Transcript Contact Dermatitis Part 1 - Osteopathic Medical School

Contact Dermatitis Part One
Ben Adams, D.O.
12-6-05
Irritant contact dermatitis (ICD)



This 37-year-old woman developed a contact
irritant dermatitis from obsessive-compulsive hand
washing 20-30 times a day. www.drmatlas.org
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
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
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
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

Bilateral shoe irritant dermatitis resulting from chronic
occlusive footwear
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%
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.
Pathogenesis of ICD

Denaturation of epidermal keratins

Disruption of the permeability barrier

Damage to cell membranes

Direct cytotoxic effects
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
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
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
Cumulative Irritant Contact
Dermatitis




Consequence of multiple subthreshold 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
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
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
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
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
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
Frictional Irritant Contact
Dermatitis



Results from repeated lowgrade 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
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
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
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
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
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
Hand dermatitis due to contact with cement

Can accompany allergic contact
dermatitis
dermnetnz.org/dermatitis/chrome
Metal Salts


Include arsenic trioxide, beryllium compounds, calcium
oxide, copper salts, inorganic mercury, thimerosal, and
selenium
Signs ranging from ulceration to folliculitis
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
Professional
paint and crayon illustrator with bilateral palmar dermatitis
secondary to repeated contact with paint solvents. Extensive patch testing excluded
allergic contact dermatitis
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
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.
Plastics



Three categories: thermoplastics, thermosettings,
elastomers
Skin damage is attributed to monomer ingredients,
hardeners, and stabilizers
Final hardened plastic product is generally considered
inert
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
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
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
Fiberglass dermatitis www.cdc.gov/niosh/ocderm

Wool and rough clothing cause
dermatitis in atopic individuals
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
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
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
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
Allergic contact dermatitis (ACD)



Allergic contact dermatitis. Linear streaks seen with ACD to poison ivy.
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
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

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.

Allergic contact
dermatitis to leather
shoes. Note the
correspondence to sites
of exposure. Courtesy of Yale
Residents Slide Collection.

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
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
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

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.

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.
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
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

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.
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
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
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
True Test



Preimpregnated test that screens
for 23 allergens
Application of TRUE test.
www.truetest.com
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 nonscreening allergens


Additional allergens come in
multiuse syringes
Allergens contained
within syringes being
placed by nurse into
Finn chambers
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
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
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.
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
Patch Test Scoring

A positive patch test reaction to nickel.
This is an example of a 3+ reaction
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
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
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
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
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
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
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
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
Fragrance Mix




Contains eight different components:
cinnamic etoh, cinnamic aldehyde,
hydroxycitronellal, isoeugenol,
eugenol, oak moss absolute, alphaamyl 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 ‘fragrancefree’ 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.
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
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 rosealike reactions and papular eruptions with systemic reactions
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-2nitropropane-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
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
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
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
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)
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
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

Airborne contact dermatitis. Example of the
airborne contact dermatitis pattern seen in a patient
allergic to sesquiterpene lactones. Note involvement
on the anterior neck, which would not be expected if
this were a photodermatitis. Courtesy of Dirk Elston,
M.D.
55-year-old farm worker developed a chronic
allergic contact dermatitis to airborn allergens
(compositae).
Anacardiacea Dermatitis
Poison
Ivy vine growing up a tree
www.dermatlas.org
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
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 (1,3dihydroxybenzenes)

Urushiol self-melanizes on
exposure to oxygen

Avidly binds to skin but is readily
degraded by water

Poison Ivy www.dermatlas.org
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
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

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.
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
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
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.org
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