as specific topical and systemic treatments. A relapsingremitting nature is not uncommon, given the nature of some dermatoses and that the conditions that led to the pedal disease may not be easily avoided.

Online resources
Australasian College of Dermatologists: www.dermcoll.asn.au DermNet NZ: www.dermnet.org.nz

Some pedal dermatoses and appropriate first-line therapies

Disease Tinea pedis Clinical features Scaly, erythematous, marginated rash Interdigital maceration and scale Moccasin-type: scale on entire sole Excessive sweating of feet, leading to odour, tinea, pitted keratolysis, etc Investigations Scrapings for fungal MCS; nail clippings if appropriate Rule out systemic causes (uncommon) Treatment Deliberate drying and ventilation Terbinafine spray, lotion, drops Oral terbinafine if extensive Open shoes Topical Driclor Iontophoresis Botulinum toxin Deliberate drying and ventilation Topical clindamycin lotion Keratolytics (Uptons paste) and paring Cryotherapy Formalin paint Combination of treatments Potent topical steroidocclusion Oral corticosteroid if severe Potent topical steroid Tar ointment* Use both at separate times, under occlusion Potent topical steroid Allergen-avoidance strategies Change to natural fibres for socks and ventilated footwear Keratolytic moisturisers Topical steroid if inflamed Warm socks and footwear Treat associated conditions Potent topical steroids Calcium-channel blockers Topical minoxidil (5%) lotion Occlusive footwear Regular debridement/pumicing Heel balms and keratolytics

Plantar hyperhidrosis

Pitted keratolysis Plantar warts

Pale, oedematous plantar skin with small punched-out pits Discrete, flat-topped, verrucous papules and nodules with punctate, thrombosed capillaries Large mosaic warts Acute pruritic vesicopapular eruption on palms and sides of fingers Erythematous, scaly, discrete plaque studded with vesicopustules Eczematous features Peculiar pattern associated with contact Associated with particular footwear Dry, erythematous, glazed appearance Affecting load-bearing areas Spares webspaces and instep Painful, pruritic, violaceous nodules on toes and extremities

Look out for hyperhidrosis Nil

Pompholyx Palmoplantar pustulosis Allergic contact dermatitis

Swabs for bacterial MCS if appropriate Scrapings for fungal MCS Swabs for bacterial MCS Biopsy Refer for epicutaneous patch testing (not prick test or RAST) Nil

Juvenile plantar dermatosis

Perniosis

Connective tissue disease screening Cryoprecipitate screening Diabetes screening Fasting lipids Peripheral vascular disease imaging Nil

Heel fissures

Dry, hyperkeratotic, cracked and fissured heels

*Tar ointment: Liquor picis carbonis (LPC) 10%, salicylic acid 10% in petrolatum Urea 10% cream, salicylic 8% in emulsifying ointment Peripherally vasodilating types: diltiazem, nifedipine MCS = microscopy, culture, sensitivities

GPs contribution
Case study
TONY, 40, is morbidly obese and has metabolic syndrome. He probably weighs about 150kg, but my scales only weigh up to 135kg! He cannot reach his toes to wear shoes and tie laces, cut his toe nails or dry his feet after showering. He had swollen legs with venous eczematous skin changes. About a year ago he had leg oedema associated with oozing and a few ulcers. He was also seen by a vascular surgeon, who suggested he have four-layer compression bandaging. Although the dressings were done by the community nurses, sometimes, Tony would remove the compression bandaging himself (before the end of the week) because he did not tolerate them. Unfortunately his ulcers then became infected and swabs revealed pseudomonas. I decided to treat him with oral ciprofloxacin. However, the surgeon suggested I was essentially wasting my time with oral antibiotics if he did not also address the underlying venous return issues. This patient also had cracked heels and in the past I had suggested using urea 10% creams. But because of his size he could not apply them himself. After reading your article, I wonder if he also has tinea between his toes because he was not able to effectively dry his feet himself. He also has pitted keratolysis on the soles of his feet.

Questions for the author

Obviously Tonys excessive weight and therefore difficulty with personal hygiene is the underlying problem here. However, how would you tackle his multiple pedal skin problems? Indeed, the above patients problem is complex and multifactorial, and improvement
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DR PHILIP LYE
Sutherland, NSW

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rather than full resolution may be seen as successful management. Apart from the obesity, the venous insufficiency and ulceration are the most pressing issues, while the potential tinea and pitted keratolysis may be dealt with in due course. Although four-layer compression is the gold standard in terms of effective compression bandaging, it may be difficult to tolerate when there is inflammation, infection and oedema. I would suggest twicedaily applications of a potent topical steroid under wet dressings for 1-2 weeks, with plenty of leg elevation and rest without too much compression. The topical steroid (eg Diprosone cream) may be mixed three parts with one part Hydroform cream (clioquinol with hydrocortisone), to combine a topical antiseptic property with the anti-inflammatory intent. Once much of the inflammation has settled, the wet dressings should stop and the topical steroid only be applied, followed by regular moisturising. Over the steroids and moisturisers, light compression

may be applied in the form of grade I compression stockings (up to 20mmHg), which is much more tolerable for larger oedematous legs (light compression being better than no compression). The stockings may be removed for sleep. As the patients clinical state improves, more aggressive stockings (or four-layer compression) may be applied. My preference is for compression stockings, as they may be applied by the patient (sometimes requiring assistance), are less cumbersome and can be reused after laundering. Arterial compromise needs to be excluded, especially in a patient with metabolic syndrome. Once the venous insufficiency and secondary eczema have settled, drying the feet becomes easier. Compression stockings with open toes rather than four-layer bandaging would be less occlusive and sweaty, thus facilitating dessication of the feet. Perhaps the community nurses can assist with drying the feet when applying the steroids and stockings. The pitted keratolysis will settle with drying, while the fissures may well improve with the occlusion of

the most appropriate narrowspectrum antibiotic to use. The empirical mixture of a topical steroid (three parts) with clioquinol (Hydroform cream, one part) used twice daily under occlusion can be a quite effective adjunct in treating infected venous eczema.

General questions for the author

the compression stockings. What is your opinion about using oral ciprofloxacin? All chronic wounds are typically colonised, with Pseudomonas being a commonly isolated organism. Clinical correlation is required to determine whether the swab result indicates infection is present. Ciprofloxacin is a useful antibiotic, especially for Pseuomonas. However, it is also quite broad spectrum and, although this may initially be an attractive attribute, it is often said that a narrow-spectrum antibiotic is desirable to prevent antibiotic resistance. Culture sensitivities should give guidance to What brand of waterproof tape do you use when applying Uptons paste to plantar warts? Is there anything to watch out for (as a GP) when doing this? In my experience, patients are not very impressed by the macerated tissue when the tape is taken off a week later. I routinely treat warts with Uptons paste and paring, and if applied carefully the maceration is only found where one applied the paste. The surrounding normal skin has to be protected with Leukoplast Waterproof fabric-based white tape. I typically use one or two strips with a hole cut in the middle appropriately sized for the wart and a small rim of surrounding skin. A mound of paste is applied, covering the entire wart and more water-

proof tape applied over the top. Patients are advised to take care of the dressing to avoid it lifting off. Patients are advised that the maceration is indeed the intent. The Uptons paste will dissolve not only the wart-infested tissue, but also allow relatively easy and painless paring of the wart so that the base of the wart may more effectively treated with cryotherapy. I have an elderly Chinese patient with pompholyx involving both feet. In the past she had been treated with Condys solution. Is this still suggested? Soaking with Condys crystals (potassium permanganate) in solution is an effective astringent and antiseptic treatment traditionally used as a wet-to-dry dressing for weepy wounds. It can be used in pompholyx if there is a lot of weeping and wet maceration. Topical steroids can be more effectively applied after the weeping is removed with Condys solution. When making up the solution it is important to dissolve the crystals parsimoniously, to produce a preparation with a

relatively pale colour. An overly concentrated batch will stain skin and nails purple. Could you briefly explain the difference between patch and prick testing? Prick testing is performed to discover immediate hypersensitivity to agents that cause urticaria, angioedema and anaphylaxis. Allergens in solution are placed onto the skin and the stratum corneum breached by scratching lightly with a lancet to expose the allergen to the skin. A wheal reaction is anticipated within minutes. Patch testing (epicutaneous patch testing) is used for delayed hypersensitivity, which typically manifests as allergic contact dermatitis. Allergens in solution or paraffin wax are placed on specialised aluminium chambers and stuck onto the skin for two days. An initial reading is made after removal of the allergens to observe for irritation, and a second reading made at day seven to reveal any delayed allergic response. Agents that cause immediate- and delayed-type hypersensitivity are typically quite different.

How to Treat Quiz

Pedal dermatoses 19 March 2010
1. Which TWO statements are correct? a) In patients with recurrent pedal cellulitis, identification and treatment of coexistent tinea pedis can prevent bacterial re-infection b) Fine scale and erythema of the entire plantar surface suggests a diagnosis other than tinea pedis c) Keeping the feet dry by careful drying and footwear with adequate ventilation is the key to preventing tinea pedis d) Topical corticosteroids should never be used in the treatment of tinea pedis 2. Which TWO statements are correct? a) Topical antifungals are the treatment of choice for onychomycosis b) Possible adverse events associated with oral terbinafine include loss of taste, loss of appetite, severe drug rashes and hepatic impairment c) Plantar hyperhidrosis may uncommonly be associated with serious neurological and vascular conditions d) In the treatment of hyperhidrosis, aluminium chloride hexahydrate lotion should be applied to moist skin 3. Which THREE statements are correct? a) Iontophoresis and botulinum toxin are treatment options for hyperhydrosis b) Lumbar sympathectomy for plantar hyperhidrosis is often associated with ejaculatory failure, impotence and anorgasmia c) Pitted keratolysis is caused by the overgrowth of dermatophyte fungi d) Treatment for pitted keratolysis includes clindamycin lotion and 2% formalin soaks 4. Which THREE statements are correct? a) Paediatric plantar warts typically resolve spontaneously over time b) To be effective, plantar wart treatments should not inflame the wart c) Persistence with treatments and regular paring of the warty tissue are essential in the treatment of plantar warts d) A combination of keratolytics and cryotherapy is an effective treatment of plantar warts 5. Which TWO statements are correct? a) Cryotherapy to plantar warts should not result in blistering b) Preparations containing formalin should be avoided in the treatment of plantar warts c) Cryotherapy is not suitable for the large skin area involved with mosaic warts d) Treatments for plantar warts unresponsive to conventional therapy include immunotherapy, bleomycin injections and laser therapy 6. Which THREE statements are correct? a) Palmoplantar pustulosis is a form of infected eczema

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b) Palmoplantar pustulosis is associated with smoking, diabetes and thyroid disease c) Topical treatments used in psoriasis are also used for palmoplantar pustulosis d) Treatments that may be used in palmoplantar pustulosis unresponsive to topical therapy include psoralen with ultraviolet A [PUVA], oral acitretin, methotrexate, cyclosporin and the biologicals 7. Which TWO statements are correct? a) Pompholyx presents as an acute eruption of intensely pruritic vesicopapules on the glabrous skin of the palms and soles and often on the sides of the fingers and toes b) Pompholyx is a form of contact dermatitis c) Oral corticosteroids are contraindicated for pompholyx d) Topical treatment for chronic endogenous hyperkeratotic foot eczema is identical to that for palmoplantar pustulosis 8. Which TWO statements are correct? a) Allergic contact dermatitis on the feet often involves a delayed hypersensitivity reaction to one of the components of shoes or socks b) The allergens in contact dermatitis can include rubber, glues, fabric dyes, chromate in leathers, or nickel from buckles or studs c) The rash of contact dermatitis is always confined to the skin in immediate contact with the allergen d) Skin prick testing or RAST are required to make the diagnosis of contact dermatitis 9. Which THREE statements are correct? a) In juvenile plantar dermatosis the skin has a dry glazed appearance with fissuring and scaling, affecting only the load-bearing areas of the feet b) Juvenile plantar dermatosis typically settles by puberty c) Heel fissures can be sealed and soothed with twice-daily applications of Tinc Benz Co 3% in petrolatum d) Occlusive footwear should be avoided in patients with heel fissures 10. Which THREE statements are correct? a) Perniosis (chilblains) is associated with anorexia, connective tissue diseases, myelodysplastic disease, peripheral vascular disease or cryoproteins in children b) Calcium-channel blockers are contraindicated in people with perniosis c) Palmoplantar keratoderma is a clinical description for when both the palmar and plantar surfaces are affected by gross hyperkeratosis d) In people with palmoplantar keratoderma, the differential diagnosis of underlying causes includes inherited, acquired and malignant conditions

CPD QUIZ UPDATE

The RACGP now requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2008-10 triennium. You can complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept the quiz by post or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online.

HOW TO TREAT Editor: Dr Giovanna Zingarelli Co-ordinator: Julian McAllan Quiz: Dr Giovanna Zingarelli

NEXT WEEK The next How to Treat tackles malignant glioma in adults. The authors are Dr Elizabeth Hovey, senior staff specialist in medical oncology, Prince of Wales Hospital, Randwick, and senior conjoint lecturer, University of NSW, Kensington, NSW; Dr Eng-Siew Koh, staff specialist in radiation oncology, Liverpool Hospital Collaboration for Cancer Outcomes Research and Evaluation (CCORE), and senior conjoint lecturer, south western Sydney clinical school, University of NSW; Dr Lindy Jeffree, consultant neurosurgeon, Macquarie Neurosurgery and Dalcross Private Hospital, and clinical senior lecturer, Australian School of Advanced Medicine, Macquarie University, North Ryde, NSW; and Associate Professor Andrew Cole, senior consultant in rehabilitation medicine, rehabilitation department, St George Hospital, Kogarah, and conjoint associate professor, University of NSW, Kensington, NSW.

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| Australian Doctor | 19 March 2010

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