This author details the diagnosis and management of a patient who presented with severe cracks and fissures on both heels.
An anxious middle-aged caregiver presented to the clinic complaining of very painful heels. Her limping was not due to the typical heel spur syndrome we see. She had severe cracks and fissures on both of her heels. Her soles had gradually become thicker over the last six months and felt hot and painful to the touch.
She was the primary caregiver for her disabled spouse and seriously ill son. She was unaware of any other family members with a similar condition and had tried cocoa butter and abrasive instruments to reduce the hyperkeratosis. Several deep painful cracks had developed in recent weeks. She denied any significant past medical history.
The patient had a height of 5’2” and weighed 140 lbs for a body mass index (BMI) of 25.63 kg/m2. She was a former smoker and denied taking any medication other than vitamins A and D, magnesium and calcium at simple supplement dosages. Remarkably, the soles were quite warm at 97°F. Sole temperatures can vary individually but generally range between 75 and 80°F when one measures this with an infrared thermometer.
The general examination of the skin revealed opaque, yellow-to-white plaques on the palms and knees as well as the soles. The arms and scalp were otherwise clear. The weightbearing plaques were quite thick with multiple deep fissures that tended to spare the arches and sulci. The toenails were dystrophic and thickened with subungual hyperkeratosis while the fingernails exhibited transverse onycholysis with several longitudinal spikes and superficial pits.
Dermoscopic examination of the right knee plaque found red dots on a homogenous pink background with white scales consistent with psoriasis.
I stained the sole scrapings with chlorazol black E, potassium hydroxide and a dimethylsulfoxide fungal stain. The examination of these scrapings under a light microscope failed to detect segmented branching hyphae. I collected nail clippings and sent them to pathology for examination with periodic acid Schiff and Gomori’s methenamine silver stains. This subsequently revealed hyphae within the nail plate consistent with a dermatophyte infection.
In order to make a differential diagnosis, it is useful to organize our thinking into four areas. What is our first impression, a mimicking condition, the worst case scenario and finally, one esoteric disease?
In this case, considering the opaque keratin, palmar plantar hyperkeratosis and significant stress history, psoriasis was the first impression. A mimicking condition might be atopic eczema but the history and distribution fail to support that diagnosis. The worst case scenario could be a paraneoplastic disorder like Bazex syndrome, which is an erythrosquamous eruption of the fingers and toes associated with lung cancer. Hopefully, a good review of systems would help to rule this out.
Finally, the rare differential condition could be arsenical keratosis of the palms and soles. One could investigate this differential diagnosis by exploring the patient’s travel history and possible exposure to well water contaminated with arsenic. In these cases, laboratory investigation could reveal hemolysis or electrolyte disturbances.
The initial management should focus on symptom relief and the most likely scenario of psoriasis pending results of the workup of the differential diagnosis. For this patient, the painful, deep fissures limiting walking were the primary issue and initial treatment in the office consisted of lidocaine ointment to allow debridement and flattening of the vertical edges of the sole splits with a wetting agent and tissue nippers. In order to relieve the weightbearing pain, I applied loose Unna paste gauze dressings to the feet for 48 hours. At home, the patient applied triamcinolone 0.5% ointment twice daily followed by urea 40% cream at night. Once the fissures healed and the plaques thinned, the concurrent onychomycosis had cleared with an 84-day course of oral terbinafine (Lamisil, Novartis).
The clinical diagnosis of psoriasis relies on searching for the essential disease characteristics. Most hyperkeratosis of the soles, which is due to excessive intermittent pressure as in tylomas, corns and calluses, is relatively clear and translucent while psoriatic hyperkeratosis is commonly opaque and white to yellow. Accelerated psoriatic keratinization produces the opaque hyperkeratosis of psoriasis. Accumulated immature keratinocytes retain their nuclei and therefore are not translucent like the more mature keratin of pressure keratoses.
The prevalence of onychomycosis is actually higher in patients with psoriasis. Eighteen percent of patients with lower extremity psoriasis have concurrent onychomycosis.1 When it comes to moderate to severe onychomycosis, oral terbinafine is the drug of choice with long-term topical antifungal prophylaxis against re-infection.
Another symptom of plantar psoriasis is increased sole temperature. Although there is no single normal foot temperature, sole temperatures do vary within a daily circadian rhythm between morning vasodilation and a cooler vasoconstricted state. Clinical examination usually occurs in a cool examination room when anxious patients exhibit moist and cool feet. Increased sole temperature can be a sign of diabetic neuropathy.2 A typical sole temperature is about 75°F while this patient’s sole measured 95°F. Plantar psoriasis may present with significant vasodilation and palpable heat along with the typical erythematous plaques.
As far as the dermoscopy examination goes, Lallas and colleagues studied 83 patients with psoriasis and 86 patients with dermatitis, lichen planus or pityriasis rubra.3 The authors found dotted vessels in a regular arrangement over a light red background and white scales to be highly predictive of psoriasis. Dermatitis patients more commonly showed yellow scales and dotted vessels in a patchy arrangement. Pityriasis rubra was characterized by a yellowish background, dotted vessels and peripheral scales while whitish lines (Wickham striae) were visible exclusively in patients with lichen planus.4
In the Manual of Dermatologic Therapeutics, Hsu discusses the various approaches to plantar psoriasis management.5 Traditional treatments include salicylic acid, corticosteroids and tars. Salicylic acid and urea are keratolytic in higher concentrations, serving not only to thin the hyperkeratotic plaques by keratolysis but also to facilitate the penetration of topical medications.
Topical corticosteroids have three useful mechanisms of action. First, they are potent cutaneous vasoconstrictors that slow epidermal proliferation. Secondly, they are strong immune blockers of this T-cell mediated disease. Finally, corticosteroids are anti-inflammatory by slowing lymphocyte and cytokine mediators. Initially, patients can use a class I steroid like halobetasol (Ultravate) for a maximum of two weeks with a class III mid-potency ointment such as triamcinolone (Kenalog, Bristol-Myers Squibb)after initial improvement.
Hydration of the skin before application increases corticosteroid absorption fivefold while plastic wrap occlusion increases hydration 40 percent and increases corticosteroid efficacy up to 100-fold.5 The optimal frequency of application is two to three times per day. Patients can significantly reduce the risk of adverse drug reactions such as tachyphylaxis, atrophy and striae by suspending applications one day per week.5 Patients should avoid systemic steroids because a severe rebound reaction often occurs upon cessation.
Coal tars inhibit DNA synthesis. Coal tar 5% applications transiently trigger hyperplasia but after 40 days of application reduce epidermal thickness by 20 percent.5 Salicylic acid ointment or gels are keratolytic at 3 to 6% concentrations. They help thin the hyperkeratotic plaques by solubilizing intercellular cement and enhancing desquamation. Urea compounds have a softening and hydrating effect at lower concentrations, and are keratolytic at higher concentrations. They work by disrupting hydrogen bonds within epidermal proteins. Calcipotriene is a vitamin D3 analogue that induces terminal epidermal differentiation and inhibits keratinocytes production. The efficacy of calcipotriene matches class II topical steroids without their adverse effects.5
It is useful to remember that combinations of these agents can synergistically potentiate each other’s actions. Some effective products exploit this effect by combining calcipotriene (Dovonex, Warner Chilcott) with a potent corticosteroid. Phototherapy combining oral retinoids with PUVA or UVB administered with special light boxes for the soles and palms can be effective.
Psoriasis typically follows a chronic and recurrent course. Patients with generalized involvement are best served by dermatology consultation. In addition to phototherapy, dermatologists can employ oral immunosuppressive therapies like acitretin (Soriatane, Stiefel Laboratories), methotrexate (Trexall) and cyclosporines. Methotrexate with folic acid supplementation can clear many cases of palm and sole psoriasis within four to six weeks.
A topical retinoid, tazarotene (Tazorac, Allergan), modulates differentiation and proliferation of epithelial tissue, and perhaps has anti-inflammatory and immunomodulatory activities. There are several protocols but the least irritating is to apply the medication for 15 to 20 minutes and then wash it off. Topical retinoids are effective but childbearing females must avoid them because the retinoids are teratogenic and carry a class X warning.6
New biologic therapies like etanercept (Enbrel, Amgen) and tumor necrosis factors are available for severe unresponsive psoriasis and may be tertiary care choices. Richetta and coworkers found that adalimumab (Humira, AbbVie) for 12 weeks was safe and efficacious in an open-label clinical trial of patients with palmoplantar psoriasis.7
It is widely accepted that psychosocial stress can trigger exacerbations of psoriasis so one should consider stress reduction exercise and behavioral counseling recommendations.8 Even in patients with mild psoriasis, there is a significant increase in the risk of myocardial infarction and stroke from this chronic inflammatory disease so internal medicine consultation is also appropriate.9,10 Patients should be aware of the recurring course of psoriasis with its periods of improvement followed by acute flares. It is also important to screen for underlying inflammatory arthritis with foot radiographs.11
Dr. Bodman is an Associate Professor at the Kent State University College of Podiatric Medicine. He is a Diplomate of the American Board of Podiatric Medicine. Dr. Bodman is in private practice in Ohio.
1. Klaassen KM, Dulak MG, van de Kerkhof PC, Pasch MC. The prevalence of onychomycosis in psoriatic patients: a systematic review. J Eur Acad Dermatol Venereol. 2013 Aug 19, epub ahead of print.
2. Houghton VJ, Bower VM, Chant DC. Is an increase in skin temperature predictive of neuropathic foot ulceration in people with diabetes? A systematic review and meta-analysis. J Foot Ankle Res. 2013; 6(1):31.
3. Lallas A, Kyrgidis A, Tzellos TG, Apalla Z, Karakyriou E, Karatolias A, Lefaki I, Sotiriou E, Ioannides D, Argenziano G, Zalaudek I. Accuracy of dermoscopic criteria for the diagnosis of psoriasis, dermatitis, lichen planus and pityriasis rosea. Br J Dermatol. 2012; 166(6):1198-205.
4. Micali G, Lacarrubba F, Massimino D, Schwartz RA. Dermatoscopy: alternative uses in daily clinical practice. J Am Acad Dermatol. 2011; 64(6):1135-46.
5. Hsu SP. Formulary. In (Arndt A, Hsu J, eds.) Manual of Dermatologic Therapeutics, seventh edition, Lippincott Williams & Wilkins, Philadelphia, 2007, chapter 40, pp. 315-318.
6. Mehta BH, Amladi ST. Evaluation of topical 0.1% tazarotene cream in the treatment of palmoplantar psoriasis: an observer-blinded randomized controlled study. Indian J Dermatol. 2011; 56(1):40-3.
7. Richetta AG, Mattozzi C, Giancristoforo S, D'Epiro S, Cantisani C, Macaluso L, Salvi M, Calvieri S. Safety and efficacy of Adalimumab in the treatment of moderate to severe palmo-plantar psoriasis: an open label study. Clin Ter. 2012; 163(2):e61-6.
8. Hunter HJ, Griffiths CE, Kleyn CE. Does psychosocial stress play a role in the exacerbation of psoriasis? Br J Dermatol. 2013; 169(5):965-74.
9. Armstrong EJ, Harskamp CT, Armstrong AW. Psoriasis and major adverse cardiovascular events: a systematic review and meta-analysis of observational studies. J Am Heart Assoc. 2013; 2(2):e000062.
10. Biyik I, Narin A, Bozok MA, Ergene O. Echocardiographic and clinical abnormalities in patients with psoriasis. J Int Med Res. 2006; 34(6):632-9.
11. Lowell DL, Osher LS, Grady AF. Incidental findings of massive heel spurs in a veteran with a variant of psoriatic arthritis. J Am Podiatr Med Assoc. 2012; 102(5):422-7.