Background: Contact dermatitis can be subdivided on etiological grounds into the following types: irritant contact dermatitis, allergic contact dermatitis, photo contact dermatitis, contact urticaria, and reactions to pharmacologically active agents.

Once diagnosed, most cases of contact dermatitis are self-limited or are treated easily. However, morbidity from contact dermatitis depends on its cause and the possibility of avoiding repeated or continued exposure. Unless the diagnosis of contact dermatitis is considered and appropriate history obtained, it is rare that a correct diagnosis will be made. As a result, the patient may have chronic or recurrent episodes of dermatitis.

A comprehensive review of the topic of contact dermatitis is beyond the scope of this reference. There are several major textbooks dedicated to this subject. One of the more comprehensive textbooks on this subject is Fisher's Contact Dermatitis. It contains over 1100 pages discussing contact dermatitis associated with numerous products, occupations, hobbies, and other environmental sources. In addition, new contactants are created as part of our industrial society and reported in the literature on a daily basis.

Pathophysiology: Irritant contact dermatitis (ICD) is a condition caused by direct injury of the skin. An irritant is any agent that is capable of producing cell damage in any individual if applied for sufficient time and in sufficient concentration.

Immunological processes are not involved and dermatitis occurs without prior sensitization. Irritants cause damage by breaking or removing the protective layers of the upper epidermis. They denature keratin, remove lipids, and alter the water-holding capacity of the skin. This leads to damage of the underlying living cells of the epidermis. ICD is a spectrum of disease ranging from a mild dryness, redness, or chapping to various types of eczematous dermatitis or an acute caustic burn. The severity of dermatitis produced by an irritant depends upon the type of exposure, vehicle, and individual propensity. Normal, dry, thick skin is more resistant to irritant effects than moist, macerated, or thin skin. Cumulative irritant dermatitis most commonly affects thin, exposed skin, such as the backs of the hands, the webspaces of the fingers, or the face and eyelids.

Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction only affecting previously sensitized individuals. A common example of ACD is rhus dermatitis, the allergic reaction to plants, such as poison ivy, poison oak, and poison sumac. The 2 distinct phases in a type IV hypersensitivity reaction are the induction (ie, sensitization) phase and the elicitation phase.

During the induction phase, an allergen, or hapten, penetrates the epidermis where it is picked up and processed by an antigen-presenting cell. Most allergens in contact dermatitis are of low molecular weight and require minimal processing. However, many have a complicated structure and are altered significantly by the antigen-presenting cell. Antigen-presenting cells include Langerhans cells, dermal dendrocytes, and macrophages. The processed antigen is presented to T-lymphocytes, which undergo blastogenesis in the regional lymph nodes. One subset of these T cells differentiates into memory cells, while others become effector T-lymphocytes that are released into the bloodstream.

The elicitation phase occurs when the sensitized individual again is exposed to the antigen. The antigen penetrates the epidermis and is picked up and processed by an antigen-presenting cell. The processed antigen is presented to the circulating effector T-lymphocytes that in turn produce lymphokines. These lymphokines mediate the inflammatory response that is characteristic of an allergic contact dermatitis. The elicitation phase requires several hours to develop, and, as a result, symptoms of allergic contact dermatitis usually develop hours to days following exposure. Once acquired, contact sensitivity tends to persist. The degree of sensitivity may decline unless boosted by repeated exposure, but with a high initial level of sensitivity it may remain demonstrable throughout life.

With photo contact dermatitis, irradiation of certain substances by light results in the transformation of the substance into allergens (photoallergic) or irritants (phototoxic). This transformation usually is wavelength specific for any individual substance. Dermatitis may develop only following exposure to UV-A, UV-B, or white light.

Contact urticaria may be defined as a wheal and flare reaction occurring after topical exposure to an agent. It may be immunologic, nonimmunologic, or of unknown mechanism. The immunologic type may be severe with associated anaphylaxis. Nonimmunologic contact urticaria is the most common and is caused by agents that directly stimulate the release of vasoactive substances from mast cells. Other forms of urticaria may mimic contact urticaria and include cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, and exercise-induced urticaria.

Contact reactions occur to pharmacologically active agents in some plants, most commonly plants in the family Urticaceae. Stinging nettles are in this family and are densely covered with coarse, stinging hairs. The hairs consist of a tiny capillary tube with a small bladderlike base. Pressure on the bladderlike base injects fluid containing histamine, acetylcholine, and serotonin into the skin. The result is a typical triple response with itching noted in seconds and pruritus that lasts a few hours. Most stings are benign and require little or no therapy.

Frequency:

• In the US: Contact dermatitis is exceedingly common, accounting for 4-7% of all dermatological consultations and consistently is among the top 10 causes for patient visits in primary care clinics. Each year 10-50 million Americans develop an allergic rash after contact with poison ivy, poison sumac, or poison oak. Incidence of contact dermatitis in the pediatric age group is debated, but allergic contact dermatitis affects approximately 20% of all children at some time. Approximately 20-35% of healthy children react to 1 or more allergens on standard patch tests. Among workman's compensation claims for dermatological conditions, 90% are due to contact dermatitis. Children of contact dermatitis sufferers are 60% more likely to have positive patch tests.

• Internationally: The most common environmental allergens appear to be the same in Europe and the United States. Allergens such as benzocaine, neomycin, and lanolin are common in all countries. However, each country has a small number of locally unique topical medications, which are a source of allergens. Rhus dermatitis is extremely common in the United States but virtually nonexistent in Europe. The level of sensitivity to a specific allergen in a population changes over time. Some allergens come and go, and the perceived incidence of sensitivity to an individual substance depends on many variables.

Mortality/Morbidity: Most cases of contact dermatitis are treated easily. However, morbidity from contact dermatitis depends on its cause and the possibility of avoiding repeated or continued exposures. Some ubiquitous allergens, such as rubber or nickel, are impossible to avoid completely. Exposure can be reduced with careful instruction, but occult exposures may produce chronic or recurrent symptoms. In a study of the prevalence of dermatitis of the hands, half the patients had suffered from their dermatitis for more than 5 years. Relapses or chronicity are due not only to reexposure to allergens and irritants, but also to other contributory mechanisms. The barrier function of the skin is impaired for months or even years after significant dermatitis. Recovery may be prevented by exposure to irritants or allergens in concentrations, which are tolerated by normal skin. Overzealous use of cleansers and antiseptics and/or use of various popular or herbal remedies also may prolong the course of dermatitis.

• Latex allergy is common among dentists and surgeons. In rare cases, this may have a significant impact on their medical practice.

• Anaphylaxis and death can occur following epidermal exposure to some antigens. Antigens in products such as latex rarely produce an immunoglobulin E (IgE)-mediated immediate hypersensitivity reaction resulting in anaphylactic shock.

Race: Contact dermatitis is thought to affect whites more frequently than other races. People with fair skin and red hair are the most vulnerable.

Sex: Both allergic and irritant reactions are twice as common in females as in males.

• Nickel is the most frequent contact allergen in females older than 8 years. In one study, reactions to nickel sulfate occurred in 16% of children but occurred 25% of girls aged 14-15 years, and in only 4.5% of boys aged 6-13 years.

• What is the chief complaint? Mild pruritus or a burning sensation is more common than the intense pruritus usually associated with allergic contact dermatitis.

• When did the symptoms start? If a suspected irritant exists, how long prior to the symptoms did the exposure occur? Symptoms may occur within minutes of the exposure. Mild irritants require prolonged or repeated exposure before inflammation is noted, while strong irritants, such as strong acids and alkalis, can produce an immediate reaction similar to a thermal burn.

• Is this the first time this has occurred? When symptoms are episodic, an accurate diary of exposures occurring shortly prior to symptoms may help narrow the list of possible irritants.

• Many substances will produce a nonallergic inflammatory reaction. Examples of irritants include acids, alkalis, metal salts, bromine, chlorine (commonly used in hot tubs and swimming pools), hydrocarbons, and harsh soaps or detergents. Soaps and detergents are the most common causes of an irritant reaction, but may produce an allergic reaction to perfumes, dyes, lanolin, deodorants, or antiperspirants. Some plants may cause an irritant dermatitis. The history must include exposure to these products.

• Allergic contact dermatitis usually is more severe and acute in onset than irritant contact dermatitis. Again, a detailed history may help confirm the dermatitis is being produced by an allergen and help to identify that allergen. The history should cover the following areas:

• What is the chief complaint? ACD frequently is very pruritic. Mild pruritus or a burning sensation is more common in irritant contact dermatitis.

• When did the symptoms start? If a suspected allergen exists, how long prior to the symptoms did the exposure occur? Type IV hypersensitivity reactions usually take 6-24 hours to produce symptoms.

• Has the dermatitis been spreading? Allergic contact dermatitis frequently will appear to spread over time. In fact, this represents delayed reactions to the allergens. Heavily contaminated areas may break out first, followed by areas of less exposure. Thick skin may react much later than thin skin or may not react at all. Different sites may have come in contact with the allergen at different times. Gloves and other clothing contaminated with sap from poison ivy may expose the skin days, weeks, or months later. All these factors may give the false impression the dermatitis is spreading or is contagious.

• Is this the first time the symptoms have occurred? When symptoms are episodic, an accurate diary of exposures occurring shortly prior to symptoms may help narrow the list of possible allergens.

• Many substances can produce an allergic contact dermatitis. The patient's age and the location and appearance of the dermatitis frequently will lead the history in a particular direction. For example, if the dermatitis is perioral, the history might include exposure to pacifiers, bubble gum, musical instruments played with a mouthpiece, toothpaste, mouthwashes, lip licking habits, hobbies with mouthpieces (eg, snorkeling, diving), lipstick, lip balms, products applied to treat the symptoms, sucking limes and lying in the sun, and eating foods such as mangos (specifically exposure to the skin rind of the mango). On occasion, simply asking about some of these possible allergens may stimulate the patient or parent to recall an exposure they had forgotten.

• Photo contact dermatitis usually occurs on sun-exposed areas. At some beaches or in tanning booths that may include most, if not all, of the skin surface. A detailed exposure history, including a detailed history of types and quantity of light exposure, is required. Did the reaction occur following exposure through window glass or on a cloudy day? This would suggest photo dermatitis related to UV-A light. The history also should include the following questions:

• What is the chief complaint? Pruritus is the main complaint in photoallergic reactions. Phototoxic reactions produce a primary complaint of burning. Reactions range from sunburns to bullous eczematous dermatitis and usually occur on sun-exposed areas of the body.

• Many plants can cause a phototoxic response. These include the citrus family (limes), the mulberry family (figs), and the Umbelliferae family (parsnip, celery). Lime juice exposure most commonly occurs when limes are squeezed into beverages. Excess juice dribbles down the arm or neck. Sun exposure of this lime juice on the skin produces linear streaks of dermatitis or hyperpigmentation. Perfumes also are common sources of photo contact dermatitis.

• Contact urticaria usually is very pruritic and rapid in onset. Because symptoms occur so rapidly following exposure, the etiology for contact urticaria usually is obvious. If the etiology is not apparent, an exposure history may include the following items:

• Agents that can produce allergic contact urticaria include silk, wool, rubber, animal hair, dander, saliva, serum, seminal fluid, cockroaches, moths, insect stings, milk, eggs, fish, meat, fruits, potatoes, beer, penicillin, neomycin, nickel, formaldehyde, and rubber. Contact urticaria from rubber occurs almost exclusively from the use of rubber gloves.

• Agents, which produce a nonimmunologic contact urticaria, include jellyfish, Portuguese man-of-war, balsam of Peru, caterpillar hair, moths, insect stings, benzoic acid, and nettles (plants).

• Contact reactions to pharmacologically active agents occur most commonly following exposure to plants in the family Urticaceae (eg, stinging nettles). Itching is noted in seconds and lasts a few hours.

• The exposure history also is important to rule out other forms of urticaria, such as cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, and exercise-induced urticaria.

Physical: Many cases of contact dermatitis have a similar appearance regardless of the mechanism or cause of the inflammation. Other than distribution and severity, most cases of acute irritant contact dermatitis look similar and the clinical appearance does not suggest the etiologic agent. However, some distributions are highly suggestive of the etiologic agent. For example, pruritic dermatitis of the ear lobes or near the umbilicus almost always is the result of nickel allergy. Inflammatory responses can be categorized into acute, subacute, and chronic phases.

• In acute contact dermatitis the skin is bright red and edematous. Clear fluid-filled vesicles or bullae may develop in these areas. As lesions break, they weep clear serum. Yellow crusts form as this serum dries. These may suggest that the area is infected. Although secondary infection can occur, it usually takes several days to develop and usually is more purulent than the yellow crusts. Most healthy patients do not require antibiotic therapy unless significant purulent drainage is noted or the healing of the wound is not progressing as expected.

• Subacute contact dermatitis is less edematous and erythematous. Little or no drainage of serum is present. Superficial papules and excoriations are common.

• Chronic contact dermatitis is characterized by scaling, fissuring, and lichenification with minimal edema. Mild erythema and excoriations are common.

• The clinical appearance of the dermatitis may suggest the type of contact dermatitis. This may help to narrow the list of possible causes.

• Irritant contact dermatitis: (1) Rash often is localized to the site of exposure. (2) Severity is dependent upon the irritant, concentration, dwell time, site, and condition of the skin. (3) Thick, dry skin is the most resistant to the effects of irritants. (4) Maceration makes skin more vulnerable to irritants. (5) Xerosis can predispose to irritant dermatitis. (6) The most common site is the hands.

• Allergic contact dermatitis: (1) Condition may extend beyond the borders of the region exposed to the allergen. (2) Generally much more edematous than irritant contact dermatitis, and vesiculation is more common. Clues by distribution include the following:
  • Scalp and ears - Shampoo, hair spray, hair dyes, earrings, eyeglasses, ear plugs, headphones, telephones, bathing caps, ear drops (Cerumenex)

  • Eyelids - Nail polish (transferred by rubbing), cosmetics, contact lens solution, sport goggles

  • Face - Airborne allergens (poison ivy from burning leaves, ragweed), cosmetics, sunscreens, nose clips, perfumes

  • Lips - Lip balms, lipstick, toothpaste, mouthwash, bubble gum (rosin or cinnamates), nickel in musical instrument mouthpiece, rubber in snorkeling mouthpiece, cane reed in a clarinetist, food (mango)

  • Neck - Necklaces, perfumes, aftershave lotion (men or women from their beau), rubber or leather straps

  • Trunk - Topical medication, sunscreens, poison ivy, clothing, undergarments (eg, spandex bras, elastic waistbands), metal belt buckles, dive suits

  • Axilla - Deodorant (axillary vault), clothing (axillary folds)

  • Hands - Soaps and detergents, foods, poison ivy, solvents and oils, cement, metal topical medications, gloves, athletic tape

  • Wrists - Same as hands; watch, watchband, bracelets

  • Genitals - Poison ivy (transferred by hand), rubber condoms, nickel allergy from a bed-wetting alarm was confused with herpes genitalis and child abuse

  • Anal region - Hemorrhoid preparations (benzocaine, Nupercaine)

  • Lower legs - Typical medication (benzocaine, lanolin, neomycin, paraben), dye in socks

  • Feet - Shoes and sandals (rubber, leather, glues, dyes, nickel snaps), topical medications, swim fins, athletic tape

• Photo contact dermatitis: (1) Phototoxic photo contact dermatitis essentially is a bad sunburn or an allergic reaction to the sun, with primary complaint of burning. (2) In photoallergic photo contact dermatitis, the primary complaint is of pruritus; this occurs on sun-exposed areas of the body with direct exposure of skin to photosensitizing agent, and ranges from sunburns to eczematous dermatitis or hyperpigmentation. On occasion, aerosolized contactants may produce a similar clinical appearance.

• Contact urticaria - Hives or whelps; edematous pale or pink plaques

• Contact reactions to pharmacologically active agent - Typical triple response noted in seconds

Causes: The causes of contact dermatitis are innumerable and increase daily. The items listed below are some of the more common causes and may help expand the list of possible etiologies, which might need to be researched. Items identified in the history can be researched further either in the medical literature or in one of the extensive textbooks on contact dermatitis.

• Irritant contact dermatitis (ICD)
  • ICD is a direct local cytotoxic effect of an irritant on the cells of the epidermis, with a subsequent inflammatory response in the dermis.

  • Examples of irritants include acids, alkalis (sodium, potassium, ammonium, calcium hydroxide compounds, which frequently are associated with hand eczemas following exposure to soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, toilet bowl cleaners, oven cleansers), bromine and chlorine (commonly used in hot tubs and swimming pools), hydrocarbons (eg, crude petroleum, lubricating oils, and cutting oils [chronic exposure may cause pruritus, folliculitis, calcifications, or acneiform eruptions; creosote, asphalt, and other tar products may result in melanoderma; creosote is a contact irritant, sensitizer, and photosensitizer]).

  • Irritant dermatitis from plants usually occurs after exposure to a particular part of the plant and the degree of toxicity may vary with the season, type of exposure, stage of maturity of the plant, and locality.

  • The spurge plant family includes the most plants capable of producing ICD and includes the poinsettia, crown-of-thorns, candelabra cactus, and pencil tree. These plants contain a highly irritating white milky sap that may cause erythema, desquamation, and bulla formation. Calcium oxalate is an irritant found in a number of plants, including Dieffenbachia, daffodils, hyacinths, and pineapples.

• Allergic contact dermatitis
  • This type of dermatitis is an acquired, type IV, hypersensitivity response generated after exposure to an allergen.

  • Causes include plants of the family Anacardiaceae (eg, poison ivy, poison oak, poison sumac, mango), nickel sulfate (eg, earrings, buckles, zippers, buttons, metal clips, various metal alloys), potassium dichromate (eg, cements, household cleansers, leather, some matches, paints, antirust products), formaldehyde (common preservative in creams), ethylenediamine (eg, dyes, medications), mercaptobenzothiazole (rubber), thiram (fungicides) and paraphenylenediamine (eg, hair dyes, photographic chemicals).

  • As mentioned above, harsh soaps most commonly cause an irritant reaction, but allergic reactions to perfumes, dyes, lanolin, deodorants, or antiperspirants can occur.

• Allergic plant dermatitis
  • The family Anacardiaceae, which includes poison ivy, probably accounts for more cases of allergic contact dermatitis than all other plant families combined. The antigen in these plants is in an oleoresin known as urushiol (you-ROO-shee-ol).

  • In poison ivy and poison oak, the antigen in urushiol is pentadecylcatechol. Slight molecular variations in catechols may result in large variations in the degree of antigenicity. Poison ivy and poison oak sap contain a near maximal percentage of the most allergenic catechols.

  • Uninjured plants do not induce a dermatitis. The plant must be injured or bruised before the oleoresin containing the urushiol can contact the skin. Smoke from burning plants may cause a severe dermatitis. All parts of the plant are antigenic, and under controlled conditions, more than 70% of the population in the United States will react to the urushiol in poison ivy and oak.

  • The plant family Anacardiaceae contains other species that also contain urushiol and cross-reacts withpoison ivy. Mango contact dermatitis develops most commonly in the perioral region and on the hands, and it results from exposure to the peel, not the juice. Poison sumac is highly antigenic, resulting in severe contact dermatitis in sensitized patients.

• Photo contact dermatitis
  • Symptoms occur as a result of direct exposure of skin to photosensitizing agent followed by direct sun exposure.

  • Many plants are known to cause a phototoxic response. These include the citrus family (eg, limes), the mulberry family (eg, figs) and the Umbelliferae family (eg, parsnip, celery). Lime juice exposure is most common when limes are squeezed into beverages. Excess juice dribbles down the arm or neck. Sun exposure of this lime juice produces linear streaks of dermatitis or hyperpigmentation. Perfumes also are common sources of photo contact dermatitis.

• Contact urticaria
  • Agents that can produce allergic contact urticaria include silk, wool, rubber, animal hair, dander, saliva, serum, seminal fluid, cockroaches, moths, insect stings, milk, eggs, fish, meat, fruits, potatoes, beer, penicillin, neomycin, nickel, formaldehyde, and rubber.

  • Contact urticaria from rubber occurs almost exclusively from the use of rubber gloves. Nonimmunologic contact urticaria results in local edema and erythema. It is more common than the immunologic mechanism.

  • Agents that produce nonimmunologic contact urticaria include jellyfish, Portuguese man-of-war, balsam of Peru, caterpillar hair, moths, insect stings, benzoic, sorbic, cinnamic or nicotinic acid, and nettles (plants). In one report, 18 out of 20 children aged 1-4 years developed perioral contact urticaria after a rather undisciplined lunch when having fun smearing the food around their mouths. This was traced to sorbic acid and benzoic acid in a salad dressing.

  • Contact urticaria must be distinguished from environmentally associated urticaria including cold urticaria, cholinergic urticaria, dermatographism, pressure urticaria, aquagenic pruritus, aquagenic urticaria, solar urticaria, heat urticaria, papular urticaria, and exercise-induced urticaria.

• Contact reactions to pharmacologically active agents: Most of these reactions are produced by plants in the family Urticaceae (eg, stinging nettles).

Other Tests:

• Patch testing may suggest or confirm the etiologic agent in allergic contact dermatitis. By placing standard concentrations of common allergens or specific ingredients of an implicated product on the skin and leaving them covered for 2 days, one may identify the allergen. If the patient has been previously sensitized to one of the agents under occlusion, this reexposure will produce the elicitation phase of a type IV hypersensitivity reaction resulting in pruritus, erythema, and vesiculation.

• Biopsies are of little diagnostic help in contact dermatitis. Most types of contact dermatitis show very similar pathological changes, and allergic and irritant contact dermatitis may not be distinguished with certainty in all cases. A skin biopsy may serve to eliminate some conditions included in the differential diagnosis.

Histologic Findings: Histologic findings in contact dermatitis usually are not helpful in identifying the specific cause of the contact dermatitis. Findings in acute contact dermatitis include intercellular edema in the epidermis and vesiculation or blister formation. Mast cells may be increased in urticarial reactions. Chronic contact dermatitis will show signs of lichenification and varying degrees of nonspecific inflammation.

Medical Care: Once the correct diagnosis has been established, many patients will improve with adequate hygiene and avoidance of the contactant. Depending upon the degree of involvement, duration, and presence or absence of secondary infection, each of the following therapies may be considered.

• Removal of the contactant: In acute irritant dermatitis the first goal must be to prevent further damage by removal of the irritant. Immediately rinse the site of both acid and alkali burns the site with large quantities of water. Acid burns can be treated with weak alkali solutions, such as sodium bicarbonate or soap solutions. Following irrigation, alkalis, such as soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, and toilet bowl and oven cleansers, may be buffered by rinsing the skin with a weak acid solution, such as vinegar or lemon juice. Alkalis cause tissue destruction by dissolving keratin. Oral and topical steroid therapies are of no benefit in irritant contact dermatitis. Thoroughly wash skin exposed to significant allergens, such as poison ivy, and remove and wash contaminated clothing. Patients may be able to minimize or eliminate allergic contact dermatitis if the skin is adequately washed as soon as possible following exposure.

• Topical nonsteroidal therapy: Many cases of localized mild contact dermatitis will respond well to cool compresses and adequate wound care. Cool wet soaks applied for 5-10 minutes followed by air-drying may reduce serous drainage significantly from the site. Clean water, isotonic saline, and Burow solution all can be used with good success. Application of topical Calamine usually is of minimal benefit. Gently clear the loose crusts from the affected sites and apply a thin coat of Vaseline ointment or antibacterial ointment. Most episodes of contact dermatitis will not require antibiotic therapy if treated promptly and adequate wound care can be provided. Secondary infection usually takes at least 2-3 days to develop. Initial yellow crusts are simply dried serum from ruptured bullous lesions. If a significant degree of purulent material is present, a wound culture may be done and oral antibiotics may be of benefit. Adequate coverage for staphylococci and streptococci usually can be achieved with a 5-10
  day course of erythromycin, dicloxacillin, or a cephalosporin.

• Steroids

• Low strength topical steroids, such as hydrocortisone, may be effective in decreasing inflammation and symptoms associated with very mild contact dermatitis in infants, but are useless as therapy for significant areas of allergic contact dermatitis. Potent topical steroids, such as clobetasol propionate (Temovate) or betamethasone dipropionate (Diprolene) applied twice daily for 1-2 weeks, are effective for treating small areas of moderate allergic contact dermatitis.

• Systemic steroids are the mainstay of therapy in acute episodes of severe, extensive allergic contact dermatitis. Without therapy, an episode of rhus dermatitis may be expected to persist up to 3-4 weeks. Early adequate use of prednisone can shorten this course significantly. The duration of prednisone therapy generally is 7-10 days, but severe episodes of allergic contact dermatitis may recur when therapy is stopped, thus, an additional few days of systemic therapy may be required. In otherwise healthy individuals, a tapering dose of prednisone is not required for short courses of systemic therapy (7-10 d). In adolescents and adults an alternative to oral therapy is a single IM dose of 4 mg (1 cc) of betamethasone sodium phosphate (Celestone) mixed with 40-60 mg of triamcinolone (Kenalog). This provides rapid onset and prolonged action over 2-4 weeks.

• Severe pruritus may respond to antihistamines, such as hydralazine (Atarax) or diphenhydramine (Benadryl).

Consultations: A primary care provider can treat most cases of contact dermatitis on an outpatient basis. Deep chemical burns, extensive bullous reactions, or pulmonary symptoms related to inhaled agents may require admission and consultation as appropriate. Refer the patients who have recurrent episodes of dermatitis with unclear etiology to a dermatologist.

Drug Category: Antihistamines -- May be used as adjunctive therapy to relieve pruritus. Used to treat minor allergic reactions and anaphylaxis. May be used to pretreat patients with prior documentation of minor allergic reactions. May control itching by blocking effects of endogenously release of histamine.

Drug Category: Topical corticosteroids -- Decreases inflammatory reaction associated with allergic contact dermatitis.

Drug Category: Superpotent topical corticosteroids -- Low- or moderate-strength topical corticosteroids are useless as therapy for moderate-to-severe allergic contact dermatitis. Superpotent topical corticosteroids, such as clobetasol propionate (Temovate) or betamethasone dipropionate (Diprolene), applied 2-3 times/d for 1-2 wk may be effective in small areas of acute allergic contact dermatitis or in lichenified areas of chronic contact dermatitis.

Drug Category: Systemic corticosteroids -- Reserved for severe cases of allergic contact dermatitis with >20% total body surface area (TBSA), significant bullae, or significant facial involvement. They have anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids cause profound and varied metabolic effects and modify the body's immune response.

Drug Category: Barrier products -- Barrier creams, such as zinc oxide or Desenex, are common, effective agents to treat or prevent irritant diaper dermatitis. In the past, barrier creams or preexposure treatments offered little hope for protection from poison oak and ivy. However, new over-the-counter products, such as a lotion containing bentoquatam (IvyBlock), may offer some protection. Bentoquatam creates a clay-like barrier on the skin that protects against urushiol, the oily resin in poison ivy, oak, and sumac. Bentoquatam is not a replacement for accepted protective devices, such as gloves, boots, and clothing. When exposure cannot be avoided completely, barrier products may protect areas of exposed skin, such as the neck and face.

Deterrence/Prevention:

• Prevention is better than cure. The most important part of the treatment is to identify and eliminate further exposure to the causative agent.

• Urushiol is the oily resin in poison ivy, poison sumac, and poison oak, which causes an allergic reaction. Keep in mind this resin can remain active for years on virtually any surface. Thoroughly wash everything that might have brushed against the plants, including clothing, shoes, tools, camping equipment, and pets.

• Wearing a long-sleeved shirt, pants, gloves, and boots when in an infested area and bathing as soon as possible after exposure are effective methods to limit rhus dermatitis.

• The only places in the United States where poison ivy is not found are areas above 4000 feet elevation, Alaska, Hawaii, and some desert areas of California and Nevada. Poison ivy usually grows east of the Rocky Mountains and in Canada. Poison oak grows in the western United States, Canada, and Mexico (western poison oak), and in the southeastern states (eastern poison oaks). Poison sumac grows in the eastern states and southern Canada.