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Keys To Diagnosing And Treating Contact Dermatitis

Given that contact dermatitis can have numerous inciting causes, this author discusses how to determine the allergen sources in cases of allergic contact dermatitis and irritant contact dermatitis, and proposes practical treatment strategies.

For many practitioners, this is a common scenario: a patient with a red and scaly rash walks into the office. The physician has a working differential diagnosis of tinea pedis, psoriasis and perhaps some type of eczema. After a history and physical, you surmise that the patient is having a skin reaction to something he has been exposed to, but the patient relates nothing new that he has come into contact with, leaving a perplexing situation.

he reality is that many products can cause a contact dermatitis reaction. Often the things we touch and use on a daily basis have the potential to cause an allergic reaction. Accordingly, let us take a closer look at both allergic contact dermatitis and irritant contact dermatitis in relation to the lower extremity.  

Before discussing contact dermatitis specifically, it is important to define the entities known as eczema and dermatitis. The words eczema and dermatitis are interchangeable terms that refer to an inflammatory condition of the skin. Common skin signs of inflammation are calor (heat), rubor (redness), tumor (swelling) and pruritus (itching), which ultimately point to skin barrier dysfunction. The skin barrier, which is the stratum corneum with the lipid-enriched extracellular matrix surrounding the corneocytes, is the body’s protective wall and regulates homeostasis and transepidermal water loss, and prevents the entry of foreign particles and pathogens into the body.  

In general, eczema has acute, subacute and chronic phases that result from either exogenous or endogenous conditions. During the acute phase, patients experience intense pruritus with an erythematous scaling and oozing skin rash with or without vesicles. Histologically, one would see this as epidermal intercellular edema or spongiosis as well as a perivascular infiltrate of lymphocytes, macrophages and eosinophils in the dermis.1 Clinically, this can also appear as contact dermatitis (allergic or irritant), stasis dermatitis or even a dermatophyte infection. Other differential diagnoses include psoriasis, lichen planus and tinea pedis.

Subacute forms of dermatitis present as less intense pruritic, erythematous, scaling and fissured skin rash. Chronic eczema can present as lesions that are pruritic, hyperpigmented and/or hypopigmented, well-defined plaques of previously inflamed skin, a scaly appearance and lichenification. Recognizing the phase of eczema the patient is experiencing is important when determining the age or chronicity of the rash, and the corresponding treatment plan.

In the eczematous skin condition family, contact dermatitis is an inflammatory skin reaction due to direct contact with noxious agents in the environment. Inflammation is visible on the body parts that have come in contact with the agent and is most often present around the hands. There are two types of contact dermatitis: non-immunologic irritant contact dermatitis and immunologic allergic contact dermatitis. With irritant contact dermatitis, no previous exposure to the irritant is necessary. Alternatively, a sensitization process of the inciting agent occurs in the development of allergic contact dermatitis.  

Pertinent Insights On Allergic Contact Dermatitis

Affecting approximately 7 percent of the general population, allergic contact dermatitis is an eczematous skin reaction that occurs after one or more exposures to a potential allergen.2 The reaction may take anywhere from 14 to 21 days to manifest and occur as acute, subacute or chronic forms. In acute allergic contact dermatitis, symptoms include erythema, edema, vesicle and pruritus of the skin. As I described previously, with chronic allergic contact dermatitis, the skin may become lichenified, fissured or pigmented. Episodes of oozing and crusting may arise.  

Allergic contact dermatitis is a form of Type IV delayed, cell-mediated hypersensitivity reaction caused by exposure to exogenous chemical and/or physical agents. It is a response caused by skin contact with haptens that activate antigen-specific T cells in sensitized patients. It generally begins with a skin sensitizer that has an intrinsic ability to induce an allergy. These chemicals then react with self-proteins that subsequently create a hapten-protein complex that the Langerhans cells process. These complexes are then presented to major histocompatibility complex (MHC) class II molecules that are recognized as foreign by native T cells. The T cells are further induced, activating more T cells and going on to produce memory T cells that end up in the dermis. We refer to this as the sensitization phase. Further exposure to the same, similar or cross-reactive chemical leads to antigen presentation to memory T cells in the dermis. Cytokines release and enhance the inflammatory response. The process of sensitization takes 10 to 14 days. Sensitization occurs as a result of prolonged contact with haptens in both occupational and non-occupational environments.3,4  

Only a small amount of allergen is required to trigger the inflammatory reaction and spreading of the reaction may also occur. The allergic contact dermatitis skin reaction may spread beyond the initial point of contact of the allergen, which is a useful sign for the practitioner. A patient who is allergic to a component in nail polish and subsequently develops a rash on the face from scratching with that polished nail would be an example of that phenomenon.  

Pinpointing The Source Of The Allergen

The most common allergens for allergic contact dermatitis include agents found in adhesives, topical antibiotics, fabrics, clothing, fragrances, cosmetics, soaps, moisturizers, nail polish, hair dyes, hair perms, nickel and poison ivy. During the patient’s initial visit, after determining the start of the rash, the practitioner should take a detailed environmental history that includes the following potential contributing factors.

• Everyday personal products used (shampoo, soap/body wash, hand sanitizer use, detergent, cleansers, diaper balms and wipes [if the patient is pediatric], and lotions)
• Any current or previous medications
• Other non-prescription products (i.e. over-the-counter topical creams), play mats (in the pediatric population)
• Pets, outdoor yard work or environment during outdoor workouts.

Knowledge of these potential allergens aids in creating an in-office test known as a patch test, which allergists or dermatologists can perform to determine the source.  

Poison ivy is the most common Type IV allergen with 50 to 70 percent of the population sensitized. Interestingly, urushiol, the offending agent in poison ivy leaves, stems and roots, is also in mango peel and sap. For those sensitized to poison ivy, they may have a reaction to mango, which leads to a mango dermatitis.1 Researchers note that 5.8 percent of the U.S. population is sensitized to nickel, which may be in costume jewelry, suspenders and button-fly jeans.5 Bacitracin and neomycin, which people frequently use to coat wounds and ulcers, are also potent sensitizers. After identifying the allergen, it is important to remove its exposure to the patient and avoid/reduce future contact.  

If a post-surgical patient develops a rash or a loosening of a metal implant, consider as potential allergens the product used to scrub or prep the foot, the glue/Steri-Strips, the topical antibiotic and even the implanted metal hardware.6

Mesinkovska and colleagues did a retrospective review of two groups of patients: those who had complained of metal sensitivity and had patch testing prior to implantation of an orthopedic device, and those who had patch testing postoperatively.7 Those who complained of metal sensitivity self reported sensitivity to costume jewelry, belts, buckles and dental implants. They received referrals to dermatology for patch testing prior to their procedure and the patch testing result factored into the surgeon’s decision to use a different implant from their device of choice. The most common allergen was nickel, of course, followed by palladium, gold, cobalt and chromium. Patients who then had their procedure did not have any dermatitis or loosening of the implant postoperatively.

In the post-implantation group, patients had procedures ranging from ankle fracture fixation to total hip replacement. Most of these patients complained of redness, swelling and rash that continued long after the surgical procedure. Nickel was the most common culprit in their patch test results and dermatitis was the most frequent concurrent complaint. Several of the patients with documented patch test allergies had implant explantation, which alleviated their skin symptoms. This study could have implications in the podiatric physician’s preoperative interview and decision making, even though it was a small sample size and cutaneous patch testing cannot “recreate the environment in which the metal resides.”8

Podiatric surgeons will have to determine the necessity of patch testing on a case-by-case basis. Certainly, as further studies occur in this area, we as a profession can refer patients who fit this metal sensitive profile to the local dermatologist or allergist for patch testing and further evaluation.

In both adult and pediatric patients whose lower extremity rash is chronic, severe and not responding to the typical therapeutic agents, clinicians should consider a diagnosis of allergic contact dermatitis as repeated exposure to an environmental agent may continue the skin’s reaction. Especially when the feet are involved, one should suspect an allergic reaction to a component in shoes or socks.

Shoe allergic contact dermatitis reportedly occurs in 1.5 to 24 percent of patch-tested patients.9,10 Men seem predisposed due to their wearing of occlusive footwear for long periods of time (as is the case with factory workers and military personnel) whereas women develop it due to a variation in footwear.10,11 Shoe allergy is often indicated by the presence of erythema, papules and vesicles, oozing, scaling, or crusting at the site of contact plantarly or dorsally. Shoe allergic contact dermatitis is an area of needed research as the moist, enclosed environment of the shoe seems to contribute to the susceptibility of the skin developing a reaction.12,13 Any part of the foot can be affected but it is more common dorsally.13

Common allergens in shoes include leather chemicals such as potassium dichromate, glues, rubber compounds such as thiuram, paraphenylenediamine (PPD)-containing dyes, and metals containing nickel sulfate or cobalt chloride. Rubber and dyes in socks can also contribute to foot allergic contact dermatitis (see “A Quick Guide To Possible Shoe Allergens” at left).1

What You Should Know About Irritant Contact Dermatitis

Irritant contact dermatitis accounts for approximately 80 percent of all cases of contact dermatitis. Unlike an allergen inciting allergic contact dermatitis in a certain patient, irritant contact dermatitis usually occurs in most cases in which the chemical is exposed to the skin. Irritant contact dermatitis arises as a result of contact with highly irritating chemicals that induce activation of the innate immune system through hyperproduction of cytokines and chemokines, and infiltration of inflammatory cells.

Irritant contact dermatitis differs from allergic contact dermatitis in that irritant contact dermatitis is an inflammatory response to an external stimulus without a sensitization phase. After an irritation to the skin and disruption to the epidermal barrier, there is a release of interleukin-1 (IL-1) and transforming necrosis factor alpha (TNF-a) from keratinocytes. This triggers the release and cascade of pro-inflammatory cytokines that further activate the dendritic cells, T cells and other pro-inflammatory molecules that modulate the skin’s inflammatory response. Concurrently, exposure to irritants will activate endothelial cells, which subsequently allows for the passage of the aforementioned pro-inflammatory cells toward the site of cutaneous irritation. In comparison to allergic contact dermatitis, which is mediated by memory T cells and humoral response, irritant contact dermatitis is mediated by the innate immune system.14  

The reaction can look like a red, dry and scaly rash, or can appear more like a burn. There are two types of irritant contact dermatitis: chronic cumulative insult reaction and acute toxic eruptions. The chronic cumulative insult reaction involves multiple exposure of low level irritants while acute eruptions take a single exposure to a strong toxic chemical. An irritant such as a caustic acid or alkali will provide instant damage to the epithelial cells, and does not require prior sensitization.1 Irritants include acids, alkaline materials such as soaps and detergents, chlorine in swimming pools, fabric softeners, solvents, tobacco smoke, paints and astringents. In infants, it is common to see irritant contact dermatitis in the diaper area due to exposure of stool, urine and maceration, and friction from the diaper itself.15 Unlike allergic contact dermatitis, skin reaction is generally limited to the point of contact and will be more severe with longer exposure of the irritant.

It can be difficult to distinguish clinically between allergic contact dermatitis and irritant contact dermatitis. A patch test will assist the clinician with this distinction. As with allergic contact dermatitis, once one has identified the aggravating irritant, the patient should avoid or reduce exposure to the irritant.

Key Pointers On General Management Of Eczematous Conditions

With the advent of focusing on the epidermal barrier as being problematic in eczematous skin, a paradigm shift has occurred.

The first focus should be on improving the skin barrier with moisturizers, emollients and ceramide-based creams. These creams decrease transepidermal water loss, which enhances the function of the epidermal skin barrier.

The second focus is decreasing inflammation and itching with the gold standard being topical corticosteroids. However, clinicians are now using topical calcineurin inhibitors for the steroid-phobic, weak responders to topical corticosteroids and for facial use.

Third, preventing infection in these patients is paramount as researchers have documented Staph aureus colonization and possible pathogenic involvement in patients with atopic dermatitis.16 Staph aureus can be isolated from 90 percent of skin lesions in people with atopic dermatitis although it is rarely present on healthy skin.17

Oral antibiotics, topical antibiotics, antibacterial soaps and bath additives, and dressings have all been in use with varying success. For example, one study found that the use of dilute bleach baths (concentration of 0.005%) with periodic intranasal application of mupirocin ointment decreases the eczema severity in those who frequently develop Staph superinfections.18 Avoiding triggers in these patients involves identifying food allergies, airborne allergies (pet dander and dust), and, in the case of allergic contact dermatitis, the offending allergens. Also, changing body and laundry soap to mild fragrance-free preparations without the addition of bleach or fabric softeners can be useful. Patients should wear cotton clothing and avoid wool or rough fabrics. Finally, if external environment is a trigger for patients, they should avoid severe heat and low humidity.  

How To Address Contact Dermatitis

Beyond general eczema skin care, there are two aspects to addressing contact dermatitis. First, one should treat the irritated skin. Skin barrier creams such as over-the-counter and prescription moisturizers, as well as topical steroids appropriate for the level of inflammation, are useful in the treatment of contact dermatitis.

However, one should closely monitor topical steroid use, due to the fact that irritant contact dermatitis may be caused by irritation due to propylene glycol in the formulation of a topical steroid (and many other personal products). Allergic contact dermatitis can result from the fragrance or a preservative itself in the topical steroid. One can use topical antihistamines and calamine/oatmeal soaks as well. If it is a severe reaction, then one may use systemic steroids like an oral prednisone taper.  

Second, determine the cause of the reaction so the patient can avoid that allergen or irritant in the future. It is important to address specific questions concerning the patient’s reaction, such as his or her daily skin care routine, topical products used, occupation and hobbies. Irritant contact dermatitis and allergic contact dermatitis can be difficult to distinguish clinically and histologically.

A patch test, which exposes the skin to various allergens in a controlled time period, can aid in distinguishing the difference between irritant contact dermatitis and allergic contact dermatitis. Physician office applied patch tests may involve allergens tailored to the patient’s history (Finn Chamber, SmartPractice) or the commercially prepared most common allergens (T.R.U.E. Test®, SmartPractice and allergEAZE, SmartPractice). Either one may assist in pinpointing the offending agent. In the case of shoe dermatitis, one can use a piece of the patient’s shoe or an extract of the chemicals from the shoe on non-involved skin to elucidate the cause.13

Authors recommend using patch testing in children with new onset foot dermatitis or those whose skin condition is spreading to other body sites and do not have a personal or family history of atopy (asthma, allergic rhinitis, skin disease).19 Although some are concerned that patch testing may precipitate allergic contact dermatitis, patch testing should include the most common allergens (nickel, cobalt, neomycin/antibiotics, fragrance and rubber).19 Once one has identified the allergen, institute an avoidance regimen of the aggravating allergen.  

For our patients with shoe allergic contact dermatitis, avoidance of an allergen can be challenging, especially if it involves continual use of footwear that is necessary for one’s profession. Some patients who are able to wear two pairs of socks and alternate work boots report success.13 If hyperhidrosis is present, treat it as sweat can create an ideal environment for allergic contact dermatitis to develop. A new barrier fabric (Microair barrier socks, Alpretec) is under development to keep out allergens, irritants and liquids.20 For those who are allergic to rubber, consider cork-based insoles. Custom-made shoes are an expensive option but may be necessary for a certain population (see “An Overview Of Socks And Shoes For Patients With Shoe Allergic Contact Dermatitis” at left).  

In Conclusion

Ultimately, contact dermatitis in the lower extremity is a manageable, yet challenging, condition especially when it is related to footwear allergy. Once one suspects the diagnosis, it is important to refer the patient for patch testing, manage the inflammation topically and systemically if warranted, and recommend lifestyle changes in order to ultimately improve the patient’s quality of life.

Dr. Vlahovic is a Clinical Associate Professor in the Department of Podiatric Medicine at the Temple University School of Podiatric Medicine.

References

  1.     Vlahovic TC, Schleicher SM. Skin Disease of the Lower Extremities: A Photographic Guide. HMP Communications, Malvern, PA, 2012.   
  2.     Wilkinson M, Orton D. Allergic contact dermatitis. In (Griffiths C, Barjer J, Bleiker T, et al, eds.): Rook’s Textbook of Dermatology, Ninth Edition, John Wiley & Sons, Indianapolis, 2016, p. 128.4.
  3.     Janeway C. Delayed-type hypersensitivity reactions are mediated by TH1 cells and CD8 cytotoxic T cells. In Immunobiology: The Immune System in Health and Disease. Harcourt Brace, London, 1999, p. 12-17.
  4.     Divkovic M, Pease CK, Gerberick GF, Basketter DA. Hapten-protein binding: from theory to practical application in the in vitro prediction of skin sensitization. Contact Dermatitis. 2005; 53(4):189–200.
  5.     Van Joost T, van Everdingen JJ. Sensitization to cobalt associated with nickel allergy: clinical and statistical studies. Acta Derm Venereol. 1982;62(6):525-9.
  6.     Hood CR Jr, Cornell RS, Greenfield B. Liquid adhesive contact dermatitis after bunionectomy: a case report and literature review. J Foot Ankle Surg. 2016;55(1):209-14.
  7.     Atanaskova Mesinkovska N, Tellez A, Molina L, et al. The effect of patch testing on surgical practices and outcomes in orthopedic patients with metal implants. Arch Dermatol. 2012; 148(6):687-693.
  8.     Mowad CM. The role of patch testing in the selection and management of metal device implants. Comment on “The effect of patch testing on surgical practices and outcomes in orthopedic patients with metal implants.” Arch Dermatol. 2012; 148(6):693-694.
  9.     Freeman S. Shoe dermatitis. Contact Dermatitis. 1997;36(5):247-251.
  10.     Saha M, Srinivas CR, Shenoy SD, et al. Footwear dermatitis. Contact Dermatitis. 1993;28(5):260-264.
  11.     Rani Z, Hussain I, Haroon TS. Common allergens in shoe dermatitis: our experience in Lahore, Pakistan. Int J Dermatol. 2003;42(8):605-607.
  12.     Onder M, Atahan AC, Bassoy B. Foot dermatitis from the shoes. Int J Dermatol. 2004;43(8):565-567.
  13.     Matthys E1, Zahir A, Ehrlich A. Shoe allergic contact dermatitis. Dermatitis. 2014;25(4):163-71.
  14.     Lee HY, Stieger M, Yawalkar N, Kakeda M. Cytokines and chemokines in irritant contact dermatitis. Mediators Inflamm. 2013; 916497.
  15.     Alberta L, Sweeney SM, and Wiss K. Diaper dye dermatitis. Pediatrics. 2005; 116(3):e450-e452.
  16.     Birnie AJ, Bath-Hextall FJ, Ravenscroft JC, Williams HC. Interventions to reduce Staphylococcus aureus in the management of atopic eczema: an updated Cochrane review. Br J Dermatol. 2011; 154(1):228.
  17.     Leyden JJ, Marples RR, Kligman AM. Staphylococcus aureus in the lesions of atopic dermatitis. Br J Dermatol. 1974; 90(5):525-30.
  18.     Gelmetti C, Frasin A, Restano L. Innovative therapeutics in pediatric dermatology. Dermatol Clin. 2010; 28(3):619-629.
  19.     Jacob SE, Burk CJ, Connelly EA. Patch testing: another steroid-sparing agent to consider in children. Pediatr Dermatol. 2008;25(1):81-87.
  20.     Corazza M, Baldo F, Ricci M, et al. Efficacy of new barrier socks in the treatment of foot allergic contact dermatitis. Acta Derm Venereol. 2011;91(1):68.

For further reading, see the DPM Blog “What Kind Of Dermatitis Is This?” by Dr. Vlahovic at http://tinyurl.com/np4ctpm or “What You Should Know About Atopic Dermatitis” in the September 2005 issue of Podiatry Today.  

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Tracey C. Vlahovic, DPM, FFPM, RCPS (Glasg)
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