1. Contact Dermatitis Part One
Boris Ioffe, D.O., Pharm.D.

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 times a day.

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
Host factors
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
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
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
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%

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

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

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.

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

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.

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

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

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
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
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
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
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
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. Irregular 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.

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
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
Application of TRUE test.
Allergens contained within syringes being placed by nurse into Finn chambers

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

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.

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/quaternium

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.

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)

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

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

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

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

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

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
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

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

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