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S1PodiatryNow Supplement June 2008

ContinuingProfessional Development Supported by an educational grant from Galderma UK Limited

The Society of Chiropodists and Podiatrists

Hyperkeratosis of the foot: part 1Ivan Bristow, Lecturer, School of Health Professions & Rehabilitation Sciences,University of Southampton.

IntroductionThe plantar surface of the foot is a specialised area of skin.Despite its relatively small surface area, its integrity is essentialfor normal locomotion and health. The key to its role, in part,is the thickened, keratinised epidermis. The process ofkeratinisation is a normal physiological mechanism whichmaintains viability by the generation of new epidermal cells inthe basal layer and differentiation of the cells ascending throughthe epidermis. By the time they have reached the stratumcorneum, cells have matured and finally desquamate from thesurface of the epidermis.

When an area of skin shows thickening of the stratum corneumbeyond that which is appropriate for the site, it is termed

“hyperkeratosis”1. The most common cause of the condition onthe foot is as a response to the intermittent forces of locomotionalthough many dermatological conditions may demonstratehyperkeratosis as part of their pathophysiology. This article willreview some of the causes of plantar hyperkeratosis and howthey may be recognised clinically.

Approach to assessmentAs with all assessments, when approaching a patient withhyperkeratosis, a standard procedure should be followed:

HistoryExaminationFurther Tests

History should encompass the normal details including medicalhistory, family history (with particular attention to skindisorders), and medication. In addition, inspection of thepatient’s footwear, an often neglected area, is important. Badlyworn or incorrectly fitting shoes can lead to the development oraggravation of hyperkeratosis (see case study 1). Attentionshould be paid to the insock and lining as well as the sole andheel areas.


• Mechanically induced

• Dermatological disease

• Infection

• Drugs

Table 1. Common causes of PlantarHyperkeratosis

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Examination should be carried out in a methodical fashion.Firstly, it is important to assess the skin of the foot and wherepossible legs, palms and arms. Many conditions may affect thepalms concurrently and recognition of this can aid diagnosis. Itis also pertinent to question the patient about other areas ofskin which may not be available for examination. Other keyaspects are bulleted below.

• Pattern of hyperkeratosis: symmetrical, asymmetrical, archsparing?

• Appearance of lesions elsewhere on the skin?• Texture: does this feel like normal mechanical keratosis? • Is the hyperkeratosis easily lifted or well attached? • Visual examination of individual lesions - magnifying lamp or

dermatoscope.• Fungal infection ruled out? Take skin scrapings if suspected.

Causes of HyperkeratosisIn routine podiatry practice, mechanically induced skin changesare the most common cause of hyperkeratosis on the foot (ascorns and callus). Thickening of the stratum corneum may beregarded as a physiological response to mechanical trauma2.Burzykowski and colleagues3 in a study of over 70 000 adultfeet found that around 10% suffered with the condition with anincreased prevalence in women and with ageing. Such lesionscan be a source of high pressure and lead to complications suchas ulceration in the diabetic foot4. Mechanically inducedhyperkeratosis will be discussed further in a future CPD article.

Non-mechanical hyperkeratosis Although no specific data is available, non-mechanicallyinduced hyperkeratosis is probably less common in podiatricpractice. From a clinician’s point of view, it is important toestablish the differentiation between the mechanically inducedand non-mechanically induced lesions as therapeutic successrelies on elucidating the cause and selecting an appropriatetreatment. For example, chronic, hyperkeratotic eczema on the

plantar surface will not benefit from operative reduction andmay lead to other complications (see case study 2). Table 3 listssome of the causes of non-mechanical hyperkeratosis. Due tothe restrictions on the length of this publication it is not possibleto cover all these in detail and the reader is encouraged toresearch the topic further if it is of relevance to their CPD needs.

Skin DiseasePsoriasis affects around 2-3% of the population and in a subsetof patients may affect the plantar surfaces either as part ofwidespread eruption or as localised disease. Classically, itpresents as erythematous scaly plaques. Clues to its presencerely on its symmetrical presentation with sharply demarcatedborders with a tendency to relapse and remit. Examination mayreveal the disease elsewhere including the scalp, extensorsurfaces of the elbows and knees. Fingernail involvement mayinclude pitting, whilst toenails tend to show onycholysis, sub-ungual hyperkeratosis and rapid growth. Lifting the scale maylead to pinpoint bleeding known as “Auspitz sign” which canaid diagnosis. On that basis, scalpel debridement of psoriaticlesions is not recommended. Management of the condition onthe foot can be difficult although emollients may be helpful insoftening the lesions. Topical steroids may be used to treat thecondition, but withdrawal from them often leads to a worsening

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PodiatryNow Supplement June 2008

Continuing Professional Development


• Plantar surface• Non-weight bearing or weight bearing areas?• Symmetry• Texture and characteristics• Background erythema

• Legs and arms• Examine where possible

• Palms• Signs of hyperkeratosis may be more subtle here

• Footwear• Inspect the shoes most frequently worn• Internal and external assessment of the shoe

Table 2. Examination of the patient withhyperkeratosis

• Skin Disease• Psoriasis• Eczema / dermatitis• Keratoderma blennorrhagica• Keratoderma climactericum• Lichen planus• Pityriasis rubra pilaris• Palmo-plantar keratoderma (PPK)

• Infection• Tinea pedis• Plantar warts• Scabies• Syphilis

• Drugs• Lithium• Verapamil• Bleomycin

• Systemic Disease• Hypothyroidism• Lymphoedema

• Malnutrition• Zinc deficiency

• Internal malignancies• Idiopathic

Table 3. Causes of non-mechanical hyperkeratosis


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of the psoriasis (a “rebound” phenomenon) and so they areseldom used. Dermatological management may include topicalvitamin D derivatives, oral retinoids, ciclosporin and PUVA5.

Eczema is another common skin disorder which may affect thefoot. Causes can be internal or external (such as allergens,irritants or skin infections). Chronic eczema of the foot ishallmarked by hyperkeratosis and lichenification (exaggerationof skin creases with a leathery texture)6. Anecdotally, it maypresent as a diffuse plantar hyperkeratosis but with a brittletexture which bleeds when debridement is undertaken. Heelfissures are a common accompaniment to the disorder (see casestudy 2). Where fissuring and weeping are present, secondarybacterial infection, with staphylococcus aureus, is very commonin patients with eczema7. Management, like psoriasis, requiresemollients and topical steroids although antibacterial measureswill be required to treat any co-existing infection if steroids areto be applied.

Contact dermatitis can occur anywhere on the feet, most typicallyas a result of sensitivity to adhesives, rubber, nickel buckles andleather dyes. Most commonly it is seen as symmetrical,hyperkeratotic areas on the dorsum of the feet, corresponding tothe points of contact with the allergen. A thorough history andpatch testing can help rule out other causes such as mechanicalirritant dermatitis, eczema and psoriasis8.

Keratoderma blennhorragica is an uncommon hyperkeratoticeruption of the soles which is virtually indistinguishable fromplantar psoriasis. The condition is a cutaneous manifestation ofReiters disease, a seronegative polyarthritis seen particularly inyoung men with the B 27 haplotype.

Keratoderma climactericum is a hyperkeratosis of the soleswhich slowly develops in the heel and forefoot area anddevelops into non-itchy, hyperkeratotic plaques whichsubsequently fissure and become painful. With time, lesionsmay develop on the palms. Generally, the lesions are round oroval in shape and are light in texture (See figure 1). Fungalinfection should be ruled out by microscopy and fungal culture.

The disease was first described in 1934 by Hauxthausen whodescribed the condition in menopausal women. SubsequentlyGram9 noted that typically women sufferers were moderatelyoverweight, hypertensive and had arthritis of the knees9. Studies sofar have been unable to show a link to fluctuating oestrogen levelsalthough collagen structure has been demonstrated to beinfluenced by sex hormones10 and may explain the disease.Management of the condition as a first step should includeintensive emollient therapy11. Fissuring can be managedsuccessfully with topical steroids as a cream/ointment or as animpregnated adhesive tape (Haelan®, Typharm Ltd). Undercurrent access and supply, podiatrists are only able to access mildlypotent topical corticosteroids (1% hydrocortisone) and so referralwill be necessary to obtain the more potent steroid preparations.

Other dermatological conditions which may give rise tohyperkeratosis include lichen planus and pityriasis rubra pilaris.The former is characterised by itchy, purple, flat topped papulesaround the ankles and wrists of adults. Occasionally, thecondition may involve the plantar surface and present asdiffuse, yellow hyperkeratosis. Rarely, ulcerations may developon the sole12. Pityriasis rubra pilaris is an uncommon follicularhyperkeratosis which affects adults between the ages of 40 and60 leading to scaly plaques with yellow-red appearance. Palmo-plantar involvement causes a diffuse hyperkeratosis (Figure 2).Most cases spontaneously resolve in 2-3 years, but oralretinoids may hasten its remission. Retinoids are describedunder the Section ‘Palmo-plantar Keratoderma’ (page 5).

InfectionsWarts commonly affect the foot and plantar lesions in particularmay develop an overlying hyperkeratosis hampering topicaltreatment. Diagnosing the lesion is straightforward but lesionsin immuno-suppressed individuals (such as transplantrecipients) may be larger and more hyperkeratotic and requirecareful assessment, as malignant transformation is notuncommon in these patients13. Tinea pedis occasionally may

Hyperkeratosis of the foot: part 1

PodiatryNow Supplement June 2008

Figure 2 : Pityriasis rubra pilaris

Figure 1: Keratoderma climactericum


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S4 PodiatryNow Supplement June 2008

result in a mild plantar hyperkeratosis, particularly T rubruminfections. Diagnostically, a number of clues should be sought.Firstly, the skin appears dry with a chalky white appearanceaccentuated in skin creases14. Itching is often absent. Theinfection is usually asymmetrical, affecting one foot and can beconfirmed by mycology. Management requires the use of topicalantifungal agents or oral agents in more chronic infections.Attention should also be paid to the hands and groin which mayharbour co-existing infection.

Secondary syphilis, although uncommon, produces a psoriasis-like eruption on the soles of the feet15. Typically beginning ascoppery colour papules and macules, that develop ahyperkeratotic surface and central keratinous plugs.

Scabies is a contagious infestation of the skin by the Sarcoptesscabei mite. Symptoms of severe itching develop around 4 weeksafter exposure, worse when the patient is warm. Typically, it mayoccur around the arch of the foot, mimicking eczematous-likeeruptions in the very young. Debilitated and immuno-compromised patients may develop crusted scabies which presentsas hyperkeratotic patches on the feet which are home to millionsof active mites. Treatment in such cases is oral ivermectin.

Hyperkeratosis due to drugs and other chemical agentsAny patient presenting with a recent skin problem should bequestioned about medications and other chemical agents whichmay be applied to the skin as a medicine or in the course of theiroccupation or recreational pursuits. Particular attention shouldbe paid to any agents that were first used around the time theeruption began. Causation can only be confirmed if the drug isdiscontinued and the symptoms then subside. Drugs includinglithium, gold salts, bleomycin, methyldopa and verapamil haveall been implicated as occasional causes. Arsenic intoxicationhas also been shown to lead to the development of small,punctuate plantar keratoses identical to seed corns16.

LymphoedemaChronic swelling of the leg has many causes. Typicallylymphatic failure leads to a painless swelling of the leg and foot.Water logging of the dermis leads to a hyperplasia of overlyingskin due to the presence of growth factors and cytokines. Thisin turn can lead to hyperplasia of the skin with velvety or wartylike changes17. A brown coloured hyperkeratosis may occuroverlying these plaques. Treatment for the underlying cause andreduction of the oedema along with good skin care canfrequently reverse these changes (Figure 3).

HypothyroidismRarely, hypothyroidism can lead to a diffuse plantarhyperkeratosis of the palms and soles. Typically the patients aremiddle aged with a more severe eruption on the palms than onthe soles. The plantar surfaces may show patchy hyperkeratosiswith fissuring. The condition appears to be unresponsive totopical steroids but shows rapid improvement upon thyroxinereplacement therapy19.

Palmo-plantar KeratodermaThe term palmo-plantar keratoderma (PPK) is given to a diversegroup of conditions which describe a hyperkeratosisconcurrently affecting the palms and the soles of the sufferer.Traditionally, the term was used to describe those conditionssuspected to be genetic in origin, although it is generallyaccepted that acquired types of PPK do occur as well.Conditions causing PPK are distinguished by their genetics,clinical appearance, symptoms and features additional to thepalmo-plantar involvement. Stevens et al.20 attempted to classifythe disease by its presentation and described it as:

• Diffuse (widespread plantar involvement, usually archsparing)

• Focal (discrete foci of thick hyperkeratosis on the plantarsurface)

• Punctate (multiple corn-like presentation across the soles)• PPK with ectodermal dysplasias (such as altered sweat

functioning, deafness, abnormal dentition, nail deformitiesand neurological deficits)

Over 50 types have been described and many of the inheritabletypes have been well documented and readers are directed to areview article by Itin and Fistarol21 for further information ofspecific conditions. Clinically, when confronted with suspectedPPK it is important to obtain a full family history and examinethe hands. Hyperkeratosis of the palms with these conditionsmay not be so obviously affected and subtle scaling and similarchanges should be noted. Referral to a dermatologist may berequired if a definitive diagnosis is being sought. Managementof PPK can be frustrating and difficult. Owing to the thicknessof the hyperkeratosis, emollients and other topical therapieshave little effect. Oral retinoids are occasionally used to managethe condition under the direction of a consultant dermatologist.These drugs reduce cell turnover and as a result cause thinningof the epidermis, relieving symptoms for the patient. However,

Figure 3 : Hyperkeratosis due to lymphatic failure (taken from Dawber, Bristow & Turner18)




the frequent side effects of the drug often mean a proportion ofthe patients are unable to sustain the drug regime long term.Typical side effects include dryness of the mouth, nose bleeds,hair thinning, altered liver function and skeletal hyperostosis.

Internal Malignancy and HyperkeratosisHyperkeratosis of the palms and soles has been recognised as amarker of internal malignancy. A number of rare forms of PPKare known to be associated with an increased risk of developing internal cancers. For example, Howel-Evanssyndrome is a familial form of PPK present in a small numberof families. Of those members of the family who develop thepalmo-plantar keratoderma, they hold a 95% chance ofdeveloping an oesophageal carcinoma in later life22. Othersimilar associations have been reported in patients withhereditary diffuse gastric cancer23 and in a population withcancer of the oesophagus24.

Aside from inheritable forms of PPK, a number of papers havepublished cases where PPK of the palms and soles has been amarker for internal malignancies of the lung, bladder, stomachand colon25-27 often preceding any internal symptoms. Any adultpatient presenting with a recent onset hyperkeratosis where adiscernable cause is not apparent should be referred for medicalassessment.

MalnutritionZinc deficiency has been cited as a cause of plantarhyperkeratosis28. The condition itself is usually hereditary (as anautosomal recessive trait) or acquired through malnutrition.Weissman28 has also presented cases of zinc deficiency occurringin patients with alcoholic cirrhosis of the liver whodemonstrated plantar involvement.

SummaryHyperkeratosis is the most common disorder of the adult foot.In most cases the causes are mechanical in nature and should bemanaged appropriately. A minority of cases are caused by arange of other conditions. Effective treatment for these requiresa firm diagnosis. Where the aetiology is uncertain referral to aspecialist should be sought.

References1. MacDonald D. Histopathology of the skin. In: Hall-Smith

P, Cairns R, eds. Dermatology:current concepts andpractices. London: Butterworth; 1981.

2. Thomas SE, Dykes PJ, Marks R. Plantar hyperkeratosis: astudy of callosities and normal plantar skin. J InvestDermatol. Nov 1985;85: 394-397.

3. Burzykowski G, Molenberghs D, Abeck E, et al. Highprevalence of foot diseases in Europe: results of the Achillesproject. Mycoses. 2003;46: 496-505.

4. Young MJ, Cavanagh PR, Thomas G, Johnson MM,Murray H, Boulton AJ. The effect of callus removal ondynamic plantar foot pressures in diabetic patients.Diabetic Med. Jan-Feb 1992;9: 55-57.

5. Spuls PI, Hadi S, Rivera L, Lebwohl M. Retrospectiveanalysis of the treatment of psoriasis of the palms and soles.J Dermatolog Treat. 2003;14 Suppl 2: 21-25.

6. Gong JQ, Lin L, Lin T, et al. Skin colonization byStaphylococcus aureus in patients with eczema and atopicdermatitis and relevant combined topical therapy: adouble-blind multicentre randomized controlled trial.British Journal of Dermatology. 2006;155: 680-687.

7. Hauser C, Wuethrich B, Matter L, Wilhelm JA, SonnabendW, Schopfer K. Staphylococcus aureus skin colonization inatopic dermatitis patients. Dermatologica. 1985;170: 35-39.

8. Onder M, Atahan AC, Bassoy B. Foot dermatitis from theshoes. Int J Dermatol. Aug 2004;43: 565-567.

9. Gram H. Keratoderma Climactericum. Archives DermatolSyph. 1943;40.

10. Shuster S, Black M, McVitie E. The influence of age and sexon skin thickness, skin collagen and density. Brit JDermatol. 1975;93: 639-643.

11. Robinson H. Keratoderma climactericum: a case study. JBrit Pod Med. 1997;52: 178-190.

12. Cram DL, Kierland RR, Winkelmann RK. Ulcerative lichenplanus of the feet. Bullous variant with hair and naillesions. Arch Dermatol. Jun 1966;93: 692-701.

13. Iraji F, Kiani A, Shahidi S, Vahabi R. Histopathology ofSkin Lesions With Warty Appearance in Renal AllograftRecipients. American Journal of Dermatopathology.2002;24: 324-325.

14. Bristow I. Tinea Pedis:diagnosis and management. PodiatryNow. 2004;7: S1-S8.

15. So SG, Kovarik CL, Hoang MP. Skin clues to a systemicillness. Secondary syphilis. Arch Pathol Lab Med. May2006;130: 737-738.

16. Brown KG, Ross GL. Arsenic, Drinking Water, and Health:A Position Paper of the American Council on Science andHealth. Regulatory Toxicology and Pharmacology.2002;36: 162-174.

17. Stoberl C, Partsch H. [Congestive lymphostaticpapillomatosis]. Hautarzt. Jul 1988;39: 441-446.

18. Dawber R, Bristow I, Turner W. A text atlas of podiatricdermatology. London: Martin Dunitz; 2000.

19. Miller J, Roling D, Spiers E, Davies A, Rawlings P, Leyden J. Palmoplantar keratoderma associated withhypothyroidism. British Journal of Dermatology.1998;139: 741-742.

20. Stevens HP, Kelsell DP, Bryant SP, et al. Linkage of anAmerican pedigree with palmoplantar keratoderma andmalignancy (palmoplantar ectodermal dysplasia type III) to17q24. Literature survey and proposed updatedclassification of the keratodermas. Arch Dermatol. Jun1996;132: 640-651.

21. Itin PH, Fistarol SK. Palmoplantar keratodermas. ClinDermatol. Jan-Feb 2005;23: 15-22.

22. Howel-Evans W, McConnell R. Carcinoma of theoesphagus with keratosis palmaris and plantaris (tylosis).Quart J Med. 1958;27: 413.


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23. Robertson EV, Jankowski JA. Genetics ofGastroesophageal Cancer: Paradigms, Paradoxes, andPrognostic Utility. The American Journal ofGastroenterology. 2007;102: 1-7.

24. Ilhan M, Erbaydar T, Akdeniz N, Arslan S. Palmoplantarkeratoderma is associated with esophagus squamous cellcancer in Van region of Turkey: a case control study. BMCCancer. 2005;5: 90.

25. Murata I, Ogami Y, Nagai Y, Furumi K, Yoshikawa I,Otsuki M. Carcinoma of the stomach with hyperkeratosispalmaris et plantaris and acanthosis of the esophagus. AmJ Gastroenterol. Mar 1998;93: 449-451.

26. Cuzick J, Harris R, Mortimer PS. Palmar keratoses andcancers of the bladder and lung. Lancet. Mar 10 1984;1:530-533.

27. Powell F, Mackey JP. Bronchial carcinoma andhyperkeratosis palmaris et plantaris. Postgrad Med J. Jan1981;57: 57-59.

28. Turgut S, Ergin S, Turgut G, Erdogan BS, Aktan S. The roleof essential and non-essential elements in Mal de Meleda. JBasic Clin Physiol Pharmacol. 2007;18: 11-19.

29. Weismann K, Hoyer H, Christensen E. Acquired zincdeficiency in alcoholic liver cirrhosis: report of two cases.Acta Derm Venereol. 1980;60: 447-449.

Case Study 1A 70 year old womanpresented to the clinicwith a scaly, symmetricalhyperkeratosis affectingboth heels. The conditionhad been graduallyworsening, but now wasbecoming uncomfortablefor the patient whoenjoyed walking (Figure4). Her medical historyrevealed nothing of note.Examination of thehyperkeratosis showed aclose relationship to theheel area of the insock ofher favourite shoes, which showed a high sheen (Figure 5).It was suspected that the motion of the sole over the insockwas leading to inflammation of the skin and thedevelopment of the hyperkeratosis. The insole was removedand replaced with a simple cushioning insole. Thehyperkeratosis subsided within a few weeks.

Case Study 2A 45 year old man presented with hyperkeratosis andfissuring to the plantar surface of the feet. Prior to this, hehad had regular debridement and reduction with a Mooresdisc but this had proven unsatisfactory as the callus wouldfrequently bleed (Figure 6). The patient’s history revealedthat he had suffered intermittently with eczema elsewhereon the body. Moreover, the hyperkeratosis on the foot wasvariable and not related to activity levels. On examination,the soles of the feet were hyperkeratotic with a vagueerythema and fissuring around the heels. The texture of thehyperkeratosis was light and brittle. A diagnosis of chronicplantar eczema was made and he was treated for 10 daysusing a potent topical steroid and emollients*.

* For guidance on the use of emollients, please refer to the earlier CPD article on “Emollients: selection andapplication” in the September 2005 edition of PodiatryNow.

Figure 4

Figure 5

Figure 6




Post-reading activity

After reading this CPD article spend some time reflecting on its content, using the sub-headings as prompts. Keep the reflections, notesand key points in your CPD portfolio

Reflection

1. How would you define hyperkeratosis?

2. What are the main causes of hyperkeratosis on the feet?

3. What percentage of my own caseload may have hyperkeratosis attributable to causes other than mechanical?

4. Will this article change my practice at all? If so how?

5. How will this impact on the care of my patients / service users?

6. After reading this, have I identified any new CPD needs (for example revision of specific topics, acquisition of new skills etc).


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Key points Learning outcomes

Notes

CPD Series No. 2

Title: Hyperkeratosis: Part 1. Author: Ivan Bristow

Editorial Board: Professor Kate Springett (Canterbury Christ Church University, UK), Ian Reilly (Podiatric Surgeon, Northamptonshire, UK),Ivan Bristow (University of Southampton, UK), Mike Potter (University of Southampton, UK).

Published in association with the Society of Chiropodists and Podiatrists.This work is supported by an unrestricted educational grant from Galderma (UK) Ltd.

The opinions, statements, assertions and data which are presented in this article are those of the author(s). The author(s), the Society of Chiropodists and Podiatrists, the editorial board, sponsors and their respective employers, officers and agents accept no liability for the consequences of inaccurate, misleading, incorrect statements, opinions, assertions or data. As new knowledge and research evidence is madeavailable there will be changes to treatment, management, advice provided, procedures and equipment used. Readers of this article are advised to check and confirm that information they are utilising conforms to the latest standards of practice and legislation.

© 2008

If readers have any feedback, comments or suggestions for future articles please contact the Editorial board at the Offices of the Society ofChiropodists and Podiatrists.


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