AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.

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 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 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

• ACD is most common during adulthood, but it affects all ages.
• 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. For related CME, see CME - Presentation, Prognosis, Treatment of Most Common Newborn Rashes.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.
  • 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.
  • 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), potassium dichromate (cements, household cleaners), formaldehyde, ethylenediamine (dyes, medications), mercaptobenzothiazole (rubbers), thiram (fungicides), and paraphenylenediamine (dyes, photographic chemicals).
  • 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), plants (eg, hot peppers, garlic, tobacco) have also been implicated.
  • 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.

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.⁴
 
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

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

Lab Studies

• Laboratory examination of ACD centers 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

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.

Consultations

Patients with recurrent episodes of contact dermatitis or rash of unclear etiology may benefit from an outpatient dermatologic consultation.

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.

Drug Category: Wet compresses with an astringent

These compresses are soothing, have a mild antipruritic effect, and keep affected areas clean.

Drug Category: 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.

Drug Name	Hydrocortisone valerate 0.2% (LactiCare HC, DermaGel, Cortaid, Dermacort)
Description	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.
Adult Dose	Apply tid initially; reduce as lesions remit
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity; viral, fungal, and bacterial skin infections
Interactions	None reported
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

Drug Category: 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.

Drug Category: Antihistamines

These agents may be used as adjuncts to relieve pruritus associated with contact dermatitis.

Drug Name	Hydroxyzine HCl (Atarax, Vistaril)
Description	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.
Adult Dose	25-50 mg PO tid/qid prn
Pediatric Dose	<6 years: 30-50 mg/d PO divided tid >6 years: 50-100 mg/d PO divided tid
Contraindications	Documented hypersensitivity
Interactions	CNS depression may increase with alcohol or other CNS depressants
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

Drug Category: Emollients

These agents may be used as adjuncts to moisturize dry skin in subacute and chronic contact dermatitis.

Drug Name	Mineral oil (Fleet, Zymenol)
Description	Promotes removal of excess keratin in conditions of hyperkeratosis.
Adult Dose	Apply to affected area prn
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	None reported
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

Drug Category: Barrier creams

These are the primary agents for diaper dermatitis.

Drug Category: Dry skin agents

Moisturize dry skin in subacute and chronic contact dermatitis.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

In/Out Patient Meds

• 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 ICD and 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.

FURTHER READING

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

See Contact Dermatitis for an excellent review of contact dermatitis with a focus on the pediatric population.⁵

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.⁴

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

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.
	View Full Size Image
Media type:  Photo

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.
	View Full Size Image
Media type:  Photo

Media file 3:  Subacute contact dermatitis, in this case due to bacitracin. Image courtesy of Julie Cantatore.
	View Full Size Image
Media type:  Photo

Media file 4:  Contact dermatitis with bullous formation caused in this case by a new pair of shoes. Image courtesy of Julie Cantatore.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Further Reading
• Acknowledgments
• Multimedia
• References

1. Wolff K, Johnson RA, Suurmond D. Contact dermatitis. In: Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology. 5^th 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. Edwards L. Acute allergic contact dermatitis. In: Dermatology in Emergency Care. New York: Churchill Livingstone; 1997:53-55.
5. Ong PY, Boguniewicz M. Atopic dermatitis and contact dermatitis. Clin Pediatr Emerg Med. 2007;8(4):81-86.
6. Arndt KA. Archives of Dermatology. Second century. Arch Dermatol. Jan 1984;120(1):42-3. [Medline].

Article Last Updated: Feb 28, 2008