Contact Dermatitis


Article Author:
Graham Litchman
Pragya Nair
Amber Atwater


Article Editor:
William Gossman


Editors In Chief:
David Wood
Andrew Wilt
Hajira Basit


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
10/27/2019 12:17:40 PM

Introduction

Contact dermatitis is an inflammatory eczematous skin disease. It is caused by chemicals or metal ions that exert toxic effects without inducing a T-cell response (contact irritants) or by small reactive chemicals that modify proteins and induce innate and adaptive immune responses (contact allergens).[1][2][3][4]

Contact dermatitis is divided into irritant contact dermatitis and allergic contact dermatitis. Irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage that releases mediators of inflammation predominantly from epidermal cells while allergic contact dermatitis is a delayed (type 4) hypersensitivity reaction to exogenous contact antigens. Immunological responses are due to the interaction of cytokines and T cells. In photo contact, allergic dermatitis lesions are confined to sun-exposed areas even though the allergen is in contact with covered areas.

Until recently it was believed that allergic contact dermatitis was rare, unfortunately, data indicate that it is very common and affects close to 20% of children. 

The good news is that the majority of cases of contact dermatitis are self-limited and managed with simple supportive measures. However, in some patients, the disorder is chronic and can significantly affect the quality of life.

Etiology

Irritant contact dermatitis 

The likelihood of developing irritant contact dermatitis (irritant contact dermatitis ) increases with the duration, intensity, and concentration of the substance. Chemical or physical agents and microtrauma may produce skin irritation thus causing Irritant contact dermatitis. Physical irritants like friction, abrasions, occlusion, and detergents like sodium lauryl sulfate produce more irritant contact dermatitis in combination than alone.[5][6]

The factors which determine the severity of irritant contact dermatitis include the quantity and concentration of the irritant, duration, and frequency of exposure. It also depends on the type of skin if it is thick, thin, oily, dry, very fair, previously damaged skin, or having a pre-existing atopic tendency. Environmental factors like high or low temperature and humidity also determine the severity.

Allergic contact dermatitis

Common etiological allergens for allergic contact dermatitis are nickel, balsam of Peru, chromium, neomycin, formaldehyde, thiomersal, fragrance mix, cobalt, and parthenium.[7] Poison Ivy (Toxicodendron, formerly known as Rhus), in the United States, is considered to be the most common cause of allergic contact dermatitis.[8] As much as 50-70% of the adult population is sensitive to poison ivy or poison oak.[8] Once exposed to the skin, urushiol (the allergin responsible for the skin reaction), should be diligently removed by washing the affected area as soon as possible. Studies have shown that washing with regular soap, e.g. Dial, is sufficient and should be done within a 2-hour window.[8] If the patient has not removed the urushiol oil from their skin within the appropriate time frame, high-potency topical steroids may be used to reduce inflammation in early stages, i.e. within 12 hours of exposure.[9] It should be noted that low-potency topical steroids are of little use and even high-potency steroids do not significantly relieve symptoms once vesicles have formed.[9]

Epidemiology

Females, infants, elderly, and individuals with atopic tendencies are more susceptible to irritant contact dermatitis.  It is reported that up to 80% of cases of occupational dermatitis are irritant contact dermatitis.[10]

All individuals are at risk of developing allergic contact dermatitis.  Risk factors for allergic contact dermatitis include age, occupation, and history of atopic dermatitis.

Overall contact dermatitis is most common in people with red hair and fair skin. Women are more likely to develop contact dermatitis because of the use of jewelry and fragrances.

Pathophysiology

Irritant contact dermatitis 

It is due to sufficient inflammation arising from the release of proinflammatory cytokines from keratinocytes, usually in response to chemical stimuli. It mainly causes skin barrier disruption, epidermal cellular changes, and cytokine release.

Irritants can be classified as cumulatively toxic (e.g., hand soap causing irritant dermatitis in a hospital employee), subtoxic, degenerative, or toxic (e.g., hydrofluoric acid exposure at a chemical plant).

Allergic contact dermatitis

It is T-cell mediated inflammation of the skin caused by repeated skin exposure to haptens in a sensitized individual.

Allergic contact dermatitis has two phases. The sensitization phase in which antigen-specific effector T cells are induced in the draining lymph nodes by antigen captured cutaneous dendritic cells that migrate from the skin. The elicitation phase includes effector T cells that are activated in the skin by antigen captured cutaneous dendritic cells and produce various chemical mediators, which create antigen-specific inflammation.

Photo contact dermatitis occurs when an allergen becomes an irritant in the presence of light.

Contact urticaria usually presents with a 'wheal and flare' reaction after exposure to the offending topical agent. While most cases are mild, anaphylactic reactions can occur. Some common types of contact urticaria include exposure to cold, dermatographism, pressure, exercise, solar, heat and cholinergic.

Contact dermatitis can also occur after exposure to plants of the Urticaceae family.

Histopathology

Contact irritant dermatitis presents with mild spongiosis, epidermal cell necrosis, and neutrophilic infiltration of the epidermis, while in allergic contact dermatitis dermal inflammatory infiltrates predominately contains lymphocytes and other mononuclear cells.

History and Physical

Symptoms of irritant contact dermatitis may include burning, itching, stinging, soreness, and pain, particularly at the beginning of the clinical course, while pruritus is more common in allergic contact dermatitis. Patients with a history are at increased risk for developing nonspecific hand dermatitis and irritant contact dermatitis.

Both irritant contact dermatitis and allergic contact dermatitis can present with three morphological patterns.

  • Acute phase: erythema, edema, oozing,  crusting, tenderness, vesicles or pustules
  • Subacute phase: crusts, scales, and hyperpigmentation
  • Chronic phase: Lichenification. 

Hands are the common site of contact allergic dermatitis.

No pathognomonic clinical signs and symptoms can differentiate between allergic contact dermatitis and irritant contact dermatitis.

The acute irritant reaction usually reaches its peak quickly, within minutes to few hours after exposure, and then starts to heal, while in allergic contact dermatitis, the elicitation time depends on the characteristics of the sensitizer, the intensity of exposure, and degree of sensitivity. Lesions usually appear 24 to 72 hours after the exposure to the causative agent and reach their peak at approximately 72 to 96  hours. Allergic contact dermatitis improves more slowly than irritant contact dermatitis and then recurs faster (in a few days) when exposure is re-established.

Common allergens causing allergic contact dermatitis include the following -

  1. Paraphenylenediamine (PPD) present in hair dye; a common cause of allergic contact dermatitis on the scalp, face, ears
  2. Neomycin and bacitracin applied to the areas of stasis dermatitis and leg ulcers may be the cause of allergic contact dermatitis on the legs and feet
  3. Topical neomycin and corticosteroids can lead to allergic contact dermatitis in patients with otitis externa
  4. In women with lichen sclerosus et atrophicus, benzocaine applied in pruritus ani and pruritus vulvae may develop allergic contact dermatitis
  5. Nickel is the most common metal present in artificial jewelry which is the cause of allergic contact dermatitis.

Different clinical patterns of allergic contact dermatitis include erythema multiforme, urticarial papular plaques, lichen-planus, lichenoid eruptions, purpuric petechial reactions, dermal reactions, lymphomatoid contact dermatitis, granulomatous and pustular reactions, pigmentation disturbances, or pemphigoid.

Evaluation

History regarding occupation, hobbies and any topical or oral medications is important in diagnosing contact dermatitis. Patch testing is considered to be the gold standard in diagnosing contact allergic dermatitis and is used to determine the exact cause. A patch test mainly relies on the principle of a. The chemicals included in the patch test kit are chemicals present in metals (e.g., nickel), rubber, leather, formaldehyde, lanolin, fragrance, toiletries, hair dyes, medicine, pharmaceutical items, food, drink, preservative, and other additives.  Patch testing helps identify which substances may be causing a delayed-type allergic reaction.  It produces a local allergic reaction on a small area of the patient's back, where the diluted chemicals are applied.[11][12]

Allergens are placed on Finn chambers and applied on the back. Patches are removed at 48 hours, and final results are read 48-72 hours later. Grading of the reactions is completed based on the International Contact Dermatitis Research Group guidelines.

  • Negative (-)
  • Irritant reaction (IR)
  • Equivocal / uncertain (+/-)
  • Weak positive (+)
  • Strong positive (++)
  • Extreme reaction (+++)

In patients with nickel allergy, a few drops of dimethylgloxime and hydroxide solutions are on a cotton tip applicator and rubbed on the metallic surface of the jewelry. If the color pink appears on the applicator, this is a positive test for nickel. Women with nickel allergy can perform the test at home on jewelry for the presence of nickel.

Treatment / Management

Compliance with avoidance is important. The key to avoidance is proper evaluation and detection of causative allergen. Wear appropriate clothing to protect against irritants at home and in a work environment.[13][14]

High-potency topical corticosteroids, e.g. clobetasol propionate 0.05% cream, may be used to reduce the inflammation.[9] As a general rule, high-potency corticosteroids should not be used on thin skin, e.g. face, genitals, intertriginous areas, to avoid the risk of skin atrophy. Antihistamines such as hydroxyzine and cetirizine are recommended to control pruritus. Systemic steroids are advised in severe cases but should be tapered gradually to prevent recurrences. Friction should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus ointment and pimecrolimus cream are immunomodulating drugs that inhibit calcineurin and are helpful in allergic contact dermatitis.

Prognosis

The prognosis of patients with contact dermatitis depends on the cause and lifestyle. Isolated cases usually resolve if the offending agent exposure is discontinued. Those who do not remain compliant and continue to wear jewelry with metal or are exposed to plants because of lifestyle generally tend to have a chronic course. Relapses are very common. In healthcare, latex allergy is a very common form of contact dermatitis and can have an impact on clinical practice. Cases of anaphylaxis are reported all the time.

Enhancing Healthcare Team Outcomes

Contact dermatitis is a relatively common disorder encountered in clinical practice. However, the condition is best managed by an intradisciplinary team that includes a dermatologist, allergist, primary care provider, nurse practitioner, and a pharmacist. The key is compliance with avoidance is important. The key to avoidance is proper evaluation and detection of causative allergen. Wear appropriate clothing to protect against irritants at home and in a work environment.

The pharmacist should educate the patient on over the counter products that can be used to ease symptoms. Topical corticosteroids may be used to reduce the inflammation. Antihistamines such as hydroxyzine and cetirizine are recommended to control pruritus. Systemic steroids are advised in severe cases but should be tapered gradually to prevent recurrences. Friction should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus ointment and pimecrolimus cream are immunomodulating drugs that inhibit calcineurin and are helpful in allergic contact dermatitis.

The nurse and primary care physician should educate the patient on avoidance of the offending agents and maintain some type of barrier protection. Patients should be educated that contact dermatitis can recur if repeated exposure occurs. When going hiking, long-sleeved garments are recommended for individuals with an allergy to plants.

Unfortunately, recurrence is common and people with no identifiable cause have a poor quality of life.[15] A nurse educator specializing in dermatology and dermatology should work together to assist in patient education, particularly for challenging cases. [Level V]


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Contact Dermatitis - Questions

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A teenage girl complaining of scaly rashes on her earlobes, neck, and umbilical region may likely be experiencing which condition?



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A 27-year-old female with no significant past medical history presents to your office with a chief complaint of a pruritic rash on her neck and chest for the past week. She reports having several significant life events in the past month: job promotion, engagement, mother's cancer diagnosis. She often "breaks out in hives" when she is stressed, but the rash is usually not very itchy, and the redness will subside fairly quickly. Over the counter medications help to alleviate the itching, but the rash is progressively worsening. Upon physical examination, the physician notes erythematous, indurated, scaly plaques scattered across the anterior chest wall and circumferentially around her neck. She denies a personal or family history of asthma, seasonal allergies, or scaly plaques on flexor or extensor surfaces. Based on the information provided, which of the following inflammatory cells are involved in this patient's current condition?



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A 22-year-old female collegiate soccer player with no significant past medical history and is 5 months status post left “knee surgery” secondary to a severely displaced patella fracture presents to your office with a chief complaint of an evolving erythematous, edematous “rash” over her chest and back. She reports that she has noticed blistering last week, which is why she made the appointment. Over-the-counter topical agents have not been successful in treating the rash. Which of the following is the most common cause of the underlying diagnosis and what is the most suitable treatment?



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A 2-year-old boy presents to your clinic with erythematous eruption around the buttocks and genitals. There are some superficial erosions present, as the child's mother was unable to schedule an appointment before the weekend, and the child is clearly experiencing pain and discomfort. Upon further inspection, you note that skin folds are spared and you do not appreciate any satellite lesions. What are the acute clinical descriptions of the two most common forms of the condition described above as it pertains to the pediatric population?



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A 32-year-old male landscaper with a past medical history of gout, treated with allopurinol, stage 1 chronic kidney disease, and mild hypertension presents with a 6-day history of a progressively worsening, severely pruritic rash on his hands. Upon physical examination, you appreciate erythematous and edematous underlying skin with linear groups of small vesicles extending from his fingers to his elbows, bilaterally. Based on the information provided, what is the treatment and type of hypersensitivity reaction is associated with the most likely diagnosis?



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A 16-year-old female with a past medical history significant for mild asthma and a seizure disorder, successfully treated with carbamazepine for 6 years, presents to the physician's office complaining of pruritic, well-demarcated, scaly, erythematous rashes on her earlobes. Upon further questioning, she reports recently getting her ears pierced. Based on her history and physical examination, which of the following is the most likely diagnosis?



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Contact Dermatitis - References

References

Basketter DA,Huggard J,Kimber I, Fragrance inhalation and adverse health effects: The question of causation. Regulatory toxicology and pharmacology : RTP. 2019 Mar 20;     [PubMed]
Romita P,Foti C,Calogiuri G,Cantore S,Ballini A,Dipalma G,Inchingolo F, Contact dermatitis due to transdermal therapeutic systems: a clinical update. Acta bio-medica : Atenei Parmensis. 2018 Oct 26;     [PubMed]
Esser PR,Mueller S,Martin SF, Plant Allergen-Induced Contact Dermatitis. Planta medica. 2019 Mar 15;     [PubMed]
Anderson LE,Treat JR,Brod BA,Yu J,     [PubMed]
Bingham LJ,Tam MM,Palmer AM,Cahill JL,Nixon RL, Contact Allergy and Allergic Contact Dermatitis to Lavender: A Retrospective Study from an Australian Clinic. Contact dermatitis. 2019 Feb 18;     [PubMed]
Kimyon RS,Warshaw EM, Airborne Allergic Contact Dermatitis: Management and Responsible Allergens on the American Contact Dermatitis Society Core Series. Dermatitis : contact, atopic, occupational, drug. 2019 Mar/Apr;     [PubMed]
Shane HL,Long CM,Anderson SE, Novel cutaneous mediators of chemical allergy. Journal of immunotoxicology. 2019 Mar 1;     [PubMed]
Zander N,Sommer R,Schäfer I,Reinert R,Kirsten N,Zyriax BC,Maul JT,Augustin M, Epidemiology and Dermatological Comorbidity of Seborrhoeic Dermatitis - Population-based Study in 161,000 Employees. The British journal of dermatology. 2019 Feb 25;     [PubMed]
Stingeni L,Bianchi L,Hansel K,Corazza M,Gallo R,Guarneri F,Patruno C,Rigano L,Romita P,Pigatto PD,Calzavara-Pinton P, Italian guidelines in patch testing adapted from the European Society of Contact Dermatitis (ESCD). Giornale italiano di dermatologia e venereologia : organo ufficiale, Societa italiana di dermatologia e sifilografia. 2019 Feb 4;     [PubMed]
DeKoven JG,Warshaw EM,Zug KA,Maibach HI,Belsito DV,Sasseville D,Taylor JS,Fowler JF Jr,Mathias CGT,Marks JG,Pratt MD,Zirwas MJ,DeLeo VA, North American Contact Dermatitis Group Patch Test Results: 2015-2016. Dermatitis : contact, atopic, occupational, drug. 2018 Nov/Dec;     [PubMed]
Soltanipoor M,Kezic S,Sluiter JK,de Wit F,Bosma AL,van Asperen R,Rustemeyer T, Effectiveness of a skin care programme for the prevention of contact dermatitis in healthcare workers (the Healthy Hands Project): A single-centre, cluster randomized controlled trial. Contact dermatitis. 2019 Jan 16;     [PubMed]
Nedorost S, A diagnostic checklist for generalized dermatitis. Clinical, cosmetic and investigational dermatology. 2018;     [PubMed]
Bennike NH,Heisterberg MS,White IR,Mahler V,Silvestre-Salvador JF,Giménez-Arnau A,Johansen JD, Quality of life and disease severity in dermatitis patients with fragrance allergy - a cross-sectional European questionnaire study. Contact dermatitis. 2019 Feb 25;     [PubMed]
Stibich AS,Yagan M,Sharma V,Herndon B,Montgomery C, Cost-effective post-exposure prevention of poison ivy dermatitis. International journal of dermatology. 2000 Jul;     [PubMed]
Vernon HJ,Olsen EA, A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally induced Rhus dermatitis. Journal of the American Academy of Dermatology. 1990 Nov;     [PubMed]

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