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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
www.australiandoctor.com.au
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.
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.
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19 March 2010 | Australian Doctor |
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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 meas-
Figure 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.
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
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.
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.
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| Australian Doctor | 19 March 2010
• 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 accord-
ing 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 surcont’d page 28
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HOW TO TREAT Pedal dermatoses
from page 26
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).
• Horner’s 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 ‘Upton’s
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.
small stellate scar can result
occasionally. If needed, the
cryotherapy can be repeated
at four-weekly intervals, but
without the Upton’s 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
Palmoplantar pustulosis
PALMOPLANTAR pustulosis is a relatively common
relapsing–remitting 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.
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| Australian Doctor | 19 March 2010
Figure 7: Multiple plantar warts, coalescing into a large
aggregate on an HIV-positive man.
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.
Pompholyx and dermatitis
Figure 8: Palmoplantar pustulosis. Note the broad sheets of scaly
erythema studded with vesicopustules, with a discrete border.
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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 relapsing–remitting 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 relapsing–remitting
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
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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.
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Allergic contract
dermatitis on the
feet results from
a delayed
hypersensitivity
to one of the
components of
shoes or socks.
Figure 9: Chronic foot eczema as part of generalised eczema.
Note the associated hyperpigmentation in Asian skin.
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 sponta-
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 straight-
forward. 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 10: Allergic contact dermatitis to the rubber strap of
thongs/flip-flops.
Heel fissures
neous 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.
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.
• Reiter’s-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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HOW TO TREAT Pedal dermatoses
from previous page
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 Weber–Cockayne-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
Online resources
thematous 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 sys-
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 ery-
temic treatments.
A relapsing–remitting 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.
Australasian College of
Dermatologists:
www.dermcoll.asn.au
DermNet NZ:
www.dermnet.org.nz
Some pedal dermatoses and appropriate first-line therapies
Disease
Clinical features
Investigations
Treatment
Tinea pedis
Scaly, erythematous, marginated rash
Interdigital maceration and scale
Moccasin-type: scale on entire sole
Scrapings for fungal MCS; nail clippings
if appropriate
Deliberate drying and ventilation
Terbinafine spray, lotion, drops
Oral terbinafine if extensive
Plantar hyperhidrosis
Excessive sweating of feet, leading
to odour, tinea, pitted keratolysis, etc
Rule out systemic causes (uncommon)
Open shoes
Topical Driclor
Iontophoresis
Botulinum toxin
Pitted keratolysis
Pale, oedematous plantar skin with small
‘punched-out’ pits
Look out for hyperhidrosis
Deliberate drying and ventilation
Topical clindamycin lotion
Plantar warts
Discrete, flat-topped, verrucous papules
and nodules with punctate,
thrombosed capillaries
Large ‘mosaic’ warts
Nil
Keratolytics (Upton’s paste) and paring
Cryotherapy
Formalin paint
Combination of treatments
Pompholyx
Acute pruritic vesicopapular eruption
on palms and sides of fingers
Swabs for bacterial MCS if appropriate
Potent topical steroid±occlusion
Oral corticosteroid if severe
Palmoplantar
pustulosis
Erythematous, scaly, discrete plaque
studded with vesicopustules
Scrapings for fungal MCS
Swabs for bacterial MCS
Biopsy
Potent topical steroid
Tar ointment*
Use both at separate times, under occlusion
Allergic contact dermatitis
Eczematous features
Peculiar pattern associated with contact
Associated with particular footwear
Refer for epicutaneous patch testing
(not prick test or RAST)
Potent topical steroid
Allergen-avoidance strategies
Juvenile plantar dermatosis
Dry, erythematous, glazed appearance
Affecting ‘load-bearing’ areas
Spares webspaces and instep
Nil
Change to natural fibres for socks and
ventilated footwear
Keratolytic moisturisers†
Topical steroid if inflamed
Perniosis
Painful, pruritic, violaceous nodules on
toes and extremities
Connective tissue disease screening
Cryoprecipitate screening
Diabetes screening
Fasting lipids
Peripheral vascular disease imaging
Warm socks and footwear
Treat associated conditions
Potent topical steroids
Calcium-channel blockers‡
Topical minoxidil (5%) lotion
Heel fissures
Dry, hyperkeratotic, cracked and
fissured heels
Nil
Occlusive footwear
Regular debridement/pumicing
Heel balms and keratolytics
*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
GP’s contribution
Case study
DR PHILIP LYE
Sutherland, NSW
30
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
| Australian Doctor | 19 March 2010
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.
www.australiandoctor.com.au
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 Tony’s 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 patient’s
problem is complex and multifactorial, and improvement
cont’d page 32
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HOW TO TREAT Pedal dermatoses
from page 30
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 patient’s 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
How to Treat Quiz
What brand of waterproof
tape do you use when applying
Upton’s 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
Upton’s 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 Upton’s 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 Condy’s solution. Is this
still suggested?
Soaking with Condy’s 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
Condy’s 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.
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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.
32
| Australian Doctor | 19 March 2010
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