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Keys To Differentiating Eczematous Eruptions In The Pedal Skin
Eczema can arise in various permutations ranging from nummular eczema and atopic dermatitis to xerotic eczema and hyperkeratotic plantar eczema. Accordingly, these authors review key clinical signs, possible etiologies and exacerbating factors, and appropriate treatment considerations.
Eczema, a form of dermatitis or inflammation of the superficial layers of the skin, is the most common skin reaction that podiatrists encounter.1 It is an acute inflammatory cutaneous eruption characterized by itching, redness, papules, vesicles, edema, serous discharge, dryness, flaking, blistering, cracking, oozing, bleeding and crusting.
There is a tendency to use the terms eczema and dermatitis interchangeably. When it comes to pedal skin, physicians frequently use dermatitis to describe any itchy, red skin problem. However, dermatitis merely refers to an inflammation of the skin that may result in a spectrum of lesions varying from acute necrosis and ulceration to simple erythema. In an effort to identify the specific eruption, we have terms such as contact dermatitis, seborrheic dermatitis, nummular dermatitis and atopic dermatitis.2
Simply diagnosing patients with “dermatitis/eczema” is inadequate as one should more clearly define the condition with further diagnostic effort.
Classification of the underlying diseases has been haphazard and unsystematic as physicians often use many synonyms to describe the same condition. One may describe a type of eczema by specific appearance (eczema craquele, which has the appearance of cracked porcelain or discoid eczema, which is in the shape of a “disc”) or by the possible cause (varicose eczema).3
However, the morphological and pathologic changes in all forms of eczema are similar. The skin disease will usually pass through the following three stages: acute eczema, subacute eczema and chronic eczema.
Acute eczema is marked by pruritus, erythema, edema (with or without vesicles) and oozing. With subacute eczema, one may see pruritus, erythema, scaling and crusting. Patients with chronic eczema will have pruritus and lichenification.
Therefore, when you see a patient for an initial evaluation, it is important to note whether he or she is in an acute or chronic phase or somewhere in the middle. The patient may also have rubbed or scratched the affected area, and that will change the appearance of the dermatoses. While we only deal with the pedal skin, it is important to observe the other skin areas (legs, arms, hands, trunk) to gain more insight into the diagnosis.
A Guide To Different Types Of Pedal Eczema
Atopic eczema/dermatitis. There may be a hereditary component with this condition. One will often see this condition in families whose members also have hay fever, allergic rhinitis and asthma. Itching is the outstanding feature of this disease. Many of the clinical signs are secondary to the scratching and rubbing of the skin. Family members may also have a history of atopic dermatitis.
An itchy rash is particularly noticeable on the face and scalp, neck, inside the elbows, behind the knees and buttocks. Isolated involvement of the feet without lesions elsewhere is rare. Due to the rubbing of the skin and the breakdown of the barrier function of the stratum corneum, one can get secondary bacterial, fungal and viral infections.
Causes include extreme heat/cold, sweating, occlusive clothing, fragrances, oils, soaps and environmental allergens. Exacerbating factors include over-washing, contact irritants, allergens, illness, perspiration, excessive heat, rough fibers (wool sweaters), dry air, tight clothing, and dust mite allergies.
Nummular eczema. Also known as discoid eczema, nummular eczema is characterized by round to oval erythematous plaques that are most common on the arms, legs, hands and feet. Lesions begin as papules but then coalesce into plaques. Early lesions may start out as vesicles containing a serous exudate and result in a yellowish crust around the lesion. Nummular eczema is commonly associated with xerosis and intense pruritus. Patients with nummular eczema are at a higher risk of developing secondary allergic contact dermatitis, which contributes to the severity and chronicity of their dermatitis. Therefore, some studies advocate patch testing in these patients.4
Cold or dry climates may be exacerbating factors as flares are most common in the winter. The etiology is unknown and most likely multifactorial. Other causes include occupational irritation and stress.
Contact dermatitis. Irritant contact dermatitis makes up 80 percent of contact dermatitis cases. It results from a direct reaction to a solvent or chemical (sodium lauryl sulfate for example) on the skin, and causes inflammation.5 This form of dermatitis is the most common occupational skin disease. Podiatrists will see this mainly on the dorsal aspects of the feet. Usually irritant contact dermatitis is due to allergens in the uppers of shoes or the lining. It usually starts on the dorsal aspect of the hallux and spreads from there. Other causes include latex and rubber hypersensitivity, topical steroid dermatitis, topical products and dyes.
The second type of contact dermatitis is allergic contact dermatitis, which results from a delayed reaction to some allergen, such as poison ivy or nickel. This requires a period of sensitization. It is itchier and often appears with linear streaks.
Recurrent focal plantar peeling. Previously known as keratolysis exfoliativa, recurrent focal plantar peeling is a chronic, noninflammatory bilateral peeling of the palms and soles. The etiology is unknown. However, the condition has been associated with sweating and most commonly occurs in the summer months.
Scaling of the skin starts simultaneously in several areas on the soles and palms. It begins as 2- to 3-mm round scales that continue to peel and extend to the periphery, which forms larger areas of scaling with coalescence of the borders. Central areas may become red and tender. Treatment for this condition usually just involves lubrication and resolves within a couple of weeks.6
Juvenile plantar dermatitis. This condition occurs in children as dry fissured dermatitis of the plantar aspect of the feet with a red, dry, glazed appearance.
Hyperkeratotic plantar eczema. This is usually due to mechanical trauma. Hyperkeratotic eczema is a chronic condition that occurs almost exclusively in men and consists of a dense, thick form of eczema that occurs on the hands and feet.6,7 The dense scaling forms deep, interconnected cracks over the surface. These yellow-brown plaques are firmly adherent to the epidermis. Unlike a callus, these dense plaques are moist underneath and are not easy to debride with a blade. The etiology of hyperkeratotic eczema is unknown but it may be related to an allergy or irritant. Consider patch testing with recurrent conditions.
Treatment for this condition is the same as for the other eczematous conditions. Researchers have looked at the use of topical vitamin D3 derivatives (calcipotriol 50 microg/g and maxacalcitol 25 microg/g) in the treatment of hyperkeratotic eczema and noted some success.8
Infective eczema. This happens when bacteria provokes the eczema. Bear in mind that this can imitate an acute vesiculous form of tinea pedis.
Xerotic eczema. This is dry skin that turns into eczema. The skin becomes rough, flaky or scaly. The water content of the stratum corneum is of prime importance in maintaining the normal appearance and texture of human skin. The hydration depends on three factors including: the rate of water transport from dermis to stratum corneum, the rate of surface loss of water and the water-binding ability of the stratum corneum.9
This condition becomes worse in dry winter weather. The limbs and trunk are most often affected. It is common in all age groups but more common in the elderly. The itchy, tender skin resembles a dry, cracked riverbed. On the dorsum surface of the foot, follicular accentuation is prominent as well as scale formation. On the plantar skin or sole where the stratum is thick, one may note cracks or fissures due to the shrinking of the top layer of skin. Ichthyosis is a related disorder.
Dyshidrotic eczema. Also known as dyshidrosis, dyshidrotic eczema is characterized by recurrent flares of vesicles or blisters on palms and soles appearing over non-erythematous skin. It is associated with moderate to severe pruritus that gets worse at night. During the acute stage, clear to pink vesicles form on the palms, soles, fingers and toes. Vesicles are deep seated with a tapioca-like appearance. One would commonly see these vesicles on the lateral aspects of fingers and toes. Larger bulla can form on the palms and soles. In the chronic stage, the vesicles are replaced by scaling, fissuring and lichenification.
In 1999, researchers developed the Dyshidrotic Eczema Area and Severity Index, which is based on severity grades for the number of vesicles per square centimeter, erythema, desquamation, itch and the extent of affected areas. 10 Other researchers have found the index to be a simple standardized method for assessing the condition and have used it to assess disease severity and treatment effectiveness in clinical studies. 11,12
The treatment of dyshidrotic eczema involves decreasing stress, perspiration and avoiding known contact irritants. The etiology is unknown but may be associated with emotional stress, hyperhidrosis or exposure to contact irritants. A recent study in the Archives of Dermatology found that 40 percent of patients with dyshidrotic eczema had a tendency to palmar-plantar hyperhidrosis, 48.3 percent of the patients smoked and in 24 percent of the patients, researchers suspected that stress played a role in the disease.13
Pompholyx. Pompholyx presents as tiny tapioca-like vesicles on the sides of the toes and soles. The affected areas may become red, scaly and weep with intense itching. There may be an overlap between contact dermatitis and pompholyx, but bear in mind that contact dermatitis treatment requires emollients and pompholyx requires steroids.14
Discoid eczema. This is characterized by round spots of oozing or a dry rash with clear boundaries. One will often see this on the lower legs. It is usually worse in winter. The cause is unknown and the condition tends to come and go.
Venous eczema/stasis dermatitis. This condition occurs in people with impaired circulation, varicose veins and edema. It is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the skin and itching. The disorder predisposes patients to leg ulcers.
Neurodermatitis. Also known as lichen chronicus simplex (LCS), neurodermatitis is a thickening of the skin with scaling that arises secondary to repetitive scratching or rubbing due to an insect bite, clothing irritation, contact dermatitis and psoriasis. Usually, with this condition, there is only one spot on the foot whereas all other types of eczema show more widespread involvement. A thick plaque can form with well demarcated lichenification.
Pruritus provokes rubbing that produces clinical lesions but the underlying pathophysiology is unknown. However, a relationship likely exists between central and peripheral neural tissue and inflammatory cell products when it comes to the perception of itch and ensuing changes in the skin secondary to chronic rubbing.15
Lichen chronicus simplex is one of the hyperkeratotic processes from which a cutaneous horn may grow. Causes that can develop into or exacerbate LCS include atopic dermatitis; psychological factors such as anxiety, depression or OCD; insect bites; scars and xerosis.
What You Should Know About Overlapping Dermatitis
When diagnosing eczema, podiatrists have to keep in mind that often a mixed eczema is present with more than one causative factor in play.
Patients with atopic dermatitis often react more quickly to constant irritation of the skin (e.g. due to working in a wet environment) and may display an overlap of atopic dermatitis and irritant contact dermatitis. In patients with irritant contact dermatitis, allergens may penetrate the skin more quickly due to the barrier damage and allergic contact dermatitis may develop in these patients as well. Patients with stasis dermatitis and possibly ulcers may develop an additional allergic contact dermatitis due to topical treatments of the open wounds.16
Eczema may also be due to other causes such as: an allergic reaction to the excrement from house dust mites, allergy to foodstuffs including dairy products, coffee, soybean products, eggs, nuts, wheat and maize.
How Age Factors Into Eczema Treatment
Atopic dermatitis is the most common cause of eczema in children. Although its cause remains unknown, the disorder represents an eczematous disorder of characteristic distribution, a hereditary symptom complex in individuals with paradoxical physiologic responses to pharmacologic stimuli, a constitutional predisposition to develop dry skin and pruritus, and/or a personal or family history of allergy.
Elderly patients on the whole have drier skin than younger patients. The skin becomes drier as we become older and this is exacerbated by age, illness, malnutrition, skin cleansers, trauma, low humidity and dry, cold windy weather.17 The elderly are more prone to loss of the stratum corneum and a host of skin problems. The usual types of eczema in these patients include asteatotic eczema (a.k.a. eczema craquele), winter eczema, stasis/varicose eczema, allergic/contact eczema, discoid (nummular) eczema and eczematous drug eruptions. One recent study showed that calcium channel blockers can trigger skin reactions.18
Pertinent Considerations With Treating Eczema In Patients With Ethnic Skin
When it comes to treating African-Americans and those with ethnic skin, eczema features include follicular prominence and a tendency toward hyperpigmentation and hypopigmentation. Chronic rubbing and scratching of ethnic skin produces epidermal thickening and greater pigmentation than what one may see for the same amount of trauma in non-ethnic skin.
In areas of longstanding eczema and scratching, there may be a patchy area of complete depigmentation that will not repigment. Areas of hypopigmentation should repigment but areas of complete depigmentation will not repigment. Patients can also get post-inflammatory hyperpigmentation and lichenification.19
Darker skin becomes “ashy” white when the skin is dry and scaly. The same scaling appears in lighter skin but is not as apparent.
Management of atopic dermatitis in those with ethnic skin varies only slightly from managing the condition in lighter skinned people. One must not cause hypopigmentation by using very strong topical corticosteroids in patients with ethnic skin.
Patients should use steroids at bedtime and once during the day. Long-term application can cause atrophy and hypopigmentation in dark-skinned patients. When there is more scaling than erythema, patients should use a keratolytic prior to the use of the steroid.
Essential Tips To Educating Patients On Self-Care Treatment Regimens
While the treatment regimen varies for different types of eczema, there are some general measures one can recommend to patients.
For acute eczema, one should consider the following modalities.
• Apply Burrows solution (diluted 1:20) cold compresses for 20 minutes four to six times a day (or soak in an oatmeal bath such as Aveeno).
• Use soothing lotions such as calamine.
• After vesiculation subsides, use a topical steroid.
• Use antihistamines PO and avoid topical antihistamines.
Patients should take short five-minute showers with cool water and use a mild soap such as Dove, Tone, Basis or Cetaphil.
Emollients add moisture to the skin. This is the single most important treatment. Many of the available emollients are emulsions of oil in water. They provide an inert oily layer on the skin surface to impede evaporation of water from the skin. Patients should apply emollients within three minutes after bathing in order to trap the water in the skin. Frequent application soothes the skin. Ointments are better than creams and creams are better than lotions.
When Should You Consider Steroid Agents?
Remind patients that emollients do not resolve inflammation. If there is inflammation, the patient must use a steroid as well. If patients are using emollients and a topical steroid, advise them to use the emollients between steroid applications. It is important to lubricate the skin often for chronic conditions.
In regard to steroids, patients should avoid intertriginous use. The ideal time to apply them is on a b.i.d. basis after bathing or application of wet compresses or a spray mist of water. Steroids work to suppress the inflammation and the pruritus, and interrupt the inflammation-itch-scratch-inflammation cycle.5
When using steroids, several factors come into play: the age of patient, severity of eczema and the thinness of skin. Based on these attributes, one can pick the correct topical steroid.
In children as young as 1 year, one may use low to mid-potency steroids including fluticasone propionate 0.05% lotion (Cutivate, PharmaDerm) qd to b.i.d. Mid-potency creams or ointments include flucocinonide (Lidex, Medicis) or desoximetasone (Topicort, Taro), qd to b.i.d.
It is recommended that patients use a high potency steroid initially to lessen the acute eruption. Then patients use the steroids less often and the emollients more often. One high potency ointment or foam qd is clobetasol (Temovate).
To increase the effect of a high-potency steroid, one may consider application under plastic or hydrocolloid dressings such as DuoDerm Extra Thin (Convatec) or Actiderm (Convatec) overnight or for three-day periods. Cordran tape works well for areas of smaller size (around a digit). The senior author has also used Silipos gel in an elastic bandage as a way to occlude the area.
In severe acute cases, patients should use systemic steroids. These include either a Depo Medrol dose pack (Pfizer) or 14 days of tapered oral prednisone. Patients should use 40 to 60 mg of steroid with tapering to 0 in 10 to 14 days. Alternately, one may opt for one injection of 6 mg of Celestone Soluspan (Schering-Plough) or 40 to 80 mg of Depo-Medrol.5 Another approach with steroids includes the use of intralesional steroids such as triamcinolone acetonide (Kenalog, Bristol-Myers Squibb) 10 mg/mL with injection in 0.1 mL amounts in a checkerboard pattern throughout the involved area.
Other Pertinent Treatment Tips
When it comes to topical antipruritic preparations, possible options include camphor/menthol (Sarna, Sarnol, Stiefel Laboratories), pramoxine (Pramosone, Ferndale Laboratories), Caladryl (Johnson and Johnson) and doxepine (Zonalon, DPT Laboratories). If patients are already using Benadryl due to allergic sensitization, they should avoid using Caladryl. Patients should also avoid using topical benzocaine as it induces allergic contact dermatitis.
In regard to reducing the risk of steroid side effects, one may use 1% tacrolimus (Protopic ointment, Astellas Pharma) or 1% pimecrolimus (Elidel Cream, Novartis).
When there are secondary infections with acute and/or subacute lesions, physicians may consider topical antibiotics including mupirocin ointment b.i.d. (Bactroban, GlaxoSmithKline). Oral agents include cephalexin (Keflex, MiddleBrook Pharmaceuticals) and dicloxacillin (Dynapen).
An Overview Of Antihistamine Options
Sedating antihistamines promote sleep and, in turn, facilitate less pruritus and decreased anxiety. Possible options include:
• hydroxyzine (Atarax, Watson Labs) 10 to 25 mg PO q6 prn or qd
• diphenhydramine (Benadryl) 25 to 50 mg PO q6 prn or hs
• chlorpheniramine 4 mg PO q6 prn or hs
Non-sedating antihistamines include Claritin and Zyrtec with dosing at 10 mg PO qhs.
In Conclusion
Recognizing one of these eczematous eruptions in the pedal skin is of fundamental importance when it comes to treatment options and recurrence prevention. Although most of the aforementioned conditions have unknown etiologies and can become chronic in nature, it is important for podiatric physicians to familiarize themselves with the current treatment options to offer patients the best overall outcome.
While patients may get eczema of the feet only, they will usually get lesions/dermatitis on others areas of the body as well. One must be able to identify those other areas to aid in the diagnosis.
Dr. Morse is the President of the American Society of Podiatric Dermatology. He is a Fellow of the American College of Foot and Ankle Surgeons, and the American College of Foot and Ankle Orthopedics and Medicine. Dr. Morse is board certified in foot surgery.
Dr. Cornell is a third-year resident within the Podiatric Surgery Residency Program at the Washington Hospital Center in Washington, DC.
References:
1. Schalock PC. Dermatitis/eczema. In: Arndt KA, Hsu JT (eds.): Manual of Dermatologic Therapeutics, seventh edition, Ch. 8. Lippincott Williams and Wilkins, Philadelphia, 2007. 2. Hurwitz S. Eczematous eruptions in childhood. Pediatrics in Review 3(1):23-30, 1981. 3. Chandak P. Eczema and its homoeopathic approachwww.modernhomoeopathy.com/july_2008.htm 4. Krupa Shankar DS, Shrestha S. Relevance of patch testing in patients with nummular dermatitis. Indian J Dermatol Venereol Leprol 2005 Nov-Dec; 71(6):406-8. 5. Krivda S. Managing atopic dermatitis in practical dermatology for primary care providers. Presented May 1, 2008 at Uniformed Services University of the Health Sciences, Bethesda, Md. 6. Habif T. Clinical dermatology: a color guide to diagnosis and treatment, fourth edition. Elsevier, 2004, pp 55-59. 7. Dockery GL, Crawford ME. Color atlas of foot and ankle dermatology. Lippincott-Raven, Philadelphia, 1999, pp 12-13. 8. Egawa K. Topical vitamin D3 derivatives in treating hyperkeratotic palmoplantar eczema: a report of five patients. J Dermatol 2005 May; 32(5):381-6. 9. Siddappa K. Dry skin conditions, eczema and emollients in their management. Indian J Dermatol Venereol Leprol 2003; 69(2):69-75. 10. Vocks E, Plötz SG, Ring J. The dyshidrotic eczema area and severity index- a score developed for the assessment of dyshidrotic eczema. Dermatology 1999; 198(3):265-9. 11. Schnopp C, et al. Topical tacrolimus (FK506) and mometasone furoate in treatment of dyshidrotic palmar eczema: a randomized, observer-blinded trial. J Am Acad Dermatol 46(1):73-77, Jan 2002. 12. Wollina U. Pompholyx: what’s new? Expert Opin Investig Drugs. June 2008, 17(6):897-904. 13. Guillet MH, Wierzbicka E, Guillet S, Dagregorio G, Guillet G. A 3-year causative study of pompholyx in 120 patients. Arch Dermatol 2007;143(12):1504-1508 14. Johnson BL, Moy RL, White GM. Ethnic skin: medical and surgical. Mosby, St. Louis, 1998, p. 96. 15. Hogan DJ, Mason SH, Bower, SM. Lichen simplex chronicus. Emedicine. https://emedicine.medscape.com/article/1123423-overview. 16. Burgin S. Nummular eczema and lichen simplex chronicus/pruigo nodularis. In Wolff K, Goldsmith LA, Katz S, Gilchrest BA, et al., (eds.): Fitzpatrick’s Dermatology in General Medicine, seventh edition, Ch. 15, McGraw-Hill, New York, 2007. 17. Bryden AM. Eczema in the Elderly www.eczema.org/Eczema-elderly.pdf 18. Joly P, Benoit-Corven C, Baricault S, et al. Chronic eczematous eruptions of the elderly are associated with chronic exposure to calcium channel blockers: results from a case–control study. J Invest Dermatol. 2007 Dec; 127(12): 2766-71. 19. Johnson BL, Moy RL, White GM: Ethnic skin: medical and surgical. Mosby, St. Louis, 1998, pp 129-140.