Background

Irritant contact dermatitis (ICD) is inflammation of the skin typically manifested by

erythema, mild edema, and scaling. Irritant contact dermatitis is a nonspecific
response of the skin to direct chemical damage that releases mediators of
inflammation predominately from epidermal cells. A corrosive agent causes the
immediate death of epidermal cells, manifested by chemical burns and cutaneous
ulcers. Note the image belo.
Chronic irritant contact dermatitis of the hands in an older orker! the condition resulted in early
retirement.
"he hands are the most important sites of irritant contact dermatitis. Irritant contact
dermatitis from repeated orkplace e#posure of the hands to soaps, cleansers, and
solvents is the source of most occupational skin disorders.
Irritant contact dermatitis remains understudied compared ith allergic contact
dermatitis. $ost articles on contact dermatitis concern allergic contact dermatitis. "his
largely reflects the fact that ith history and patch testing, a specific hypersensitivity
and a probable cause of dermatitis can be identified in most cases of allergic contact
dermatitis.
No diagnostic test e#ists for irritant contact dermatitis. "he diagnosis rests on the
e#clusion of other cutaneous diseases (especially allergic contact dermatitis) and on
the clinical appearance of dermatitis at a site sufficiently e#posed to a knon
cutaneous irritant. %aboratory studies may be of value in eliminating some disorders
from the differential diagnosis. (&ee 'orkup).
"he definitive treatment of irritant contact dermatitis is the identification and removal of
any potential causal agents. Advise individuals to use ceramides creams or bland
emollients after ashing hands ith soap and before sleep. (&ee "reatment.)
Although the term hypoallergenic is used idely in the marketing of consumer
products, no (ood and Drug Administration)approved definition of *hypoallergenic*
e#ists. Individuals ith susceptible skin (eg, atopic dermatitis, facial skin of individuals
ith rosacea) ould benefit greatly from hypoirritating cleansers, cosmetics,
moisturi+ers, and protectants, but there is no standard method for identifying such
products.
,o to Allergic Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact
Dermatitis for complete information on these topics.
Pathophysiology
Irritant contact dermatitis is the clinical result of sufficient inflammation arising from the
release of proinflammatory cytokines from skin cells (principally keratinocytes), usually
in response to chemical stimuli. Different clinical forms may arise. "he . main
pathophysiological changes are skin barrier disruption, epidermal cellular changes,
and cytokine release.
'ith sufficient concentration or duration of e#posures, a ide range of chemicals can
act as cutaneous irritants. Common cutaneous irritants include solvents, microtrauma,
and mechanical irritants.
Cumulative irritant contact dermatitis from repeated mild skin irritation from soap and
ater is common. (or e#ample, hand/ashing fre0uency of more than .1 times per
shift as associated strongly ith occupational hand dermatitis in intensive care unit
orkers (odds ratio 2 3.4.). &imilarly, most cases of *homemaker5s* ec+ema are
irritant contact dermatitis resulting from repeated skin e#posure to lo/grade
cutaneous irritants, particularly soaps, ater, and detergents.
&olvents cause cutaneous irritation because they remove essential fats and oils from
the skin, hich increases transepidermal ater loss and renders the skin susceptible
to the increased direct to#ic effects of other previously ell/tolerated cutaneous
e#posures. "he alcohol propanol is less irritating to the skin than the detergent sodium
lauryl sulfate.
p K
a
, an acid dissociation constant, is a 0uantitative measure of the strength of an acid
in solution. p K
a
has been shon to be highly predictive of acute skin irritation for acids
and bases6 acids ith a p K
a
of less than 3 and bases ith a p K
a
of less than 7 are
highly irritative.849
$icrotrauma may produce skin irritation. A common e#ample is fiberglass, hich may
produce pruritus ith minimal visible inflammation in susceptible individuals. $any
plant leaves and stems bear small spicules and barbs that produce direct skin trauma.
-hysical irritants (eg, friction, abrasive grains, occlusion) and detergents such as
sodium lauryl sulfate produce more irritant contact dermatitis in combination than
singly.8:9 -ropanol and sodium lauryl sulfate are not additive irritants, hoever.
&kin irritation predisposes the skin to develop sensiti+ation to topical agents. &kin
irritation by both nonallergenic and allergenic compounds induces %angerhans cell
migration and maturation.8.9 An e#acerbation of irritant contact dermatitis may reflect
development of allergic contact dermatitis to topical creams, medications, or rubber
gloves.
"he pathogenesis of irritant contact dermatitis involves resident epidermal cells,
dermal fibroblasts, endothelial cells, and various leukocytes interacting ith each other
under the control of a netork of cytokines and lipid mediators. ;eratinocytes play an
important role in the initiation and perpetuation of skin inflammatory reactions through
the release of and responses to cytokines. <esting keratinocytes produce some
cytokines constitutively.
A variety of environmental stimuli (eg, ultraviolet light, chemical agents) can induce
epidermal keratinocytes to release the folloing cytokines6
Inflammatory cytokines (interleukin 4, tumor necrosis factor/alpha)
Chemotactic cytokines (interleukin 7, interleukin 4=)
,roth/promoting cytokines (interleukin >, interleukin ?, interleukin 41, granulocyte/
macrophage colony/stimulating factor, transforming groth factor)alpha)
Cytokines regulating humoral versus cellular immunity (interleukin 4=, interleukin 4:,
interleukin 47)
Intercellular adhesion molecule 4 promotes the infiltration of leukocytes into the
epidermis in cutaneous inflammatory reactions, including irritant contact dermatitis.
&ignificantly increased numbers of dividing keratinocytes are present 37 and @> hours
after e#posure to the anionic emulsifying agent sodium lauryl sulfate (used in
shampoos, skin cleansers, acne treatments, and toothpastes and in laboratories as an
e#perimental irritant). Aoever, Aeinemann et al found that repeated occlusive
application of =.1B sodium lauryl sulfate over . eeks often resulted in adaptation
(the so/called hardening phenomenon), ith an increase in ceramide 4 in the lipid
composition of the stratum corneum.839
All irritants provoke a similar pattern of cellular infiltration in the dermis! the densities of
most of the cell types rise in proportion to the intensity of inflammation. 'ithin the
epidermis, marked differences e#ist in the patterns of cellular infiltration among
different irritants.
Individuals ith a history of atopic dermatitis are prone to develop irritant contact
dermatitis of the hands. -olymorphisms in the filaggrin (FLG) gene, hich result in
loss of filaggrin production, may alter the skin barrier and are a predisposing factor for
atopic dermatitis. FLG null alleles are associated ith increased susceptibility to
chronic irritant contact dermatitis.819
Etiology
Almost any material may be a cutaneous irritant, if the e#posure is sufficiently
prolonged andCor the concentration of the substance sufficiently high. Dnvironmental
factors may enhance the effect of other irritants.
Dry air and temperature variation
Dry air renders the skin more susceptible to cutaneous irritants. &ufficiently dry air
alone may provoke irritant contact dermatitis. $ost cases of inter itch are a result of
dry skin from the drier air found during sustained periods of cold eather.
An increase in temperature (up to 3.EC from :=EC) increases the cutaneous effect of
an irritant.8>9
Water
Continual e#posure to ater may produce maceration or repeated evaporation of
ater from the skin may produce cutaneous irritation by desiccation of the skin. Dven
distilled ater e#perimentally provokes increased CD44c
F
cells and neutrophils in the
epidermis.
Solvents
$any individuals are e#posed to solvents, particularly at ork. &olvents such as
alcohol or #ylene remove lipids from the skin, producing direct irritant contact
dermatitis and rendering the skin more susceptible to other cutaneous irritants, such
as soap and ater.
Irritant contact dermatitis from alcohol most often is cumulative. $anual orkers may
ash their hands inappropriately ith solvents to remove oil, grease, paints, or other
materials! thus, they develop irritant contact dermatitis.
Inappropriate skin cleansing is a primary cause of irritant contact dermatitis in the
orkplace. 'ashing facilities and methods must be inspected hen investigating the
orkplace for 4 or more cases of occupational irritant contact dermatitis. "he irritating
agents include aromatic, aliphatic, and chlorinated solvents, as ell as solvents such
as turpentine, alcohol, esters, and ketones. &ome organic solvents produce an
immediate erythematous reaction on the skin and remove lipids from the stratum
corneum.
Metalworking fluids
Neat oils most commonly produce folliculitis and acne. "hey may cause irritant contact
dermatitis (as ell as allergic dermatitis). 'ater/based metalorking fluids often cause
irritant contact dermatitis in e#posed orkers! surfactants in these fluids are the main
culprit.
Cumulative irritant contact dermatitis
"his is common in many occupations that often are termed *et ork.* Aealthcare
orkers ash their hands :=/3= times a day, producing cumulative irritant contact
dermatitis. &imilar e#posures occur among individuals ho ash hair repeatedly or in
cleaners or kitchen orkers.
$ultiple skin irritants may be additive or synergistic in their effects. Alcohol/based
hand/cleansing gels cause less skin irritation than hand ashing and therefore are
preferred for hand hygiene from the dermatological point of vie. An alcohol/based
hand/cleansing gel may even decrease, rather than increase, skin irritation after a
hand ash, oing to a mechanical partial elimination of the detergent.8?9
Microtrauma
(iberglass produces direct damage to the skin, usually manifested by pruritus that
may result in e#coriation and secondary skin damage. Cutaneous irritation primarily is
caused by fiberglass ith diameters e#ceeding 3.1 Gm.
Controversy surrounds hether individuals ith dermatographism are more
susceptible to fiberglass dermatitis.
$ost orkers ith irritant contact dermatitis resulting from fiberglass develop
hardening, in hich they tolerate further cutaneous e#posure to fiberglass.
$any plant leaves and stems bear small spicules and barbs that produce direct skin
trauma
Mechanical trauma
-ressure produces callus formation. -ounding produces petechia or ecchymosis.
&udden trauma or friction produces blistering in the epidermis. <epeated rubbing or
scratching produces lichenification. &eating and friction appear to be the main cause
of dermatitis that appears under soccer shin guards in children.879
Ruer gloves
&ome rubber gloves may provoke direct cutaneous irritation. $any orkers complain
of irritation from the poder in rubber gloves.
<emember that gloves compromised by a hole may allo an irritant to enter! occlusion
dramatically increases skin damage from the irritant. Hcclusion accentuates the
effects, good or bad, of topical agents. ;erosene may produce skin changes similar to
that of to#ic epidermal necrolysis folloing occluded cutaneous e#posure. D#cessive
amounts of ethylene o#ide in surgical sheets also may produce similar changes.
Sodium lauryl sulfate
"his chemical is found in some topical medications, particularly acne medications, as
ell as a range of soaps and shampoos. It is also a classic e#perimental cutaneous
irritant.
!ydrofluoric acid
A hydrofluoric acid burn is a medical emergency. <emember that onset of clinical
manifestations may be delayed after the acute e#posure (this is crucial to diagnosis).
Infortunately, hydrofluoric acid burns are most fre0uent on the digits, here the pain
is most severe and management is most difficult (see Aydrofluoric Acid Jurns).
"lkalies
&kin surfaces normally have an acidic pA, and alkalies (eg, many soaps) produce
more irritation than many acids. "he *acid mantle* of the stratum corneum seems to be
important for both permeability barrier formation and cutaneous antimicrobial defense.
Ise of skin cleansing agents, especially synthetic detergents ith a pA of
appro#imately 1.1 rather than alkaline pA, may help prevent skin disease.8@9
Epidemiology
#nited States statistics
Irritant contact dermatitis is common in occupations that involve repeated hand
ashing or repeated e#posure of the skin to ater, food materials, and other irritants.
Aigh/risk occupations include cleaning, hospital care, food preparation, and
hairdressing.
"he prevalence of occupational hand dermatitis as found to be 11.>B in : intensive
care units and as >@.?B in the most highly e#posed orkers. Aand/ashing
fre0uency of more than .1 times per shift as associated strongly ith occupational
hand dermatitis.84=9
$nternational statistics
In Denmark, cleaners comprise the greatest number of affected orkers, but culinary
orkers have the highest incidence. A higher proportion of prolonged sick leave is
seen among those in food/related occupations compared ith those in et
occupations.8449
"he incidence rates of contact dermatitis in ,ermany ere 3.1 per 4=,=== orkers for
irritant contact dermatitis, compared ith 3.4 per 4=,=== orkers for allergic contact
dermatitis. "he highest irritant contact dermatitis annual incidence rates ere found in
hairdressers (3>.@ cases per 4=,=== orkers per year), bakers (:..1 cases per 4=,===
orkers per year), and pastry cooks (4>.@ cases per 4=,=== orkers per year.84:9
Se%ual differences in incidence
Irritant contact dermatitis is significantly more common in omen than in men. "he
high fre0uency of hand ec+ema in omen in comparison ith men is caused by
environmental factors, not genetic factors.
Hccupational irritant contact dermatitis affects omen almost tice as often as men, in
contrast to other occupational diseases that predominantly affect men. 'omen are
e#posed more highly to cutaneous irritants from their disproportionately greater role in
housecleaning and the care of small children at home. In addition, omen
predominantly perform many occupations at high risk for irritant contact dermatitis (eg,
hairdressing, nursing).
"ge&related differences in incidence
Irritant contact dermatitis may occur at any age. $any cases of diaper dermatitis are
irritant contact dermatitis resulting from direct skin irritants present in urine and,
especially, feces. Hlder persons have drier and thinner skin that does not tolerate
soaps and solvents as ell as younger individuals. Hccupational hand ec+ema often is
associated ith persistent dermatitis and prolonged sick leave, ith substantially
greater severity among those ith occupational irritant contact dermatitis and atopic
dermatitis and age older than 1= years.
Prognosis
-rognosis is good for nonatopic individuals in hom irritant contact dermatitis is
diagnosed and managed promptly. Individuals ith atopic dermatitis remain highly
susceptible to irritant contact dermatitis and may find that the tasks of many common
occupations (eg, nursing, hairdressing) produce too much direct skin inflammation to
continue ith these careers.
Aardening may be specific to the irritant inducing the hardening phenomenon and
does not occur in all persons e#posed long term to an irritant.849 Aardened skin may
also have a thickened stratum granulosum, ith changes in the e#pression of various
inflammatory mediators and markers.849 An induction of an increase in the stratum
corneum lipid ceramide 4 may play a key role as a protection mechanism against
irritation by repeated application of sodium lauryl sulfate.8:, 39
Activities of daily living and ork may be reduced by severe irritant contact dermatitis.
Acute irritant contact dermatitis reactions to potent irritants (eg, acids, alkaline
solutions) are comparable to a chemical burn and can be graded like thermal burns
(ie, first/, second/, or third/degree burns). 'ith appropriate symptomatic management,
the prognosis for this type of irritant contact dermatitis is usually good, and, unless the
dermis is damaged, no permanent scarring should occur. &ee Chemical Jurns for
more information.
Mortality
Aydrofluoric acid is a potent cutaneous irritant used in lo/technology and high/
technology industries and at home in rust removal.84.9 Death from hypocalcemia may
ensue if as little as 4B of the skin5s surface area is e#posed sufficiently to this strong
inorganic acid and if complications are not managed optimally (see Aydrofluoric Acid
Jurns).
Patient Education
<emind individuals that they must continue to avoid cutaneous irritants! they ill
redevelop or aggravate dermatitis if they continue to have the same skin care
e#posures that resulted in irritant contact dermatitis. "he possibility of secondary or
complicating allergic contact dermatitis alays must be borne in mind.
(or patient education information, see the &kin, Aair, and Nails Center, as ell as
Contact Dermatitis.
Proceed to Clinical Presentation!istory
A detailed history is re0uired because the diagnosis of irritant contact dermatitis rests
on the history of e#posure of the affected body site to the cutaneous irritant. -atch
testing also is used in severe or persistent cases to e#clude allergic contact dermatitis
as a component of the individual5s cutaneous manifestations.
Hnset of symptoms occurs ithin minutes to hours of e#posure in simple acute irritant
contact dermatitis. Acute delayed irritant contact dermatitis is characteristic of certain
irritants, such as ben+alkonium chloride (eg, +ephiran, a preservative and
disinfectant), hich elicits a deferred (7/:3 h after e#posure) inflammatory reaction.8439
"he onset of signs and symptoms may be delayed by eeks in cumulative irritant
contact dermatitis. Cumulative irritant contact dermatitis is a conse0uence of multiple
incidents of subthreshold damage to the skin, ith the time beteen e#posures being
too short for a full resolution of skin barrier function. -atients ith sensitive skin (ie,
atopic individuals) have a decreased irritant threshold or a prolonged restoration time,
making them more vulnerable to clinical irritant contact dermatitis.
Cumulative irritant contact dermatitis typically occurs ith e#posure to eak irritants
rather than strong ones. Hften, the e#posure (eg, ater) is not only at ork but also at
home.
"hese patients report both itching and pain caused by fissuring of the hyperkeratotic
skin (chapping). -ain, burning, stinging, or discomfort e#ceeding pruritus occur early in
the clinical course.
%ess important subKective criteria for irritant contact dermatitis include the onset of
dermatitis ithin : eeks of e#posure, and reports of many other coorkers or family
members affected.
'ccupational history
Irritant contact dermatitis is a maKor occupational disease! skin disorders comprise up
to 3=B of occupational illnesses. "he physician needs to take an occupational history
from adults ith suspect irritant contact dermatitis.
Hccupational irritant contact dermatitis typically affects orkers ho are ne to a Kob,
ho are constitutionally more susceptible to irritant contact dermatitis, or ho have not
learned to protect their skin from cutaneous irritants. Individuals ith history of atopic
dermatitis (especially of the hands) are more susceptible to irritant contact dermatitis,
particularly of the hands.
$ost affected orkers have a degree of permanent inKury that is loer than that of
other occupational diseases! hoever, the compensation pay as higher for skin
diseases than for diseases of the respiratory system or musculoskeletal disorders,
according to a study in Denmark.
Physical E%amination
<ietschel and (oler proposed the folloing as primary diagnostic criteria for irritant
contact dermatitis8419 6
$acular erythema, hyperkeratosis, or fissuring predominating over vesiculation
,la+ed, parched, or scalded appearance of the epidermis
Aealing process beginning promptly on ithdraal of e#posure to the offending agent
Negative results on patch testing that includes all possible allergens
$inor obKective criteria for irritant contact dermatitis include the folloing6
&harp circumscription of the dermatitis
Dvidence of gravitational influence such as a dripping effect
%oer tendency for the dermatitis to spread than in cases of allergic contact dermatitis
$orphologic changes suggesting small differences in concentration or contact time
producing large differences in skin damage
Individuals may develop a habit of continuing to rub a site initially affected by irritant
contact dermatitis and may develop secondary neurodermatitis or lichen simple#
chronicus (lichenification). "his may be accepted as a se0uela of an occupational
inKury.
Complications
&kin lesions may become coloni+ed secondarily andCor infected, particularly by
Staphylococcus aureus. &econdary neurodermatitis (lichen simple# chronicus) may
develop in individuals ith irritant contact dermatitis, particularly in those ith
orkplace e#posures or under psychological stress.
-ostinflammatory hyperpigmentation or hypopigmentation may occur in areas affected
by irritant contact dermatitis or persist after resolution of irritant contact dermatitis in
individuals ith more pigmented skin.
&carring may occur after corrosive agent e#posure, e#coriation, or artifact, causing
ulceration.
Irritant contact dermatitis increases the risk of sensiti+ation to topical medications.
Proceed to Differential Diagnoses
Diagnostic Considerations
Hther causes of contact dermatitis must be e#cluded. Dlements of the history andCor
patch testing to relevant allergens can identify allergic contact dermatitis. &cabies may
resemble fiberglass dermatitis.
Differential Diagnoses
Atopic Dermatitis
Dermatologic $anifestations of <enal Disease
Dermatologic $anifestations of &cabies
Drug Druptions
Drysipelas
Drythema Infectiosum ((ifth Disease)
Id <eaction (Autoec+emati+ation)
%ichen &imple# Chronicus
-erioral Dermatitis
-hytophotodermatitis
&eborrheic Dermatitis
"pproach Considerations
No diagnostic test e#ists for irritant contact dermatitis. "he diagnosis rests on the
e#clusion of other cutaneous diseases (especially allergic contact dermatitis) and on
the clinical appearance of dermatitis at a site sufficiently e#posed to a knon
cutaneous irritant. %aboratory studies are generally of little value in proving a diagnosis
of contact dermatitis. Aoever, they may be of value in eliminating some disorders
from the differential diagnosis.
(indings of significantly elevated serum immunoglobulin D occasionally are useful to
substantiate an atopic diathesis in the absence of a personal or family history of atopy.
,o to Allergic Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact
Dermatitis for complete information on these topics.
Bacterial and (ungal Studies
A bacterial culture can be obtained in cases complicated by secondary bacterial
infection. A potassium hydro#ide (;HA) e#amination of scrapings may be performed
and samples for mycology may be obtained to e#clude superficial tinea infections or
candidal infections, depending on site and morphology of lesions.
Patch )esting
-atch testing can be performed to diagnose contact allergies, but no patch test e#ists
that proves that a cutaneous irritant is responsible for a particular case of irritant
contact dermatitis. Diagnosis rests on e#clusion of allergic contact dermatitis and
history of sufficient e#posure to a cutaneous irritant. Also see the folloing summaries
of clinical guidelines from the Loint Council of Allergy, Asthma and Immunology6
Allergy diagnostic testing6 an updated practice parameter. -art 4 84>9
Allergy diagnostic testing6 an updated practice parameter. -art : 84?9
Skin Biopsy
&kin biopsy can help e#clude other disorders, such as tinea, psoriasis, or cutaneous "/
cell lymphoma. All clinical cases of dermatitis are similar histologically.
&kin biopsy of skin lesions of the palms and soles has several potential pitfalls. "he
stratum corneum and epidermis are particularly thick there, hich makes the histologic
diagnosis of psoriasis more difficult and increases the possibility that the specimen
lacks sufficient dermis for optimal diagnosis. In the thenar area, an overly deep biopsy
can cut the recurrent branch of the median nerve. A biopsy from the sole may leave a
chronic painful scar on hich the patient must alk. A sauceri+ed shave biopsy is
usually the most suitable method.
Direct Microscopy
&kin scrapings of cutaneous lesions may help e#clude scabies or may reveal
fiberglass fibers as a cause of a patient5s pruritus.
!istologic (indings
"he histopathology of acute e#perimental irritant contact dermatitis has been studied
to a greater e#tent than chronic irritant contact dermatitis, hich is the primary clinical
complaint. Cellular changes seen in the skin vary according to the chemical nature
and concentration of the irritant applied, duration of e#posure, severity of ensuing
response, and time of sampling for acute irritant contact dermatitis. $any primary
irritants cause overt necrosis if applied in a sufficiently high concentration for sufficient
time.
$ost histologic e#aminations of irritant contact dermatitis reveal some degree of
intercellular edema or spongiosis in the epidermis. &pongiosis usually is less
pronounced than that seen in allergic contact dermatitis reactions.
-arakeratosis also is observed idely in irritant contact dermatitis reactions.
"he histology of chronic irritant contact dermatitis is one of hyperkeratosis ith areas
of parakeratosis, moderate/to/marked epidermal hyperplasia (acanthosis), and
elongation of the rete ridges.
Proceed to )reatment * Management
Emergency Department Care
Dmergency department treatment may include the folloing6
"opical soaks ith cool tap ater, Juro solution (463= dilution), saline (4 tspCpint)
%ukearm ater baths (antipruritic)
Aveeno (oatmeal) lukearm baths
Dmollients (eg, hite petrolatum, Ducerin) may be beneficial chronic cases.
%arge vesicles may benefit from therapeutic drainage (but not removing the vesicle
tops).849 "hese lesions should then be covered ith antibiotic dressing or a dressing
soaked in Juro solution.
Aospital admission is re0uired only in severe cutaneous irritant contact dermatitis, ie,
chemical burns from hydrofluoric acid or, occasionally, from freshly mi#ed -ortland
cement.
Barrier Creams
Creams containing ceramides (eg, Impruv, Cerave) may be particularly helpful in
restoring the epidermal barrier in persons ith irritant contact dermatitis and atopic
dermatitis. Creams containing dimethicone (eg, Cetaphil cream) can be helpful in
restoring the epidermal barrier in persons ith et ork)related irritant contact
dermatitis.
Cleansers
$ost soaps and detergents are alkaline and induce an increase in cutaneous pA,
hich affects the physiologic protective acid mantle of the skin by decreasing the fat
content. Disruption of stratum corneum and changes in pA are key elements in the
induction of irritant contact dermatitis and pruritus by soaps. "hese conditions are
e#acerbated in the inter months in patients ith dry, sensitive skin.
&yndets, ith a pA appro#imately 1.1, do not modify skin pA. $ost bar soaps and
li0uid detergents available on the market are a mi#ture of soap and syndet. A study
found that Dove and Cetaphil had a loer irritant effect than the other soaps tested.
Interestingly, no significant correlation as made beteen the price of the products
and their irritation potential.
Irritant contact dermatitis is a fre0uent problem in health care orkers, due to fre0uent
hand ashing. "he best antimicrobial efficacy can be achieved ith ethanol (>=/71B),
isopropanol (>=/7=B), and N /propanol (>=/7=B). "he antimicrobial efficacy of
chlorhe#idine (:/3B) and triclosan (4/:B) is both loer and sloer and carries a
potential risk of bacterial resistance.
"he use of alcohol/based hand rubs containing various emollients instead of irritating
soaps and detergents is one strategy to reduce skin damage, dryness, and irritation in
health care orkers. Irritant contact dermatitis occurs most fre0uently ith
preparations containing 3B chlorhe#idine gluconate, less fre0uently ith
nonantimicrobial soaps and preparations containing loer concentrations of
chlorhe#idine gluconate, and least fre0uently ith ell/formulated alcohol/based hand
rubs containing emollients and other skin conditioners.
"pproach Considerations
"he definitive treatment of irritant contact dermatitis is the identification and removal of
any potential causal agents. An inflammatory reaction from acute delayed irritant
contact dermatitis to an agent such as ben+alkonium chloride (eg, +ephiran) rarely
needs treatment and usually resolves ith cessation of e#posure. (urther symptomatic
therapy depends on the degree of involvement and the presence or absence of
secondary infection.
Advise individuals to use ceramides creams or bland emollients after ashing hands
ith soap and before sleep. Cleansers may be ranked by their irritancy.8479
<ecommend mild skin cleansers (eg, A0uanil, Cetaphil cleanser, Hilatum AD,
Neutrogena cleanser) in place of soap on affected areas. Instruct individuals to refrain
from the use of inappropriate solvents (eg, gasoline) or abrasives (eg, pumice stone)
to cleanse hands! these directly defat or traumati+e the skin.
A clinical guideline summary from the American Academy of Allergy, Asthma and
Immunology, Contact Dermatitis6 A -ractice -arameter, may be helpful.84@9
,o to Allergic Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact
Dermatitis for complete information on these topics.
Steroids and $mmunomodulators
"opical corticosteroids and immunomodulators are of unproven use in treating irritant
contact dermatitis. Corticosteroids ere found ineffective in treating the surfactant/
induced irritant dermatitis hen compared ith the vehicle and ith the untreated
control.8:=9 Aoever, topical steroids may be helpful for superimposed ec+ematous
features.
-otential complications center on the use of steroids, particularly around the eye. "he
avoidance of long/term steroid use is essential, because such use may cause
cataracts, glaucoma, corneal thinningCperforation, and loss of the eye, as ell as other
problems.
"opical tacrolimus is an irritant that may produce further stinging and irritation in
persons ith irritant contact dermatitis.8:49
Consultations
$ultidisciplinary consultations may be re0uired hen many orkers become affected
ith irritant contact dermatitis in a orkplace. Identifying and remediating the causes
of idespread irritant contact dermatitis interfering ith orkplace productivity and
orker 0uality of life is important.
Any patient ith hydrofluoric acid burn should be evaluated as a medical emergency
by a physician e#perienced in the management of hydrofluoric e#posures and burns.
Consider regional intravenous infusion of calcium gluconate as a therapeutic option in
hydrofluoric acid burns to forearm, hand, or digits hen topical therapy fails.
Proceed to Medication
Medication Summary
After the identification and removal of any potential causal agents, the use of
ceramides creams or bland emollients and bland barrier creams such as those
containing dimethicone are the mainstays of medical treatment for irritant contact
dermatitis.
A number of agents commonly found in therapeutic products for the skin (eg,
propylene glycol, lactic acid, urea, salicylic acid) may produce further skin
inflammation and may need to be avoided in these individuals. "opical corticosteroids
play a limited role in the treatment of irritant contact dermatitis. "hey do not address
the process directly, but they may be helpful for superimposed ec+ematous features.
Corticosteroids+ topical
Class Summary
Corticosteroids are immunosuppressives ith anti/inflammatory properties that modify
the body5s immune response to diverse stimuli. Hther actions include vasoconstriction
and antiproliferation. "hese agents have limited use in the treatment of irritant contact
dermatitis.
Mie full drug information
"mcinonide

A highly potent, fluorinated corticosteroid (class :/.), amcinonide suppresses mitotic
activity and causes vasoconstriction. It stimulates synthesis of en+ymes needed to
decrease inflammation and may suppress histamine release associated ith pruritus.
Mie full drug information
(luocinolone ,Cape%+ Derma&Smoothe-(S.

(luocinolone is a fluorinated corticosteroid of mid potency at the =.=:1B concentration
(class 3/1) and mild potency at the =.=4B concentration (class >).
Practice Essentials
Individuals ith allergic contact dermatitis may have persistent or relapsing dermatitis,
particularly if the material(s) to hich they are allergic is not identified or if they
practice inappropriate skin care. "he longer an individual has severe dermatitis, the
longer, it is believed, that the dermatitis ill take to resolve once the cause is
identified.
Essential update/ "llergic contact dermatitis caused y non&late% ruer gloves
In a study of surgery personnel in &eden ith occupational allergic contact
dermatitis, -ontNn et al found evidence that the condition as caused by 4,./
diphenylguanidine (4,./D-,) in non/late# rubber gloves.849 Ising patch tests, the
investigators found that 4: of 4> patients reacted to 4,./D-,. "he 4,./D-, as
present in the gloves orn by the patients in the study, ith a higher concentration on
the inside of the gloves than on the outside. In ? of 7 patients, contact allergy to
cetylpyridinium chloride as also found849
Signs and symptoms
Acute allergic contact dermatitis is characteri+ed by pruritic papules and vesicles on
an erythematous base. %ichenified pruritic pla0ues may indicate a chronic form of the
condition.
Individuals ith allergic contact dermatitis typically develop the condition ithin a fe
days of e#posure, in areas that ere e#posed directly to the allergen. Certain
allergens (eg, neomycin), hoever, penetrate intact skin poorly! in such cases, the
onset of dermatitis may be delayed for up to a eek folloing e#posure.
Individuals may develop idespread dermatitis from topical medications applied to leg
ulcers or from cross/reacting systemic medications administered intravenously.
Intraoral metal contact allergy may result in mucositis that mimics lichen planus, hich
has an association ith intraoral s0uamous cell carcinoma.
&ee Clinical -resentation for more detail.
Diagnosis
Diagnostic studies for allergic contact dermatitis include the folloing6
-otassium hydro#ide preparation andCor fungal culture6 "o e#clude tinea! these tests
are often indicated for dermatitis of the hands and feet
-atch testing6 "o identify e#ternal chemicals to hich the person is allergic
<epeat open application test (<HA")6 "o determine hether a reaction is significant in
individuals ho develop eak or 4F positive reactions to a chemical
Dimethylglo#ime test6 "o determine hether a metallic obKect contains enough nickel
to provoke allergic dermatitis
&kin biopsy6 $ay help to e#clude other disorders, particularly tinea, psoriasis, and
cutaneous lymphoma
&ee 'orkup for more detail.
Management
"he definitive treatment for allergic contact dermatitis is the identification and removal
of any potential causal agents! otherise, the patient is at increased risk for chronic or
recurrent dermatitis. "reatments also include the folloing6
Corticosteroids6 "opical corticosteroids are the mainstay of treatment, although acute,
severe allergic contact dermatitis, such as from poison ivy, often needs to be
treated ith a :/eek course of systemic corticosteroids
"opical immunomodulators ("I$s)6 Approved for atopic dermatitis, but they are also
prescribed for cases of allergic contact dermatitis hen they offer safety
advantages over topical corticosteroids
-hototherapy6 Administered to individuals ith chronic allergic contact dermatitis that
is not controlled ell by topical corticosteroids! these patients may benefit from
treatment ith a combination of psoralen (a photosensiti+er) and ultraviolet/A
(-IMA)
Immunosuppressive agents6 Chronic immunosuppressive agents are, in rare
instances, used to treat recalcitrant cases of severe, chronic, idespread
allergic contact dermatitis or severe hand dermatitis that prevents a patient from
orking or performing daily activities
Disulfiram6 Hccasionally, an individual ho is highly allergic to nickel and has severe
vesicular hand dermatitis ill benefit from treatment ith disulfiram (Antabuse)!
the drug has a chelating effect
&ee "reatment and $edication for more detail.
$mage lirary
Chronic stasis dermatitis ith allergic contact dermatitis to 0uaternium/41, a preservative in
moisturi+er. Allergic contact dermatitis produces areas of erythema in areas of atrophie blanche and
varicose veins.
Background
Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity (allergy)
resulting from cutaneous contact ith a specific allergen to hich the patient has
developed a specific sensitivity. "his allergic reaction causes inflammation of the skin
manifested by varying degrees of erythema, edema, and vesiculation.
"he term contact dermatitis sometimes is used incorrectly as a synonym for allergic
contact dermatitis. Contact dermatitis is inflammation of the skin induced by chemicals
that directly damage the skin (see Irritant Contact Dermatitis) and by specific
sensitivity in the case of allergic contact dermatitis.
Ladassohn first described allergic contact dermatitis in 47@1. Ae developed the patch
test to identify the chemicals to hich the patient as allergic. &ul+berger populari+ed
patch testing in the Inited &tates in the 4@.=s. "he (inn chamber method for patch
testing as designed in the 4@?=s! these chambers consist of small metal cups,
typically attached to strips of tape, filled ith allergens dispersed in either petrolatum
or ater. "he thin/layer rapid use epicutaneous ("<ID) test for patch testing became
available in the Inited &tates in the 4@@=s.
"he importance of specific substances as causes of allergic contact dermatitis varies
ith the prevalence of that substance in the environment. $ercury compounds once
ere significant causes of allergic contact dermatitis but rarely are used as topical
medications and, currently, are uncommon as a cause of allergic contact dermatitis.
Dthylenediamine, hich as present in the original $ycolog cream, declined as a
primary cause of allergic contact dermatitis once $ycolog cream as reformulated to
no longer contain this allergen.
A detailed history, both before and after patch testing, is crucial in evaluating
individuals ith allergic contact dermatitis. Jefore patch testing, the history identifies
potential causes of allergic contact dermatitis and the materials to hich individuals
are e#posed that should be included in patch testing. After patch testing, the history
determines the clinical significance of the findings. (&ee Clinical.)
"opical corticosteroids are the mainstay of treatment, hile a variety of symptomatic
treatments can provide short/term relief of pruritus. Aoever, the definitive treatment
of allergic contact dermatitis is the identification and removal of any potential causal
agents! otherise, the patient is at increased risk for chronic or recurrent dermatitis.
(&ee "reatment.)
,o to Irritant Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact
Dermatitis for complete information on these topics.
Pathophysiology
Appro#imately .=== chemicals are ell documented as specific causes of allergic
contact dermatitis. $ost of the chemicals able to provoke allergic contact dermatitis
are small molecules (O 1== d). "hese molecules must bind to carrier proteins on
%angerhans cells, hich are situated ithin the suprabasilar layer of the epidermis.
%angerhans cells are the antigen/presenting cells ithin the skin. %angerhans cells
interact ith CD3
F
" cells (helper " cells). &kin irritation by both nonallergenic and
allergenic compounds induces %angerhans cell migration and maturation. In contrast,
only allergenic compounds induce CD4a
F
CD7.
F
%angerhans cell migration ith
partial maturation at subto#ic concentrations.8:9
Cytokines also play an important role in allergic contact dermatitis because they
regulate accessory/adhesion molecules, such as intercellular adhesion molecule 4.
Interleukin 7 may be a cytokine indicating allergic contact dermatitis, not irritant
contact dermatitis.
%angerhans cells can migrate from the epidermis to the regional draining lymph nodes.
&ensiti+ation to a chemical re0uires intact lymphatic pathays.
"he initial sensiti+ation typically takes 4=/43 days from initial e#posure to a strong
contact allergen such as poison ivy. &ome individuals develop specific sensitivity to
allergens folloing years of chronic lo/grade e#posure! for e#ample, sensitivity to
chromate in cement can eventually develop in individuals ith chronic irritant contact
dermatitis resulting from the alkaline nature of cement. Hnce an individual is sensiti+ed
to a chemical, allergic contact dermatitis develops ithin hours to several days of
e#posure.
CD3
F
CC<4=
F
memory " cells persist in the dermis after clinical resolution of allergic
contact dermatitis.
(ilaggrin barrier defects that predispose individuals to atopic dermatitis might also
predispose them to allergic contact dermatitis by alloing greater penetration of
chemical haptens.8.9
Etiology
Appro#imately :1 chemicals appear to be responsible for as many as one half of all
cases of allergic contact dermatitis. "hese include nickel, preservatives, dyes, and
fragrances.
Poison ivy
-oison ivy (Toxicodendron radicans) is the classic e#ample of acute allergic contact
dermatitis in North America. Allergic contact dermatitis from poison ivy is characteri+ed
by linear streaks of acute dermatitis that develop here plant parts have been in direct
contact ith the skin.
0ickel
Nickel is the leading cause of allergic contact dermatitis in the orld. "he incidence of
nickel allergic contact dermatitis in North America is increasing! in contrast, ne
regulations in Durope have resulted in a decreasing prevalence of nickel allergy in
young and middle/aged omen.83, 19
Allergic contact dermatitis to nickel typically is manifested by dermatitis at the sites
here earrings or necklaces (see the image belo) containing nickel are orn or
here metal obKects (including the keypads of some cell phones8>9 ) containing nickel
are in contact ith the skin.
Nickel may be considered a possible occupational allergen. 'orkers in hom nickel
may be an occupational allergen primarily include hairdressers, retail clerks, caterers,
domestic cleaners, and metalorkers. Individuals allergic to nickel occasionally may
develop vesicles on the sides of the fingers (dyshidrotic hand ec+ema or pompholy#)
from nickel in the diet.
Allergic contact dermatitis to nickel in a necklace.
Ruer gloves
Allergy to 4 or more chemicals in rubber gloves is suggested in any individual ith
chronic hand dermatitis ho ears them, unless patch testing demonstrates
otherise. Allergic contact dermatitis to chemicals in rubber gloves typically occurs
ma#imally on the dorsal aspects of the hand. Isually, a cutoff of dermatitis occurs on
the forearms here skin is no longer in contact ith the gloves. Individuals allergic to
chemicals in rubber gloves may develop dermatitis from other e#posures to the
chemicals (eg, under elastic aistbands).
!air dye and temporary tattoos
p/-henylenediamine (--D) is a fre0uent component of and sensiti+er in permanent
hair dye products and temporary henna tattoos8?9 ! e#posure in to it in hair dye
products may cause acute dermatitis ith severe facial edema. &evere local reactions
from --D may occur in black henna tattoos in adults and children. Dpidemiologic data
indicate that the median prevalence of positive patch test reactions to --D among
dermatitis patients is 3..B (increasing) in Asia, 3B (plateau) in Durope, and >.:B
(decreasing) in North America.879
)e%tiles
Individuals allergic to dyes and permanent press and ash/and/ear chemicals added
to te#tiles typically develop dermatitis on the trunk, hich occurs ma#imally on the
lateral sides of the trunk but spares the vault of the a#illae. -rimary lesions may be
small follicular papules or may be e#tensive pla0ues.
Individuals in hom this allergic contact dermatitis is suspected should be tested ith
a series of te#tile chemicals, particularly if routine patch testing reveals no allergy to
formaldehyde. Ne clothing is most likely to provoke allergic contact dermatitis, since
most allergens decrease in concentration in clothing folloing repeated ashings.
Preservatives
-reservative chemicals added to cosmetics, moisturi+ers, and topical medications are
maKor causes of allergic contact dermatitis (see the image belo). "he risk of allergic
contact dermatitis appears to be highest to 0uaternium/41, folloed by allergic contact
dermatitis to isothia+olinones (;athon C,). Although parabens are among the most
idely used preservatives, they are not a fre0uent cause of allergic contact dermatitis.
&evere allergic contact dermatitis resulting from preservatives in sunscreen. -atch testing as
negative to the active ingredients in the sunscreen.
&chnuch et al estimated that preservatives found in leave/on topical products varied
over : orders of magnitude in relative sensiti+ation risk.8@9
(ormaldehyde is a maKor cause of allergic contact dermatitis (see the image belo).
Certain preservative chemicals idely used in shampoos, lotions, other moisturi+ers,
and cosmetics are termed formaldehyde releasers (ie, 0uaternium/41 8Doicil :==9,
imida+olidinyl urea 8,ermall 4419, and isothia+olinones8@9 ).
Hnycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.
(ragrances
Individuals may develop allergy to fragrances. (ragrances are found not only in
perfumes, colognes, aftershaves, deodorants, and soaps, but also in numerous other
products, often as a mask to camouflage an unpleasant odor. Inscented products
may contain fragrance chemicals used as a component of the product and not labeled
as fragrance.
Individuals allergic to fragrances should use fragrance/free products. Infortunately,
the e#act chemicals responsible for a fragrance in a product are not labeled. (our
thousand different fragrance molecules are available to formulate perfumes. "he
fragrance industry is not re0uired to release the names of ingredients used to
compose a fragrance in the Inited &tates, even hen individuals develop allergic
contact dermatitis to fragrances found in topical medications.
Deodorants may be the most common cause of allergic contact dermatitis to
fragrances because they are applied to occlude skin that is often abraded by shaving
in omen.
$assage and physical therapists and geriatric nurses are at higher risk of occupational
allergic contact dermatitis to fragrances.
Corticosteroids
In the last decade, it has become clear that some individuals ith chronic dermatitis
develop allergy to topical corticosteroids. $ost affected individuals can be treated ith
some topical corticosteroids, but an individual can be allergic to all topical and
systemic corticosteroids. Judesonide and ti#ocortol pivalate are useful patch test
corticosteroids for identifying individuals allergic to topical corticosteroids.
0eomycin
"he risk of allergy to neomycin is related directly to the e#tent of its use in a
population. "he risk of allergy to neomycin is much higher hen it is used to treat
chronic stasis dermatitis and venous ulcers than hen it is used as a topical antibiotic
on cuts and abrasions in children. Assume that individuals allergic to neomycin are
allergic to chemically related aminoglycoside antibiotics (eg, gentamicin, tobramycin).
84=9 Avoid these drugs both topically and systemically in individuals allergic to
neomycin.
Ben1ocaine
Avoid topical use of ben+ocaine. Jen+ocaine is included in most standard patch test
trays. Individuals allergic to ben+ocaine may safely use or be inKected ith lidocaine
(Pylocaine), hich does not cross/react ith ben+ocaine.
$any individuals complain of adverse reactions to sunscreens, but many of these
individuals are not allergic to the sunscreen materials. "hey may be allergic to
preservatives in these products or may have nonspecific cutaneous irritation from
these products.
Photoallergy
Hccasionally, individuals develop photoallergic contact dermatitis. Allergic contact
dermatitis may be accentuated by ultraviolet (IM) light, or patients may develop an
allergic reaction only hen a chemical is present on the skin and hen the skin is
e#posed sufficiently to ultraviolet light A (IM/A! .:=/3== nm).
Epidemiology
#nited States statistics
"he National Aealth and Nutrition D#amination &urvey (NAAND&) estimated the
prevalence of contact dermatitis to be 4..> cases per 4=== population, using physical
e#aminations by dermatologists of a selected sample of patients. NAAND&
underreported the prevalence compared ith the physical e#amination findings.
"he National Ambulatory $edical Care &urvey conducted in 4@@1 estimated 7.3
million outpatient visits to American physicians for contact dermatitis. "his as the
second most fre0uent dermatologic diagnosis. Hf office visits to dermatologists, @B
are for dermatitis. At a student health center dermatology clinic, ..4B of patients
presented for allergic contact dermatitis, and :..B presented for irritant contact
dermatitis.
"he "<ID test 'eb site can provide accurate basic information on common allergens.
"he Contact Allergen $anagement -rogram is provided as a service to the American
Contact Dermatitis &ociety (ACD&) members and is particularly valuable for allergens
found in topical skin care products. "he Contact Allergen <eplacement Database
(CA<D) contains more than 74== knon ingredients cataloged in more than 11==
commercial skincare products and is available as a &martphone application.
$nternational statistics
A &edish study found that prevalence of allergic contact dermatitis of the hands as
:.? cases per 4=== population. A Dutch study found that prevalence of allergic contact
dermatitis of the hands as 4: cases per 4=== population.
Race+ se%+ and age&related demographics
No racial predilection e#ists for allergic contact dermatitis. Allergic contact dermatitis is
more common in omen than in men. "his predominantly is a result of allergy to
nickel, hich is much more common in omen than in men in most countries.
Allergic contact dermatitis may occur in neonates. In elderly individuals, the
development of allergic contact dermatitis may be delayed somehat, but the
dermatitis may be more persistent once developed. Contact allergy to topical
medicaments is more common in persons older than ?= years.8449
Prognosis
Individuals ith allergic contact dermatitis may have persistent or relapsing dermatitis,
particularly if the material(s) to hich they are allergic is not identified or if they
continue to practice skin care that is no longer appropriate (ie, they continue to use
harsh chemicals to ash their skin, they do not apply creams ith ceramides or bland
emollients to protect their skin).
"he longer an individual has severe dermatitis, the longer it is believed it ill take the
dermatitis to resolve once the cause is identified.
&ome individuals have persistent dermatitis folloing allergic contact dermatitis, hich
appears to be true especially in individuals allergic to chrome.
A particular problem is neurodermatitis (lichen simple# chronicus), in hich individuals
repeatedly rub or scratch an area initially affected by allergic contact dermatitis.
Mortality
Death from allergic contact dermatitis is rare in the Inited &tates. Allergic contact
dermatitis to the eed ild feverfe caused deaths in India hen the seeds
contaminated heat shipments to India. "his plant then became idespread and a
primary cause of severe airborne allergic contact dermatitis.
Patient Education
-atients have the best prognosis hen they are able to remember the materials to
hich they are allergic and ho to avoid further e#posures. -rovide patients ith as
much information as possible concerning the chemical to hich they are allergic,
including all knon names of the chemical. 'eb sites, &martphone applications,
standard te#tbooks, and the "<ID test kit contain basic information about the
chemicals.
&usceptible individuals need to read the list of ingredients before applying cosmetic
products to their skin, since preservative chemicals are used idely in consumer,
medical, and orkplace products. "he same chemical may have different names hen
used for consumer or industrial purposes.
-rovide pamphlets ith color pictures of poison ivy to individuals allergic to the plant.
"he American Academy of Dermatology also has pamphlets on allergic contact
dermatitis and hand ec+ema.
(or patient education information, see the &kin, Aair, and Nails Center, as ell as
Contact Dermatitis.
Proceed to Clinical Presentation
!istory
A detailed history, both before and after patch testing, is crucial in evaluating
individuals ith allergic contact dermatitis. -otential causes of allergic contact
dermatitis and the materials to hich individuals are e#posed should be included in
patch testing. Dvaluation of allergic contact dermatitis re0uires a much more detailed
history than most other dermatologic disorders.
Aistory is e0ually important after patch testing. Hnly history and 0uestioning can
determine hether the materials to hich a patient is allergic are partly or holly
responsible for the current dermatitis. A positive patch reaction may indicate only a
sensitivity and not the cause of current dermatitis.
Pree%isting skin diseases
Individuals ith stasis dermatitis are at high risk for developing allergic contact
dermatitis to materials and agents applied to the areas of stasis dermatitis and leg
ulcers. Neomycin is an important cause of allergic contact dermatitis in these
individuals because it is used fre0uently despite the lack of documentation of its
efficacy in the treatment of stasis ulcers.
Individuals ith otitis e#terna fre0uently are allergic to topical neomycin and topical
corticosteroids.
Individuals ith pruritus ani and pruritus vulvae may become sensiti+ed to ben+ocaine
and other medications applied to chronic pruritic processes.
'omen ith lichen sclerosus et atrophicus fre0uently develop allergic contact
dermatitis, complicating the severe chronic vulvar dermatosis. -atch testing these
patients may provide important information that can help in the management of
recalcitrant and difficult/to/manage dermatosis.
"topic dermatitis
-atients ith a history of atopic dermatitis are at increased risk for developing
nonspecific hand dermatitis and irritant contact dermatitis. Aoever, they do not
appear to be at an increased risk for allergic contact dermatitis, despite the ide range
of topical medications and moisturi+ers used by individuals ith chronic atopic
dermatitis. "hey are at loer risk of allergic contact dermatitis to poison ivy. &ome
Duropean studies indicate that patients ith atopic dermatitis may have increased
incidence of allergic contact dermatitis to nickel.
'nset of symptoms
Individuals ith allergic contact dermatitis typically develop dermatitis, ithin a fe
days of e#posure, in areas that ere e#posed directly to the allergen. Certain
allergens (eg, neomycin) penetrate intact skin poorly, and the onset of dermatitis may
be delayed up to a eek folloing e#posure.
A minimum of 4= days is re0uired for individuals to develop specific sensitivity to a
ne contactant. (or e#ample, an individual ho never has been sensiti+ed to poison
ivy may develop only a mild dermatitis : eeks folloing the initial e#posure but
typically develops severe dermatitis ithin 4/: days of the second and subse0uent
e#posures.
<emember that removing the poison ivy allergen from the skin is difficult, and unless
an individual ashes e#posed skin ithin .= minutes of e#posure, allergic contact
dermatitis ill develop. "he hallmark of the diagnosis of poison ivy is linear dermatitic
lesions. "he possibility of an e#ternal cause of dermatitis alays must be considered if
the dermatitis is linear or sharply defined.
"he immediate onset of dermatitis folloing initial e#posure to material suggests either
a cross/sensiti+ation reaction, prior forgotten e#posure to the substance, or
nonspecific irritant contact dermatitis provoked by the agent in 0uestion.
Eyelid dermatitis
Individuals may develop dermatitis on eyelids and other e#posed skin folloing
e#posure to airborne allergens or allergens transferred to that site by the fingers.
Contact dermatitis may also result from allergy to eyelid makeup.
Contact urticaria
Immediate reactions, ie, visible lesions developing less than .= minutes after
e#posure, indicate contact urticaria (not allergic contact dermatitis). "his is particularly
true if the lesions are urticarial in appearance and if the skin reaction is associated
ith other symptoms, such as distant urticaria, hee+ing, ophthalmedema, rhinorrhea,
or anaphyla#is.
2ate%
<ubber late# currently is the most important source of allergic contact urticaria (see
%ate# Allergy). "he term hypoallergenic may refer to gloves that do not contain
sensiti+ing chemicals added to rubber late# but may not indicate hether the gloves
are rubber late# free.
&ome individuals may have delayed specific contact sensitivity to rubber late#, but
contact urticaria to rubber late# is much more common than allergic contact dermatitis
to late#. Individuals ith hand dermatitis, hospital orkers, children ith spina bifida,
and atopic individuals are at increased risk of developing contact urticaria to rubber
late#. Individuals may have allergic contact dermatitis to chemicals added to rubber
gloves and have contact urticaria to late#. Individuals earing rubber gloves should be
evaluated carefully for both possibilities.
<are reports e#ist of immediate anaphylactic reactions to topical antibiotics (eg,
bacitracin).
'ccupational dermatitis
Contact dermatitis is 4 of the 4= leading occupational illnesses. It may prevent
individuals from orking. "he hands are the sites e#posed most intensely to contact
allergens and irritants, both at ork and at home. Allergic contact dermatitis in
response to orkplace materials may improve initially on eekends and during
holidays, but individuals ith chronic dermatitis may not demonstrate the classic
history of eekend and holiday improvement.
Irritant contact dermatitis is more likely if multiple orkers are affected in the
orkplace. $ost allergens rarely sensiti+e a high percentage of the population.
!oies
Aobbies may be the source of allergic contact dermatitis. D#amples include
oodorking ith e#otic tropical oods or processing film using color/developing
chemicals that may provoke cutaneous lesions of lichen planus from direct skin
e#posure.
Medications
$edications (both self/prescribed and physician/prescribed) are important causes of
allergic contact dermatitis. "he orkplace nurse may dispense ineffective and
sensiti+ing topical preparations, such as thimerosal ($erthiolate), hich may change a
simple abrasion into a severe case of allergic contact dermatitis. Individuals may
develop allergy to preservatives in medications andCor to the active ingredients in
topical medications, especially neomycin and topical corticosteroids.84:, 4.9
-atients ith dermatitis that did not clear ith topical corticosteroid treatment should
be considered for patch testing ith a corticosteroid series and the commercial
preparations of corticosteroids and their vehicles.
Physical E%amination
Acute allergic contact dermatitis is characteri+ed by pruritic papules and vesicles on
an erythematous base. %ichenified pruritic pla0ues may indicate chronic allergic
contact dermatitis. Hccasionally, allergic contact dermatitis may affect the entire
integument (ie, erythroderma, e#foliative dermatitis). "he initial site of dermatitis often
provides the best clue regarding the potential cause of allergic contact dermatitis. Note
the folloing.
!ands
Aands are an important site of allergic contact dermatitis, particularly in the orkplace.
Common causes of allergic dermatitis on the hands include the chemicals in rubber
gloves.
)opical medication sites
Allergic contact dermatitis is fre0uent in the perianal area as a result of the use of
sensiti+ing medications and remedies (eg, topical ben+ocaine). "opical medications
are also important causes of allergic contact dermatitis in cases of otitis e#terna.
Allergy to chemicals in ophthalmologic preparations may provoke dermatitis around
the eyes.
"irorne allergic contact dermatitis
Chemicals in the air may produce airborne allergic contact dermatitis. "his dermatitis
usually occurs ma#imally on the eyelids, but it may affect other areas e#posed to
chemicals in the air, particularly the head and the neck.
!air dyes
Aair dyeQin particular, the component p/phenylenediamine (--D)Qmay trigger
allergic contact dermatitis. Individuals allergic to hair dyes typically develop the most
severe dermatitis on the ears and adKoining face rather than on the scalp.
Stasis dermatitis and stasis ulcers
Individuals ith stasis dermatitis and stasis ulcers are at high risk for developing
allergic contact dermatitis to topical medications applied to inflamed or ulcerated skin
(see the image belo). "he chronicity of this condition and the fre0uent occlusion of
applied medications contribute to the high risk of allergic contact dermatitis to
medicament (eg, neomycin) in these patients.
Individuals may develop idespread dermatitis from topical medications applied to leg
ulcers or from cross/reacting systemic medications administered intravenously. (or
e#ample, a patient allergic to neomycin may develop systemic contact dermatitis if
treated ith intravenous gentamicin.
Chronic stasis dermatitis ith allergic contact dermatitis to 0uaternium/41, a preservative in
moisturi+er. Allergic contact dermatitis produces areas of erythema in areas of atrophie blanche and
varicose veins.
Erythema multiforme
Drythema multiforme (D$) is a severe cutaneous reaction ith targetoid lesions that
occurs primarily after e#posure to certain medications or is triggered by infection, most
commonly by herpes simple# virus. <are cases of D$ have been reported after
allergic contact dermatitis resulting from e#posure to poison ivy,8439 tropical oods,
nickel, and hair dye (see the image belo).
Drythema multiformelike reaction that developed acutely folloing hair dying.
Intraoral metal contact allergy may result in mucositis that mimics lichen planus, hich
has an association ith intraoral s0uamous cell carcinoma. Intraoral s0uamous cell
carcinoma adKacent to a dental restoration containing a metal to hich the patient as
allergic has been reported.8419
Allergic contact dermatitis may be a direct trigger for skin ulceration in patients ith
venous insufficiency. Darly diagnosis and treatment of allergic contact dermatitis may
prevent the development of venous ulcers.
Complications
Darkly pigmented individuals may develop areas of hyperpigmentation or
hypopigmentation from allergic contact dermatitis. Hccasionally, they may develop
depigmentation at sites of allergic contact dermatitis to certain chemicals.
Hccasionally, allergic contact dermatitis is complicated by secondary bacterial
infection, hich may be treated by the appropriate systemic antibiotic.
Proceed to Differential Diagnoses
Diagnostic Considerations
Contact dermatitis from allergy must be differentiated from contact dermatitis due to
irritation, as ell as other forms of dermatitis. In addition, the specific substance to
hich the patient is sensitive needs to be identified.
Differential Diagnoses
Asteatotic Dc+ema
Contact Dermatitis, Irritant
Drug/Induced Jullous Disorders
Drug/Induced -hotosensitivity
Nummular Dermatitis
Hnycholysis
-erioral Dermatitis
-hytophotodermatitis
-rurigo Nodularis
&eborrheic Dermatitis
"inea Corporis
"ransient Acantholytic Dermatosis
Irticaria, Contact &yndrome
Proceed to Workup
"pproach Considerations
,uideline summaries are available as follos6
American Academy of Allergy, Asthma and Immunology, American College of Allergy,
Asthma and Immunology /Allergy diagnostic testing6 an updated practice
parameter. -art 4 84>9
American Academy of Allergy, Asthma and Immunology, American College of Allergy,
Asthma and Immunology /Allergy diagnostic testing6 an updated practice
parameter. -art : 84?9
,o to Irritant Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact
Dermatitis for complete information on these topics.
2a Studies
-otassium hydro#ide preparation andCor fungal culture to e#clude tinea are often
indicated for dermatitis of the hands and feet. "his ill identify disorders such as tinea
pedis.
Patch )esting
-atch testing847, 4@, :=9 is re0uired to identify the e#ternal chemicals to hich the
person is allergic. "he greatest 0uality/of/life benefits from patch testing occur in
patients ith recurrent or chronic allergic contact dermatitis (ACD). -atch testing is
most cost/effective and reduces the cost of therapy in patients ith severe allergic
contact dermatitis.
-atch testing must be performed by health care providers trained in the proper
techni0ue. $ost dermatologists can perform patch testing using the "<ID test, hich
can identify relevant allergies in as many as one half of affected patients. $ore
e#tensive patch testing is indicated to identify allergies to chemicals not found in the
"<ID test. &uch testing typically is available only in a limited number of dermatology
offices and clinics.
"he patch testing procedure is as follos6
&mall amounts of appropriate labeled dilutions of chemicals are applied to the skin
and occluded for : days
-atch tests may be left on for . days before removal
(or reasons of scheduling, a chemical must remain under a skin patch for a minimum
of 4 day to produce a positive patch test reaction :/? days folloing initial
application
"he patch test must be read not only at 37 hours, hen the patch tests customarily are
removed, but again beteen ?: hours and 4 eek folloing initial application
Individuals ith suspected allergic contact dermatitis ithout positive reactions on the
"<ID test or ith chronic dermatitis or relapsing dermatitis, despite avoiding
chemicals to hich they are allergic (identified on "<ID test), need additional patch
testing. $any individuals have more than 4 contact allergy and may be allergic to 4 or
more chemicals found on the "<ID test and on special allergen trays or series.
"esting reactions to more allergens increases accuracy of the diagnosis of allergic
contact dermatitis. &election of allergens for testing re0uires consideration of the
patient5s history and access to appropriate environmental contactants.
Certain chemicals (eg, neomycin) typically produce delayed positive patch test
reactions at 3 days or later folloing initial application. A tendency e#ists for elderly
patients to manifest positive patch test reactions later than younger patients. Do not
perform patch testing on patients taking more than 41 mgCd of prednisone. Hral
antihistamines may be used during the patch test period if re0uired.
Angry back syndrome or e#cited skin syndrome may occur. If a patient has a large
number of positive patch test reactions, retesting the patient se0uentially to a small
series of these allergens may be necessary to e#clude nonspecific false/positive
reactions. "he syndrome most likely occurs in individuals ho have active dermatitis at
the time of patch testing or ho have a strong positive patch test reaction, both of
hich may induce local skin hyperreactivity in the area here patches ere applied.
Additional patch test series or sets include the folloing6
Corticosteroids, particularly ti#ocortol pivalate and budesonide
Ingredients in cosmetics not found in the "<ID test
Chemicals used in dentistry that may produce mucosal and lip dermatitis in dental
clients or that may produce chronic dermatitis of the hands in dentists and
dental team members
Chemicals used in hairdressing that may produce facial, ear, and neck dermatitis in
clients or chronic hand dermatitis or eyelid dermatitis in hairdressers
(ragrances found in cosmetics and a ide range of consumer products
Important allergens not found in the "<ID test that are fre0uent causes of allergic
contact dermatitis are as follos6
Jacitracin
Acrylates used in dentistry, artificial nails, and printing
Chemicals used in baking
-esticides (many cases of dermatitis attributed to pesticides result from other causes,
particularly from plants such as poison ivy)
Chemicals used in machining, eg, cutting oils and fluids
-hotographic chemicals used by photographers and photographic developers
-lants e#cluding poison ivy
Chemicals in plastics and glues
Chemicals found in rubber products not included in the "<ID test
Chemicals in shoes and clothing
Iltraviolet (IM) protective ingredients in sunscreens
Hther chemicals producing photo allergic contact dermatitis
$iscellaneous allergens
"he chemicals listed above are tested under (inn chambers, allergDARD chambers, or
the IS Chamber patch test. In photopatch testing, the chemicals are applied in
duplicate sets. Hne set receives 4= LCcm
:
of IM/A (or 4 LCcm
:
less than the minimum
erythema dose, hichever is loest) :3 hours after application of the allergens. "he
other series is protected from IM e#posure to differentiate allergic contact dermatitis
and photo/accentuated allergic contact dermatitis from photo/allergic contact
dermatitis. Joth sets are read at 37 hours after application, as ell as at an additional
time point as in routine patch testing.
"he safety of patch testing in pregnancy has not been studied! hoever, the minute
amounts of allergens applied appear unlikely to be absorbed in sufficient amounts to
harm the fetus. Nonetheless, as ith all treatments in pregnant omen, the benefits of
testing should be eighed against any potential, albeit undocumented, risk.
Repeat 'pen "pplication )est
(or individuals ho develop eak or 4F positive reactions to a chemical, the repeat
open application test (<HA") is useful in determining hether the reaction is
significant. <HA" is most useful hen an individual has a 4F reaction to a chemical
found in a leave/on consumer product.
(or e#ample, an individual ith a eak reaction to a preservative found in a
moisturi+er may apply the moisturi+er tice a day for a eek to the side of the neck or
behind an ear! if clinical dermatitis does not develop, the 4F reaction likely as not
meaningful. Conversely, if dermatitis develops after a fe days of repeated application
of the suspected product, then the eak patch test reaction is highly relevant.
Dimethylglo%ime )est
"he dimethylglo#ime test is a useful and practical ay to identify metallic obKects that
contain enough nickel to provoke allergic dermatitis in individuals allergic to nickel.
Dermatology staff may test suspected metal products in the office, or the individual
may purchase a test kit and test obKects at home or at ork, particularly Keelry or
metallic surfaces.
Hther chemical tests are available for other suspected allergens (eg, formaldehyde,
cobalt, chromate). Hccasionally, chemical analyses may be necessary to determine
hether a material contains a suspected allergen or to identify ne unknon
allergens.
Skin Biopsy
&kin biopsy may help e#clude other disorders, particularly tinea, psoriasis, and
cutaneous lymphoma. &kin biopsy of skin lesions of the palms and soles has several
potential pitfalls, hoever.
"he stratum corneum and epidermis are particularly thick on the palms and soles. "his
makes the histologic diagnosis of psoriasis more difficult and increases the possibility
that the biopsy specimen ill lack sufficient dermis for optimal diagnosis.
An overly deep skin biopsy of the thenar area can cut the motor nerve, hich is the
recurrent branch of the median nerve. A biopsy from the sole may leave a chronic
painful scar on hich the patient must alk.
!istologic (indings
"he histology of allergic contact dermatitis is similar to that found in other forms of
ec+ematous dermatitis. A pattern of subacute chronic dermatitis or acute dermatitis
may be seen. "he inflammatory infiltrate in the dermis predominately contains
lymphocytes and other mononuclear cells.
Dpidermal edema (ie, spongiosis and microvesicle formation) may be seen, but these
changes may be absent in long/standing dermatitis in hich thickening of the
epidermis (acanthosis) ith hyperkeratosis and parakeratosis may be seen in the
epidermis and stratum corneum. Allergic contact dermatitis may provoke atypical "/cell
infiltrates, simulating mycosis fungoides.
Proceed to )reatment * Management
Background
%eprosy is a chronic infection caused by the acid/fast, rod/shaped bacillus
Mycobacterium leprae. %eprosy can be considered : connected diseases that
primarily affect superficial tissues, especially the skin and peripheral nerves. Initially, a
mycobacterial infection causes a ide array of cellular immune responses. "hese
immunologic events then elicit the second part of the disease, a peripheral neuropathy
ith potentially long/term conse0uences.
"he social and psychological effects of leprosy, as ell as its highly visible debilities
and se0uelae (as seen in the image belo), have resulted in a historical stigma
associated ith leprosy. "o minimi+e the preKudice against those ith leprosy, the
condition is also knon as Aansen disease, named after ,.A. Aansen, ho is credited
ith the 47?. discovery of M leprae. "his mycobacterium gros e#tremely sloly and
has not been successfully cultured in vitro.
Aands ith R/thumbs, claing, contractures, and shortening of fingers due to repetitive inKury and
healing. Ao Chi $inh City, Mietnam. (Courtesy of D. &cott &mith, $D)
In the 4@@=s, the 'orld Aealth Hrgani+ation ('AH) launched a campaign to eliminate
leprosy as a public health problem by :===. Dlimination, as defined by the 'AH, as
defined as a reduction of patients ith leprosy re0uiring multidrug therapy to feer
than 4 per 4=,=== population. "his goal as achieved in terms of global prevalence by
:==:, but 41 of the 4:: countries here leprosy as endemic in 4@71 still have
prevalence rates of greater than 4 per 4=,=== population.849
Although multidrug regimens have been used globally to cure nearly 43 million
patients ith leprosy since 4@71, the number of ne leprosy cases remained relatively
unchanged from 4@7= to :===, ranging from 1==,===/?==,=== orldide per year.8:9
Access and delivery of antibiotics continues to be a problem in the most endemic
nations. 'ith the precise transmission mechanism of leprosy still unknon and a lack
of an effective vaccine, leprosy ill probably continue to pose an ongoing public health
problem in the coming decades.
Pathophysiology
%eprosy can manifest in different forms, depending on the host response to the
organism.
Individuals ho have a vigorous cellular immune response to M leprae have the
tuberculoid form of the disease that usually involves the skin and peripheral nerves.
"he number of skin lesions is limited, and they tend to be dry and hypoesthetic. Nerve
involvement is usually asymmetric. "his form of the disease is also referred to as
paucibacillary leprosy because of the lo number of bacteria in the skin lesions (ie, O 1
skin lesions, ith absence of organisms on smear). <esults of skin tests ith antigen
from killed organisms are positive in these individuals.
Individuals ith minimal cellular immune response have the lepromatous form of the
disease, hich is characteri+ed by e#tensive skin involvement. &kin lesions are often
described as infiltrated nodules and pla0ues, and nerve involvement tends to be
symmetric in distribution. "he organism gros best at :?/.=EC! therefore, skin lesions
tend to develop in the cooler areas of the body, ith sparing of the groin, a#illa, and
scalp. "his form of the disease is also referred to as multibacillary leprosy because of
the large number of bacteria found in the lesions (ie, T> lesions, ith possible
visuali+ation of bacilli on smear). <esults of skin tests ith antigen from killed
organisms are nonreactive.
-atients may also present ith features of both categories! hoever, over time, they
usually evolve to one or the other (indeterminate or borderline leprosy). Interestingly,
most individuals ho are e#posed to leprosy never develop the disease.
Classification of leprosy6 %eprosy has : classification schemas6 the 1/category <idley/
Lopling system and the simpler and more commonly used 'AH standard.
<idley/Lopling6 Depending on the host response to the organism, leprosy can manifest
clinically along a spectrum bounded by the tuberculoid and lepromatous forms
of the disease. $ost patients fall into the intermediate classifications, hich
include borderline tuberculoid leprosy, midborderline leprosy, and borderline
lepromatous leprosy. "he classification of the disease typically changes as it
evolves during its progression or management. "he <idley/Lopling system is
used globally and forms the basis of clinical studies of leprosy. It may also be
more useful in guiding treatment regimens and assessing risk of acute
complications. -hysical findings in each subtype are presented in the Clinical
section.
'AH system6 "he 'AH recommends classifying leprosy according to the number of
lesions and the presence of bacilli on a skin smear. "his method is useful in
countries here biopsy analysis in unavailable.
-aucibacillary leprosy is characteri+ed by 1 or feer lesions ith absence of
organisms on smear. -aucibacillary leprosy generally includes the
tuberculoid and borderline lepromatous categories from the <idley/Lopling
system.
$ultibacillary leprosy is marked by > or more lesions ith possible visuali+ation of
bacilli on smear. %epromatous leprosy, borderline lepromatous leprosy,
and midborderline leprosy on the <idley/Lopling scale are included in the
multibacillary leprosy category.
Epidemiology
(re3uency
#nited States
In the Inited &tates, an average of 41= cases are diagnosed each year. In :==3, >@
ne cases of leprosy ere detected and 4.4 total persons ere reported to have the
disease, according to the 'AH. $ost cases of leprosy in the Inited &tates are found
in immigrants, although endemic foci e#ist in parts of %ouisiana, (lorida, and "e#as
along the ,ulf of $e#ico! in $e#ican and Asian California populations! and in &panish
Americans in Ne Uork City. Around 71B of these detected leprosy cases involve
patients ho have lived in foreign countries, primarily Asia, Africa, and %atin America.
8.9
Jased on genetic analysis studies, ild armadillos and many patients ith leprosy in
the southern Inited &tates are infected ith the same strain of M leprae.839 %eprosy
may be a +oonosis in the southern Inited &tates because armadillos are a large
reservoir for this disease.
$nternational
According to 'AH figures, the global registered prevalence of leprosy at the start of
:==1 as :7>,=>. cases. ,lobal annual detection rates have declined from :==4 to
:==3, hen ?>.,:>: and 3=?,?@4 ne cases ere reported, respectively. %eprosy is
still deemed a public health problem in @ countries6 Angola, Jra+il, Central African
<epublic, Democratic <epublic of the Congo, India, $adagascar, $o+ambi0ue, Nepal,
and the Inited <epublic of "an+ania. "hese countries account for 73B of reported
cases. (urthermore, more than @3B of ne cases of leprosy in %atin America are
reported in Jra+il.849
Mortality-Moridity
%eprosy is rarely fatal, and the primary conse0uence of infection is nerve impairment
and debilitating se0uelae. According to one study, ../1>B of nely diagnosed patients
already displayed signs of impaired nerve function.819 According to estimates, . million
people ho have completed multidrug therapy for leprosy have sustained disability
due to nerve damage. Although both lepromatous leprosy and tuberculoid leprosy
involve the skin and peripheral nerves, tuberculoid leprosy has more severe
manifestations. Nerve involvement results in loss of sensory and motor function, hich
may lead to fre0uent trauma and amputation. "he ulnar nerve is most commonly
involved.
Damage in the folloing nerves is associated ith characteristic impairments in
leprosy6
Ilnar and median / Claed hand
-osterior tibial / -lantar insensitivity and claed toes
Common peroneal /(oot drop
<adial cutaneous, facial, and greater auricular nerves (may also be involved! as seen
in the image belo)
-atient ith facial nerve palsy and contractures of the hand. Daloa, Ivory Coast.
(Courtesy of D. &cott &mith, $D)
Infiltration by bacteria may lead to destruction of nasal cartilage (lepromatous leprosy),
ocular involvement, and diffuse thickening of the skin. Advanced cases of
leprosy involve the loss of eyebros and lashes, but these deformities are less
common today.
'orldide, leprosy is considered the most common cause of crippling of the hand,
hich is caused by ulnar nerve involvement.8>9 -eroneal nerve involvement can
lead to foot drop, posterior tibial nerve involvement, and claed toes.
Race
%eprosy as once endemic orldide, and no racial predilection is knon. In the late
47==s, the incidence of leprosy in northern Durope and North America dropped
dramatically, and the disease is no reported primarily in tropical areas.
Se%
%eprosy is generally more common in males than in females, ith a male/to/female
ratio of 4.164. In some areas in Africa, the prevalence of leprosy among females is
e0ual to or greater than that in males.8:9
"ge
%eprosy can occur at any age, but, in developing countries, the age/specific incidence
of leprosy peaks in children younger than 4= years, ho account for :=B of leprosy
cases. %eprosy is very rare in infants! hoever, they are at a relatively high risk of
ac0uiring leprosy from the mother, especially in cases of lepromatous leprosy or
midborderline leprosy.!istory
&ymptoms
-ainless skin patch accompanied by loss of sensation but not itchiness (%oss of
sensation is a feature of tuberculoid leprosy, unlike lepromatous leprosy,
in hich sensation is preserved.) Chronic insensate patch is seen in the
mage belo.
Chronic insensate patch due to leprosy infection. Ao Chi $inh City, Mietnam. (Courtesy
of D. &cott &mith, $D)
%oss of sensation or paresthesias here the affected peripheral nerves are distributed
'asting and muscle eakness
(oot drop or claed hands (may result from neuritic pain and rapid peripheral nerve
damage! as seen in the image belo)
Characteristic claed hand deformity caused by ulnar involvement in leprosy. Daloa,
Ivory Coast. (Courtesy of D. &cott &mith, $D)
Ilcerations on hands or feet (ulcer at the metatarsal head is seen in the image belo)
Chronic nonhealing ulcer at the metatarsal head resulting from loss of sensation in the
feet. ;arigiri, "amil Nadu, India. (Courtesy of "ara <amachandra)
%agophthalmos, iridocyclitis, corneal ulceration, andCor secondary cataract due to
nerve damage and direct bacillary skin or eye invasion8?9
&ymptoms in reactions
"ype 4 (reversal) / &udden onset of skin redness and ne lesions
"ype : (erythema nodosum leprosum 8DN%9! as seen in the image belo) / $any skin
nodules, fever, redness of eyes, muscle pain, and Koint pain
-atient ith erythema nodosum leprosum type : reaction several eeks after initiation
of drug therapy. "his photograph as taken after tendon release. <edood City,
California. (Courtesy of D. &cott &mith, $D)
"ravel6 %eprosy should be considered in anyone ho has lived in the tropics or
ho has traveled for prolonged periods to endemic areas.
D#posure6 "he incubation period of leprosy is long, ranging from a fe months
to :=/1= years. "he mean incubation time is estimated to be 4= years for
lepromatous leprosy and 3 years for tuberculoid leprosy. "he organism5s slo
dividing time (once every : k) contributes to the challenge of epidemiologically
linking e#posures to the development of disease.
Jecause of immunologic reasons, only around 1/4=B of the population is
estimated to be susceptible to infection.
Physical
"he cardinal signs of leprosy include hypoesthesia, skin lesions, and peripheral
neuropathy. "he first physical signs of leprosy are usually cutaneous. "he subtype of
leprosy often determines the degree of skin involvement.
-hysical e#amination should include the folloing6
Dvaluation of skin lesions
Careful sensory and motor e#amination
-alpation of peripheral nerves for pain or enlargement, ith particular attention paid to
the folloing locations6
Dlbos / Ilnar nerve
'rist / &uperficial radial cutaneous and median nerves
-opliteal fossa / Common peroneal nerve
Neck / ,reat auricular nerve
-hysical findings in specific leprosy subtypes include the folloing6
"uberculoid leprosy
"he initial lesion is often a sharply demarcated hypopigmented macule that is ovoid,
circular, or serpiginous. "he lesions may be somehat elevated
ith a dry scaly center and erythematous borders.
Common lesion sites include the buttocks, face, and e#tensor surfaces of limbs. "he
perineum, scalp, and a#illa are not normally involved because of
the temperature differential in these +ones, as predilection is toard
cooler +ones.
As the disease progresses, lesions tend to destroy the normal skin organs such as
seat glands and hair follicles.
&uperficial nerves that lead from the lesions tend to enlarge and are sometimes
palpable. "he patient may e#perience severe neuropathic pain.
Nerve involvement can also lead to trauma and muscle atrophy.
%epromatous leprosy
"his form is characteri+ed by e#tensive bilaterally symmetric cutaneous involvement,
hich can include macules, nodules, pla0ues, or papules. $ultiple
flat hypopigmented lesions are seen in the image belo.
$ultiple flat hypopigmented lesions on shoulder and neck, suggestive of
multibacillary leprosy. Note ulceration of hypothenar area of hand, indicative of
ulnar neuropathy. <edood City, California, Inited &tates. (Courtesy of D. &cott
&mith, $D)
Inlike lesions in tuberculoid leprosy, those in lepromatous leprosy have poorly defined
borders and raised and indurated centers. As in all forms of leprosy,
lepromatous lesions are orst on cooler parts of the body. Common
areas of involvement include the face, ears, rists, elbos,
buttocks, and knees.
Aoarseness, loss of eyebros and eyelashes, and nasal collapse secondary to septa
perforation may occur in advanced cases of disease. Involvement
of the eye may include keratitis, glaucoma, or iridocyclitis as seen in
the image belo.
$an ith advanced deformities caused by unmanaged leprosy. ;eratitis, loss of
eyebro, thickened skin, and typical hand impairments. Ao Chi $inh City,
Mietnam. (Courtesy of D. &cott &mith, $D)
"he leonine facies associated ith leprosy develop as the disease progresses, and
the facial skin becomes thickened and corrugated.
A#illary and inguinal adenopathy may develop, in addition to scarring of the testes and
subse0uent gynecomastia and sterility.
Nerve involvement in lepromatous leprosy is not as severe as in tuberculoid leprosy,
since nerves, although visibly thickened and highly infected, still
function reasonably ell in early stages of the disease.
Jorderline tuberculoid leprosy6 "he lesions are fe or moderate and asymmetric ith
almost complete anesthesia. -eripheral nerves are often involved and
thickened asymmetrically, and cutaneous nerves are sometimes enlarged.
$idborderline leprosy6 "he number of skin lesions is moderate, and they are
asymmetrical and somehat anesthetic. -eripheral nerves may be
somehat symmetrically enlarged, but cutaneous nerves are not.
Jorderline lepromatous leprosy6 $oderate to numerous slightly asymmetrical skin
lesions appear ith minor or no anesthesia. -eripheral nerves are often
enlarged symmetrically, but cutaneous nerves are not.
Indeterminate leprosy6 &kin lesions are typically either hypopigmented or
hyperpigmented macules or pla0ues. -atients may note that these lesions
are anesthetic or paresthetic.
Causes
M leprae is the causative agent associated ith leprosy, hich has been
recogni+ed as an infectious disease for the last : millennia. M leprae as
discovered as the causative agent in 47?.. "he acid fast, gram/positive bacillus
is an obligate intracellular organism ith a predilection for &chann cells and
macrophages. M leprae has not been successfully gron using artificial media.
"he route of transmission has not been definitively established, although
human/to/human aerosol spread of nasal secretions is thought to be the most
likely mode of transmission in most cases. %eprosy is not spread by touch, since
the mycobacteria are incapable of crossing intact skin. %iving near people ith
leprosy is associated ith increased transmission. Among household contacts,
the relative risk for leprosy is increased 7/ to 4=/fold in multibacillary and :/ to 3/
fold in paucibacillary forms. Animal reservoirs do e#ist (armadillos, certain
nonhuman primates), and cases of suspected +oonotic transmission have been
reported.
Proceed to Workup
2aoratory Studies
"he 'AH case definition of leprosy is M leprae infection in an individual ho has not
completed a course of treatment and has one or more of the folloing6
Aypopigmented or reddish skin lesions ith loss of sensation
Involvement of the peripheral nerves as demonstrated by their thickening and
associated loss of sensation
&kin smear positive for acid/fast bacilli
%aboratory studies include the folloing6
&kin biopsy, nasal smears, or both are used to assess for acid/fast bacilli using (ite
stain. Jiopsies should be full dermal thickness taken from an edge of the lesion
that appears most active.879
&erologic assays can be used to detect phenolic glycolipid/4 (specific for M leprae)
and lipoarabinomannan (commonly seen in mycobacteria).879
$olecular probes detect 3=/1=B of cases missed on prior histologic evaluation. &ince
probes re0uire a minimum amount of genetic material (ie, 4=
3
DNA copies), they
can fail to identify paucibacillary leprosy.
%aboratory tests related to drug treatment follo/up include the folloing6
CJC count
Creatinine level
%iver function tests
'ther )ests
Immunologic tests include the folloing6
%epromin skin test (not available in the Inited &tates)6 Although not diagnostic of
e#posure to or infection ith M leprae, this test assesses a patient5s ability
to mount a granulomatous response against a skin inKection of killed M
leprae. -atients ith tuberculoid leprosy or borderline lepromatous
leprosy typically have a positive response (T1 mm). -atients ith
lepromatous leprosy typically have no response.
-henolic glycolipid/46 "his is a specific serologic test based on the detection of
antibodies to phenolic glycolipid/4. "his test yields a sensitivity of @1B for
the detection of lepromatous leprosy but only .=B for tuberculoid leprosy.
-olymerase chain reaction (-C<)6 -C< and recombinant DNA technology have
alloed for the development of gene probes ith M leprae )specific
se0uences. "his technology can be used to identify the mycobacterium in
biopsy samples, skin and nasal smears, and blood and tissue sections.
%ymphocyte migration inhibition test (%$I")6 As determined by a lymphocyte
transformation and %$I", cell/mediated immunity to M leprae is absent in
patients ith lepromatous leprosy but present in those ith tuberculoid
leprosy.
Contact or family screening for history of leprosy
Procedures
&kin biopsy samples stained ith hemato#ylin/eosin and (ite/(araco are the
primary basis for laboratory diagnosis and categori+ation. A full/thickness skin
biopsy sample should be taken from an advancing border of an active lesion
and should include dermis and epidermis. &kin smears that demonstrate acid/
fast bacilli strongly suggest a diagnosis of leprosy, but the bacilli may not be
demonstrable in tuberculoid (paucibacillary) leprosy.
A nerve biopsy can be beneficial in ruling out diseases such as hereditary
neuropathies or polyarteritis nodosa. Nerve biopsies may also help identify
abnormalities in patients ith subclinical leprosy and may be the only ay to
definitively diagnose completely neuropathic forms of leprosy. If a nerve biopsy
is needed to confirm diagnosis, a purely sensory nerve (eg, sural or radial
cutaneous nerve) should be used. "his procedure is rarely necessary.8?9
!istologic (indings
(indings vary but can include dermatitis, giant cells, infiltration of nerve bundles ith
mononuclear cells, and granulomas. %epromatous lesions generally contain numerous
acid/fast bacilli and fat/laden macrophages ith a paucity of lymphocytes.
Aistopathology of leprosy is seen in the image belo.
Aistopathology of leprosy6 %arge numbers of acid/fast bacilli (in clusters) in histiocytes and ithin
nerves. (ite/(araco stain 1== P. (Courtesy of "ara <amachandra and D. &cott &mith, $D)
In contrast, tuberculoid lesions contain fe/to/no acid/fast bacilli but manifest
granulomatous changes ith epithelial cells and lymphocytes. "he immunopathologic
spectrum of leprosy has been delineated in the Neurologic $anifestations of %eprosy
topic in $edscape <eference5s Neurology volume.
Staging
%eprosy is staged or graded based on microscopy findings to classify cases as
paucibacillary or multibacillary so that duration and type of drug therapy can be
determined.
Proceed to )reatment * ManagementMedical Care
In response to the increased incidence of dapsone resistance, the 'AH introduced a
multidrug regimen in 4@74 that includes rifampicin, dapsone, and clofa+imine. &ome
clinical studies have also shon that certain 0uinolones, minocycline, and
a+ithromycin have activity against M leprae. "he 'AH recently recommended single/
dose treatment ith rifampin, minocycline, or oflo#acin in patients ith paucibacillary
leprosy ho have a single skin lesion. Aoever, the 'AH still recommends the use of
the long/term multidrug regimens henever possible because they have been found to
be more efficacious.
"able. $ultidrug "herapy -lan <ecommended by the 'AH (Hpen "able in a ne
indo)
)ype of 2eprosy
Daily+ Self&
"dministered
Monthly Supervised Months of )reatment
-aucibacillary Dapsone 4== mg <ifampicin >== mg >/4:
$ultibacillary Dapsone 4== mg,
Clofa+imine 1= mg
<ifampicin >== mg,
Clofa+imine .== mg
:3
-ediatric Dapsone : mgCkg,
Clofa+imine 4 mgCkg
<ifampicin 4= mgCkg,
Clofa+imine > mgCkg
&ame as in adults
I& regimens emphasi+e the use of rifampin, hich is the most bactericidal drug used
to treat leprosy. Although a single dose of >== mg once monthly (the 'AH standard) is
considered bactericidal, treatment plans in the Inited &tates may include doses of >==
mgCday.
-aucibacillary leprosy should be treated for >/4: months ith dapsone 4== mgCday
unsupervised plus rifampin >== mgCmonth supervised. "his regimen should be
folloed by treatment ith dapsone as monotherapy for . years in patients ith
tuberculoid leprosy or 1 years in patients ith borderline lepromatous leprosy.
$ultibacillary leprosy should be treated for :3 months ith dapsone 4== mgCday
unsupervised, clofa+imine 1= mgCday unsupervised, and rifampin >== mg plus
clofa+imine .== mgCmonth supervised.
Corticosteroids have been used to treat nerve damage associated ith leprosy, but a
recent revie of . randomi+ed controlled trials shos no significant long/term
effect.8@9 -rednisolone is believed to minimi+e pain and acute inflammation. "he
recommended initial dose is prednisolone 3= mg daily.
Hbservations of increasing resistance in patients treated for leprosy have been
reported in &outheast Asia, notably in Mietnam.84=9 "he drug most commonly
found to be resistant is dapsone, often in the conte#t of prior e#posure or
treatment attempts ith monotherapy. Although drug resistance is an ongoing
concern, it is difficult to assess in this slo/groing organism. In a study of M
leprae strains from &outh America, fe of :.= strains subKected to molecular
drug/susceptibility analysis ere drug/resistant. Hf the :.= strains, . ere
identified as clinically relapsing and ere found to be resistant by genetic
testing! : of the . ere dapsone/resistant! and 4 as dapsone/resistant and
rifampin/resistant using genetic testing for point mutation.8449
Surgical Care
"he goals of surgical treatment in patients ith leprosy are to prevent further
deterioration, to improve motor function, and, in some cases, to improve
sensation.
-reoperative re0uirements6 (irst, a full sensory and motor appraisal ith
functional and occupational assessment must be completed to determine the
e#tent of damage. Additionally, patients must have completed the multidrug
therapy and should have negative skin smear results. "he patient should not
use steroids a fe months before surgery, and acute neuritis should not be
evident. &tiffness of hands and feet should be minimi+ed ith preoperative
therapy.
Neural surgery
Attempts to restore autonomic function and sensation are rarely undertaken since little
evidence shos that function is significantly regained. Draining of acute
nerve abscesses and fascicular dissection can reduce the pressure on
nerves and may improve sensation. In some cases, longitudinal
epineurotomy may relieve some sensory loss. Considerable nerve
function can be regained in the posterior tibial nerve ith neurovascular
decompression via release of the fle#or retinaculum. Calcaneal bands can
be slit to relieve distal compression of branches on the sole of the foot.
Nerve grafts may be of some benefit in patients ith locali+ed lesions. Neural surgery
may also be indicated in patients ith unremitting nerve pain.
<econstruction and functional restoration8>9
In leprosy management, the goal of most surgical procedures is to remedy motor
paralysis due to primary nerve impairment. Cla fingers and R/thumbs
caused by ulnar nerve paralysis are among the most common deformities.
Claed hands are repaired ith arthrodesis or ith a tendon transfer to 4
of 3 insertion sites on the finger6 interosseus tendons, pro#imal phalan#,
dorsal e#tensor e#pansion, or fle#or sheath annular pulleys. "he palmaris
longus, fle#or digitorum superficialis, e#tensor carpi radialis longus, and
e#tensor indices are tendons that can be used for transfer. "endon
transfers are also used to repair abduction and opposition of the thumb,
dorsifle#ion of the foot, and fle#ion and e#tension of the
metacarpophalangeal and pro#imal interphalangeal Koints, respectively.
Contractures of the hand, such as the thumb eb contracture, can be repaired ith R/
plasty, and Koint stability can be improved ith tenodesis.
"he constrictions caused by repetitive inKury and healing in patients ith leprosy can
be treated ith several methods. -ossible treatment options include
removal of the carpal tunnel roof, ulnar nerve transposition anteriorly, and
epicondylectomy.
-rocedures that limit hypere#tension of the metacarpophalangeal Koint or keep it in
fle#ion are not indicated in the insensate hands of patients ith leprosy,
ho suffer from continued eakness.
Amputation is a last resort and is reserved for cases of e#tremely diseased tissue.
Dye procedures6 %oss of eyelid function may be treated ith passing a strip from
the temporalis muscle through the eyelid and connecting it to the inner canthus.
"arsorrhaphy may help narro the opening of the eyelid, and canthoplasty
reduces sagging of the eyelids.
Cosmetic surgery6 After the disease is controlled medically, the folloing
cosmetic procedures may also be considered6
Nasal reconstruction
<emoval of e#cess skin
<eplacement of eyebros using transplants of scalp hair
<emoval of breast tissue formation due to gynecomastia
Consultations
Consultations may include an orthopedic surgeon, dermatologist, neurologist, and
physical therapist, based on the needs of the individual patient.

Medication Summary
"he goals of pharmacotherapy are to eradicate the infection, to prevent complications,
and to reduce morbidity.
"he multidrug therapy plan recommended by the 'AH can be used to plan therapy
based on the type of leprosy (paucibacillary or multibacillary) and hether it is
supervised monthly or self/administered daily (see $edical Care).
"ntimycoacterial "gents
Class Summary
"hese agents have bactericidal and bacteriostatic activity against mycobacteria.
Mie full drug information
Dapsone ,"vlosulfon.

Jactericidal and bacteriostatic against mycobacteria! mechanism of action is similar to
that of sulfonamides, in hich competitive antagonists of -AJA prevent formation of
folic acid, inhibiting bacterial groth. -art of a :/drug regimen for treatment of
paucibacillary leprosy! part of a ./drug regimen for treatment of multibacillary leprosy.
Mie full drug information
Rifampin ,Rifadin+ Rimactane.

(or use in combination ith at least 4 other antituberculous drug! inhibits DNA/
dependent bacterial but not mammalian <NA polymerase. $ost bactericidal drug used
against M leprae. Cross/resistance may occur.
"reat for >/@ mo or until > mo have elapsed from conversion to sputum/culture
negativity.
-art of :/drug regimen for treatment of paucibacillary leprosy! part of ./drug regimen
for treatment of multibacillary leprosy.
Mie full drug information
Clofa1imine ,2amprene.

Inhibits mycobacterial groth, binds preferentially to mycobacterial DNA. Aas
antimicrobial properties, but mechanism of action is unknon. -art of ./drug regimen
for treatment of multibacillary leprosy.
Mie full drug information
Minocycline

Ised to treat leprosy in patients ho cannot tolerate clofa+imine.
Proceed to (ollow&up
(urther 'utpatient Care
"he 'AH recommends that the monthly doses of rifampin be administered
under direct observation during the visit.
$onthly outpatient follo/up is recommended during treatment, although eekly
visits may be necessary if the patient e#periences a leprosy reaction.
(ollo/up laboratory studies during treatment include the folloing6
Irinalyses
CJC count
Creatinine
%iver function tests
Uearly skin scrapings taken from the . or 3 most active lesions are
recommended.
<esponse to treatment
&uccessful treatment can result in flattening and elimination of nodules, papules, and
pla0ues, as ell as improved nerve function. Jacillary load is rarely a
convenient method of assessing response to treatment. Noncompliance
or drug resistance should be suspected if intact organisms are present
after several months of treatment.
Hnce treatment is completed, the patient should be monitored for the ne#t 1/4= years
to evaluate for signs of relapse. "o date, the relapse rate folloing
completion of multidrug therapy has been 4B for both types of leprosy. In
such cases, ne bacillus/positive lesions may develop and should be
treated ith a thorough I& regimen that incorporates once/daily rifampin
(see "reatment).
-atients ho have been successfully treated occasionally develop reversal reactions
and further neuropathy. If skin biopsy samples are bacillus/negative,
these patients are deemed to have a reversal reaction (see
Complications).
Complications
Careful attention to the development of reversal reactions during treatment and prompt
and proper management ill minimi+e long/term neurologic se0uelae.
"ype 4 reaction
<eversal reaction, or lepra type 4 reaction, is a delayed/type hypersensitivity reaction
that arises hen borderline leprosy shifts toard borderline lepromatous
leprosy ith treatment. "hese types of reactions reflect the development
of an appropriate immune response and the local generation of tumor
necrosis factor/alpha and interferon/gamma. "he reaction is characteri+ed
by edema and erythema of e#isting skin lesions, formation of ne skin
lesions, neuritis, and additional sensory and motor loss.
"he likelihood of a type 4 reaction in patients ith borderline leprosy is .=B.8?9
"reatment includes nonsteroidal anti/inflammatory drugs (N&AIDs) and high/dose
steroids. -rednisone is given at a dose of 3=/>= mgCday ith a decreasing
taper of 1 mg every :/3 eeks after improvement is demonstrated.
"ype : reaction
Drythema nodosum leprosum (DN%), also knon as lepra type : reaction, is a
complication of lepromatous leprosy. It is characteri+ed by the
development of inflamed subcutaneous nodules accompanied at times by
fever, lymphadenopathy, and arthralgias. Aigh levels of tumor necrosis
factor/alpha and immune comple# deposition are associated ith DN%.8?9
"reatment includes prednisolone, clofa+imine, or thalidomide. Drythema
nodosum leprosum reaction is seen in the image belo.
-atient ith multibacillary leprosy shoing subse0uent erythema nodosum leprosum
reaction. &anta Clara, California. (Courtesy of D. &cott &mith, $D)
$ild DN% reactions are treated ith aspirin >==/4:== mgCday in 3/> doses per day.
&evere DN% reactions are treated ith prednisone >=/7= mgCday ith a slo taper,
reducing by 1/4= mg every :/3 eeks, depending on response and
severity, to prevent residual deformity and nerve damage.
Alternatively, thalidomide 4== mg -H 3 times per day (if available and in the absence
of contraindications) can be used in cases that involve large
subcutaneous pla0ues, arthritis, and temperature that e#ceeds .7.7EC.
%ucio phenomenon is a severe complication of multibacillary leprosy that is marked by
blue hemorrhagic pla0ues and necrotic ulcerations. "he bacilli may e#tend to
the endothelial cells along ith the appearance of necrotic epidermis and
vasculitis ith thrombus formation and endothelial proliferation.
Prognosis
<ecovery from neurologic impairment is limited, but skin lesions generally clear
ithin the first year of therapy. Discoloration and skin damage typically persist.
-hysical therapy, reconstructive surgery, nerve and tendon transplants, and
surgical release of contractures have all contributed to increasing the functional
ability in patients ith leprosy. A common residual deformity is insensitive feet,
as seen in persons ith diabetes.
Patient Education
<egional ambulatory clinics6 "he National Aansen5s Disease -rograms (NAD-)
provide outpatient services and medical care to patients ith leprosy in the
Inited &tates and -uerto <ico. 'ith the goals of prevention and early detection,
the program supports delivery of services in areas ith considerable populations
of patients ith leprosy. (or additional information about these free services,
contact the NAD- directly at 4/7==/>3:/:3??. "he NAD- Center in Jaton
<ouge, %a, provides free histopathologic services to facilitate diagnosis. Dleven
outpatient AD clinics are located at hospitals, universities, and public health
departments in Ari+ona, California, (lorida, Illinois, $assachusetts, Ne Uork,
-uerto <ico, "e#as, and 'ashington. "hese clinics provide the folloing
services6
&kin biopsy diagnostic confirmation
Additional medical care
Aospitali+ation for treatment complications
Consultations
$aterials for professional and patient education
-atients ith leprosy should be advised about the importance of continuing
long/term therapy until the course of antibiotics is completed. "he 'AH
recommends that the monthly administration of rifampin be directly observed.
In patient ith leprosy ho have advanced nerve damage, self/care techni0ues
are of utmost importance in maintaining function and preventing further
disability. "he use of visual input to regulate activity, self/inspection, hygiene,
and proper footear can help prevent ulcer formation and tissue damage.
"he 'AH recommends e#amination of all household contacts of patients ith
leprosy, ith careful instructions to seek medical care if signs and symptoms of
leprosy appear.
-regnancy in patients ith leprosy can result in hormonal changes that
lead to suppression of cell/mediated immunity, hich may e#acerbate symptoms of
leprosy. (urthermore, pregnant omen ith leprosy are at greater risk of developing
reactions and relapses. "ype 4 reactions are more likely during the first fe months
folloing childbirth, hereas type : reactions typically occur during the third trimester
of pregnancy and during lactation.8?9