Pediatric Contact Dermatitis

Contact dermatitis can be subdivided on etiologic grounds into various types, including the following:

• Irritant contact dermatitis

• Allergic contact dermatitis

• Photo contact dermatitis

• Contact urticaria

• Reactions to pharmacologically active agents

Go to Irritant Contact Dermatitis, Allergic Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.

Examples of contact dermatitis are shown in the images below.

Allergic contact dermatitis in childhood was considered rare until recently.[1] However, reports of this condition are increasing, which may reflect an increased incidence, more frequent patch testing of children, or both.[2, 3] Allergen exposure in children has also likely changed over time.

Allergic contact dermatitis may affect as many as 20% of the pediatric population. It occurs less frequently in the first few months of life and increases in prevalence with increasing age.

In the adolescent age group, females have significantly higher rates of allergic contact dermatitis on the face. This is likely explained by increased exposures to nickel in piercings and to preservative and fragrance chemicals in cosmetic products.[2]

Once diagnosed, most cases of contact dermatitis are self-limited or are easily treated. 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 is obtained, a correct diagnosis is rarely 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 article. Several major textbooks are dedicated to this subject. One of the more comprehensive textbooks on this subject is Fisher's Contact Dermatitis.[4] It contains over 1100 pages discussing contact dermatitis associated with numerous products, occupations, hobbies, and other environmental sources. In addition, industry continues to create new contactants on a daily basis.

Irritant contact dermatitis

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

Immunologic 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.

Irritant contact dermatitis consists of a spectrum of disease that ranges 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 on the type of exposure, vehicle, and individual propensity. Normal, dry, or 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.

Irritant contact dermatitis most commonly produces symptoms of pain or burning. With severe irritant contact dermatitis, symptoms may develop within seconds or minutes following exposure. Patients with allergic contact dermatitis usually report itching, and, following exposure to an antigen, symptoms require several hours to develop.

Allergic contact dermatitis

Allergic contact dermatitis is a type IV (ie, delayed) hypersensitivity reaction that affects previously sensitized individuals only. A common example of allergic contact dermatitis 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 significantly altered 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, whereas others become effector T lymphocytes that are released into the blood stream.

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.

Data on the role of atopy in the development of allergic contact dermatitis are mixed but favor a true association in more severe disease. Although some studies suggest an increased incidence of allergic contact dermatitis exists in atopic patients, most recent studies suggest that the incidence of allergic contact dermatitis in atopic patients is similar to that of patients experiencing other conditions, such as seborrheic dermatitis. Patients with severe atopic dermatitis, in fact, may have a diminished capacity for dinitrochlorobenzene (DNCB) sensitization.[5, 6]

Photo contact dermatitis

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

Contact urticaria

Contact urticaria may be defined as a wheal-and-flare reaction that occurs after topical exposure to an agent.[7, 8] 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 (eg, bee venom).

Other forms of urticaria may mimic contact urticaria. These include the following:

• Cold urticaria

• Cholinergic urticaria

• Dermatographism

• Pressure urticaria

• Aquagenic pruritus

• Aquagenic urticaria

• Solar urticaria

• Heat urticaria

• Papular urticaria

• Exercise-induced urticaria

Reactions to pharmacologically active agents

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 (ie, erythema, flare, and wheal formation) with itching noted in seconds and pruritus that lasts a few hours. Most stings are benign and require little or no therapy.

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 further researched either in the medical literature or in one of the extensive textbooks on contact dermatitis.

Irritant contact dermatitis

Irritant contact dermatitis 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 (eg, sodium, potassium, ammonium, calcium hydroxide compounds), which are frequently associated with hand eczemas following exposure to soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, toilet bowl cleaners, or oven cleansers; bromine and chlorine, which are commonly used in hot tubs and swimming pools[9] ; and hydrocarbons such as crude petroleum, lubricating oils, and cutting oils. Long-term 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. 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 irritant contact dermatitis 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. The most common allergens are fragrance, metals, and preservatives.[10]

Causes include the following:

• 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, devices such as tablets)

• Potassium dichromate (eg, cements, household cleansers, leather, some matches, paints, antirust products)

• Formaldehyde (common preservative in creams)

• Methylisothiazolinone/methylchloroisothiazolinone (preservative in wipes, cleansers, and house paints)[11]

• Ethylenediamine (eg, dyes, medications)

• Mercaptobenzothiazole (eg, diaper wipes, rubber)

• Thiuram (eg, fungicides)

• Paraphenylenediamine (PPD; eg, hair dyes, photographic chemicals, "black" henna tattoos)

• Acrylates and methacrylates (manufacturing, nail acrylics, wound dressings)[12, 13, 14]

Henna extract has long been used as a stain or dye that produces a temporary tattoo when applied to the skin. Sensitivity to ordinary henna tattoos that are brown in color is rare. However, PPD may be added to henna extract to darken the tattoo and reduce fixation time. PPD in the black henna tattoo mixture is at a significantly higher concentration than is found in commercial hair dye preparations and can induce severe sensitivity to PPD and severe allergic reactions.

In almost all studies, nickel is the most common allergen and is even more common in females. Depending on the study population, the most common allergens following nickel are as follows:

• Fragrance mix

• Rubber accelerators

• Thimerosal

• PPD

• Cobalt

• Lanolin

• Neomycin

Allergic reaction to topical steroids used to treat eczema is not rare. As with any topical therapy, it may initially be soothing, but if the eczema continues to worsen, the patient may have developed a sensitivity to the active ingredient or a preservative. In patients suspected of having corticosteroid allergy, patch testing is required to confirm the diagnosis.

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

The family Anacardiaceae, which includes poison ivy, probably accounts for more cases of 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 contains a near maximal percentage of the most allergenic catechols.

Uninjured plants do not induce 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 reacts to the urushiol in poison ivy and oak.

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

Atopic dermatitis can be complicated by allergic contact dermatitis to agents such as nickel sulfate, and patch testing should be considered in severe, persistent cases.[15]

Diaper or allergic contact dermatitis in the perineal area can cause or aggravate persistent diaper dermatitis. Culprit allergens in this setting include botanical extracts, including members of the Compositae family, α-tocopherol, fragrances, propylene glycol, parabens, iodopropynyl butylcarbamate, and lanolin.[16]

Methylchloroisothiazolinone and methylchloroisothiazolinone (Kathon CG) has been described as an important allergen in personal care wipes, including makeup removal and those used even by adults in the bathroom setting.[17]

In a 2021 review of allergens identified in the North American Contact Dermatitis Group, 237 children were identified to have hand eczema, 14.5% of the total population of 1634 children.[18] In the hand eczema group, about half were found to have allergic contact dermatitis (49.4%), atopic dermatitis (37.1%), and irritant contact dermatitis (16.9%). The five most relevant allergens in hand eczema were nickel, methylisothiazolinone, propylene glycol, decyl glucoside, and lanolin. Significantly higher odds of relevant allergen reactions were to lanolin, quaternium -15, Compositae mix, thiuram mix, 2-mercaptonezothiazole, and colophony.

Photo contact dermatitis

Symptoms occur as a result of direct exposure of skin to a 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

A wide range of agents can produce allergic contact urticaria. These include the following:

• Silk, wool, animal hair, dander

• Saliva, serum, seminal fluid

• Cockroaches, moths, insect stings

• Milk, eggs, fish, meat, fruits, potatoes, beer

• Penicillin, neomycin

• Nickel

• Formaldehyde

• 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 smearing a salad dressing around their mouths.[19] This was traced to sorbic acid and benzoic acid in the dressing.

Contact urticaria must be distinguished from environmentally associated urticaria. These include the following:

• Cold urticaria

• Cholinergic urticaria

• Dermatographism

• Pressure urticaria

• Aquagenic pruritus

• Aquagenic urticaria

• Solar urticaria

• Heat urticaria

• Papular urticaria

• Exercise-induced urticaria

Contact reactions to pharmacologically active agents primarily involve plants in the family Urticaceae (eg, stinging nettles).

United States statistics

Contact dermatitis is exceedingly common, accounting for 4-7% of all dermatologic consultations, and is consistently among the top 10 causes for patient visits in primary care clinics. Each year, 10-50 million people in the United States develop an allergic rash after contact with poison ivy, poison sumac, or poison oak.

The 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 one or more allergens on standard patch tests.

Among worker's compensation claims for dermatologic conditions, 90% are due to contact dermatitis. Children of parents who experience contact dermatitis are 60% more likely to have positive patch test results.

International statistics

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.

Race-, sex-, and age-related demographics

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

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 in 25% of girls aged 14-15 years and in only 4.5% of boys aged 6-13 years.[20]

Contact dermatitis is most common during adulthood, but it affects people of all ages. The type of contact dermatitis is frequently age related. Infants are most likely to have irritant contact dermatitis in the diaper area. Toddlers and older children become increasingly exposed to poison ivy, poison oak, and poison sumac.

Adolescents are more likely to develop irritant reactions from excessive exposure to soaps and allergic reactions to nickel and to preservatives in creams and lotions. The recent trend of piercing ears in infants and body piercing by adolescents can be expected to lower the average age at which nickel allergy occurs.

The prognosis in patients with contact dermatitis depends on the cause and the possibility of avoiding repeated or continued exposure to the causal allergen or irritant. Most contact dermatitis resolves without intervention in 4-6 weeks if further exposure is prevented. Obviously, long-term success in treatment is poor if the correct diagnosis and offending agent are not identified.

Numerous individual factors are also important in prognosis. Although an alert patient can reduce contact, some ubiquitous allergens, such as rubber or nickel, are impossible to totally avoid. Exposure can be reduced with careful instruction, but occult exposures may produce chronic or recurrent symptoms. Some allergens probably are still unknown, and the significance of others may not be fully realized yet.

New sensitivities to topical medications or other substances may develop during the course of dermatitis. Sensitivity to rubber gloves may complicate dermatitis of the hands. Sensitivity to neomycin may complicate the course when applied to an infected dermatitis. During a long course of relapsing dermatitis, sensitivity to various allergens may accumulate, increasing the risk of recurrence.

Contact dermatitis of the hands is generally of mixed origin, caused by alternating or simultaneous exposure to allergens and irritants. Half of patients with hand dermatitis have had symptoms of dermatitis for more than 5 years.[21] When followed up after 6-22 months, one quarter of the patients heal completely, half of the patients improve, and one quarter of the patients are unchanged or worse. No difference in prognosis between irritant and allergic dermatitis is observed.

Relapses or chronicity is 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 an episode of dermatitis. Recovery can be prevented by exposure to irritants or allergens in concentrations that may be tolerated by normal skin.

Inappropriate treatment with irritants or allergens, such as overzealous use of cleansers and antiseptics, use of various popular or herbal remedies, or both, may prolong the course.

Secondary infection is common in chronic contact dermatitis, preventing normal recovery.

Latex allergy is common among medical professionals, such as 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 such as latex rarely produce an immunoglobulin E (IgE)–mediated immediate hypersensitivity reaction that results in anaphylactic shock.

Extensively counsel patients with documented contact dermatitis on possible sources of future exposure. If possible, provide a written list of potential sources. Although listing every potential source of exposure is impossible, provide the patient with the name of the contactant and related chemical compounds. Failure to do so may result in the patient experiencing unnecessary exposure and dermatitis. In cases of extreme sensitivity, exposure may produce severe or fatal reactions.

Patch testing can be extremely important in diagnosing the cause of allergic contact dermatitis; however, patients forget more than 40% of identified allergens. Provide a printed list of sources of allergic contact to the patient. Discuss sources of allergic contact with the same or cross-reacting allergens.

Discuss prognosis. Acute allergic contact dermatitis may take several weeks to completely resolve. Recurrences are common unless the contactant is identified and avoided.

Provide instructions for reduction of further contact, identification of sources of contactant, barrier protection, good skin care, and hygiene. Advise patients that allergy does not disappear when the dermatitis clears. Risk of relapses usually persists throughout life.

Following significant episodes of dermatitis, the area of involved skin may be especially sensitive to recurrences for several months. Allergic contact dermatitis may be prolonged by subsequent contact with weak irritants. Conversely, patients with irritant dermatitis may develop an undetected secondary allergy to an ingredient of creams or rubber gloves being used to treat the initial dermatitis.

Secondary infection is common in subacute or chronic contact dermatitis. If the contact dermatitis is resistant to appropriate therapy or suddenly worsens for no particular reason, secondary bacterial infection should be considered.

Urushiol, the allergen in poison ivy, can remain active for months. Exposed clothing, shoes, tools, camping equipment, and pets must be washed thoroughly.

If rhus dermatitis is a problem, patients must learn to recognize the plants and have them removed from areas where children are likely to play. The American Academy of Dermatology has handouts with color photographs available for purchase or viewing on their web site.

Wearing a long-sleeved shirt, pants, gloves, and boots when in areas infested with poison ivy and bathing as soon as possible after exposure are effective methods for reducing rhus dermatitis.

Occupational contact dermatitis is a major problem.[22] Patients may need assistance with positively identifying irritants or allergens in the work place. Once identified, the patient's environment must be appropriately adjusted. Patients may need assistance with documentation for worker's compensation claims.

For patient education information, see Skin, Hair, and Nails Center, as well as Contact Dermatitis and Eczema.

When contact dermatitis is suspected, the history must include a detailed list of environmental exposures. Determine whether the patient has had any exposure to materials such as plants, paints, dyes, cleaning solutions, soaps, and protective gear such as eyewear and athletic gloves. Ask whether any new products or plants are present in the home or during recreational activities. Toys are possible sources of allergen exposure, particularly electronic devices, and a careful history of exposures is needed.[23]

Query patients regarding hobbies that might be the source of an irritant or allergen. Determine whether the patient is applying any products or treatments to the involved area. If the lesions or symptoms appear to be primarily in exposed areas, determine how much sun exposure has occurred recently. Ask the patient if symptoms improve over weekends or vacations.

A detailed history may help determine whether the patient has irritant, allergic, or photo contact dermatitis or contact urticaria. The history should include the following questions:

What is the chief symptom? Irritant contact dermatitis, which is the most common form of contact dermatitis, usually causes mild pruritus or a burning sensation. Allergic contact dermatitis and contact urticaria are usually very pruritic. Pruritus is the main symptom in photoallergic reactions, whereas a burning sensation on affected (ie, sun-exposed) areas of the body is the primary symptom of phototoxic reactions.

When did the symptoms start? If a suspected substance is recognized, how long prior to the symptoms did the exposure occur? With irritant contact dermatitis, 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.

Allergic (type IV hypersensitivity) reactions usually take 6-24 hours to produce symptoms. Contact urticaria is usually rapid in onset. Because symptoms occur so rapidly following exposure, the etiology for contact urticaria is usually obvious. If the etiology is not apparent, an exposure history should include items commonly associated with this disorder (see Etiology).

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 or allergens.

Has the dermatitis been spreading? Allergic contact dermatitis frequently appears to spread over time. In fact, this represents delayed reactions to the allergens.

Several factors may produce the false impression that the dermatitis is spreading or is contagious. Heavily contaminated areas may break out first, followed by areas of lesser 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.

The patient's age and the location and appearance of the dermatitis frequently lead the history in a particular direction. For example, if the dermatitis is perioral, the history might include exposure to the following:

• Pacifiers

• Bubble gum

• Musical instruments played with a mouthpiece

• Toothpaste

• Mouthwashes

• Lip-licking habits

• Sports involving mouthpieces (eg, snorkeling, diving)

• Lipstick

• Lip balms

• Products applied to treat the perioral symptoms

• Sucking limes and lying in the sun

• Eating foods such as mangos (specifically, exposure to the skin rind of the mango)

Occasionally, simply asking about some of these possible allergens may stimulate the patient or parent to recall an exposure they had forgotten. It is important to consider allergic contact dermatitis in children with dermatitis that is poorly responsive to therapy or in unusual distributions.[24]

Additionally, certain sites are more likely to be associated with identifiable contact allergen in childhood, including hands, feet, and eyelids.

Photo contact dermatitis usually occurs on sun-exposed areas (at some clothing-optional beaches or in tanning booths, sun-exposed areas 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. Determine whether the reaction occurred following exposure through window glass or on a cloudy day. This would suggest photo dermatitis related to ultraviolet A light.

Although the possible causes of contact dermatitis are virtually endless, identification of the probable type can help direct the search for a provoking agent. For a listing of the more common causes of contact dermatitis, see Etiology.

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 appear 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 develops over several days and is usually 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. Pediatric patients of color may develop lichenified lesions, lichenoid papules, and/or postinflammatory hyperpigmentation more often than their white counterparts.

Patients with severe allergies may experience anaphylaxis. Anaphylaxis occurs most commonly in patients who are extremely sensitive to latex and is less common in patients sensitive to exposure to other antigens. Consequently, equipment and gloves should be latex-free during clinical examinations and surgical procedures of patients with whose history suggests extreme sensitivity to latex.

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

Rash is often localized to the site of exposure. The most common site is the hands.

Severity depends on the irritant, concentration, dwell time, site, and condition of the skin. Thick dry skin is the most resistant to the effects of irritants. Maceration makes skin more vulnerable to irritants. Xerosis can predispose to irritant dermatitis.

Allergic contact dermatitis

In allergic contact dermatitis, skin involvement may extend beyond the borders of the region exposed to the allergen. Edema is generally much more pronounced with allergic contact dermatitis than with irritant contact dermatitis, and vesiculation is more common.

Clues to the allergen suggested by the distribution of the dermatitis 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, fragrances, metals, neomycin, oleamidopropyl dimethylamine, tosylamide formaldehyde resin, benzalkonium chloride, other preservatives

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

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

• Neck - Necklaces, perfumes, aftershave lotion (men or women from contact with someone wearing aftershave), 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, metals, topical medications, gloves, athletic tape, rubber additives, innumerable occupational exposures, “slime” (a novelty toy)

• 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), feminine hygiene products. One study noted that toilet seat dermatitis is more common than previously recognized and should be considered in children who present with dermatitis that involves the buttocks and posterior thighs.[25] Diaper wipes, diapers, and toilet paper may also be sources of buttock allergic contactants.

• Anal region - Hemorrhoid preparations (eg, benzocaine, Nupercaine)

• Lower legs - Topical medication (eg, benzocaine, lanolin, neomycin, paraben), dye in socks, latex/rubber in socks

• Feet - Rubber, leather, glues, dyes, or nickel snaps in shoes and sandals; topical medications; swim fins; athletic tape

Photo contact dermatitis

Phototoxic photo contact dermatitis is essentially a severe sunburn or an allergic reaction to the sun, with a primary symptom of burning. In photoallergic photo contact dermatitis, manifestations on sun-exposed areas of the body range from sunburns to eczematous dermatitis or hyperpigmentation. Occasionally, aerosolized contactants may produce a similar clinical appearance.

Contact urticaria

Contact urticaria appears as hives or wheals or edematous pale or pink plaques. (See the image below.)

Contact reactions to pharmacologically active agent

Typical triple response (ie, erythema, flare, and wheal formation) is noted in seconds. Pruritus may last several hours.

Risks of contact dermatitis are manifold and include the following:

• Pain
• Stigma
• Stress/psychological distress
• Scarring/discoloration
• Superinfection
• Aggravation of underlying dermatitis (eg, atopic dermatitis)

Secondary bacterial infections are uncommon in the acute stages of contact dermatitis. They may occur several days after damage to the skin and should be treated with systemic antibiotics.

Generalized eruptions secondary to autosensitization may occur in association with severe localized allergic contact dermatitis.

Pulmonary symptoms may occur following inhalation of irritants or potent allergens.

Scar formation may result from deep chemical burns or significant secondary infection.

Phytophotodermatitis usually resolves with extensive postinflammatory pigmentary alteration. Pain and superinfection of blistered regions can also be seen.

In contact urticaria, symptoms of anaphylaxis and systemic reactions can occur with increasing exposures, and sometimes without warning. Therefore, children should strictly avoid known contact allergens and carry an epinephrine autoinjector in the event of severe symptoms with accidental exposure. Patch testing is to be avoided in such cases, owing to the risk of systemic symptoms.

Allergic contact dermatitis in children has significant morbidities, including pain, discomfort, truancy/missed school, itch, disfigurement, and sometimes scarring. For these and many other reasons, early identification and elimination of allergen exposures is important.

Irritant contact dermatitis is often triggered by specific irritants under specific settings, such as the interaction of urine and stool to create irritating products. Recurrence of irritation is not uncommon. In addition, irritation from fragrance contributes to the severity of conditions such as atopic dermatitis. Irritant contact dermatitis can be quite uncomfortable and difficult to manage. Superinfection of irritated skin is not uncommon.

Patch testing may suggest or confirm the etiologic agent in allergic contact dermatitis.[26, 27, 28] Laboratory studies are generally of little value in proving a diagnosis of contact dermatitis. However, they may be of value in eliminating some disorders from the differential diagnosis.

Go to Irritant Contact Dermatitis, Allergic Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.

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 produces the elicitation phase of a type IV hypersensitivity reaction resulting in pruritus, erythema, and vesiculation. There are a variety of panels that are used in patch testing, including the True Test and the North American Contact Dermatitis Series; however, because of the small size of a child's back, small or limited panels based on suspected agents are often used. In 2018, a Pediatric Baseline Patch Test series was validated in children.[29]

Anaphylaxis may occur shortly after application of antigens used in patch testing. This finding is particularly true when testing for latex allergy but may occur with exposure to other antigens. 

Monitor patients for anaphylactic reactions to antigens used in patch testing. Appropriate resuscitation must be available should anaphylaxis occur during the early stages of patch testing. Patch testing is contraindicated in the setting of angioedema and/or contact-induced anaphylaxis and should be avoided in patients with contact urticaria.

Atopic patients are more susceptible to irritant patch test reactions, especially when testing with metals. This may lead to false-positive results from routine patch testing. In a study of 101 sets of twins, no correlation was found between positive patch test results and atopy.

Erythema can be more difficult to spot on patch testing in patients who are Black. Tangential lighting, palpation, and comparison to surrounding skin can aid in reading 1+ patch tests in Black children.[30]

For patients with nickel allergy, a simple procedure exists to test jewelry for the presence of nickel. Trace amounts of nickel can be detected using the dimethylgloxime (DMG) spot test.

Two or 3 drops of 1% DMG and 10% hydroxide solution are placed on a white cotton-tipped applicator. The applicator tip is then rubbed against metallic areas of the jewelry. The appearance of a pink color on the applicator tip is a positive result and proof of the presence of nickel. This test is nondestructive. DMG test kits are inexpensive and available from many medical supply stores.

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

Histologic findings in contact dermatitis are not usually 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 shows signs of lichenification and varying degrees of nonspecific inflammation.

Once the correct diagnosis has been established, many patients improve with adequate hygiene and avoidance of the contactant. Further therapy depends on the degree of involvement, duration, and presence or absence of secondary infection.

In acute contact dermatitis, contaminated clothing must be removed and the contactant rinsed from the skin with large quantities of water. Mild-to-moderate acute allergic contact dermatitis responds to topical care with astringents in a wet compress, topical corticosteroids, and systemic antipruritics. Acute severe allergic contact dermatitis with marked edema and bullae should receive the same treatment but may also require the addition of systemic corticosteroids.[31]

Acute irritant contact dermatitis from acids or alkalis should be treated with vigorous irrigation with water to remove the irritant and then should be treated as a thermal burn. Treatment of chronic contact dermatitis requires identification and removal of the contactant.

Chronic allergic contact dermatitis should be treated with midpotency topical corticosteroids and general skin care with emollients. Chronic irritant dermatitis is extremely common. Irritant dermatitis of the hands secondary to soaps or volatile solutions is exceedingly common in adolescents and adults.

Patients should be educated about the cause of the dermatitis and instructed in methods of skin protection and care with emollients.

Investigators have found that most people could be immunized against poison ivy through prescription pills; however, this procedure can take months to achieve a reasonable degree of hyposensitization and must be continued over a long period. Immunization can cause uncomfortable side effects and should only be considered for individuals, such as firefighters, who must live or work in areas where they come into constant contact with poison ivy.

In systemic contact dermatitis, contact urticaria, and any time when systemic symptoms are noted, caution is required. In acute severe cases, emergency care can be required. Comanagement with an allergist when type I allergy is suspected in addition to type IV, as well as in cases that are severe, may benefit the patient.

The American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology have established a practice parameter for the management of contact dermatitis.[32]

Go to Irritant Contact Dermatitis, Allergic Contact Dermatitis, and Protein Contact Dermatitis for complete information on these topics.

The definitive treatment of both irritant contact dermatitis and allergic contact dermatitis is the identification and removal of any potential causal agents. Emergency department treatment may include the following:

• Topical soaks with cool tap water, Burow solution (1:40 dilution), or saline (1 tsp/pint)

• Lukewarm water baths (antipruritic)

• 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.

In acute irritant dermatitis, the first goal must be to prevent further damage by removal of the irritant. Remove clothing and accessories that the contactant touched. Immediately rinse the site of both acid and alkali burns with large quantities of water. Acid burns can be treated with weak alkali solutions, such as sodium bicarbonate or soap solutions. If believed to be a poison, poison control can be consulted in the United States through the website http://poisonhelp.hrsa.gov/what-can-you-do/ or by calling 800-222-1222.

Following irrigation, alkalis (eg, soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaners, 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.

Many cases of localized mild contact dermatitis respond well to cool compresses and adequate wound care. Cool wet soaks applied for 5-10 minutes followed by air-drying may significantly reduce serous drainage from the site. Clean water, isotonic sodium chloride solution, and Burow solution can all be used with good success. Application of topical calamine is usually of minimal benefit.

Gently clear the loose crusts from the affected sites and apply a thin coat of petroleum jelly (Vaseline) or antibacterial ointment. Most episodes of contact dermatitis do not require antibiotic therapy if treated promptly and if 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 performed and oral antibiotics may be of benefit. Adequate coverage for staphylococci and streptococci can usually be achieved with a 5- to 10-day course of erythromycin, dicloxacillin, or a cephalosporin.

In long-lasting contact dermatitis cases, topical tacrolimus can be used long-term to control symptomatology.

Low-strength topical steroids, such as hydrocortisone, may be effective in decreasing inflammation and symptoms associated with very mild contact dermatitis in infants. However, they 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. Usage of a midpotency agent is often more appropriate in children for milder disease. In the setting of proven allergic contact dermatitis due to topical corticosteroids, the choice of product must be modified to avoid the allergen and known cross-reactive agents.

Topical steroid therapy is of no benefit in irritant 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 as long as 3-4 weeks. Early adequate use of prednisone can significantly shorten this course.

The duration of prednisone therapy is generally 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 the setting of proven allergic contact dermatitis due to topical corticosteroids, the choice of product must be modified to avoid the allergen and known cross-reactive agents.

In adolescents and adults, an alternative to oral therapy is a single intramuscular (IM) dose of 4 mg (1 mL) 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. Popular choices include hydroxyzine (Atarax) or diphenhydramine (Benadryl).

Warm weather, hot showers, and activities vigorous enough to cause perspiration increase pruritus. Individuals with severe acute allergic contact dermatitis may be incapacitated temporarily

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 patients who have recurrent episodes of dermatitis with unclear etiology to a dermatologist.

When procedures involving metal rods are needed (eg, the Nuss procedure), prescreening for nickel and other metal allergies is needed to identify children requiring alternative alloys.

Dietary modifications are controversial, particularly in children. However, food preservatives have been identified as a source of allergic contact dermatitis and high-nickel diets can worsen some patients, Therefore, judicious food avoidance based on documented allergens and relevant reduction in symptoms with withdrawal can aid some children. Avoidance diets are known to trigger malnutrition in some children. Comanagement with a nutritionist may benefit children on avoidance diets.

Prevention of contact dermatitis 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 ft 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.

Patients should learn to recognize poison ivy, poison sumac, and poison oak and have them removed from areas where children are likely to play. Several features of poison ivy, oak, and sumac are useful in identification.

Poison ivy and oak may be shrubs or climbing vines. All species of poison ivy and oak have 3 leaflets per leaf, hence the reminder, "Leaves of 3, let them be." The leaf stalk has a groove where it attaches to the branch. Blooms and fruits arise in the angle between the leaf and the branch. Young leaves frequently are reddish in color, and the mature fruit is tan or cream colored.

Poison sumac is a shrub or small tree usually 5-10 feet tall and grows in swampy areas or peat bogs. Poison sumac contains 7-13 paired leaflets in a row. The American Academy of Dermatology has handouts with color photographs available for purchase or viewing on their web site.

Poison ivy, poison sumac, and poison oak are most dangerous in the spring and summer when sap is plentiful. The leaves, branches, and trunk may show black marks where they have been injured, as the sap turns black after exposure to air.

Do not let pets run through wooded areas where poison ivy, poison sumac, and poison oak grow. After contacting these plants, pets may carry urushiol on their fur, causing contact dermatitis in family members who come in contact with the animal. Urushiol can travel in smoke if it burns in a fire; do not burn plants that look like poison ivy, poison sumac, or poison oak.

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 claylike 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.

Allergic contact dermatitis profiles can change with age, and repeat testing every 5 years may benefit children with more severe and recalcitrant dermatitis, or new flares in an unusual distribution.

Guidelines for the identification and management of nickel-allergic contact dermatitis (Ni-ACD) in children have been published in the subsection on dermatology by the American Academy of Pediatrics.[33] These guidelines are quoted below:

"The broad goals of medical therapy in Ni-ACD are as follows:

1. identification and avoidance of nickel;
2. treatment of skin inflammation; and
3. restoration of the skin barrier and skin protection."

"The following are recommended to reduce the US pediatric burden of Ni-ACD:

1. To minimize nickel-induced ACD in children, use of nickel in the manufacture of items that have direct or prolonged contact with the skin (eg, jewelry, electronic devices, toys, etc) should be limited. Regulations similar to the EU Nickel Directive that limit the weekly allowable release of nickel to less than 0.5 µg/cm2/week should be adopted.
2. Additional safety and toxicity studies are needed to better understand the complex relationship between nickel exposure and population health.
3. Companies and industries using metal in products should voluntarily create labeling for low–nickel-release products and Web-based resources to identify those items in the United States that follow EU legislation guidelines, allowing individuals who are nickel allergic to shop more wisely. Ideally, the development of trustable resources for those with Ni-ACD can be met through physician and industry partnership to develop educational resources about nickel allergy that can be easily understood and accessed by children, parents, and teachers.
4. Physicians and other health care providers can support the reduction of Ni-ACD by encouraging parents to request that posts for piercings in their children’s ears be made of surgical-grade steel with low nickel release, per EU standards. It is recommended that all individuals who perform piercing services mention Ni-ACD as a potential complication of piercing.
5. Nickel allergy can be genetic; therefore, physicians and other providers should consider educating at-risk groups to avoid nickel-based body piercings. There is further genetic reason to believe that children from families with a history of Ni-ACD would benefit from reduced exposure in childhood through the universal use of low–nickel-releasing jewelry.
6. It is likely that most children would benefit from lower exposure to such contact, even in the absence of family history of Ni-ACD, because such family history is only present in approximately half of cases of documented disease.
7. If orthodontic metal braces are anticipated, families should consider delaying ear piercing until after dental work is completed."

Therapy depends on the etiology and severity of contact dermatitis. Mild-to-moderate acute allergic contact dermatitis responds to topical care with astringents in a wet compress, topical corticosteroids, and systemic antipruritics. Acute severe allergic contact dermatitis with marked edema and bullae should receive the same treatment but may also require the addition of systemic corticosteroids.

Chronic allergic contact dermatitis should be treated with midpotency topical corticosteroids and general skin care with emollients.

Numerous emollients are available as creams, ointments, or lotions. Use ointments on dry or cracked skin and creams on inflamed or weeping lesions. Most patients prefer creams. These may be helpful in subacute and chronic contact dermatitis because they help add moisture to skin, minimize moisture loss, or both. Brand names include Eucerin, Lubriderm, Moisturel, and Vaseline Intensive Care, among many others.

Class Summary

These agents are used to reduce pain, pruritus, and serous drainage in acute weeping contact dermatitis.

Aluminum acetate solution (Burow solution, Domeboro)

Moist compresses are soothing, have a mild antipruritic effect, reduce serous drainage, and gently débride the wound. They are effective in the early stages of acute contact dermatitis when serous drainage is most severe.

Class Summary

These agents may be used as adjunctive therapy to relieve pruritus. They are used to treat minor allergic reactions and anaphylaxis and may be used to pretreat patients with prior documentation of minor allergic reactions. These agents may control itching by blocking effects of endogenously released histamine.

Hydroxyzine HCl (Vistaril, Atarax)

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in subcortical region of the central nervous system. This agent is available in 10 mg/5 mL syrup and as 10- and 25-mg tablets.

Diphenhydramine (Benadryl, Allerdryl)

Diphenhydramine is used for symptomatic relief of allergic symptoms caused by released histamine.

Class Summary

These agents decrease the inflammatory reaction associated with allergic contact dermatitis.

Triamcinolone topical (Triderm, Kenalog)

Use ointments on dry or cracked skin and creams on inflamed or weeping lesions. Most patients prefer creams. A moderate-potency topical corticosteroid, triamcinolone is available in both ointment (0.1%) and cream (0.1% or 0.5%). This agent decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Hydrocortisone topical (Cortaid, Dermarest, Westcort)

Lower-potency topical steroids such as hydrocortisone are useful on the face and intertriginous areas.

Class Summary

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 daily for 1-2 weeks may be effective in small areas of acute allergic contact dermatitis or in lichenified areas of chronic contact dermatitis.

Clobetasol propionate (Temovate)

Clobetasol decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Betamethasone dipropionate (Diprolene, Celestone, Luxiq)

Betamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Class Summary

These agents are reserved for severe cases of allergic contact dermatitis with involvement of more than 20% of the 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.

Prednisone (Deltasone)

Approximately 7-10 d of therapy is usually adequate and does not require a tapering dosage schedule. Lesions occasionally recur following a course of therapy, and an additional few days of therapy may be required.

Prednisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisolone (Pedia-Pred, Delta-Cortef)

Prednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Betamethasone (Betamethasone IM/PO, Betaject, Celestone)

In adolescents and adults, an alternative to oral therapy is an IM dose of betamethasone sodium phosphate (Celestone) mixed with triamcinolone (Kenalog). This provides rapid onset and prolonged action over 2-4 weeks.

Triamcinolone (Aristospan, Kenalog IV, Trivaris)

In adolescents and adults, an alternative to oral therapy is an IM dose of betamethasone sodium phosphate (Celestone) mixed with triamcinolone (Kenalog). This provides rapid onset and prolonged action over 2-4 weeks.