Atypical Wounds - Contact Dermatitis

In summary, at least 20% of the general population are contact-allergic to common environmental allergens. Early detection and removal of the offending agent are the primary approach to treatment, followed by topical applications to decrease the inflammatory or immunologic symptoms that occur.
Atypical Wounds - Contact Dermatitis

Allergic reactions can be either contact (the offending substance touches the skin) or systemic (the offending substance is injected or ingested). In either case, the substance, termed an antigen, causes an immunological response that results in the production of antibodies and a subsequent inflammatory response. The reaction can actually cause wounds to develop, or in the case of existing wounds, prevent healing from progressing.

Contact dermatitis can be either allergic or irritant, depending on the host immune system and the concentration of the irritant. In allergic contact dermatitis (ACD), the offending substance or contact allergen (ie, a non-protein, low-molecular-weight chemical termed hapten[i]) reacts with the skin barrier to activate the innate immune response. The allergen binds to the carrier protein and creates a sensitizing antigen, the Langerhans cells or dendritic cells engulf and carry the antigen to the T cells (specifically CD8+ T cells that are primed in lymphoid organs during sensitization and recruited in the skin upon re-exposure to the hapten),[ii] and the T cells cause the release of lymphokines.[iii] Thus develops the inflammatory symptoms of erythema, rash, itching, and in some cases vesicular lesions, followed by scaling and dry skin (See photo) The allergic response can be either immediate or delayed, and can involve both the skin and the subcutaneous tissue. Usually the response increases in severity after repeated exposures; sensitization upon first exposure may last 10–15 days with no clinical consequence and upon re-exposure clinical symptoms may appear within 24–72 hours.2

The irritant type of contact dermatitis (ICD) is not an immunological response but an inflammatory reaction to a caustic substance, the severity of which depends on the concentration of the substance, for example, a chemical or topical liquid.  During ICD, keratinocytes initiate the inflammatory cascade by producing cytokines, including IL-6.[iv]  Some antiseptics, e.g. acetic acid or Dakin’s solution, may cause irritant contact dermatitis if used repeatedly or in strong concentrations.

Patients with chronic leg wounds have an increased susceptibility to allergic contact dermatitis, especially if they are being treated with compression therapy, a condition sometimes referred to as stasis dermatitis. If contact dermatitis is suspected or if the patient reports a history of allergies to other substances, patch testing can be performed to confirm the diagnosis.[v]  Common allergens for ACD include the following:

  • Alcohol
  • Bacitracin
  • Formaldehyde
  • Latex
  • Metals
  • Neomycin
  • Parabens
  • Perfumes
  • Tape adhesives
  • Wool

The most common metallic allergen is nickel, and it has been the experience of this clinician that any patient who reports an allergy to silver or latex will be more likely to develop an allergic reaction to many of the dressings used in wound care.  Also, many tattoo inks contain metallic pigments, potentially causing allergic contact dermatitis.[vi]  A meta-analysis by Bonitsis reported the five most common allergens for the pediatric population are nickel sulfate, ammonium persulfate, gold sodium thiosulfate, thimerosal, and toluene-2,5-diamine (p-toluenediamine).[vii]

Some of the most common irritant allergens include soap and detergents, especially those that contain surfactants; cleansing solvents; poison ivy or oak; and pesticides.[viii]

Signs of dermatitis include erythema, weeping, scaling of the periwound area, and itching. It can occur at any age; however, in the older population it can easily be misdiagnosed. In severe cases, shiny skin and alopecia may develop. A visible determining factor is that the symptoms occur only in areas of direct contact with the irritating material.  In patients receiving lower extremity total joint arthroplasty, signs of an allergic reaction to the implant metal include chronic eczema, joint effusions, joint pain, and limited range of motion; therefore, if no other cause of a poor outcome post-surgery can be identified, the possibility of an allergic reaction should be explored.[ix]

The most important component of treating any dermatitis is the identification and discontinuation of the medication, dressing, or other substance that might be responsible for the contact dermatitis. In the acute phase, low-dose topical steroids and antihistamines may help decrease inflammation and discomfort; systemic steroids may be beneficial if there is an extensive area of contact dermatitis. Antibiotics are indicated only if there is evidence of secondary infection.3

In regard to wound management, patients usually require only supportive care and discontinuation of the irritating topical agent and, in the case of an existing wound, substitution of a dressing that has fewer or no allergens. Non-adherent hypoallergenic dressings are recommended for care of open lesions. Most products that are used for wound care are available in latex-free forms, as both patients and clinicians can suffer from latex allergies.   A systematic review by Saary et al, found the following topical treatments effective for preventing ICD: barrier creams containing demethicone or perfluoropolyethers, cotton liners, softened fabrics, topical skin protectants, and quaternium 18 bentonite (also known as organoclay).  They also reported that diethylenetriamine pentaacetic acid (chelator) cream helps prevent nickel, chrome, and copper ACD; and potent or moderately potent steroids effectively treat ACD.[x] 

In summary, at least 20% of the general population are contact-allergic to common environmental allergens.  Early detection and removal of the offending agent are the primary approach to treatment, followed by topical applications to decrease the inflammatory or immunologic symptoms that occur.

[i] Nassau S, Fonacier L.  Allergic contact dermatitis.  Med Clin N Am.  2020;104:61-76.  Accessed 2/2/20.

[ii] Vocanson M, Hennino A, Rozieres A, Poyet G, Nocolas JF.  Effector and regulatory mechanisms in allergic contact dermatitis.  Allergy.2009;64(12):1699-1714.

[iii] Al-Otaibi ST, Alqahtani H.  Management of contact dermatitis. J Dermatol Surg. 2015;19(2):86-91.

[iv] Frempah B, Luckett-Chastain LR, Calhoun KN, Gallucci RM. Keratinocyte-specific deletion of the IL-6RA exacerbates the inflammatory response during irritant contact dermatitis.  Toxicology. 2019;423:123-131.

[v] Fonacier L, Noor I.  Contact dermatitis and patch testing for the allergist.  Ann Allerg Asthma Im.  2018;120(6):592-598.

[vi] Liszewski W, Warshaw EM. Pigments in American tattoo inks and their propensity to elicit allergic contact dermatitis.  J Am Acad Derm.  2019;81(2):379-385.

[vii] Bonitsis NG, Tatsioni A, Bassioukas K, Ioannidis JP.  Allergens responsible for allergic contact dermatitis among children.  Contact Dermatitis.  2011;64(5):245-257.

[viii] Hamm R, Shah JB.  Atypical wounds.  In Hamm R. (Ed.). Text and Atlas of Wound Diagnosis and Treatment, 2nd edition. New York: McGraw Hill Education.  2019;235-268.

[ix] Jauregui JJ, Desai SJ, Hodges V, et al.  Outcomes of revision joint arthroplasty due to metal allergy and hypersensitivity: a systematic review.  Surg Technol Int. 2018;33(11):332-336.

[x] Saary J, Qureshi R, Palda V, et al.  A systematic review of contact dermatitis treatment and prevention.  J Am Acad Dermatol.  2005;53(5):845.