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Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023
| Contributor Information
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Image from Sahu S. et al. Cureus. 2022 Dec;14(12):e32119. [Open access.] PMID: 36601177, PMCID: PMC9805537.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
As the body's primary barrier against environmental insults, the skin is regularly exposed to potential noxious agents. Many of these agents can provoke an uncomfortable local inflammatory response known as contact dermatitis.
Two forms of contact dermatitis exist. Allergic contact dermatitis is caused by lymphocyte-mediated immune responses to an allergen, whereas irritant contact dermatitis ensues after a direct cytotoxic insult to the skin (eg, a chemical burn).[1,2] Because allergic and irritant contact dermatitis can have similar clinical presentations—erythema, edema, and vesiculation—it is important to identify the source of the reaction.
The image shows occupational allergic contact dermatitis due to cement exposure in a construction worker.
Image from Wikimedia Commons | Alborz Fallah. [Creative Commons Attribution-ShareAlike 3.0 Unported (CC-BY SA 3.0).]
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Acute Allergic Contact Dermatitis
Allergic contact dermatitis is a delayed-type hypersensitivity reaction that occurs when the skin is reexposed to an allergen to which it has been previously sensitized.[1,2] The reexposure activates the adaptive immune system, causing previously primed T lymphocytes to release a cascade of cytokines and proinflammatory factors.[1] This leads to the formation of a well-defined erythematous plaque and intercellular edema in the epidermis. The severity of the reaction depends on the properties of the allergen, the contact duration, and the host response, but it usually includes the formation of pruritic papules and vesicles (shown here in a 3-year-old patient 1 day after exposure to poison ivy). The vesicles can blister and ooze, with eventual crusting.[1]
Common causes of acute allergic contact dermatitis include poison ivy and nickel. Textile dyes are often overlooked sensitizing agents.[3] Although laundry detergents are frequently implicated by patients and physicians alike, allergic contact dermatitis to detergents is actually quite rare.[4] Topical corticosteroids are the first-line treatment for acute allergic contact dermatitis.[1,2] Other options include nonsedating oral antihistamines and topical moisturizers.
Image courtesy of Medscape.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Nickel is routinely used in jewelry, buckles on clothing, kitchen supplies, and even medical devices. An individual who is allergic to nickel can develop a pruritic, erythematous plaque that precisely demarcates the area of contact. In the acute phase, erythema is accompanied by edema and vesiculation, whereas chronic exposure can cause lichenification and pruritus.[5]
Although topical corticosteroids can alleviate the reaction, strict avoidance of nickel is the recommended management. Persons with extreme sensitivity may experience skin reactions after eating foods that contain nickel, such as chocolate, oatmeal, nuts, and green beans; in addition to avoiding those foods, these individuals may benefit from treatment with disulfiram, a metal-chelating agent.[5,6]
The presence of nickel in a watch and watch band produced the episode of allergic contact dermatitis shown.
Image courtesy of Medscape.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Severe Allergic Contact Dermatitis
Severe reactions to exogenous allergens can occur. Paraphenylenediamine (PPD) is a common ingredient in hair dyes that can cause allergic contact dermatitis.[2,7,8] Acute dermatitis and severe facial edema may develop following exposure to PPD in hair dye products (shown).[2] Treatment options for severe reactions include systemic corticosteroids, antibiotics, immunosuppressive agents, and hospitalization.[2] Unfortunately, many patients with PPD allergy experience cross-reactions with PPD-free hair dyes, and most affected patients must completely discontinue hair dye.
Image from Carino M, Romita P, Foti C. ISRN Prev Med. 2013;2013:864679. [Open Source.] PMID: 24971193, PMCID: PMC4045454.[11]
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Chronic Allergic Contact Dermatitis
Long-term exposure to an allergen can lead to the development of chronic allergic contact dermatitis. This condition is typically characterized by hyperpigmented, lichenified plaques that are exacerbated by scratching.[9] In affected areas, such as the hands, painful fissures and dry scaling are common. Identification of the allergen is critical to reducing the risk of repeated allergen exposure and subsequent development of chronic allergic contact dermatitis. Treatment options include topical or systemic corticosteroids, emollients, phototherapy, and immunosuppressive agents.[2]
The image shows the sequelae of repeated exposure to wet cement on the hand of a construction worker. Chromates, contained in cement, are among the most common sensitizing agents in the construction industry. [1,10-13] Additionally, exposure to the high pH of cement can result in irritant contact dermatitis.
Image from Wikimedia Commons | Blazius. (CC-BY SA 3.0).
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Acute Irritant Contact Dermatitis
Most contact dermatitis cases represent a nonimmunologically-initiated inflammatory response to localized exposure to a cytotoxic agent, called irritant contact dermatitis.[12] Hazardous agents are common in the workplace and at home and include surfactants, solvents, acids, and alkaline solutions.[15,16] The three most common exposures are to rubber, wet work, and soaps and cleansers.[16] Irritant contact dermatitis is a leading cause of occupational skin disease.[16]
Treatment options include thorough flushing of the skin with water, followed by the use of topical corticosteroids, oral antihistamines, emollients, cold/moist compresses, moisturizers, antibiotics, and/or antidotes/agents that act specifically against the offending irritant.[16]
The image shows ulcerations on the back of a hand 44 hours after exposure to sodium hydroxide solution (lye), a strong base that is frequently used as an industrial cleaning agent.
Image from Malla G, Basnet B, Vohra R, Lohani SP, Yadav A, Dhungana V. BMC Res Notes. 2013;6:524. PMID: 24321121, PMCID: PMC4029564. [Creative Commons Attribution 2.0 Generic (CC BY 2.0).]
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Acute irritant contact dermatitis is caused by direct tissue damage. After chemical or physical irritants penetrate the epidermal barrier, keratinocyte injury promotes the release of proinflammatory factors that lead to leukocyte recruitment.[15,17] The reaction will occur in minutes to hours after the initial contact, consisting of burning, stinging, or soreness at the area.[17]
The clinical features of irritant contact dermatitis include a wide range of presentations of erythema, edema, and bullae; the findings depend on the nature of the irritant. For example, inorganic acids and strong alkalis cause ulcerations, whereas contact with greases, tar, or asphalt results in folliculitis.[16] An eczematous process can occur in those who handle or clean crustaceans, such as shrimp, crabs, and lobsters.[18]
The image shows cellulitis and irritant contact dermatitis on a patient's left arm following exposure to parenteral organophosphate.
Image courtesy of Medscape.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Chronic Irritant Contact Dermatitis
Chronic irritant contact dermatitis (shown) results from repeated exposures to solvents and surfactants.[16,17] Solvents, including hexanes found in gasoline and benzene found in plastics and resins, remove surface lipids from the stratum corneum. Surfactant, found in many detergents and cleaning agents, binds to keratin and causes protein denaturation. This disruption of barrier function promotes transepidermal water loss and desquamation.
In some individuals, irritant contact dermatitis resolves spontaneously even with ongoing exposure, perhaps as a consequence of thickening of the stratum corneum resulting in improvement of the physical barrier.[19] Chronic irritant contact dermatitis develops when the irritant contact frequency is greater than the time needed for recovery through barrier restorative mechanisms, such as lipid synthesis and keratinocyte proliferation.[16,17]
Image from the National Institute for Occupational Safety and Health (US). (Public domain).
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Areas of chronic irritant contact dermatitis are less defined than those seen in the acute form. Lichenification and hyperkeratosis are characteristic features of chronic irritant contact dermatitis, and they are associated with pain and pruritus of the affected areas.[16]
The skin of the hands and wrists of this man demonstrates the sequelae of long-term exposure to kerosene, a solvent. Kerosene was routinely used to clean the skin by workers who had contact with oily products (eg, auto mechanics), resulting in eventual thickening, fissuring, and hyperpigmentation.
Image courtesy of Justin Finch, MD.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Phytodermatitis
Plants are a common cause of both allergic and irritant contact dermatitis; this is known as phytodermatitis. The characteristic skin lesions are linear eruptions.
Poison ivy
Poison ivy is the most common cause of allergic phytodermatitis[20] and is in fact the overall most common cause of any skin allergy. Over 95% of humans are allergic to poison ivy. This plant contains the compound urushiol, which causes a pruritic eruption (shown) within 2 days of contact; left untreated, the eruption can persist for 2-3 weeks. Streaks of erythema, edema, and papules are typically observed before the formation of vesicles and bullae (as shown on Slide 2). Vesicles will not develop if the antigen load is low.
It is a common misconception that the rash of poison ivy is contagious. Fluid in the bullae does not carry noxious particles; therefore, bullous eruption does not propagate the reaction.[20]
Images from Wikimedia Commons | Tinkerbelle122 (left) and Wikimedia Commons | Curtis Clark (right). (CC-BY SA 3.0) and [Creative Commons Attribution-ShareAlike 2.5 Generic (CC BY-SA 2.5).], respectively.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Glochids
Plant-induced irritant contact dermatitis can be mechanical or chemical. Mechanical insults can arise from contact with thorns or spines that penetrate the skin, with the smallest spines causing the most damage. Glochids covering the surface of prickly pears are especially notorious for these skin reactions. The collections of hundreds of short, barbed spines act like fishhooks in the skin, causing pruritic, papular eruptions.
The most common chemical cause of irritant phytodermatitis is calcium oxalate, which is found in daffodil, pineapple, rhubarb, and century plants. The skin reactions to calcium oxalate are typically a burning sensation and the formation of blistering lesions.[20]
The left image shows irritant phytodermatitis after contact with the glochids of Opuntia microdasys monstrose, a type of cactus. The right image is a scanning electron micrograph of the retrorse barbs at the margin of a Hordeum murinum spikelet. H murinum is a type of annual grass.
Images courtesy of Justin Finch, MD.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Stinging nettle
The stem and leaves of the stinging nettle plant (Urtica spp) are covered in tiny trichome hairs (shown) containing histamine. Upon contact, these trichomes inject histamine into the skin, causing an itchy reaction known as contact urticaria. The hairs also contain oxalic acid and tartaric acid, which are responsible for the stinging sensation.[21]
Image courtesy of Justin Finch, MD.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
Patch Testing
Patch testing is the gold standard diagnostic tool for the evaluation of allergic contact dermatitis.[13] Identifying the specific allergen can help clinicians to distinguish between allergic and irritant contact dermatitis, which, as previously noted, have similar clinical presentations.
Obtaining a detailed history is critical for identification of common exogenous exposures at work and at home. This information will help to direct the selection of appropriate agents to be included in an individual patch test.[2,13]
Patch testing is usually conducted on the patient's back (shown), where controlled concentrations and volumes of allergens are aliquoted into chambers and secured to the skin using tape. The area must be kept dry for the duration of the test (96 hours).
Image courtesy of Justin Finch, MD.
Contact Dermatitis: A Summary
Justin Finch, MD | February 6, 2023 | Contributor Information
After 48 hours, the patches are removed. The patch locations are marked with a gentian violet skin pen, and each site is classified and graded[1,13] on the basis of its morphologic features: 1+ for redness and induration, 2+ for vesicle formation, and 3+ for bulla formation.[13]
After 96 hours, a second, delayed assessment is performed. A positive reaction at both the 48-hour and the 96-hour evaluations is a stronger indicator of an allergy than is a transient reaction that occurs at 48 hours but resolves by 96 hours.
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Contributor Information
Justin Finch, MD
Founding Partner
Central Connecticut Dermatology
Cromwell, CT;
Associate Professor
Department of Dermatology
University of Connecticut Health Center
Farmington, CT
Disclosure: Justin Finch, MD, is an investigator for: AbbVie, Brickell Biotech, Cara, Corrona, Dermavant, Dermira, Incyte, and Novartis.
Reviewer
Brett Sloan, MD, FAAD
Professor of Dermatology
Dermatology Residency Program Director
University of Connecticut School of Medicine;
Connecticut Veterans Affairs Healthcare System;
Editor-in-Chief Journal of the American Academy of Dermatology Case Reports
Disclosure: Brett Sloan, MD, FAAD, has disclosed the following relevant financial relationships:
Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Journal of the American Academy of Dermatology; UpToDate; Medical Review Institute of America.
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References
Mowad CM et al. Allergic contact dermatitis. Bolognia JL et al, eds. Dermatology. 3rd ed. Philadelphia: Elsevier; 2012: Chap 14.
Nygaard U et al. Allergic contact dermatitis induced by textile necklace. Case Rep Dermatol. 2013 Nov 16;5(3):336-9. PMID: 24348384
Belsito DV et al. Allergic contact dermatitis to detergents: a multicenter study to assess prevalence. J Am Acad Dermatol. 2002 Feb;46(2):200-6. PMID 11807430
Kim D et al. Dermatology for the allergist. World Allergy Organ J. 2010 Jun;3(6):202-15. PMID: 23268431
Kridin K et al. Cement-induced chromate occupational allergic contact dermatitis. Dermatitis. 2016 Jul-Aug;27(4):208-14. PMID: 27331340
Carino M et al. Allergy-related disorders in the construction industry. ISRN Prev Med. 2013 Dec 5;2013:864679. PMID: 24971193
Dear K, Palmer A, Nixon R. Allergic chromate dermatitis to cement in Australia: an ongoing problem. Occup Environ Med. 2020 Sep;77(9):658. PMID: 32404532.
Wilson B et al. Chromate-induced allergic contact dermatitis treated with dupilumab. J Drugs Dermatol. 2021 Dec 1;20(12)1340-42. PMID: 34898150.
Haddad V Jr. Environmental dermatology: skin manifestations of injuries caused by invertebrate aquatic animals. An Bras Dermatol. 2013 Jul-Aug;88(4):496-506. PMID: 24068119.
Watkins SA et al. The hardening phenomenon in irritant contact dermatitis: an interpretative update. Contact Dermatitis. 2009 Mar;60(3):123-30. PMID 19260908
McGovern TW. Dermatoses due to plants. Bolognia JL et al, eds. Dermatology. 3rd ed. Philadelphia: Elsevier; 2012: Chap 17.
Fu HY et al. Identification of oxalic acid and tartaric acid as major persistent pain-inducing toxins in the stinging hairs of the nettle, Urtica thunbergiana. Ann Bot. 2006 Jul;98(1)57-65. PMID: 16675601.
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