How To Handle Common Skin Dermatoses

Author(s): 
By James Q. Del Rosso, DO, FAOCD

Dermatoses of the lower extremities are fairly common.1 These conditions include infectious, inflammatory, vascular, neoplastic and traumatic dermatoses. Many dermatologic conditions (i.e. psoriasis, lichen planus) that exhibit the potential for widespread distribution can be prone to occur on the legs, ankles or feet in some patients. Other disorders characteristically involve the lower extremities. For example, dyshidrotic eczema and pitted keratolysis are examples of dermatoses that involve the plantar surface of the foot.
With this in mind, let’s take a closer look at these conditions and the appropriate treatment regimens for each.

Diagnosing And Managing Pitted Keratolysis
Pitted keratolysis is a superficial bacterial infection that involves the weightbearing regions of the plantar surface and usually affects both feet.2 You’ll find that young adults and children are most often affected by this condition.3 Several keratinase-producing bacteria (including Corynebacterium spp, Micrococcus sedentarius and Streptomyces spp) have been implicated.1,4

These patients often have a “soggy stratum corneum” caused by prolonged exposure of the feet to closed, moisture-impermeable shoes and sweaty socks. Superficial maceration and plantar hyperhidrosis are commonly associated features. Keep in mind that this disorder is often misdiagnosed and erroneously treated as tinea pedis.
Another plantar disorder associated with hyperhidrosis is symmetrical lividity. This entity, which predominantly affects young adult males, presents as sweaty or macerated anterior and posterior soles.1,5 Unlike pitted keratolysis, plantar symmetrical lividity demonstrates a macular, purplish-red livedo-like appearance. However, be aware that pitted keratolysis and symmetrical lividity may coexist in the same patient.5
Pitted keratolysis is asymptomatic, but is often associated with malodor. The clinical features are usually always diagnostic, presenting as multiple, shallow, round or oblong, punched out-appearing depressions. The etiologic bacterial organisms are not easily cultured using standard media, but you may be able to identify them in routinely stained, formalin-fixed histologic sections of shaved stratum corneum.2 Since the clinical features are so distinctive, laboratory diagnostic testing is not needed.

The primary goals of therapy for pitted keratolysis are: (1) promotion of dryness; (2) control of hyperhidrosis; (3) minimized exposure to occlusive footwear; (4) improved hygience; and (5) eradication of bacterial overgrowth.2,4
Nightly application of aluminum chloride 20% solution is very effective. The drying effect of topical aluminum chloride may be significant enough to warrant using an emollient in the morning to prevent symptomatic irritation, chafing and fissuring. Having patients apply topical clindamycin phosphate 1% or erythromycin 2% (solution or gel) twice a day until they achieve clearance is very effective.2-4 Alcohol-based formulations of benzoyl peroxide 6–10% can be used as a cleanser. The “leave on” gel is also effective.2 It is important to inform the patient that benzoyl peroxide, specifically when it is used with a “leave on” gel, may bleach color from fabric (i.e. colored socks).
For long-term control of underlying chronic hyperhidrosis, you may emphasize intermittent use of topical aluminum chloride 20% solution, usually one to three nights per week, or topical aluminum chloride 6.25% solution, which is applied more frequently (i.e. nightly, every other night) to maintain control of pedal sweating.

Treatment Tips For Juvenile Plantar Dermatosis
Juvenile plantar dermatosis, also referred to as chapped fissured feet or sweaty sock dermatitis, most commonly affects children. The mean age of onset is 7 years with resolution usually seen by age 14 years.6 The eruption is a physical-mechanical dermatosis that is unrelated to any microbial pathogens or contact allergens.7
The typical scenario is the “wet-to-dry” cycle of events. The patient, usually a child, spends several active hours outdoors in shoes and socks, accumulating moisture due to his or her feet sweating. The same situation may occur in a cold climate when children wear heavy socks and impermeable boots or heavy shoes. This leads to moistened footwear remaining in prolonged contact with plantar skin (“artificial intertrigo”).6 Upon returning indoors, the child will remove the shoes and socks, which allows the moisture to evaporate, leading to desiccation and chafing of plantar skin.
Some authors have suggested this disorder is more likely to occur in children with atopic dermatitis or in those with a family history of atopic disorders.7 Juvenile plantar dermatosis is often misdiagnosed and erroneously treated as tinea pedis or eczematous dermatitis.
Juvenile plantar dermatosis presents as scaling, chafing and fissuring (chapped, dry appearance) of the plantar surfaces, and usually involves both feet. The eruption may be diffuse or limited to the anterior foot region. Little to no erythema (inflammation) is present, and some children may complain of associated pain or soreness.6 Pruritus is rarely present.
Historically, juvenile plantar dermatosis has been refractory to topical therapies.6,7 Using topical medications alone is minimally beneficial if the patient doesn’t change his or her approach to foot care as well. Therapeutic and preventative measures include: (a) avoiding prolonged exposure to moist socks and shoes; (b) wearing of open shoes when possible; (c) changing socks when necessary, usually once or twice daily; (d) avoiding natural evaporation of accumulated moisture; and (e) gentle cleansing of the feet with a non-irritating, non-lipid cleanser.6-8
Upon removing his or her shoes and socks, the patient should gently cleanse the feet or dry them off. Two or three times daily, the patient should proceed to use a mild topical corticosteroid and follow up by applying a non-macerating protective emollient.8 The dimethicone 1%
aluminum magnesium hydroxide stearate protectant is available OTC and may be used for feet and hands.

What You Should Know About Tinea Pedis
Tinea pedis is a dermatophyte infection involving the foot, with the two most common clinical presentations being interdigital and plantar (mocassin) tinea pedis. Vesicular tinea pedis is less common. Plantar tinea pedis, a specific presentation of Trichophyton rubrum infection, is frequently associated with concomitant or subsequent development of toenail onychomycosis (tinea unguium).9 The dermatophyte organisms migrate from pedal skin, invading below the nail plate into the nail bed and producing distal-lateral subungual onychomycosis.10
The inherited tendency to harbor Trichophyton rubrum on pedal skin has been noted in some family clusters by careful observation and kindred analysis. Such individuals are predisposed to tinea pedis, tinea unguium, tinea cruris and diffuse tinea corporis. They may present with tinea pedis or onychomycosis at an earlier age than what you would normally see and frequently experience recurrence of dermatophyte infection despite initially effective therapy.9-12
Interdigital tinea pedis presents as scaling, fissuring and erythema that involves some or all toe web spaces on one or both feet. Symptoms of irritation and pruritus are often present. Plantar tinea pedis presents as diffuse, faint to moderate pink erythema with fine scaling. You may see varying degrees of hyperkeratosis. The borders of the eruption are often well-defined along the foot margins (“moccasin foot”). Unilateral foot involvement is not uncommon with plantar tinea pedis and you may note involvement on one or both palms (tinea manuum).
Plantar tinea pedis is usually asymptomatic, however, you may see pruritus. In some cases, infection spreads onto the dorsum of the foot in a patchy or contiguous fashion. Vesicular tinea pedis presents as localized or grouped, small vesicles and/or pustules, frequently involving the distal plantar surface or in-step region. You will often notice pruritus when vesicles are eruptive and intact. Tinea pedis is uncommon among patients who are younger than 16 years old.11

The efficacy of therapy for tinea pedis is somewhat dependent on the clinical presentation. Interdigital and vesicular tinea pedis are highly responsive to topical antifungal therapy. Effective choices include the pyridine derivative ciclopirox, azole agents (i.e. econazole, oxiconazole, ketoconazole), allylamines (terbinafine, naftifine) and benzylamines (butenafine).
Most patients with interdigital tinea pedis respond within one to two weeks after you have initiated the treatment therapy. Plantar tinea pedis may also respond in some cases to topical antifungal therapy. Longer durations of therapy (i.e. four weeks) are usually needed, as the thickened stratum corneum of plantar skin produces a natural barrier that limits topical drug absorption.
In some cases, oral antifungal therapy is needed for treatment of plantar tinea pedis. The newer agents (itraconazole, terbinafine and fluconazole), although not FDA-approved for this indication, are very effective. With these agents, you’re able to employ shorter durations of therapy than what is usually required with the “older generation” oral agents, griseofulvin and ketoconazole. (See “What About Oral Antifungals For Plantar Tinea Pedis?” ).

Keys To Recognizing And Treating Localized Digital Psoriasis
While psoriasis (psoriasis vulgaris) commonly presents as erythematous plaques covered with thick, micaceous silver scales that involve any cutaneous site (including knees, legs and feet), localized digital psoriasis is a less commonly encountered variant of pustular psoriasis that involves only a single digit. For this reason, localized digital psoriasis is commonly misdiagnosed as tinea pedis, bacterial pyoderma or eczematous dermatitis. The etiology is unknown.

Localized digital psoriasis is notoriously persistent, often remaining confined to a single digit for several years.13 The characteristic appearance is vesiculation and pustulation, occurring in different stages of development, on a background of erythema, scaling, fissuring and focal erosions. You will often see serous exudation with these patients. Although pruritus is not a typical feature, tenderness is a common complaint. A high index of suspicion is warranted in order to make the diagnosis, which you can usually make on clinical grounds after ruling out other causes (i.e. fungal infection, bacterial infection, contact dermatitis).
Localized digital psoriasis is very refractory to treatment. You can try topical therapy with ultra-high potency topical corticosteroids (clobetasol propionate 0.05%, halobetasol propionate 0.05%) and you may have some success. However, the response is usually partial or temporary at best.

Two independent case reports found that applying calcipotriene 0.005% ointment twice a day for six months, and reapplying topical 5-fluorouracil 5% cream daily for 10 days under occlusion (polyethylene dressing) were successful.14,15 Case reports also suggest success with systemic therapies, including the combination of cyclosporin, acitretin with topical calcipotriene 0.005% and the combination of methotrexate with topical clobetasol propionate 0.05%. However, relapse was noted in some cases.16
Of these options, cyclosporin appears to be the most effective (albeit based on limited data), although systemic retinoid therapy is of known benefit in treating pustular psoriasis. Since the systemic agents mentioned all exhibit potential for significant adverse reactions, it’s essential to carefully weigh the risk versus benefit of therapy and review these options with the patient prior to initiating the treatment.

Assessing Antibiotic Solutions For Superficial Pyodermas
Superficial bacterial pyodermas (uncomplicated skin and soft tissue infections) of the lower extremity include folliculitis, cellulitis, ecthyma, infected eczematous dermatoses (i.e. stasis dermatitis, nummular eczema) and infected ulcers.17 The latter occur more frequently in patients with diabetes and those who have peripheral vascular disease.
With the exception of cellulitis and ecthyma, the most common organism causing superficial bacterial infection—including those infections involving the distal lower extremity—is Staphylococcus aureus. Other organisms, including gram-negative bacteria, may cause cellulitis and infection of cutaneous ulcers or wounds. The most common etiologic pathogen of cellulitis (especially recurrent lower extremity disease) and ecthyma is Streptococcus pyogenes.

Since you would initiate empiric therapy prior to receiving bacterial culture and sensitivity results (if performed), antibiotic selection is dependent upon making a correct diagnosis of the clinical presentation and determining the most likely pathogen(s) involved.
Antibiotic coverage for staphylococcal and streptococcal infection is almost always indicated.18 Many clinical situations also favor the additional “broad spectrum” coverage against gram-negative bacteria. When bacterial culture and sensitivity results are available, you may modify treatment if indicated.
Oral cephalosporins are frequently used as “first line” therapies due to their broad spectrum antibacterial activity against several gram-positive and gram-negative pathogens.19 Oral quinolones also exhibit broad spectrum activity. The older quinolones (i.e. ciprofloxacin) are especially active against Pseudomonas infection, including P. aeruginosa.
Unfortunately, the rapid development of quinolone-resistant strains of S. aureus, and the emergence of some resistant gram-negative strains, including P. aeruginosa, has limited the applicability of oral quinolones as empiric “first line” agents for uncomplicated skin and soft tissue infections.18,20 None of the available oral cephalosporin agents are effective against methicillin-resistant S. aureus (MRSA), enterococci or P. aeruginosa.18 Fortunately, skin and soft tissue infections caused by P. aeruginosa are uncommon, and would specifically warrant the use of an oral quinolone antibiotic (i.e. ciprofloxacin).18

What The Studies Reveal About Cefdinir And Cephalexin
There are currently 10 oral cephalosporins available for clinical use in the United States.19,21 Those most adaptable for empiric and directed treatment of bacterial pyodermas are cephalexin, cefdinir, cephadroxil and cefprozil, with most of the current emphasis placed upon the first two agents. Comparative studies of several cephalosporins, inclusive of 1,069 clinical isolates in adults and children, demonstrated that cefdinir was the most active against S. aureus, S. pyogenes and some gram-negative pathogens, including E. coli, K. pneumoniae and H. influenzae.22,23

In a study of pediatric patients, cefdinir activity against S. aureus was superior to cephalexin based on an eight-fold lower MIC90 requirement.24 Clinical results in uncomplicated skin and soft tissue infections have demonstrated overall comparable clinical efficacy between cefdinir 300 mg twice daily for 10 days and cephalexin 500 mg four times daily for 10 days. Eradication rates for S. aureus were 92 percent with cefdinir and 88 percent with cephalexin.24,25 Two studies have demonstrated that cefdinir effectively eradicates 88 to 100 percent of cephalexin-resistant bacterial pathogens, and is also active against erythromycin-resistant S. aureus.24-25

The pharmacokinetic properties of cefdinir, based on serum levels, half-life and suction blister penetration, allow for twice-a-day administration. The approved dosage for using cefdinir to treat cutanaeous infections is 300 mg twice daily for 10 days.26,27 The short half-life and rapid urinary excretion of cephalexin support the recommended dosage of 250 – 500 mg four times daily.20,28-30
The importance of not underdosing or shortchanging the dosing frequency with cephalexin is supported by a recent retrospective analysis evaluating outpatient treatment of uncomplicated cellulitis. Researchers observed a higher failure rate in patients treated with cephalexin as compared to other prescribed antibiotics. The calculated failure rate was 40 percent for cephalexin compared to 20 percent with other oral agents, including dicloxacillin, amoxicillin, amoxicillin-clavulanate, erythromycin and clindamycin.31

Recommendations For Treating Distal Infections On The Diabetic Foot
S. aureus, P. aeruginosa, Bacteroides fragilis and Enterobacteriacae are among the most common pathogens identified in diabetic foot infections.32,33 These infections may be polymicrobial, especially in chronic lesions, deep seated infections or in patients undergoing previous antibiotic therapy.32,33 As S. aureus is the most common pathogen identified in studies of diabetic foot infection, especially superficial presentations, effective antibiotic coverage of this pathogen is significant (see the antibiotic discussion above).33,34
Deep-seated infections necessitate parenteral antibiotic therapy, inclusive of anaerobes, such as Bacterioides fragilis and several gram-negative bacilli.32 When it comes to treating superficial infections, you may use an oral agent that exhibits clinical efficacy against both gram-positive and gram-negative pathogens, provided there is appropriate follow-up evaluation to confirm the response.32,33

Dr. Del Rosso is a Clinical Assistant Professor in the Department of Dermatology at the University of Nevada School of Medicine in Las Vegas.

CE Exam #103
Choose the single best response to each question listed below:

1. Pitted keratolysis predominantly affects:
a) the dorsal surfaces of both feet in elderly patients
b) a single digit, usually the hallux
c) the plantar surface, especially the weightbearing surfaces
d) the surfaces of several toenails, strongly suggesting a diagnosis of psoriasis

2. Symmetrical lividity is associated with:
a) pustular psoriasis
b) hyperhidrosis
c) interdigital tinea pedis
d) vesicular tinea pedis

3. Juvenile plantar dermatosis is caused by:
a) allergic contact dermatitis from shoewear chemicals
b) Corynebacterium infection of stratum corneum
c) Micrococccus sedentarius infection of macerated plantar skin
d) Evaporation of moisture from plantar skin after prolonged sweating

4. Which of the following is not true with regard to localized digital psoriasis (acrodermatitis continua)?
a) it responds rapidly to therapy to therapy with topical corticosteroid therapy
b) it is associated with a tendency to persist and relapse
c) successful treatment may require use of systemic therapy
d) it is pustular psoriasis of a single digit

5. The dosage regimen of oral terbinafine for treatment of plantar tinea pedis is:
a) 250 mg daily x 12 weeks
b) 500 mg daily x 6 weeks
c) 250 mg daily x 2 – 4 weeks
d) 500 mg once weekly until clearance of the infection is observed

6. The dosage regimen of oral itraconazole for treatment of plantar tinea pedis is:
a) 200 mg daily x 1 week
b) 200 mg twice daily x 1 week
c) 400 mg daily x 1 month
d) 200 mg twice daily x 2 - 4 weeks

7. Ecthyma is caused by:
a) Staphylococcus aureus
b) Micrococcus sedentarius
c) Steptococcus pyogenes
d) Hemophilus influenzae

8. Recurrent lower extremity cellulitis is most often caused by:
a) Staphylococcus aureus
b) Micrococcus sedentarius
c) Steptococcus pyogenes
d) Hemophilus influenzae

9. Which of the following oral cephalosporins exhibits the greatest degree of activity against S. aureus and S. pyogenes?
a) cefaclor
b) cefadroxil
c) cephalexin
d) cefdinir

10. Which of the following oral antibiotics would be most appropriate for the treatment of uncomplicated cellulitis?
a) ciprofloxacin
b) cephalexin
c) cefprozil
d) erythromycin

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Fill out the postage-paid card that appears on the following page or log on to www.podiatrytoday.com and respond electronically. Within 60 days, you will be advised that you have passed or failed the exam. A score of 70 percent or above will comprise a passing grade. A certificate will be awarded to participants who successfully complete the exam. Responses will be accepted up to 12 months form the publication date.




References:

References 1. Lauritz B. Dermatoses of the feet. Am J Clin Dermatol 2000;1(3):181-86. 2. Habif T. Pitted keratolysis. In: Habif T, Ed. Clinical Dermatology, 3rd Edition, Mosby, St Louis, 1996, p 370. 3. Shah AS, Kamino H, Prose NS. Painful, plaque-like, pitted keratolysis occurring in childhood. Pediatr Dermatol 1992;9:251-254. 4. Nordstrom KM, McGinley KJ, Capiello L, et al. Pitted keratlysis: the role of Micrococcus sedentarius. Arch Dermatol 1987;123:1320-1325. 5. Shelley WB, Shelley ED. Symmetrical lividity of the soles. Cutis 1999;64:175-176. 6. Habif T. Chapped fissured feet. In: Habif T, Ed. Clinical Dermatology, 3rd Edition, Mosby, St Louis, 1996, p 66-67. 7. Jones SK, English JS, Forsyth A, et al. Juvenile plantar dermatosis – an 8-year follow-up of 102 patients. Clin Exp Dermatol 1987;12:5-7. 8. Del Rosso JQ. What’s new in dermatologic therapy? Presented at Hawaii Dermatlogy Seminar, Maui, Hawaii, February 2002. 9. Elewski BE. Onychomycosis: treatment, quality of life, and economic issues. Am J Clin Dermatol 2000;1(1):19-26 10. Zaias N. Onychomycosis. Arch Dermatol 1972;105:263-274. 11. Gupta AK, Sibbald RG, Lynde CW, et al. Onychomycosis in children: prevalence and treatment strategies. J Am Acad Dermatol 1997;36(3):395-402. 12. Del Rosso JQ, Daniel CR, III. Diseases of the nail. WebMD Scientific American Medicine 2002, (submitted for publication). 13. Habif T. Pustular psoriasis of the digits. In: Habif T, Ed. Clinical Dermatology, 3rd Edition, Mosby, St Louis, 1996, p 198. 14. Mozzanica N, Cattaneo A. The clinical effects of topical calcipotriol in acrodermatitis continua of Hallopeau. Br J Dermatol 1998;138:556. 15. Tsuji T, Nishimura M. Topically administered fluorouracil in acrodermatitis continua of Hallopeau. Arch Dermatol 1991;127:27-28. 16. Shelley WB, Shelley ED. Acrodermatitis continua. In: Shelley WB, Shelley ED, Eds. Advanced Dermatologic Therapy II. WB Saunders, Philadelphia, 2001, pp 37-39. 17. Habif T. Bacterial infections. In: Habif T, Ed. Clinical Dermatology, 3rd Edition, Mosby, St Louis, 1996, pp 236-264. 18. Karchmer AW. Cephalosporins. In: Mandell GL, Bennett JE, Dolin R (Eds). Principles and Practice of Infectious Diseases, Fifth Edition. Churchill-Livingstone, Philadelpia, 2000, pp. 274-291. 19. Marshall WF, Blair JE. The cephalosporins. Mayo Clin Proc 1999;74:187-195. 20. Craft JC, Parish LC. Systemic antimicrobial therapy. In: Millikan LE (Ed). Drug Therapy in Dermatology, First Edition, Marcel Dekker, New York, 2000, pp. 57-78. 21. Sadick NS. Systemic antibiotic agents. Dermatol Clinics 2001;19:1-21. 22. Fung-Tomc JC, Huczko E, Stickle T, et al. Antibacterial activities of cefprozil compared with those of 13 oral cephems and 3 macrolides. Antimicrob Agents Chemother 1995;39:533-538. 23. Sultan T. In vitro activity of cefdinir (FK 482) and ten other antibiotics against gram-positive and gram-negative bacteria isolated from adult and pediatric patients. Chemother 1994;10:80-91. 24. Tack KJ, Keyserling CH, McCarty J, et al. Study of the use of cefdinir versus cephalexin for treatment of skin infections in pediatric patients. Antimicrob Agents Chemother 1997;41:739-742. 25. Tack KJ, Littlejohn TW, Mailloux G, et al. Cefdinir versus cephalexin for the treatment of skin and skin-structure infections. Clin Ther 1998;20:244-256. 26. Guay DRP. Cefdinir: An expanded-spectrum oral cephalosporin. Ann Pharmacotherapy 2000;34:1469-1477. 27. Richer M, Allard S, Manseau L, et al. Suction-induced blister fluid penetration of cefdinir in healthy volunteers following ascending oral doses. Antimicrob Agents Chemother 1995; 39:1082-1086. 28. Mandell GL, Petri WA. Antimicrobial agents: penicillins, cephalosporins and other beta-lactam antibiotics. In: Hardman JG, Limbird LE (Eds). Goodman’s & Gilman’s The Pharmacologic Basis of Therapeutics, Ninth Edition. McGraw-Hill, New York, 1996, pp. 1073-1101. 29. Craig WA, Pharmacokinetics of antibiotics with special emphasis on cephalosporins. Clin Microbiol Infect Dis 2000;6:S46-49. 30. Mazzei T, Dentico P. The pharmacokinetics of oral cephalosporins. Clin Microbiol Infect Dis 2000;6:S53-54. 31. Madaras-Kelly KJ, Arbogast R, Jue S. Increased therapeutic failure for cephalexin versus comparator antibiotics in the treatment of uncomplicated outpatient cellulitis. Pharmacother 2000;20:199-205. 32. Lipsky BA, Berendt AR. Principles and practice of antibiotic therapy of diabetic foot infections. Diabetes Metab Res Rev 2000;16:S42-S46. 33. El-Tahawy AT. Bacteriology of diabetic foot infections. Saudi Med J 2000;21:344-347. 34. Goldstein EJ, Citron DM, Nesbit CA. Diabetic foot infections: bacteriology and activity of 10 oral antimicrobial agents against bacteria isolated from consecutive cases. Diabetes Care 1996;19:638-641. 35. Del Rosso JQ. Current management of onychomycosis and dermatomycoses. Cuu Infect Dis Rep 2000;2(5):438-445.

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