Presentation is loading. Please wait.

Presentation is loading. Please wait.

Contact Dermatitis Part One Boris Ioffe, D.O., Pharm.D. 08-14-06.

Similar presentations


Presentation on theme: "Contact Dermatitis Part One Boris Ioffe, D.O., Pharm.D. 08-14-06."— Presentation transcript:

1 Contact Dermatitis Part One Boris Ioffe, D.O., Pharm.D. 08-14-06

2 Irritant contact dermatitis (ICD) Accounts for approximately 80% of all contact dermatitis ICD is the result of a local toxic effect when the skin comes in contact with irritant chemicals such as soaps, solvents, acids, or alkalis  This 37-year-old woman developed a contact irritant dermatitis from obsessive-compulsive hand washing 20-30 times a day. www.drmatlas.org

3 Introduction to Irritant Contact Dermatitis  ICD is a cutaneous inflammation resulting from a direct cytotoxic effect of a chemical or physical agent  Constitutes 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

4 Epidemiology of ICD  The US Bureau of Labor Statistics data show that occupational skin diseases accounted for 10% to 15% of all occupational illnesses  High-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

5 Epidemiology of ICD  Clinical manifestations of ICD are determined by: Properties of the irritating substance Properties of the irritating substance Host factors Host factors Environmental factors including concentration, mechanical pressure, temperature, humidity, pH, and duration of contact Environmental factors including concentration, mechanical pressure, temperature, humidity, pH, and duration of contact Cold alone may also reduce the plasticity of the horny layer, with consequent cracking of the stratum corneum Cold alone may also reduce the plasticity of the horny layer, with consequent cracking of the stratum corneum Occlusion, excessive humidity, and maceration increase percutaneous absorption of water-soluble substances Occlusion, excessive humidity, and maceration increase percutaneous absorption of water-soluble substances

6  Bilateral shoe irritant dermatitis resulting from chronic occlusive footwear

7 Epidemiology of ICD  Important predisposing characteristics of the individual include: Age, race, sex, pre-existing skin disease, anatomic region exposed, and sebaceous activity Age, race, sex, pre-existing skin disease, anatomic region exposed, and sebaceous activity Both infants and elderly are affected more by ICD because of their less robust epidermal layer Both infants and elderly are affected more by ICD because of their less robust epidermal layer Patients with darkly pigmented skin seem to be more resistant to irritant reactions Patients with darkly pigmented skin seem to be more resistant to irritant reactions Other skin disease such as active atopic dermatitis may predispose an individual to develop ICD Other skin disease such as active atopic dermatitis may predispose an individual to develop ICD The 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% The 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%

8 Pathogenesis of ICD  Denaturation of epidermal keratins  Disruption of the permeability barrier  Damage to cell membranes  Direct cytotoxic effects

9

10 Acute Irritant Contact Dermatitis  Commonly seen in occupational accidents  Irritant reaction reaches its peak quickly, within minutes to hours after exposure  Symptoms include stinging, burning, and soreness  Physical signs include erythema, edema, bullae, and possibly necrosis  Lesions restricted to the area where the irritant or toxicant damaged the tissue  Sharply demarcated borders and asymmetry pointing to an exogenous cause  Most frequent irritants are acids and alkaline solutions

11

12 Acute Delayed Irritant Contact Dermatitis  Delayed inflammatory response characteristic of certain irritants such as anthralin, benzalkonium chloride, and ethylene oxide  Visible inflammation is not seen until 8 to 24 hours after exposure  Symptoms are more frequently burning rather than pruritus  Sensitivity to touch and water are elicited  This form of ICD is commonly seen during diagnostic patch testing

13 Irritant Reaction Irritant Contact Dermatitis  Type of subclinical irritant dermatitis in individuals exposed to wet chemical environments such as hairdressers, caters, or metalworkers  Characterized by scaling, redness, vesicles, pustules, and erosions  Often begins under occlusive jewelry and then spreads over the fingers to the hands and forearms  May simulate dyshidrotic dermatitis

14 Cumulative Irritant Contact Dermatitis  Consequence of multiple sub- threshold skin insults, without sufficient time between them for complete barrier function repair  In contrast to acute ICD, the lesions of chronic ICD are less sharply demarcated  Itching and pain due to fissures of hyperkeratotic skin are symptoms of chronic ICD  Skin findings include lichenification, hyperkeratosis, xerosis, erythema, and vesicles

15 Asteatotic Dermatitis  Exsiccation eczematid ICD  Seen mainly during the winter months in elderly individuals who frequently bath without remoisturizing  Skin appears dry with ichthyosiform scale and patches of eczema craquele

16 Traumatic Irritant Contact Dermatitis  May develop after acute skin trauma, such as burns, lacerations, or acute ICD  Patients should be asked if they have cleansed with strong soaps or detergents  Characterized by eczematous lesions most commonly on the hands, that persist  Healing is delayed with redness, infiltration, scale, and fissuring in the affected areas

17 Pustular and Acneform Irritant Contact Dermatitis  Result to certain irritants such as metals, croton oil, mineral oils, tars, greases, cutting and metal working fluids, and naphthalenes  Should be considered in conditions in which folliculitis or acneform lesions develop in setting outside of typical acne  Pustules are sterile and transient  Milia may develop in response to occlusive clothing, adhesive tape, ultraviolet and infrared radiation Chloracne. Note heavy involvement of retroauricular skin with comedones and cysts

18 Subjective or Sensory Irritant Contact Dermatitis  Reports of stinging or burning in the absence of visible cutaneous signs of irritation  Response to irritants such as lactic or sorbic acid

19 Airborne Irritant Contact Dermatitis  Develops on irritant-exposed skin of the face and periorbital regions  Often simulates photoallergic reactions  Involvement of the upper eyelids, philtrum, and submental regions help to differentiate from photoallergic reaction

20 Frictional Irritant Contact Dermatitis  Results from repeated low- grade frictional trauma  Plays adjuvant role in ACD and ICD  Characterized by hyperkeratosis, acanthosis, and lichenification, often progressing to hardening, thickening, and increased toughness 9 year old girl demonstrates a lichenified hyperpigmented round plaque on the top of her thumb produced by chronic thumbsucking. www.dermatlas.org

21 Pathology of ICD  Variable mix of inflammation, necrosis of epidermal keratinocytes, and mild spongiosis  Combination 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 picture  True features of interface dermatitis are absent, and spongiosis should be focal or absent  Over time additional histologic findings include acanthosis with mild hypergranulosis and hyperkeratosis

22 Acids  Inorganic and organic acids can be corrosive to the skin  Cause epidermal damage via protein denaturation and cytotoxicity  Symptoms include erythema, vesication, and necrosis  Hydrofluoric and sulfuric acid can cause the most severe burns  Hydrofluoric acid, used in the semiconductor industry, is able to penetrate intact skin with subsequent dissociation in deeper tissues and resultant liquefactive necrosis

23 Acids  Chromic acid causes ulcerations known as ‘chrome holes’ and often perforates the nasal septum  Chemical burns and irritant dermatitis from nitric acid can cause a distinctive yellow discoloration  In general, organic acids are less irritating than inorganic acids  Formic acid has the greatest corrosive potential of the organic acids Examples of chrome holes www.cdc.gov/niosh/ocderm

24 Alkalis  Strong Alkalis include sodium, ammonium, potassium hydroxide, sodium and potassium carbonate, and calcium oxide  Found in soaps, detergents, bleaches, ammonia preparations, lye, drain pipe cleaner, toilet bowl cleansers, and oven cleaner  Often more painful and damaging than acids  No vesicles, necrotic skin that appears dark brown then black, ultimately becomes hard, dry, and cracked  Alkalis disrupt barrier lips and denature proteins with subsequent fatty acid saponification

25 Alkalis  Cement mixed with water can cause ulcerative damage due to alkalinity  Changes appear 8 to 12 hours after exposure  Chronic irritant cement dermatitis may also develop over months to years  Can accompany allergic contact dermatitis Hand dermatitis due to contact with cement dermnetnz.org/dermatitis/chrome

26 Metal Salts  Include arsenic trioxide, beryllium compounds, calcium oxide, copper salts, inorganic mercury, thimerosal, and selenium  Signs ranging from ulceration to folliculitis

27 Solvents  Act mainly by dissolving the intercellular lipid barrier of the epidermis  Prolonged skin contact can result in severe burns and well as systemic toxicity  Examples include turpentine, benzene, toluene, xylene, carbon tetrachloride, gasoline, and kerosene

28 Professional paint and crayon illustrator with bilateral palmar dermatitis secondary to repeated contact with paint solvents. Extensive patch testing excluded allergic contact dermatitis

29 Detergents and Cleansers  Include any surface active agent (surfactant) that concentrates at the oil-water interfaces and has both emulsifying and cleansing properties  Found in skin cleansers, cosmetics, and household cleaning products  Surfactants cause protein denaturation of the stratum corneum, impairing barrier function  Anionic detergents such as alkyl sulfates and alkyl carboxylate salts are the most irritating

30 Disinfectants  Include, alcohols, aldehydes, phenolic compounds, halogenated compounds, surfactants, dyes, oxidizing agents, and mercury compounds  Weak toxic agents that can cause chronic ICD Practicing 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.

31 Plastics  Three categories: thermoplastics, thermosettings, elastomers  Skin damage is attributed to monomer ingredients, hardeners, and stabilizers  Final hardened plastic product is generally considered inert

32 Food  Agriculture, fishing, catering, and food processing  Often work without gloves, in damp working conditions with frequent hand washing  Mechanical, thermal, and climatic factors  Nearly 100% of exposed persons in food handling and fishing professions may be affected by chronic irritant hand dermatitis

33 Water  Ubiquitous skin irritant  Tropical immersion foot, seen during Vietnam War  Hairdressers, hospital cleaners, cannery workers, bartenders  Irritancy of water is exacerbated by occlusion 9 year old is an habitual hand washer who develops a contact irritant dermatitis every winter. At times she washes over 10 times a day. www.dermatlas.org

34 Fabric/man-made vitreous fibers  Fibers larger than 3.5 um in diameter cause the highly pruritic contact dermatitis caused by fiberglass  Erythematous papules with superimposed excoriations on neck and dorsal hands  Wool and rough clothing cause dermatitis in atopic individuals Fiberglass dermatitis www.cdc.gov/niosh/ocderm

35 Differential Diagnosis  Allergic and ICD, especially in chronic stage appear similar by clinical appearance, histology, and immunohistology  Look identical with erythema, papules, xerosis, scaling, and lichenification with sharp borders  ICD has remained a diagnosis of exclusion when dermatitis is not explained by positive patch test to a known allergen  More frequent complaint of burning and stinging with ICD in contrast to pruritus in ACD

36

37 Treatment  Avoidance of causative irritants at home or in the workplace is the primary TX  Engineering controls to reduce exposure in the workplace  Shielding and personal protection such as gloves and special clothing  Pre-exposure protection by protective creams, removal of irritants by mild cleaning agents, and enhancement of barrier function generation by emollients and moisturizers  Emphasizing personal and occupational hygiene  Establishing educational programs to increase awareness in the workplace

38 TX Chemical Burns  Initial tx irrigation with large volumes of water, if chemical is insoluble in water a soap solution may be used  High pressure water to be avoided to prevent splashing  2.5% 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 burns  Ulcerated areas should be managed with antibacterial creams or ointments to prevent secondary infection  Frequent evaluation is required because ulcers may progress over several days  Excision, debridement and/or grafting may speed healing  Monitoring 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

39 Chronic ICD Treatment  Tx goal is to restore normal epidermal barrier function  Topical corticosteroids frequently used  Systemic corticosteroids although helpful in reducing inflammation, are not useful in treatment of chronic ICD unless offending contactants are avoided  PUVA and Grenz ray considered for chronic dermatitis that does not respond to other tx  Hyperkeratotic palmoplantar dermatitis from frictional or chronic ICD may benefit from the adjunctive use of systemic retinoids such as acitretin

40 Allergic contact dermatitis (ACD) ACD accounts for approximately 20% of all contact dermatitis ACD 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 sensitized Synonyms include contact dermatitis and contact eczema  Allergic contact dermatitis. Linear streaks seen with ACD to poison ivy.

41 ACD  Key Features ACD is a pruritic, eczematous reaction 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 allergen Acute ACD and many cases of chronic ACD are well demarcated and located to the site of contact with the allergen Prototypic reactions are ACD due to poison ivy and nickel Prototypic reactions are ACD due to poison ivy and nickel Patch testing remains the gold standard for accurate and consistent diagnosis Patch testing remains the gold standard for accurate and consistent diagnosis This healthy adolescent developed an intensely pruritic vesiculobullous allergic contact dermatitis from hair dye. Dermatlas.org

42  Classic picture of ACD is a well-demarcated erythematous vesicular and/or scaly patch or plaque with well defined margins corresponding to the area of contact  Chronic 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.

43  Allergic contact dermatitis to leather shoes. Note the correspondence to sites of exposure. Courtesy of Yale Residents Slide Collection.

44  Because 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

45 Epidemiology of ACD  Affects the old and young, individuals of all races, and both sexes  Differences in genders usually based on exposure patterns, such as nickel allergy being seen more frequently in women, presumably due to greater exposure to jewelry  Occupations and avocations play an important role  Allergens differ from region to region, e.g. preservatives used in personal care products can vary based on government legislation

46 Pathogenesis of ACD  ACD is a type IV hypersensitivity response  Requires prior sensitization to the chemical in question  Subsequent 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 eczema  Once sensitized a low concentration of causative chemical elicits a response

47  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.

48  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.

49 Clinical features of ACD  Acute blistering and weeping  Chronic lichenified and scaly plaques  Patchy and diffuse distributions may be seen with body washes and shampoos  Acute bullous allergic contact dermatitis due to poison ivy. This distribution is seen in patients who wear gloves. Courtesy of Yale Residents Slide Collection  Chronic allergic contact dermatitis due to glutaraldehyde. The patient was an optometrist

50 Pathology 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 eosinophils  Moderate to severe reactions show intraepidermal vesiculation  Subacute to chronic stages have epidermal hyperplasia, often psoriasiform

51

52 DDX of ACD  Includes many forms of dermatitis: ICD, atopic dermatitis, stasis dermatitis, and seborrheic dermatitis, as well as the erythematous form of rosacea  Hand and foot ACD need to be distinguished from psoriasis and tinea  Widespread disease needs to be differentiated from other causes of erythoderma, Sezary syndrome

53 Patch Testing  Simple office procedure upon which the diagnosis of ACD often rests  Although the procedure is simple, deciding when and what to test for requires training and experience  Patch testing is underutilized  Only 50% of all residency programs in USA have a patch test center test center  Past surveys show 27% of the responders did no patch testing

54 Patch Testing  TRUE Test  Other panels include North American Contact Dermatitis Group (NACDG) Screening Series, and the European Standard Series  Other panels are unique to specific occupations such as hairdressing tray, dental tray, and florist tray

55 True Test  Preimpregnated test that screens for 23 allergens  Extending testing beyond these 23 allergens has shown to be more beneficial  In three studies, extended testing detected 37-76% more positive reactions, and 47.3% of patients had positive reactions only to non- screening allergens  Additional allergens come in multiuse syringes  Allergens contained within syringes being placed by nurse into Finn chambers Application of TRUE test. www.truetest.com

56 Pre-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 exposures  Effect of vacations and time away form work or home should be ascertained  All personal care products should be inventoried  All hobbies should be explored

57 Patch Testing  Chemicals 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

58 Patch 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 test  Systemic corticosteroids should be avoided for 1 month prior to testing  Patches are applied to back and reinforced with Scanpor tape, patient instructed to keep back dry and patches secured until second visit at 48 hours  Fixing allergens to patient's back using Scanpor® tape.

59 Patch Testing  When the patient returns in 48 hours the patches need to be inspected to ensure that the testing technique is adequate  As patches are removed their sites of application should be marked in order to identify the locations of particular allergens

60 Patch Test Scoring  A positive patch test reaction to nickel. This is an example of a 3+ reaction

61 Patch Testing  Patient again asked to keep back dry until second reading, done from 72 hours to 1 week after the initial application of the patches  This delayed reading is necessary due to patch test responses to some allergens such as gold having a delayed reaction

62 Repeat Open Application Test (ROAT)  Poor man’s patch test  Patient applies the product in question to the same location (where there is not dermatitis), e.g. antecubital fossa, BID for 1-2 weeks  If dermatitis develops, it can be concluded that the patient is reacting to the product  Downside to this approach is that individual problem ingredients are not identified

63 Treatment and Patient Education  Once allergens are positively identified, patient should be given written information on all of these chemicals  Patient should be instructed on how to read labels on old or new products to avoid future exposure

64 Treatment of ACD  Involves identification of causative allergens  Clear the dermatitis with topical, or if necessary systemic corticosteroids  Complete and prolonged clearing can take up to 6 weeks or more, even when allergens are being avoided

65

66 Nickel  Most common allergen tested by the NACDG, with 14% of patients reacting to it  Relevance has been estimated to be 50%  Commonly used in jewelry, buckles, snaps, and other metal-containing objects  High rate of sensitivity attributed to ear piercing  Dimethylglyoxime test to determine if a particular item contains nickel  Individuals with nickel allergy should avoid custom jewelry, and can usually wear stainless steel or gold

67 Nickel Dermatitis  Common 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 snap  Eyelid dermatitis from metal eyelash curlers can be seen  Photos from dermatlas.org

68 Neomycin Sulfate  Most commonly used topical antibiotic  Most common sensitizer among topical antibiotics  Found in many OTC preparations: bacterial ointments, hemorrhoid creams, and otic and opthalmic preparations  Frequently used with other antibacterial agents, such as bacitracin and polymyxin, as well as corticosteroids  Co-reactivity is commonly seen with neomycin and bacitracin 13 year old boy developed an itchy allergic contact dermatitis from a topical antibiotic. www.dermatlas.org

69 Balsam 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 allergy  Capable of identifying 50% of those allergic to fragrance  Seen in those with allergies to spices, in particular cloves, Jamaicin pepper, and cinnamon  Patients with a positive reaction need to avoid fragrances, occasionally spices, and other sources such as colas, tobacco, wines, and vermouth

70 Fragrance Mix  Contains eight different components: cinnamic etoh, cinnamic aldehyde, hydroxycitronellal, isoeugenol, eugenol, oak moss absolute, alpha- amyl cinnamic aldehyde, and geraniol  Detects 70-80% of fragrance allergies  Patients need to read product labels and avoid anything that lists a fragrance, is labeled ‘unscented’, or has an obvious scent  Patients need to look for ‘fragrance- free’ products  ACD to fragrance found in cologne. A Patient with ACD to fragrance found in his cologne. B Patient after avoidance of fragrances and his cologne.

71 Thimerosal  Thimerosal is a combination of thiosalicylic acid and ethylmercuric chloride, and is used as a preservative  Most sensitization may be due to its use as a preservative in vaccines  Other exposures include: contact lens solution, otic and opthalmic solutions, antiseptics, and cosmetics  Positive reactions are common, relevance is low and therefore routine testing to this allergen should be reconsidered

72 Gold  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 group  Most common clinical picture is hand, facial, or eyelid dermatitis  Systemic 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

73 Formaldehyde  Is a ubiquitous, colorless gas found in the workplace, cosmetics, medications, textiles, paints, cigarette smoke, paper, and formaldehyde resins in plastic bottles  Commonly 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)nitromethane  ICD is most common, ACD, contact urticaria, and mucous membrane irritation can occur  Textile dermatitis due to formaldehyde resins in ‘wash-and-wear’ and wrinkle resistant clothes  Another source of formaldehyde is ‘formaldehyde-free’ products that are packaged in containers coated with formaldehyde resins  So widespread that avoidance is difficult and clinical relevance should be determined

74 Quaternium-15  Preservative that is an effective biocide against Pseudomonas, as well as other bacteria and fungi  Most common preservative to cause ACD  Found in shampoos, moisturizers, conditioners, and soaps  80% of those reacting to quarternium-15 are also formaldehyde sensitive Hand dermatititis due to quaternium-15 in a moisturiser dermnetnz.org/dermatitis/quaterni um

75 Cobalt  Metal that is used in association with other metals to add hardness and strength  Frequently combined with nickel, chromium, molybdenum, and tungsten  80% 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

76 Bacitracin  Topical antibiotic with activity against Gram-positive bacteria and spirochetes  Commonly used in combination with other antibiotics such as neomycin and with corticosteroids  In addition to ACD, also rarely causes anaphylaxis and contact urticaria Chronic ulcerations on the lower extremity are particularly likely to develop allergic contact dermatitis. This eruption resulted from sensitization to bacitracin. www.worldallergy.org

77 Corticosteroids  Have 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 testing  Clinical scenarios that should raise suspicion include: chronic dermatitis, failure to clear with corticosteroids, and exacerbations of dermatitis after use of corticosteroids  Tixocortol-21-pivalate and budesonide used for screening, with 91.3% of corticosteroid allergic reactions detected  Complicates patch test interpretation, due to edge effect (first reading may have erythema only at the rim of the Finn chamber)

78

79 Systemic Contact Dermatitis  Systemic exposure to a chemical may result in a diffuse dermatitis  Patient has had a prior contact allergy and then becomes exposed through a systemic route, such as injection, oral, intravenous, or intranasal administration  One of most common examples is patient with ethylenediamine allergy and subsequent reaction to aminophylline

80

81 Airborne Contact Dermatitis  Airborne allergens result in several different reactions including ICD and ACD  PhotoACD, photoICD, photoxicity, and photoallergy to systemic medications clinically resemble airborne contact dermatitis  Ragweed dermatitis is a classic example  Clinically, lichenified and dry skin located in the exposed portions of the skin: face, V of the neck, arms and legs  Most common causative agents are plants, natural resins, woods, plastics, rubbers, glues, metals, pharmaceutical chemicals, insecticides and pesticides

82 55-year-old farm worker developed a chronic allergic contact dermatitis to airborn allergens (compositae).

83 Anacardiacea Dermatitis Poison Ivy vine growing up a tree www.dermatlas.org Poison Ivy vine growing up a tree www.dermatlas.org

84 Anacardiacea ACD  Members of the Anacardiaceae cause more contact dermatitis that all other plant families combined  Most allergenic members belong to the genus Toxicodendron, including poison ivy, poison oak, and poison sumac  Tocicodendron 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 arises  Black dots of urushiol often present on leaves and fruit

85

86 Anacardiacae Allergens  Urushiol derives its name form the Japanese word for the sap (kiurushi) of the Japanese lacquer tree  Urushiol contains a mixture of catechols (1,2- dihydroxybenzenes) and resorcinols (1,3- dihydroxybenzenes)  Urushiol self-melanizes on exposure to oxygen  Avidly binds to skin but is readily degraded by water  Poison Ivy www.dermatlas.org

87 Clinical Features Anacardiacea Dermatitis  Damage is generally required for plants to release urushiol  In late fall plants release urushiol spontaneously  Urushiol may be spread by contaminated clothing, dogs, cats, lacquered furniture, sawdust, and smoke  Allergen-containing smoke can cause severe respiratory tract inflammation, severe dermatitis, and even temporary blindness  www.dermatlas.org

88 Clinical 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 days  Dermatitis may last up to 3 weeks after primary contact or within hours of secondary contact  Streaks of erythema and edematous papules typically precede vesicles and bullae  Although 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

89  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.

90 Clinical Features Anacardiacea Dermatitis  Eruption ‘progresses’ to ‘new areas’ because of variability in antigen concentration and stratum corneum/epidermis thickness, not because of bullae fluid  Over 70% of the US population reacts to poison ivy allergens after patch testing, but only 50% react to plants in the field  Only 15% atopic patients are sensitive to poison ivy  Uncommonly, eruptions resemble erythema multiforme, measles, scarlatina, or urticaria  Prolonged postinflammatory hyperpigmentation may occur in darkly pigmented individuals

91 Treatment  Entire body should be washed with copious amounts of water as soon as possible after exposure  Soap may be used afterwards, but early use of soap may expand the area of resin on the body  As 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 www.dermatlas.org

92 Treatment  Weepy 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 dressing  Topical antihistamines, anesthetics containing benzocaine, and antibiotics should be avoided to prevent sensitization  www.dermatlas.or g

93 Treatment  Most potent topical corticosteroids only help if applied during the earliest stages of the outbreak, when vesicles and blisters are not yet present  Systemic steroids are effective when given at a dose of 1-2 mg/kg/day, slowly tapered over 2-3 weeks  Many patients are referred for a ‘recurrence’ of their poison ivy dermatitis after completing a short, 6 day course of oral corticosteroids  Oral antihistamines may decrease pruritus  www.dermatlas.org


Download ppt "Contact Dermatitis Part One Boris Ioffe, D.O., Pharm.D. 08-14-06."

Similar presentations


Ads by Google