eMedicine Specialties > Emergency Medicine > Dermatology
Dermatitis, Contact
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 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 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 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 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.
Differential Diagnoses
| Bites, Insects | Herpes Zoster |
| Cellulitis | Herpetic Whitlow |
| Dermatitis, Atopic | Impetigo |
| Dermatitis, Exfoliative | Psoriasis |
| Erysipelas | Scabies |
| Erythema Multiforme | Vulvovaginitis |
| Herpes Simplex |
Other Problems to Be Considered
Properly differentiating between irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) will rarely change initial ED management, but it may aid in the identification of the offending agent and prevent reinjury. ICD can occur secondary to the first lifetime exposure to an agent, whereas ACD requires an initial sensitization to an offending antigen before an inflammatory reaction can occur. ICD is dose-dependent and has a threshold of exposure below which no reaction will occur.1 Following prior sensitization, ACD can occur after any amount of contact with an antigen. Additionally, ICD only occurs in the discreet areas of direct contact with the offending chemical, whereas ACD can involve the surrounding skin and other tissues. Pruritus is more common in ACD, whereas pain and burning are more typical of ICD.7
Before making the diagnosis of contact dermatitis, cellulitis should be excluded. On physical examination, both contact dermatitis and cellulitis can present with poorly marginated areas of erythema and occasionally edema. Cellulitis can be best differentiated by taking a focused patient history. Furthermore, cellulitis can cause pain, in contrast to the pruritic quality of ACD. Finally, cellulitis can be associated with fever, malaise, local lymphadenopathy, and leukocytosis; none of these findings are consistent with contact dermatitis. If skin blistering has occurred, herpes zoster as well as herpes simplex and impetigo should also be considered.
Atopic dermatitis (often referred to as eczema) is a chronic inflammatory skin condition most common in children. It can have a clinical presentation similar to that of ACD and ICD. Atopic dermatitis can be perpetuated by soaps, detergents, and other agents that are also implicated in contact dermatitis. However, atopic dermatitis usually presents with a flexural distribution of the limbs and neck, unlike the local distribution of ACD and ICD. See Dermatitis, Atopic for further discussion.
Nummular eczema
Lichen simplex chronicus
Stasis dermatitis
Xerosis
Workup
Laboratory Studies
- Laboratory examination of allergic contact dermatitis (ACD) focuses on patch testing. In this examination, a dermatologist or an allergist applies multiple potential allergens into the skin of the patient. The presence of erythema, papules, or vesicles can indicate a positive test. Patch testing is most accurate several weeks after the resolution of the dermatitis, and thus has no role in the ED.
Imaging Studies
- No ED imaging studies are of value in diagnosing contact dermatitis.
Other Tests
- Patch testing may be beneficial to identify the contact allergen and is usually performed in an outpatient setting.
Procedures
- Pathologic findings obtained from biopsy specimens include intercellular edema and bullae.
Treatment
Emergency Department Care
- General measures
- The definitive treatment of both irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) is the identification and removal of any potential causal agents.
- Topical soaks with cool tap water, Burow solution (1:40 dilution), saline (1 tsp/pint), or silver nitrate solution (25.5%)
- Lukewarm water baths (antipruritic)
- Aveeno (oatmeal) baths
- Emollients (eg, white petrolatum, Eucerin) may be beneficial chronic cases.
- Large vesicles may benefit from therapeutic drainage (but not removing the vesicle tops).1 These lesions should then be covered with dressing soaked in Burow solution.
Practice guidelines are available from the American Academy of Allergy, Asthma, and Immunology, and the American College of Allergy, Asthma, and Immunology.8
Consultations
Patients with recurrent episodes of contact dermatitis or rash of unclear etiology may benefit from an outpatient dermatologic consultation.
Medication
Treatment of contact dermatitis depends on the type (irritant or allergic), extent, and area of skin lesions on initial presentation. Preventative advice is as important as the prescription of medications. Once an allergen or irritant is identified as the cause of contact dermatitis, eliminate further exposure.
Wet compresses with an astringent
These compresses are soothing, have a mild antipruritic effect, and keep affected areas clean.
Aluminum acetate (Burow solution)
Dissolve aluminum acetate tabs in water for a 1:40 solution.
Dosing
Adult
Apply as compress for 20-30 min 4-6 times/d
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
For external use only
Topical steroids
Topical steroids are the mainstay of treatment of contact dermatitis. Topical agents of medium-to-high strength (class I-IV) should be adequate to treat most cases. In general, ointments are preferred over creams.
Triamcinolone acetate (Aristocort)
Treats inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. A moderate potency is available in both ointment (0.1%) and cream (0.5%).
Dosing
Adult
Apply tid initially; reduce as lesions remit
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; fungal, viral, and bacterial skin infections
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; abrupt discontinuation of glucocorticoids may cause adrenal crisis
Hydrocortisone valerate 0.2% (LactiCare HC, DermaGel, Cortaid, Dermacort)
Lower-potency cream useful on the face. An adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity.
Dosing
Adult
Apply tid initially; reduce as lesions remit
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; viral, fungal, and bacterial skin infections
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Prolonged use, applying over large surface areas, applying potent steroids, and using occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria
Systemic steroids
Use in severe cases that involve more than 10-20% of total body surface area (TBSA) or bullae. Systemic therapy may also be considered when sleep or activities of daily living are impaired.1 They have both anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
Prednisone (Deltasone, Orasone, Sterapred)
Used for treatment of a variety of diseases, including adrenocortical insufficiency. Prednisone is inactive and must be metabolized to the active metabolite prednisolone. Conversion may be impaired in patients with liver disease. Use for 2-3 weeks with taper. Too short a course results in recurrence of lesions.
Dosing
Adult
50 mg PO qd for 1 wk; taper by a 10-mg reduction in dose q3d
Pediatric
1 mg/kg PO for 1 wk; taper by a 20% reduction in dose q3d; available in 5 mg/5 mL elixir (prednisolone sodium phosphate); prolonged use in children can suppress growth
Interactions
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Contraindications
Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Antihistamines
These agents may be used as adjuncts to relieve pruritus associated with contact dermatitis.
Diphenhydramine (Benadryl)
Used for the symptomatic relief of allergic symptoms caused by histamine released in response to allergens.
Dosing
Adult
25-50 mg cap PO q6h prn
Pediatric
5 mg/kg/d (12.5 mg/5 mL elixir) PO divided qid
Interactions
Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patients taking medications that can cause disulfiramlike reactions
Contraindications
Documented hypersensitivity; glaucoma; prostatic hypertrophy
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction
Hydroxyzine HCl (Atarax, Vistaril)
Antagonizes H1 receptors in the periphery and may be used as alternative to diphenhydramine. May also suppress histamine activity in subcortical region of the CNS. Available in 10 mg/5 mL elixir.
Dosing
Adult
25-50 mg PO tid/qid prn
Pediatric
<6 years: 30-50 mg/d PO divided tid
>6 years: 50-100 mg/d PO divided tid
Interactions
CNS depression may increase with alcohol or other CNS depressants
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Associated with clinical exacerbations of porphyria (may not be safe for patients with porphyria); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness
Emollients
These agents may be used as adjuncts to moisturize dry skin in subacute and chronic contact dermatitis.
Urea cream (Ureacin, Ureaphil)
Promotes hydration and removal of excess keratin in conditions of hyperkeratosis.
Dosing
Adult
Apply to affected area prn
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; viral skin disease
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Do not use near eyes; caution if applied to broken or swollen skin
Mineral oil (Fleet, Zymenol)
Promotes removal of excess keratin in conditions of hyperkeratosis.
Dosing
Adult
Apply to affected area prn
Pediatric
Administer as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Observe for hypersensitivity reactions
Barrier creams
These are the primary agents for diaper dermatitis.
Zinc oxide paste (Desitin)
Provides relief of minor skin irritations.
Dosing
Adult
Not established
Pediatric
Apply to affected area after gentle cleansing and drying, between each diaper change
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Observe for hypersensitivity reactions
Dry skin agents
Moisturize dry skin in subacute and chronic contact dermatitis.
Camphor and menthol (0.5% each) in emollient base (Sarna Anti-Itch)
Topical drug combination that consists of mild local anesthetics, counterirritants, and antipruritic formulations. Generally safe and effective for symptomatic relief.
Dosing
Adult
Apply to affected area prn
Pediatric
<12 years: Not established
>12 years: Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
For external use only; do not apply to eyes
Follow-up
Inpatient & Outpatient Medications
- Acute contact dermatitis (mild, moderate)
- Astringents with wet compress
- Topical steroids (ointments are recommended over creams)
- Systemic antipruritics
- Acute allergic contact dermatitis (ACD) with marked edema and bullae (severe) - Above treatment with addition of systemic steroids
- Acute irritant contact dermatitis (ICD) secondary to strong acids and alkalis (severe) - Prolonged irrigation with water; further treatment same as for burns
- Chronic dermatitis - Topical steroids, emollients, and barrier agents
Deterrence/Prevention
- Prevention is better than cure.
- The most important part of treatment is to identify and eliminate further exposure to the causative agent.
- Use appropriate protective clothing. Rubber-based products protect against water-based products but not solvents.
Complications
- Treat secondary bacterial infections with systemic antibiotics.
Prognosis
- Following adequate removal of the offending agent, the prognosis for both irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) tends to be excellent.
- Most contact dermatitis resolves without intervention in 4-6 weeks if further exposure is prevented.
- Long-term success in treatment is poor if the physician does not identify the etiology.
Patient Education
- For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center.
- Also, see eMedicine's patient education article Contact Dermatitis.
Multimedia
Media file 1: 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.
Media file 2: 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.
Media file 3: Subacute contact dermatitis, in this case due to bacitracin. Image courtesy of Julie Cantatore.
Media file 4: Contact dermatitis with bullous formation caused in this case by a new pair of shoes. Image courtesy of Julie Cantatore.
References
Wolff K, Johnson RA, Suurmond D. Contact dermatitis. In: Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology. 5th ed. New York: McGraw-Hill; 2005.
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].
Spoo J, Elsner P. Cement burns: a review 1960-2000. Contact Dermatitis. Aug 2001;45(2):68-71. [Medline].
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].
[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].
Modi GM, Doherty CB, Katta R, Orengo IF. Irritant contact dermatitis from plants. Dermatitis. Mar-Apr 2009;20(2):63-78. [Medline].
Edwards L. Acute allergic contact dermatitis. In: Dermatology in Emergency Care. New York: Churchill Livingstone; 1997:53-55.
[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].
Ong PY, Boguniewicz M. Atopic dermatitis and contact dermatitis. Clin Pediatr Emerg Med. 2007;8(4):81-86.
Arndt KA. Archives of Dermatology. Second century. Arch Dermatol. Jan 1984;120(1):42-3. [Medline].
Keywords
allergic contact dermatitis, ACD, cell-mediated type IV delayed hypersensitivity reaction, contact allergen, contact urticaria, ICD, irritant contact dermatitis, diaper dermatitis, photodermatitis, photoallergic reactions, phototoxic reactions, photodermatitis, poison ivy, poison oak, poison 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.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, John A Michael, MD, to the development and writing of this article.
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
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