eMedicine Specialties > Emergency Medicine > Dermatology

Dermatitis, Contact

Author: Bradley D Shy, MD, Staff Physician, Department of Emergency Medicine, New York University School of Medicine/Bellevue Hospital Center
Coauthor(s): David Todd Schwartz, MD, Associate Professor of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center and New York University Medical Center
Contributor Information and Disclosures

Updated: Sep 22, 2009

Introduction

Background

Contact dermatitis is any inflammatory reaction of the skin that results from direct contact with an offending agent. Most cases of contact dermatitis evaluated in the ED can be classified as allergic contact dermatitis (ACD) or irritant contact dermatitis (ICD). Additional types of contact dermatitis seen in the ED include photodermatitis and contact urticaria.

For further information, see Medscape's Allergy Resource Center.

Pathophysiology

The main pathologic feature of contact dermatitis is intercellular edema of the epidermis. This initial reaction may result in intraepidermal vesicle and bullae formation in acute cases and papules, scaling, and lichenification in chronic cases. Within the dermal layer, various cells congregate around the dilated capillaries to aid in inflammatory response.

Irritant contact dermatitis (ICD) results from direct injury to the skin. It affects individuals exposed to specific irritants and generally produces a stinging or burning sensation within seconds of exposure. Alternatively, extended exposure to a mild irritant can cause a chronic form of ICD. In this case, dryness precipitates an erythematous state, which ultimately leads to cracking and the formation of painful fissures.

Allergic contact dermatitis affects only individuals previously sensitized to the contactant. It represents a delayed (cell-mediated, type IV) hypersensitivity reaction and classically requires several hours to complete the cascade of cellular immunity before symptoms manifest.

Frequency

United States

Among workers' compensation claims for dermatologic conditions, 90% are for contact dermatitis. Importantly, not all workers are at equal risk. Most workers who present with irritant contact dermatitis (ICD) have a history of atopic dermatitis.1 The greatest single risk for ICD is a history of atopic dermatitis.1 The most common allergens are nickel, potassium dichromate, and paraphenylenediamine. Contact dermatitis is the reason for 4-7% of dermatologic consultations. Hand dermatitis affects 2% of the population at a given time, and 20% of females are affected at least once in their lifetime. Children of persons with contact dermatitis are 60% more likely to have positive patch tests.

International

Contact allergens are the same in Europe as in the United States. However, dermatitis caused by Toxicodendron species is unknown in Europe.

A large, retrospective Danish study by Engkilde et al demonstrated that patients with type 1 diabetes had a significantly lower incidence of contact dermatitis, although the mechanism and causality of this association remains unclear.2

Mortality/Morbidity

Most cases of contact dermatitis are easily treated, but cases with an unrecognized etiology can result in long-term morbidity. In rare cases, epidermal contact with an allergen results in an immunoglobulin E (IgE)-mediated immediate hypersensitivity reaction causing anaphylactic shock. Anaphylactic shock, if untreated, can result in death.

Contact dermatitis can present concomitantly with chemical burns, which can be life-threatening, depending on the severity of exposure. A review of 51 patients with cement exposure found that 34% required eventual dermatologic surgery.3

Climate/weather

Low humidity and cold temperatures increase incidence of contact dermatitis. One notable contrast to this is irritant contact dermatitis (ICD) due to cement exposure, which is more common in the summer in hot and humid areas.

Race

Contact dermatitis is thought to affect whites more frequently than other races. It may be just as common in blacks but more difficult to detect. Fair-skinned redheads are the most vulnerable.

Sex

The female-to-male ratio is 2:1. Women are at highest risk following childbirth.

Age

  • Allergic contact dermatitis (ACD) is most common during adulthood, but it affects all ages.
  • Irritant contact dermatitis (ICD) affects very young and very old patients more severely.
  • A frequent cause of ACD in elderly patients is topical medication.
  • ICD is common in infants. The most common cause is diaper dermatitis.

Clinical

History

  • In acute allergic contact dermatitis (ACD), lesions appear within 24-96 hours of exposure to the allergen. 
    • The main symptom, in addition to the lesion, is pruritus.
    • Location of the dermatitis is helpful in identifying the cause.
    • Most heavily contaminated areas break out first, followed by areas of lesser exposure.
    • In more severe ACD reactions, lesions can form in adjacent areas of the skin that never had direct contact with the offending agent.
  • Irritant contact dermatitis (ICD) is divided into 2 types.
    • Mild irritants require prolonged or repeated exposure before inflammation is noted.
    • Strong irritants (eg, strong acids, alkalis) can produce immediate reactions similar to thermal burns.
    • Unlike ACD, ICD will only erupt in areas of the skin that have had direct contact with the irritant.
  • Photodermatitis is diagnosed by the presence of lesions limited to sun-exposed body areas.
    • Burning is the primary complaint in phototoxic reactions.
    • Pruritus is the main complaint in photoallergic reactions.
    • Skin contact with photosensitizing agents found in some plants (notably limes) followed by ultraviolet (UV) irradiation can precipitate a type of photodermatitis called phytophotodermatitis.
  • Contact urticaria reactions occur within 1 hour of exposure to the inciting agent.

Physical

  • Most cases of contact dermatitis have a similar appearance regardless of the mechanism or cause of inflammation. Inflammatory responses can be categorized into acute, subacute, and chronic phases. In all phases, a key feature is localization to the area of contact. 
    • Acute contact dermatitis presents with bright red edematous skin. In moderate-to-severe cases, clear fluid-filled vesicles or bullae appear. As the lesions break, skin becomes exudative and weeps clear fluid. In acute ICD, these lesions and surrounding erythema are sharply demarcated and located in the distribution of the area of contact.
Contact dermatitis on the thigh of a recreational...

Contact dermatitis on the thigh of a recreational jogger after a long run. This individual noted running through shrubs, which likely caused the rash. The linear plaques and confluent vesicles and papules on the inferior aspect of the thigh are a common presentation of rhus dermatitis. Image courtesy of Julie Cantatore.

Contact dermatitis on the thigh of a recreational...

Contact dermatitis on the thigh of a recreational jogger after a long run. This individual noted running through shrubs, which likely caused the rash. The linear plaques and confluent vesicles and papules on the inferior aspect of the thigh are a common presentation of rhus dermatitis. Image courtesy of Julie Cantatore.


Contact dermatitis with bullous formation caused ...

Contact dermatitis with bullous formation caused in this case by a new pair of shoes. Image courtesy of Julie Cantatore.

Contact dermatitis with bullous formation caused ...

Contact dermatitis with bullous formation caused in this case by a new pair of shoes. Image courtesy of Julie Cantatore.


    • Subacute contact dermatitis is characterized by the formation of papules instead of the vesicles more typical of the acute phase. Additionally, less edema is seen in the subacute phase. Dry scales are sometimes seen in subacute contact dermatitis.


Subacute contact dermatitis, in this case due to ...

Subacute contact dermatitis, in this case due to bacitracin. Image courtesy of Julie Cantatore.

Subacute contact dermatitis, in this case due to ...

Subacute contact dermatitis, in this case due to bacitracin. Image courtesy of Julie Cantatore.


    • Chronic contact dermatitis presents with scaling, skin fissuring, and lichenification but only minimal edema. Excoriations can also be observed in chronic contact dermatitis.
    • Contact urticaria has a wheal-and-flare response at the site of exposure.

Causes

Causes of contact dermatitis are classified into 4 groups according to mechanism of response: allergic contact dermatitis, irritant contact dermatitis, photodermatitis, and contact urticaria.

  • Allergic contact dermatitis 
    • A cell-mediated type IV delayed hypersensitivity reaction results from specific antigens penetrating the epidermal skin layer. The antigen combines with a protein mediator and travels to the dermis, where T lymphocytes become sensitized. On the subsequent exposure to the antigen, the allergic reaction takes place.
    • Contributing factors include allergen concentration, duration of exposure, and presence of other skin diseases.
    • The most common agents are plants of the Toxicodendron genus (eg, poison ivy, poison oak, poison sumac).
    • Other substances include nickel sulfate (various metal alloys), sunscreens, potassium dichromate (cements, household cleaners), formaldehyde, ethylenediamine (dyes, medications), mercaptobenzothiazole (rubbers), thiram (fungicides), and paraphenylenediamine (dyes, photographic chemicals).4
    • Repeated exposures to an ACD-inducing allergen tend to cause incrementally more severe reactions.
  • Irritant contact dermatitis
    • An irritant produces direct local cytotoxic effect on the cells of the epidermis, with a subsequent inflammatory response in the dermis.
    • The most common site is the hand.
    • Individuals with atopic dermatitis have an inborn constitutional skin weakness. The risk of developing irritant contact dermatitis is particularly high in individuals with eczema affecting the hands.
    • Although irritant contact dermatitis is caused mostly by chemicals (eg, acids, alkalis, solvents, oxidants, rubber, latex), plants (eg, hot peppers, garlic, tobacco) have also been implicated.5,6
Contact dermatitis from latex gloves in a health ...

Contact dermatitis from latex gloves in a health care worker. Note the sharp demarcations at the perimeter of the area of contact. Latex, in this case, is causing a type IV delayed allergic reaction. Like most types of contact dermatitis, the most important treatment is identification and avoidance of the offending agent.

Contact dermatitis from latex gloves in a health ...

Contact dermatitis from latex gloves in a health care worker. Note the sharp demarcations at the perimeter of the area of contact. Latex, in this case, is causing a type IV delayed allergic reaction. Like most types of contact dermatitis, the most important treatment is identification and avoidance of the offending agent.


    • Severity of the reaction is related to the amount and duration of exposure to the irritant.
    • Most cases of ICD are acute in onset, in which symptoms develop within seconds of exposure.
    • Alternatively, prolonged exposure to a low-level irritant can lead to chronic ICD. Soaps and prolonged exposure to water, often due to occupational soaking of the hands, are typical causes of chronic ICD.2
  • Photodermatitis
    • Irradiation of certain substances by ultraviolet light results in the transformation of the substance into allergens (photoallergic) or irritants (phototoxic).
    • A common example of this is phytophotodermatitis, in which a phototoxic reaction occurs after skin that has been in contact with citrus fruit (or another plant contact) is exposed to sunlight. This exposure to sun chemically alters a previously benign agent in citrus (called furocoumarin or psoralen) into a skin allergen.
    • Many plant families are known to cause a phototoxic response. Besides citrus, these plant families include mulberry (figs) and Umbelliferae (parsnip, celery).
    • Medications (particularly sulfa drugs, thiazides, tetracycline) have also been implicated in photodermatitis.
  • Contact urticaria (immunologic, nonimmunologic)
    • Immunologic reaction is a type I IgE-mediated process caused by the immediate release of inflammatory mediators, resulting in a wheal-and-flare reaction. In rare cases, anaphylactic shock can result. Foodstuffs and latex have been implicated.
    • Nonimmunologic contact urticaria results in local edema and erythema. It is more common than the immunologic mechanism. Substances containing benzoic, sorbic, cinnamic, or nicotinic acids often are the cause.

More on Dermatitis, Contact

Overview: Dermatitis, Contact
Differential Diagnoses & Workup: Dermatitis, Contact
Treatment & Medication: Dermatitis, Contact
Follow-up: Dermatitis, Contact
Multimedia: Dermatitis, Contact
References
Further Reading

References

  1. Wolff K, Johnson RA, Suurmond D. Contact dermatitis. In: Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology. 5th ed. New York: McGraw-Hill; 2005.

  2. Engkilde K, Menne T, Johansen JD. Inverse relationship between allergic contact dermatitis and type 1 diabetes mellitus: a retrospective clinic-based study. Diabetologia. Apr 2006;49(4):644-7. [Medline].

  3. Spoo J, Elsner P. Cement burns: a review 1960-2000. Contact Dermatitis. Aug 2001;45(2):68-71. [Medline].

  4. Agin PP, Ruble K, Hermansky SJ, McCarthy TJ. Rates of allergic sensitization and irritation to oxybenzone-containing sunscreen products: a quantitative meta-analysis of 64 exaggerated use studies. Photodermatol Photoimmunol Photomed. Aug 2008;24(4):211-7. [Medline].

  5. [Guideline] SGNA Practice Committee. Guideline for preventing sensitivity and allergic reactions to natural rubber latex in the workplace. Gastroenterol Nurs. May-Jun 2008;31(3):239-46. [Medline].

  6. Modi GM, Doherty CB, Katta R, Orengo IF. Irritant contact dermatitis from plants. Dermatitis. Mar-Apr 2009;20(2):63-78. [Medline].

  7. Edwards L. Acute allergic contact dermatitis. In: Dermatology in Emergency Care. New York: Churchill Livingstone; 1997:53-55.

  8. [Guideline] American Academy of Allergy, Asthma and Immunology, American College of Allergy, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. Sep 2006;97(3 Suppl 2):S1-38. [Medline][Full Text].

  9. Ong PY, Boguniewicz M. Atopic dermatitis and contact dermatitis. Clin Pediatr Emerg Med. 2007;8(4):81-86.

  10. Arndt KA. Archives of Dermatology. Second century. Arch Dermatol. Jan 1984;120(1):42-3. [Medline].

Further Reading

See Contact Dermatitis for an excellent review of contact dermatitis with a focus on the pediatric population. 9

An illustrated summary of contact dermatitis with special attention to the presentation in the ED can be found in the chapter on this disease in Dermatology in Emergency Care by Libby Edwards. 7

Keywords

allergic contact dermatitis, ACD, cell-mediated type IV delayed hypersensitivity reactioncontact allergen, contact urticaria, ICD, irritant contact dermatitisdiaper dermatitis, photodermatitis, photoallergic reactions, phototoxic reactions, photodermatitis, poison ivypoison oakpoison sumac, rhus dermatitis, Toxicodendron, type I IgE-mediated reaction

Contributor Information and Disclosures

Author

Bradley D Shy, MD, Staff Physician, Department of Emergency Medicine, New York University School of Medicine/Bellevue Hospital Center
Disclosure: Nothing to disclose.

Coauthor(s)

David Todd Schwartz, MD, Associate Professor of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center and New York University Medical Center
David Todd Schwartz, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Mark Louden, MD, FACEP, Assistant Medical Director, Emergency Department, Duke Raleigh Hospital
Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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