Due to varying etiologies and clinical presentations, it can be challenging at times to accurately identify rashes on the foot and ankle. With this mind, this author provides a guide to diagnosing various forms of eczema, dermatitis, infectious rashes and inflammatory rashes.
Skin rashes are common disorders that have a wide range of etiologies and frequently overlapping symptoms. Skin rashes commonly occur on the lower extremity and are frequently a presenting symptom at podiatry offices, emergency departments and primary care clinics. Despite their similarities, many rashes exhibit identifiable characteristics that can aid in diagnosis. Rashes can be a significant source of distress and morbidity with cosmetic concerns, pruritus, pain, scarring and a risk of secondary infection. Prompt identification and treatment of rashes can reduce symptoms as well as prevent complications.
Rashes are broadly defined as inflammatory skin eruptions. They may affect the subcutaneous, dermal and epidermal structures. Rashes can be generalized and include lower extremity involvement, or they can be localized to the lower extremity. Few rashes, including cutaneous larva migrans and stasis dermatitis, occur almost exclusively on the lower extremity.
Many factors, including local skin changes, underlying disease states and environmental triggers, can aid in the diagnosis of rashes. Rashes can exhibit a wide array of characteristic skin changes. While many of these skin features overlap, there are often unique characteristics or sets of characteristics that can help aid diagnosis. In addition to skin lesions, rashes may also be accompanied by other local pathologic changes, such as pruritus, edema and lymphadenopathy, which can aid in diagnosis. In severe cases, systemic symptoms such as fever, malaise, fatigue and arthralgias may accompany rashes and provide further diagnostic clues. Underlying diseases can predispose individuals to be susceptible to certain rashes. Environmental factors can serve as triggers or irritants for the development of certain rashes.
Key diagnostic criteria for rashes include a physical exam, systemic symptoms, underlying disease and environmental triggers.
Assessing Clinical Presentations, Systemic Symptoms And Clues In The Family History
linical appearance is one of the key factors in identifying lower extremity rashes. Rashes can exhibit both primary and secondary skin lesions.
Primary skin lesions are the initial pathologic skin changes while secondary skin lesions develop as the disease progresses and can be influenced by treatment and host factors. Primary skin lesions include macules, patches, papules, plaques, nodules, vesicles, bullae, pustules and wheals. Secondary skin lesions include scale, crust, excoriation, fissure, erosion, ulcer, lichenification and atrophy.
Skin lesions can be generalized or localized in their distribution. We can further break down distribution based on anatomic location and distribution of individual skin lesions. Types of distribution include symmetric, palmar/plantar, dermatome, linear, geographic, serpiginous and annular.
Primary skin lesions:
• Macule: circumscribed area of discoloration < 1 cm
• Patch: circumscribed area of discoloration > 1 cm
• Papule: solid raised lesion, < 0.5 cm diameter
• Plaque: broad raised lesion, > 0.5 cm
• Nodule: larger palpable lesion with a deep component, > 0.5 cm
• Vesicle: raised fluid filled lesion, < 0.5 cm
• Bulla: raised fluid filled lesion, > 0.5 cm
• Pustule: a raised lesion containing purulence
• Wheal: transient elevated erythematous papule
Secondary skin lesions:
• Scale: thickening and loosening of the stratum corneum
• Crust: collection of dry serum, sebum, exudate
• Excoriation: linear erosions due to injury such as scratching
• Fissure: linear cleft in the epidermis and possibly dermis
• Erosion: superficial wound resulting in loss of the epidermis
• Ulcer: wound extending to the dermis or deeper
• Lichenification: thickening of the epidermis
• Atrophy: thinning of the epidermis
Numerous aspects of a patient’s history are important in the diagnosis of lower extremity rashes. The diagnostic features of patient history include systemic symptoms, environmental exposures, disease progression, medication use, chronic disease, past medical history and family history.
Systemic symptoms, including fever and malaise, can be helpful in the diagnosis of lower extremity rashes.1,2 Environmental exposure including travel, plant exposure, insects, occupation, recreational and recent contact with illness can help to identify rash etiology, and narrow possible diagnoses. One should review medication use, especially the use of new medications. Thoroughly review the patient’s past medical history as underlying chronic disease can be associated with certain rashes.
Review the family history as many rashes have a familial component. Rashes such as atopic dermatitis are frequently associated with a personal or family history of atopy including asthma, allergic rhinitis and prior occurrence of eczema. Finally, note the time course of the rash including the initial site of presentation and progression of skin lesions. Often, treatment or mechanical factors, such as scratching, can modify primary skin lesions complicating diagnosis.
When Additional Diagnostic Testing May Be Worthwhile
One most commonly diagnoses skin rashes based on history and exam findings, but additional testing can often further aid diagnostic accuracy. Tools and techniques to aid diagnosis can include laboratory testing, skin biopsy, skin scraping and patch testing.
Laboratory testing can be useful to evaluate for associated systemic disease. Skin biopsy may provide accurate diagnosis of rashes such as lichen planus and psoriasis, but many other disorders, including atopic and contact dermatitis, yield nonspecific results.3,4 Direct or indirect immunofluorescence can be helpful in diagnosing skin lesions such as lichen planus.5 Skin patch testing can help to identify contact irritants and allergens that may be causative agents.
A Quick Primer On Classifying Rashes
There are numerous ways to classify rashes including anatomic location, depth of skin involvement, physical features and etiology. Rashes can be generalized to the entire body or localized to a specific anatomic area. One can classify rashes depending on the depth of the primary skin lesions including epidermal, dermal and subcutaneous involvement. To further classify rashes, clinicians may consider the specific skin lesions associated with a rash.
Using this classification, we can group rashes as vesicular, bullous, pustular, nodular, papular, crusted, erythematous, papulosquamous and eczematous. Finally, we can group rashes based on etiology with types including inflammatory, allergic, infectious, vascular and autoimmune. The classification of rashes can additionally aid diagnosis by similar clinical features, location, etiology and disease state.
It is difficult to review all rashes that can affect the lower extremities. For this article, I will focus on eczematous, infectious and inflammatory rashes that commonly affect the foot and ankle. I will also highlight key principles clinicians can use to diagnose rashes, including exam findings, systemic symptoms, associated past medical history and other diagnostic tools.
Differentiating The Various Forms Of Eczema And Dermatitis
We can often use the terms eczema and dermatitis interchangeably with both skin disorders representing an inflammatory skin reaction. When it comes to eczema, there are multiple etiologies including internal and external irritants. Eczema has both acute and chronic stages. Acute eczema is often characterized by erythematous, edematous plaques with vesicles or blisters. Chronic eczema is often characterized by scaling, lichenification, fissuring and excoriations. Eczema and dermatitis are frequently pruritic. Numerous forms of eczema and dermatitis can affect the lower extremity. These conditions include atopic dermatitis, contact dermatitis, dyshidrotic eczema, nummular eczema and stasis dermatitis.
Atopic dermatitis. Atopic dermatitis (atopy) is accompanied by pruritus and characterized by erythematous papules and plaques, and vesicles. Chronic forms exhibit scaling, excoriations and lichenification. Lesions are most commonly located at skin flexures.6 The diagnosis is typically based on a clinical exam, the presence of pruritus and personal or family history of atopy, allergic rhinitis or asthma. Atopic dermatitis frequently presents in children with approximately 70 percent of cases starting before 5 years of age.7
Nummular eczema. Nummular or discoid eczema is characterized by chronic or recurrent, pruritic, round or oval erythematous plaques that can contain small vesicles. Lesions can occur on the trunk, face and extremities with lesions most commonly occurring on the extensor surfaces of the extremities.8 The diagnosis of nummular eczema is largely clinical but one can use patch testing to evaluate if contact irritants are a potential cause.9 The cause of nummular eczema is unknown but it is frequently associated with dry skin, and the theory is that this may allow allergens to enter the epidermis.10,11
Dyshidrotic eczema. Dyshidrotic eczema is characterized by extremely pruritic, small vesicles that occur on the toes, fingers, palms and soles. The course and severity of dyshidrotic eczema is variable, ranging from mild, self-limiting cases to severe, chronic cases that can be very debilitating. Researchers have shown that several endogenous and exogenous factors contribute to the development of dyshidrotic eczema.12,13 Of the endogenous causes, authors have shown hyperhidrosis is present in 40 percent of cases of dyshidrotic eczema and found atopic dermatitis to be present in a large proportion of cases of dyshidrotic eczema.12,13 Exogenous factors can include cosmetic and hygiene products, mycosis and metals.13
Stasis dermatitis. Stasis dermatitis is a common lower extremity rash that is often the initial cutaneous manifestation of chronic venous insufficiency. Stasis dermatitis most commonly arises on the ankle and lower leg, and is characterized by erythematous, scaling patches often overlying the skin with brown discoloration secondary to hemosiderin deposits.14 The main focus of treating stasis dermatitis is controlling the underlying venous insufficiency and edema. This typically occurs with compression therapy.
Contact dermatitis. Contact dermatitis is common in the foot and lower leg, especially in warmer environments where shorts and sandals increase skin exposure. This rash is characterized by erythematous macules with scaling. There are numerous causes of contact dermatitis and one should obtain a complete patient history with a review of potential home, occupational and recreational contacts. Footwear dermatitis is a form of contact dermatitis that results due to contact with shoes and researchers have found it commonly occurs in children.15 Other common causative agents include adhesives, soaps, moisturizers, metals, poison ivy and poison oak. The diagnosis of contact dermatitis is based on history and exam findings as well as prompt resolution with removal of the causative agent.
What You Should Know About Infectious Rashes
Infectious rashes result from bacterial, viral and fungal skin infections. These rashes can be associated with other skin disorders and systemic disease. Atopic dermatitis may decrease the resistance of the skin barrier and can increase the risk of secondary infection. Systemic disease that affects the immune system can predispose individuals to skin infection due to the decreased host response.
Scabies. Scabies results from dermal invasion by the mite Sarcoptes scabiei hominis. This infection produces an extremely pruritic rash consisting of erythematous vesicles and papules.16 Burrows, which represent intraepidermal tunnels made by the female mites, are pathognomonic for scabies. Variations of scabies include nodular scabies, which exhibits brown nodules rather than vesicles; and crusted scabies, which presents as papules with intense scales and hyperkeratosis.17,18 The diagnosis of scabies is often clinical and based on the presence of intense pruritus and characteristic linear burrows. Light microscopy of skin scrapings can identify mites, larvae and ova, and further aid diagnosis.19
Tinea pedis. Tinea pedis is a well-known fungal skin infection that most commonly results from infection with the world’s most prevalent dermatophyte Trichophyton rubrum.20 There are multiple forms of tinea pedis including moccasin, vesicular and interdigital. Moccasin tinea pedis is characterized by scaling skin on an erythematous base distributed in a moccasin pattern on the sole of the foot. Interdigital tinea pedis can occur in isolated or all interdigital spaces, and appears as erythema, maceration, scaling and fissuring. Vesicular tinea pedis is the least common form and exhibits painful, pruritic vesicles, most commonly on the arch and anterior plantar foot.21,22 Tinea pedis, especially the vesicular form, can be complicated by secondary bacterial infections. Risk factors for tinea pedis include occlusive shoe gear, hyperhidrosis, exposure to moist environments and diabetes mellitus.23,24 The diagnosis of tinea pedis is often clinical but in uncertain cases, a KOH test of skin scrapings showing branching hyphae can help to confirm diagnosis.25
Cutaneous larva migrans. Cutaneous larva migrans is a skin disease caused by parasites of the hookworm family, most commonly Ancylostoma braziliense. Hookworm ova from dog and cat feces enter the ground, and larvae then develop in this moist environment. Transmission occurs by direct contact when larva penetrate unprotected skin.26 Foot involvement is common due to barefoot ambulation. Cutaneous larva migrans causes severe pruritus. Skin lesions begin as erythematous papules at the site of entry followed by serpiginous, red, wormlike burrows just below the epidermis.27
Pertinent Insights On Diagnosing Inflammatory Skin Rashes
Inflammation is a common cause of skin rashes. The majority of inflammatory rashes are immune-mediated. Inflammatory rashes can exist in both chronic and acute forms, and can display primary and secondary skin lesions.
Erythema nodosum. Erythema nodosum is characterized by inflammation of subcutaneous fat cells with skin lesions appearing as painful subcutaneous nodules with overlying erythema. Lesions most commonly occur on the shins. Symptoms such as fever, malaise and arthralgias typically precede skin lesions.28 Erythema nodosum is associated with a variety of systemic diseases including streptococcal infection primary tuberculosis, poststreptococcal, sarcoidosis, inflammatory bowel disease, Behçet’s disease and pregnancy.29 However, more than 50 percent of cases of erythema nodosum are idiopathic.29 The diagnosis of erythema nodosum is typically clinical but one can use a biopsy when diagnosis is uncertain.
Lichen planus. Lichen planus is a chronic inflammatory and immune-mediated disease that affects the skin, nails and mucous membranes. On the lower leg, skin lesions appear most commonly on the anterior shin. Lesions are characterized by polygonal, flat-topped, violaceous papules and plaques with overlying fine white scales known as Wickham’s striae.30 The classical clinical features of lichen planus are known as the “six Ps”: pruritic, purple, polygonal, planar, papules and plaques.31 Lichen planus also exhibits the Koebner phenomenon with the development of skin lesions due to skin trauma.32
Granuloma annulare. Granuloma annulare is a relatively common inflammatory skin disorder characterized by erythematous papules arranged in an annular pattern. Skin lesions tend to occur in areas of mild trauma including the tops of the hands and feet. Granuloma annulare is a noninfectious granulomatous disease of the skin that is frequently associated with systemic diseases including diabetes, thyroid disease, systemic lupus erythematosus, rheumatoid arthritis and Lyme disease.33 The diagnosis of granuloma annulare is based on exam findings and associated disease states. Skin biopsy of these skin lesions shows palisaded granuloma and can aid diagnosis.
An Overview Of The Key Diagnostic Features Of Common Lower Extremity Rashes
• Atopic dermatitis: personal or family of asthma, allergic rhinitis or prior eczema
• Nummular eczema: round eczematous lesions on physical exam
• Dyshidrotic eczema: vesicular lesions on palms, soles, fingers and toes
• Stasis dermatitis: associated with venous disease
• Contact dermatitis: associated with contact irritants
• Scabies: extremely pruritic, burrows on exam
• Tinea pedis: isolated to the foot, characteristic moccasin and interdigital distribution, history of hyperhidrosis/water exposure/diabetes mellitus
• Cutaneous larva migrans: serpiginous, red, wormlike burrows just below the epidermis, history of environmental exposure
• Erythema nodosum: red subcutaneous nodules on the shins, associated with systemic disease
• Lichen planus: polygonal, flat-topped, violaceous papules and plaques (six Ps) with Wickham’s striae and can exhibit the Koebner phenomenon
• Granuloma annulare: erythematous papules arranged in an annular pattern, often associated with systemic disease
Patient history and physical exam findings are key factors in the diagnosis of lower extremity rashes. Being able to identify rashes of the lower extremity quickly can provide patients with reassurance of the etiology and allow for prompt treatment.
Dr. Hoffman is the Medical Director of the Orthopedic Clinic and an Attending Physician in the Department of Orthopedics at Denver Health Medical Center. She is an Assistant Professor in the Department of Orthopedics at the University of Colorado School of Medicine.
1. Aber C, Alvarez Connelly E, Schachner LA. Fever and rash in a child: when to worry? Pediatr Ann. 2007;36(1):30-38.
2. Schlossberg D. Fever and rash. Infect Dis Clin North Am. 1996;10(1):101-110.
3. Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet. 2007;370(9583):263-271.
4. Ely JW, Seabury Stone M. The generalized rash: part I. Differential diagnosis. Am Fam Phys. 2010;81(6):726-734.
5. Boyd AS, Neldner KH. Lichen planus. J Am Acad Dermatol. 1991;25(4):593-619.
6. Aoki T, Fukuzumi T, Adachi J, Endo K, Kojima M. Re-evaluation of skin lesion distribution in atopic dermatitis. Analysis of cases 0 to 9 years of age. Acta Derm Venereol Suppl (Stockh). 1992;176:19-23.
7. Williams HC. Epidemiology of atopic dermatitis. Clin Exper Dermatol. 2000;25(7):522-529.
8. Jiamton S, Tangjaturonrusamee C, Kulthanan K. Clinical features and aggravating factors in nummular eczema in Thais. Asian Pac J Allergy Immunol. 2013;31(1):36-42.
9. Khurana S, Jain VK, Aggarwal K, Gupta S. Patch testing in discoid eczema. J Dermatol. 2002;29(12):763-767.
10. Aoyama H, Tanaka M, Hara M, Tabata N, Tagami H. Nummular eczema: An addition of senile xerosis and unique cutaneous reactivities to environmental aeroallergens. Dermatology. 1999;199(2):135-139.
11. Ozkaya E. Adult-onset atopic dermatitis. J Am Acad Dermatol. 2005;52(4):579-582.
12. Swartling C, Naver H, Lindberg M, Anveden I. Treatment of dyshidrotic hand dermatitis with intradermal botulinum toxin. J Am Acad Dermatol. 2002;47(5):667-671.
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. Sundaresan S, Migden MR, Silapunt S. Stasis dermatitis: pathophysiology, evaluation, and management. Am J Clin Dermatol. 2017;18(3):383-390.
15. Ortiz-Salvador JM, Esteve-Martinez A, Garcia-Rabasco A, Subiabre-Ferrer D, Martinez-Leborans L, Zaragoza-Ninet V. Dermatitis of the foot: epidemiologic and clinical features in 389 children. Pediatr Dermatol. 2017;34(5):535-539.
16. Huntington MK, Allison JR, Hogue AL, Shafer CW. Infectious disease: bedbugs, lice, and mites. FP Essent. 2019;476:18-24.
17. Dastgheib L, Boroujeni NH, Aslani FS. Crusted scabies masquerading as psoriasis plaques in a patient suffering from burn scars. Dermatol Online J. 2018;24(6).
18. Yanes DA, Faith EF. Nodular scabies: a persistent nodular eruption. Dermatol Online J. 2018;24(8).
19. Albrecht J, Bigby M. Testing a test: critical appraisal of tests for diagnosing scabies. Arch Dermatol. 2011;147(4):494-497.
20. Lopez-Martinez R, Manzano-Gayosso P, Hernandez-Hernandez F, Bazan-Mora E, Mendez-Tovar LJ. Dynamics of dermatophytosis frequency in Mexico: an analysis of 2084 cases. Med Mycol. 2010;48(3):476-479.
21. Moriarty B, Hay R, Morris-Jones R. The diagnosis and management of tinea. BMJ. 2012;345:e4380.
22. Hainer BL. Dermatophyte infections. Am Fam Phys. 2003;67(1):101-108.
23. Gentles JC, Evans EG. Foot infections in swimming baths. Br Med J. 1973;3(5874):260-262.
24. Akkus G, Evran M, Gungor D, Karakas M, Sert M, Tetiker T. Tinea pedis and onychomycosis frequency in diabetes mellitus patients and diabetic foot ulcers. A cross sectional - observational study. Pak J Med Sci. 2016;32(4):891-895.
25. Kutlubay Z, Yardimci G, Kantarcioglu AS, Serdaroglu S. Acral manifestations of fungal infections. Clin Dermatol. 2017;35(1):28-39.
26. Caumes E. Treatment of cutaneous larva migrans. Clin Infect Dis. 2000;30(5):811-814.
27. Leung AKC, Barankin B, Hon KLE. Cutaneous larva migrans. Recent Pat Inflamm Allergy Drug Discov. 2017;11(1):2-11.
28. Schwartz RA, Nervi SJ. Erythema nodosum: a sign of systemic disease. Am Fam Phys. 2007;75(5):695-700.
29. Mert A, Ozaras R, Tabak F, Pekmezci S, Demirkesen C, Ozturk R. Erythema nodosum: an experience of 10 years. Scand J Infect Dis. 2004;36(6-7):424-427.
30. Gorouhi F, Davari P, Fazel N. Cutaneous and mucosal lichen planus: a comprehensive review of clinical subtypes, risk factors, diagnosis, and prognosis. Scientific World Journal. 2014;2014:742826.
31. Usatine RP, Tinitigan M. Diagnosis and treatment of lichen planus. Am Fam Phys. 2011;84(1):53-60.
32. Sagi L, Trau H. The Koebner phenomenon. Clin Dermatol. 2011;29(2):231-236.
33. De Paola M, Batsikosta A, Feci L, Benedetti M, Bilenchi R. Granuloma annulare, autoimmune thyroiditis, and lichen sclerosus in a woman: randomness or significant association? Case Rep Dermatol Med. 2013;2013:289084.