Presentation on theme: "Contact Dermatitis Part One"— Presentation transcript:
1Contact Dermatitis Part One Boris Ioffe, D.O., Pharm.D.
2Irritant contact dermatitis (ICD) Accounts for approximately 80% of all contact dermatitisICD is the result of a local toxic effect when the skin comes in contact with irritant chemicals such as soaps, solvents, acids, or alkalisThis 37-year-old woman developed a contact irritant dermatitis from obsessive-compulsive hand washing times a day.
3Introduction to Irritant Contact Dermatitis ICD is a cutaneous inflammation resulting from a direct cytotoxic effect of a chemical or physical agentConstitutes nearly 80% of occupational contact dermatitis (OCD)OCD is a matter of public health importance, contributing to combined direct and indirect annual costs (in the USA) of up to $1 billion when accounting for medical costs, workers compensation, and lost time from work
4Epidemiology of ICDThe US Bureau of Labor Statistics data show that occupational skin diseases accounted for 10% to 15% of all occupational illnessesHigh-risk occupations with frequent irritant exposure in caterers, furniture industry workers, hospital workers, hairdressers, chemical industry workers, dry cleaners, metal workers, florists, and warehouse workers
5Epidemiology of ICD Clinical manifestations of ICD are determined by: Properties of the irritating substanceHost factorsEnvironmental factors including concentration, mechanical pressure, temperature, humidity, pH, and duration of contactCold alone may also reduce the plasticity of the horny layer, with consequent cracking of the stratum corneumOcclusion, excessive humidity, and maceration increase percutaneous absorption of water-soluble substances
6Bilateral shoe irritant dermatitis resulting from chronic occlusive footwear
7Epidemiology of ICDImportant predisposing characteristics of the individual include:Age, race, sex, pre-existing skin disease, anatomic region exposed, and sebaceous activityBoth infants and elderly are affected more by ICD because of their less robust epidermal layerPatients with darkly pigmented skin seem to be more resistant to irritant reactionsOther skin disease such as active atopic dermatitis may predispose an individual to develop ICDThe most commonly affected sites are exposed areas such as the hands and the face, with hand involvement in approximately 80% of patients and face involvement in 10%
8Pathogenesis of ICD Denaturation of epidermal keratins Disruption of the permeability barrierDamage to cell membranesDirect cytotoxic effects
10Acute Irritant Contact Dermatitis Commonly seen in occupational accidentsIrritant reaction reaches its peak quickly, within minutes to hours after exposureSymptoms include stinging, burning, and sorenessPhysical signs include erythema, edema, bullae, and possibly necrosisLesions restricted to the area where the irritant or toxicant damaged the tissueSharply demarcated borders and asymmetry pointing to an exogenous causeMost frequent irritants are acids and alkaline solutions
12Acute Delayed Irritant Contact Dermatitis Delayed inflammatory response characteristic of certain irritants such as anthralin, benzalkonium chloride, and ethylene oxideVisible inflammation is not seen until 8 to 24 hours after exposureSymptoms are more frequently burning rather than pruritusSensitivity to touch and water are elicitedThis form of ICD is commonly seen during diagnostic patch testing
13Irritant Reaction Irritant Contact Dermatitis Type of subclinical irritant dermatitis in individuals exposed to wet chemical environments such as hairdressers, caters, or metalworkersCharacterized by scaling, redness, vesicles, pustules, and erosionsOften begins under occlusive jewelry and then spreads over the fingers to the hands and forearmsMay simulate dyshidrotic dermatitis
14Cumulative Irritant Contact Dermatitis Consequence of multiple sub-threshold skin insults, without sufficient time between them for complete barrier function repairIn contrast to acute ICD, the lesions of chronic ICD are less sharply demarcatedItching and pain due to fissures of hyperkeratotic skin are symptoms of chronic ICDSkin findings include lichenification, hyperkeratosis, xerosis, erythema, and vesicles
15Asteatotic Dermatitis Exsiccation eczematid ICDSeen mainly during the winter months in elderly individuals who frequently bath without remoisturizingSkin appears dry with ichthyosiform scale and patches of eczema craquele
16Traumatic Irritant Contact Dermatitis May develop after acute skin trauma, such as burns, lacerations, or acute ICDPatients should be asked if they have cleansed with strong soaps or detergentsCharacterized by eczematous lesions most commonly on the hands, that persistHealing is delayed with redness, infiltration, scale, and fissuring in the affected areas
17Pustular and Acneform Irritant Contact Dermatitis Result to certain irritants such as metals, croton oil, mineral oils, tars, greases, cutting and metal working fluids, and naphthalenesShould be considered in conditions in which folliculitis or acneform lesions develop in setting outside of typical acnePustules are sterile and transientMilia may develop in response to occlusive clothing, adhesive tape, ultraviolet and infrared radiationChloracne. Note heavy involvement of retroauricular skin with comedones and cysts
18Subjective or Sensory Irritant Contact Dermatitis Reports of stinging or burning in the absence of visible cutaneous signs of irritationResponse to irritants such as lactic or sorbic acid
19Airborne Irritant Contact Dermatitis Develops on irritant-exposed skin of the face and periorbital regionsOften simulates photoallergic reactionsInvolvement of the upper eyelids, philtrum, and submental regions help to differentiate from photoallergic reaction
20Frictional Irritant Contact Dermatitis Results from repeated low-grade frictional traumaPlays adjuvant role in ACD and ICDCharacterized by hyperkeratosis, acanthosis, and lichenification, often progressing to hardening, thickening, and increased toughness9 year old girl demonstrates a lichenified hyperpigmented round plaque on the top of her thumb produced by chronic thumbsucking.
21Pathology of ICDVariable mix of inflammation, necrosis of epidermal keratinocytes, and mild spongiosisCombination of an upper dermal perivascular infiltrate of lymphocytes with minimal extension of inflammatory cells into the overlying epidermis, and widely scattered necrotic keratinocytes is most typical pictureTrue features of interface dermatitis are absent, and spongiosis should be focal or absentOver time additional histologic findings include acanthosis with mild hypergranulosis and hyperkeratosis
22Acids Inorganic and organic acids can be corrosive to the skin Cause epidermal damage via protein denaturation and cytotoxicitySymptoms include erythema, vesication, and necrosisHydrofluoric and sulfuric acid can cause the most severe burnsHydrofluoric acid, used in the semiconductor industry, is able to penetrate intact skin with subsequent dissociation in deeper tissues and resultant liquefactive necrosis
23AcidsChromic acid causes ulcerations known as ‘chrome holes’ and often perforates the nasal septumChemical burns and irritant dermatitis from nitric acid can cause a distinctive yellow discolorationIn general, organic acids are less irritating than inorganic acidsFormic acid has the greatest corrosive potential of the organic acidsExamples of chrome holes
24AlkalisStrong Alkalis include sodium, ammonium, potassium hydroxide, sodium and potassium carbonate, and calcium oxideFound in soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaner, toilet bowl cleansers, and oven cleanerOften more painful and damaging than acidsNo vesicles, necrotic skin that appears dark brown then black, ultimately becomes hard, dry, and crackedAlkalis disrupt barrier lips and denature proteins with subsequent fatty acid saponification
25AlkalisCement mixed with water can cause ulcerative damage due to alkalinityChanges appear 8 to 12 hours after exposureChronic irritant cement dermatitis may also develop over months to yearsCan accompany allergic contact dermatitisHand dermatitis due to contact with cement dermnetnz.org/dermatitis/chrome
26Metal SaltsInclude arsenic trioxide, beryllium compounds, calcium oxide, copper salts, inorganic mercury, thimerosal, and seleniumSigns ranging from ulceration to folliculitis
27SolventsAct mainly by dissolving the intercellular lipid barrier of the epidermisProlonged skin contact can result in severe burns and well as systemic toxicityExamples include turpentine, benzene, toluene, xylene, carbon tetrachloride, gasoline, and kerosene
28Professional paint and crayon illustrator with bilateral palmar dermatitis secondary to repeated contact with paint solvents. Extensive patch testing excluded allergic contact dermatitis
29Detergents and Cleansers Include any surface active agent (surfactant) that concentrates at the oil-water interfaces and has both emulsifying and cleansing propertiesFound in skin cleansers, cosmetics, and household cleaning productsSurfactants cause protein denaturation of the stratum corneum, impairing barrier functionAnionic detergents such as alkyl sulfates and alkyl carboxylate salts are the most irritating
30DisinfectantsInclude, alcohols, aldehydes, phenolic compounds, halogenated compounds, surfactants, dyes, oxidizing agents, and mercury compoundsWeak toxic agents that can cause chronic ICDPracticing dentist with moderately severe irritant hand dermatitis from chronic exposure to disinfecting solutions and antiseptics. The results of patch testing, latex challenge testing, and RAST testing were negative.
31Plastics Three categories: thermoplastics, thermosettings, elastomers Skin damage is attributed to monomer ingredients, hardeners, and stabilizersFinal hardened plastic product is generally considered inert
32Food Agriculture, fishing, catering, and food processing Often work without gloves, in damp working conditions with frequent hand washingMechanical, thermal, and climatic factorsNearly 100% of exposed persons in food handling and fishing professions may be affected by chronic irritant hand dermatitis
33Water Ubiquitous skin irritant Tropical immersion foot, seen during Vietnam WarHairdressers, hospital cleaners, cannery workers, bartendersIrritancy of water is exacerbated by occlusion9 year old is an habitual hand washer who develops a contact irritant dermatitis every winter. At times she washes over 10 times a day.
34Fabric/man-made vitreous fibers Fibers larger than 3.5 um in diameter cause the highly pruritic contact dermatitis caused by fiberglassErythematous papules with superimposed excoriations on neck and dorsal handsWool and rough clothing cause dermatitis in atopic individualsFiberglass dermatitis
35Differential Diagnosis Allergic and ICD, especially in chronic stage appear similar by clinical appearance, histology, and immunohistologyLook identical with erythema, papules, xerosis, scaling, and lichenification with sharp bordersICD has remained a diagnosis of exclusion when dermatitis is not explained by positive patch test to a known allergenMore frequent complaint of burning and stinging with ICD in contrast to pruritus in ACD
37TreatmentAvoidance of causative irritants at home or in the workplace is the primary TXEngineering controls to reduce exposure in the workplaceShielding and personal protection such as gloves and special clothingPre-exposure protection by protective creams, removal of irritants by mild cleaning agents, and enhancement of barrier function generation by emollients and moisturizersEmphasizing personal and occupational hygieneEstablishing educational programs to increase awareness in the workplace
38TX Chemical BurnsInitial tx irrigation with large volumes of water, if chemical is insoluble in water a soap solution may be usedHigh pressure water to be avoided to prevent splashing2.5% calcium gluconate gel used to tx hydroflouric acid burns, immediate application of a weak acid such as vinegar, lemon juice, or 0.5% hydrochloric acid will lessen the effect of alkali burnsUlcerated areas should be managed with antibacterial creams or ointments to prevent secondary infectionFrequent evaluation is required because ulcers may progress over several daysExcision, debridement and/or grafting may speed healingMonitoring of blood, liver, and kidney function may be needed when exposed to chemicals with potential for systemic toxicity such as hydrofluoric acid, phenolic compounds, chromic acid, and gasoline
39Chronic ICD TreatmentTx goal is to restore normal epidermal barrier functionTopical corticosteroids frequently usedSystemic corticosteroids although helpful in reducing inflammation, are not useful in treatment of chronic ICD unless offending contactants are avoidedPUVA and Grenz ray considered for chronic dermatitis that does not respond to other txHyperkeratotic palmoplantar dermatitis from frictional or chronic ICD may benefit from the adjunctive use of systemic retinoids such as acitretin
40Allergic contact dermatitis (ACD) ACD accounts for approximately 20% of all contact dermatitisACD is a type IV, delayed or cell-mediated immune reaction that is elicited when the skin comes in contact with a chemical to which an individual has been previously sensitizedSynonyms include contact dermatitis and contact eczemaAllergic contact dermatitis. Linear streaks seen with ACD to poison ivy.
41ACD Key Features ACD is a pruritic, eczematous reaction Acute ACD and many cases of chronic ACD are well demarcated and located to the site of contact with the allergenPrototypic reactions are ACD due to poison ivy and nickelPatch testing remains the gold standard for accurate and consistent diagnosisThis healthy adolescent developed an intensely pruritic vesiculobullous allergic contact dermatitis from hair dye. Dermatlas.org
42Classic picture of ACD is a well-demarcated erythematous vesicular and/or scaly patch or plaque with well defined margins corresponding to the area of contactChronic allergic contact dermatitis leading to hand dermatitis. This golfer wore one leather glove and had positive patch tests to potassium dichromate and a piece of his glove. Courtesy of Kalman Watsky, M.D.
43Allergic contact dermatitis to leather shoes Allergic contact dermatitis to leather shoes. Note the correspondence to sites of exposure. Courtesy of Yale Residents Slide Collection.
44Because ICD and ACD are not always discernable clinically, patch testing is required to help identify an allergen or exclude an allergy to a suspected allergen.Allergic contact dermatitis. Chronic hand dermatitis due to ACD to mercaptobenzothiazole found in rubber gloves
45Epidemiology of ACDAffects the old and young, individuals of all races, and both sexesDifferences in genders usually based on exposure patterns, such as nickel allergy being seen more frequently in women, presumably due to greater exposure to jewelryOccupations and avocations play an important roleAllergens differ from region to region, e.g. preservatives used in personal care products can vary based on government legislation
46Pathogenesis of ACD ACD is a type IV hypersensitivity response Requires prior sensitization to the chemical in questionSubsequent re-exposure of individual leads to allergen being presented to a primed T-cell milieu leading to release of numerous cytokines and chemotactic factors leading to the clinical picture of eczemaOnce sensitized a low concentration of causative chemical elicits a response
47Induction of contact hypersensitivity Induction of contact hypersensitivity. Application of contact allergens (Ag) induces the release of cytokines by keratinocytes, Langerhans cells and other cells within the skin. These cytokines in turn activate Langerhans cells which uptake the antigen and emigrate into the regional lymph nodes. During this process, the Langerhans cells mature into dendritic cells. In addition, the antigen is processed, re-expressed on the surface and finally presented to naïve T cells in the regional lymph node. Upon appropriate antigen presentation, T cells bearing the appropriate T cell receptor clonally expand and become effector T cells. These alter their migratory behavior due to the expression of specific surface molecules like CLA. Effector T cells recirculate into the periphery where they may later meet the antigen again. Ag, antigen; KC, keratinocyte.
48Elicitation of contact hypersensitivity Elicitation of contact hypersensitivity. Application of contact allergens (Ag) into a sensitized individual causes the release of cytokines by keratinocytes and Langerhans cells. These cytokines induce the expression of adhesion molecules and activation of endothelial cells which ultimately attracts leukocytes to the site of antigen application. Among these cells, T effector cells are present which are now activated upon antigen presentation either by resident cells or by infiltrating Langerhans cells. Antigen-specific T cell activation again induces the release of cytokines by T cells. This causes the attraction of other inflammatory cells including granulocytes and macrophages which ultimately cause the clinical manifestation of contact dermatitis. Ag, antigen; DDC, dermal dendritic cell; KC, keratinocyte; CLA, cutaneous lymphocyte antigen.
49Clinical features of ACD Acute blistering and weepingChronic lichenified and scaly plaquesPatchy and diffuse distributions may be seen with body washes and shampoosAcute bullous allergic contact dermatitis due to poison ivy. This distribution is seen in patients who wear gloves. Courtesy of Yale Residents Slide CollectionChronic allergic contact dermatitis due to glutaraldehyde. The patient was an optometrist
50Pathology of ACD ACD is the prototype of spongiotic dermatitis Acute stage: variable degree of spongiosis with mixed dermal inflammatory infiltrate containing lymphocytes, histiocytes, and variable numbers of eosinophilsModerate to severe reactions show intraepidermal vesiculationSubacute to chronic stages have epidermal hyperplasia, often psoriasiform
51Irregular psoriasiform epidermal hyperplasia with slight spongiosis Irregular psoriasiform epidermal hyperplasia with slight spongiosis. A The thick compact orthokeratotic stratum corneum is due to the acral location of the specimen. B Spongiotic, vesicular psoriasiform dermatitis due to contact dermatitis. The intraepidermal vesiculation is a consequence of marked spongiosis. C Spongiotic, psoriasiform dermatitis with areas of spongiotic microvesiculation within the epidermis. D Higher magnification of C showing eosinophils within a spongiotic microvesicle at the tip of a rete ridge. Eosinophils were also present in the dermal infiltrate.
52DDX of ACDIncludes many forms of dermatitis: ICD, atopic dermatitis, stasis dermatitis, and seborrheic dermatitis, as well as the erythematous form of rosaceaHand and foot ACD need to be distinguished from psoriasis and tineaWidespread disease needs to be differentiated from other causes of erythoderma, Sezary syndrome
53Patch TestingSimple office procedure upon which the diagnosis of ACD often restsAlthough the procedure is simple, deciding when and what to test for requires training and experiencePatch testing is underutilizedOnly 50% of all residency programs in USA have a patchtest centerPast surveys show 27% of the responders did no patch testing
54Patch Testing TRUE Test Other panels include North American Contact Dermatitis Group (NACDG) Screening Series, and the European Standard SeriesOther panels are unique to specific occupations such as hairdressing tray, dental tray, and florist tray
55True Test Preimpregnated test that screens for 23 allergens Extending testing beyond these 23 allergens has shown to be more beneficialIn three studies, extended testing detected 37-76% more positive reactions, and 47.3% of patients had positive reactions only to non-screening allergensAdditional allergens come in multiuse syringesApplication of TRUE test.Allergens contained within syringes being placed by nurse into Finn chambers
56Pre-Patch Testing Questions Exposures both at work and home to understand mechanics of the work environment, Materials Safety Data Sheets (MSDS) can be helpful for workplace exposuresEffect of vacations and time away form work or home should be ascertainedAll personal care products should be inventoriedAll hobbies should be explored
57Patch TestingChemicals brought in by patients should not be tested blindly, physician should be aware of the chemical ingredients because severe burns or ulceration may occur‘Leave on’ personal care products such as moisturizers and make-up may be tested ‘as is’‘Rinse off’ products such as soaps or shampoos need to be diluted prior to patch testing
58Patch Testing Most common site is the upper back Patients should not have a sunburn in test area, and should not apply topical corticosteroids to the patch test sites for 7 days prior to testSystemic corticosteroids should be avoided for 1 month prior to testingPatches are applied to back and reinforced with Scanpor tape, patient instructed to keep back dry and patches secured until second visit at 48 hoursFixing allergens to patient's back using Scanpor® tape.
59Patch TestingWhen the patient returns in 48 hours the patches need to be inspected to ensure that the testing technique is adequateAs patches are removed their sites of application should be marked in order to identify the locations of particular allergens
60Patch Test ScoringA positive patch test reaction to nickel. This is an example of a 3+ reaction
61Patch TestingPatient again asked to keep back dry until second reading, done from 72 hours to 1 week after the initial application of the patchesThis delayed reading is necessary due to patch test responses to some allergens such as gold having a delayed reaction
62Repeat Open Application Test (ROAT) Poor man’s patch testPatient applies the product in question to the same location (where there is not dermatitis), e.g. antecubital fossa, BID for 1-2 weeksIf dermatitis develops, it can be concluded that the patient is reacting to the productDownside to this approach is that individual problem ingredients are not identified
63Treatment and Patient Education Once allergens are positively identified, patient should be given written information on all of these chemicalsPatient should be instructed on how to read labels on old or new products to avoid future exposure
64Treatment of ACD Involves identification of causative allergens Clear the dermatitis with topical, or if necessary systemic corticosteroidsComplete and prolonged clearing can take up to 6 weeks or more, even when allergens are being avoided
66NickelMost common allergen tested by the NACDG, with 14% of patients reacting to itRelevance has been estimated to be 50%Commonly used in jewelry, buckles, snaps, and other metal-containing objectsHigh rate of sensitivity attributed to ear piercingDimethylglyoxime test to determine if a particular item contains nickelIndividuals with nickel allergy should avoid custom jewelry, and can usually wear stainless steel or gold
67Nickel DermatitisCommon presentations are dermatitis on the ears, under a necklace or a watch back, or on the mid-abdomen caused by a belt buckle, zipper, or snapEyelid dermatitis from metal eyelash curlers can be seenPhotos from dermatlas.org
68Neomycin Sulfate Most commonly used topical antibiotic Most common sensitizer among topical antibioticsFound in many OTC preparations: bacterial ointments, hemorrhoid creams, and otic and opthalmic preparationsFrequently used with other antibacterial agents, such as bacitracin and polymyxin, as well as corticosteroidsCo-reactivity is commonly seen with neomycin and bacitracin13 year old boy developed an itchy allergic contact dermatitis from a topical antibiotic.
69Balsam of Peru Naturally occurring fragrance material Prior to introduction of fragrance mix in the 1970’s, balsam of Peru was used to screen for fragrance allergyCapable of identifying 50% of those allergic to fragranceSeen in those with allergies to spices, in particular cloves, Jamaicin pepper, and cinnamonPatients with a positive reaction need to avoid fragrances, occasionally spices, and other sources such as colas, tobacco, wines, and vermouth
70Fragrance MixContains eight different components: cinnamic etoh, cinnamic aldehyde, hydroxycitronellal, isoeugenol, eugenol, oak moss absolute, alpha-amyl cinnamic aldehyde, and geraniolDetects 70-80% of fragrance allergiesPatients need to read product labels and avoid anything that lists a fragrance, is labeled ‘unscented’, or has an obvious scentPatients need to look for ‘fragrance-free’ productsACD to fragrance found in cologne. A Patient with ACD to fragrance found in his cologne. B Patient after avoidance of fragrances and his cologne.
71ThimerosalThimerosal is a combination of thiosalicylic acid and ethylmercuric chloride, and is used as a preservativeMost sensitization may be due to its use as a preservative in vaccinesOther exposures include: contact lens solution, otic and opthalmic solutions, antiseptics, and cosmeticsPositive reactions are common, relevance is low and therefore routine testing to this allergen should be reconsidered
72Gold NACDG found a positive rate of 9.5% NACDC found 90% of gold-allergic patients were women, and there was a higher rate of nickel (33.5%) and cobalt allergy (18%) in this groupMost common clinical picture is hand, facial, or eyelid dermatitisSystemic reactions to gold in patients whom it was used to tx RA, SLE, or pemphigus.Cutaneous findings of lichen planus-like reactions to pityriasis rosea-like reactions and papular eruptions with systemic reactions
73FormaldehydeIs a ubiquitous, colorless gas found in the workplace, cosmetics, medications, textiles, paints, cigarette smoke, paper, and formaldehyde resins in plastic bottlesCommonly seen in association with formaldehyde-releasing presevatives, such as quarternuim-15 imidazolidinyl urea, diazolidinyl urea, DMDM hydantoin, 2-bromo-2-nitropropane-1-3,diol, and tris(hydroxymethyl)nitromethaneICD is most common, ACD, contact urticaria, and mucous membrane irritation can occurTextile dermatitis due to formaldehyde resins in ‘wash-and-wear’ and wrinkle resistant clothesAnother source of formaldehyde is ‘formaldehyde-free’ products that are packaged in containers coated with formaldehyde resinsSo widespread that avoidance is difficult and clinical relevance should be determined
74Quaternium-15Preservative that is an effective biocide against Pseudomonas, as well as other bacteria and fungiMost common preservative to cause ACDFound in shampoos, moisturizers, conditioners, and soaps80% of those reacting to quarternium-15 are also formaldehyde sensitiveHand dermatititis due to quaternium-15 in a moisturiser dermnetnz.org/dermatitis/quaternium
75CobaltMetal that is used in association with other metals to add hardness and strengthFrequently combined with nickel, chromium, molybdenum, and tungsten80% of individuals with a cobalt sensitivity have a co-sensitivity to chromate (more common in men) or nickel (more common in women)Exposure through jewelry snaps, buttons, tools, cosmetics, hair dyes, joint replacements, ceramics, enamel, cement, paints , and resins
76BacitracinTopical antibiotic with activity against Gram-positive bacteria and spirochetesCommonly used in combination with other antibiotics such as neomycin and with corticosteroidsIn addition to ACD, also rarely causes anaphylaxis and contact urticariaChronic ulcerations on the lower extremity are particularly likely to develop allergic contact dermatitis. This eruption resulted from sensitization to bacitracin.
77CorticosteroidsHave been shown to cause ACD in anywhere from 0.2% to 5.98%It is suspected that ACD to these agents is underdiagnosed, due to insufficient testingClinical scenarios that should raise suspicion include: chronic dermatitis, failure to clear with corticosteroids, and exacerbations of dermatitis after use of corticosteroidsTixocortol-21-pivalate and budesonide used for screening, with 91.3% of corticosteroid allergic reactions detectedComplicates patch test interpretation, due to edge effect (first reading may have erythema only at the rim of the Finn chamber)
79Systemic Contact Dermatitis Systemic exposure to a chemical may result in a diffuse dermatitisPatient has had a prior contact allergy and then becomes exposed through a systemic route, such as injection, oral, intravenous, or intranasal administrationOne of most common examples is patient with ethylenediamine allergy and subsequent reaction to aminophylline
81Airborne Contact Dermatitis Airborne allergens result in several different reactions including ICD and ACDPhotoACD, photoICD, photoxicity, and photoallergy to systemic medications clinically resemble airborne contact dermatitisRagweed dermatitis is a classic exampleClinically, lichenified and dry skin located in the exposed portions of the skin: face, V of the neck, arms and legsMost common causative agents are plants, natural resins, woods, plastics, rubbers, glues, metals, pharmaceutical chemicals, insecticides and pesticides
8255-year-old farm worker developed a chronic allergic contact dermatitis to airborn allergens (compositae).
83Anacardiacea Dermatitis Poison Ivy vine growing up a tree
84Anacardiacea ACDMembers of the Anacardiaceae cause more contact dermatitis that all other plant families combinedMost allergenic members belong to the genus Toxicodendron, including poison ivy, poison oak, and poison sumacTocicodendron leaves are compound, possessing three or more leaflets. Flowers and fruit arise in an axillary positions in the angle between the leaf and the twig from which it arisesBlack dots of urushiol often present on leaves and fruit
86Anacardiacae Allergens Urushiol derives its name form the Japanese word for the sap (kiurushi) of the Japanese lacquer treeUrushiol contains a mixture of catechols (1,2-dihydroxybenzenes) and resorcinols (1,3-dihydroxybenzenes)Urushiol self-melanizes on exposure to oxygenAvidly binds to skin but is readily degraded by waterPoison Ivy
87Clinical Features Anacardiacea Dermatitis Damage is generally required for plants to release urushiolIn late fall plants release urushiol spontaneouslyUrushiol may be spread by contaminated clothing, dogs, cats, lacquered furniture, sawdust, and smokeAllergen-containing smoke can cause severe respiratory tract inflammation, severe dermatitis, and even temporary blindness
88Clinical Features Anacardiacea Dermatitis After contact with urushiol, a sensitized person typically develops and pruritic , erythematous eruption within 2 days (4-96 hours) that peaks within 1-14 daysDermatitis may last up to 3 weeks after primary contact or within hours of secondary contactStreaks of erythema and edematous papules typically precede vesicles and bullaeAlthough ACD is the most common cause of streaky, vesicular dermatitis, plants may cause this same picture by other means e.g. chemical irritant dermatitis, or the initial phase of phytodermatitis
89Clinical manifestations of Anacardiaceae dermatitis Clinical manifestations of Anacardiaceae dermatitis. A Acute, streak-like edematous and erythematous dermatitis without vesicles after poison ivy brushed across the face. Courtesy of Fitzsimons Army Medical Center Dermatology slide teaching library. B Acute, streak-like vesicular dermatitis after poison ivy (Toxicodendron radicans) contact. Courtesy of Fitzsimons Army Medical Center Dermatology slide teaching library. C Widespread erythema and edema associated with intense pruritus after carrying logs of the poisonwood tree (Metopium toxiferum) of the family Anacardiaceae. D ‘Black-spot’ poison ivy dermatitis: note the black discoloration in the central portion of the edematous plaques due to plant resin.
90Clinical Features Anacardiacea Dermatitis Eruption ‘progresses’ to ‘new areas’ because of variability in antigen concentration and stratum corneum/epidermis thickness, not because of bullae fluidOver 70% of the US population reacts to poison ivy allergens after patch testing, but only 50% react to plants in the fieldOnly 15% atopic patients are sensitive to poison ivyUncommonly, eruptions resemble erythema multiforme, measles, scarlatina, or urticariaProlonged postinflammatory hyperpigmentation may occur in darkly pigmented individuals
91TreatmentEntire body should be washed with copious amounts of water as soon as possible after exposureSoap may be used afterwards, but early use of soap may expand the area of resin on the bodyAs mentioned before, urushiol is water degradable, After 10 minutes only 50% can be removed, after 15 minutes only 25% can be removed, after 30 minutes only 10% can be removed, and after 60 minutes none of it can be removed
92TreatmentWeepy lesions are best treated with tepid baths, wet-to-dry soaks, or bland shake lotions (calamine)Stringent such as Burow’s solution (aluminum subacetate) works to cool and dry lesions when applied as a wet-to-dry dressingTopical antihistamines, anesthetics containing benzocaine, and antibiotics should be avoided to prevent sensitization
93TreatmentMost potent topical corticosteroids only help if applied during the earliest stages of the outbreak, when vesicles and blisters are not yet presentSystemic steroids are effective when given at a dose of 1-2 mg/kg/day, slowly tapered over 2-3 weeksMany patients are referred for a ‘recurrence’ of their poison ivy dermatitis after completing a short, 6 day course of oral corticosteroidsOral antihistamines may decrease pruritus