Background

Irritant contact dermatitis (ICD) is infammation of the skin typically

manifested by erythema, mild edema, and scaling. Irritant contact
dermatitis is a nonspecifc response of the skin to direct chemical damage
that releases mediators of infammation predominately from epidermal
cells. A corrosive agent cases the immediate death of epidermal cells,
manifested by chemical brns and ctaneos lcers. !ote the image belo".
Chronic irritant contact dermatitis of the hands in an older "orker# the condition reslted
in early retirement.
$he hands are the most important sites of irritant contact dermatitis. Irritant
contact dermatitis from repeated "orkplace e%posre of the hands to
soaps, cleansers, and solvents is the sorce of most occpational skin
disorders.
Irritant contact dermatitis remains nderstdied compared "ith allergic
contact dermatitis. &ost articles on contact dermatitis concern allergic
contact dermatitis. $his largely refects the fact that "ith history and patch
testing, a specifc hypersensitivity and a probable case of dermatitis can
be identifed in most cases of allergic contact dermatitis.
!o diagnostic test e%ists for irritant contact dermatitis. $he diagnosis rests
on the e%clsion of other ctaneos diseases (especially allergic contact
dermatitis) and on the clinical appearance of dermatitis at a site s'ciently
e%posed to a kno"n ctaneos irritant. (aboratory stdies may be of vale
in eliminating some disorders from the di)erential diagnosis. (*ee +orkp).
$he defnitive treatment of irritant contact dermatitis is the identifcation
and removal of any potential casal agents. Advise individals to se
ceramides creams or bland emollients after "ashing hands "ith soap and
before sleep. (*ee $reatment.)
Althogh the term hypoallergenic is sed "idely in the marketing of
consmer prodcts, no ,ood and Drg Administration-approved defnition
of .hypoallergenic. e%ists. Individals "ith ssceptible skin (eg, atopic
dermatitis, facial skin of individals "ith rosacea) "old beneft greatly
from hypoirritating cleansers, cosmetics, moistri/ers, and protectants, bt
there is no standard method for identifying sch prodcts.
0o to Allergic Contact Dermatitis, 1ediatric Contact Dermatitis, and 1rotein
Contact Dermatitis for complete information on these topics.
Pathophysiology
Irritant contact dermatitis is the clinical reslt of s'cient infammation
arising from the release of proinfammatory cytokines from skin cells
(principally keratinocytes), sally in response to chemical stimli. Di)erent
clinical forms may arise. $he 2 main pathophysiological changes are skin
barrier disrption, epidermal celllar changes, and cytokine release.
+ith s'cient concentration or dration of e%posres, a "ide range of
chemicals can act as ctaneos irritants. Common ctaneos irritants
inclde solvents, microtrama, and mechanical irritants.
Cmlative irritant contact dermatitis from repeated mild skin irritation
from soap and "ater is common. ,or e%ample, hand3"ashing fre4ency of
more than 25 times per shift "as associated strongly "ith occpational
hand dermatitis in intensive care nit "orkers (odds ratio 6 7.82). *imilarly,
most cases of .homemaker9s. ec/ema are irritant contact dermatitis
reslting from repeated skin e%posre to lo"3grade ctaneos irritants,
particlarly soaps, "ater, and detergents.
*olvents case ctaneos irritation becase they remove essential fats and
oils from the skin, "hich increases transepidermal "ater loss and renders
the skin ssceptible to the increased direct to%ic e)ects of other previosly
"ell3tolerated ctaneos e%posres. $he alcohol propanol is less irritating to
the skin than the detergent sodim laryl slfate.
p K
a
, an acid dissociation constant, is a 4antitative measre of the
strength of an acid in soltion. p K
a
has been sho"n to be highly predictive
of acte skin irritation for acids and bases: acids "ith a p K
a
of less than 7
and bases "ith a p K
a
of less than ; are highly irritative.<8=
&icrotrama may prodce skin irritation. A common e%ample is fberglass,
"hich may prodce prrits "ith minimal visible infammation in
ssceptible individals. &any plant leaves and stems bear small spicles
and barbs that prodce direct skin trama.
1hysical irritants (eg, friction, abrasive grains, occlsion) and detergents
sch as sodim laryl slfate prodce more irritant contact dermatitis in
combination than singly.<>= 1ropanol and sodim laryl slfate are not
additive irritants, ho"ever.
*kin irritation predisposes the skin to develop sensiti/ation to topical
agents. *kin irritation by both nonallergenic and allergenic componds
indces (angerhans cell migration and matration.<2= An e%acerbation of
irritant contact dermatitis may refect development of allergic contact
dermatitis to topical creams, medications, or rbber gloves.
$he pathogenesis of irritant contact dermatitis involves resident epidermal
cells, dermal fbroblasts, endothelial cells, and varios lekocytes
interacting "ith each other nder the control of a net"ork of cytokines and
lipid mediators. ?eratinocytes play an important role in the initiation and
perpetation of skin infammatory reactions throgh the release of and
responses to cytokines. @esting keratinocytes prodce some cytokines
constittively.
A variety of environmental stimli (eg, ltraviolet light, chemical agents)
can indce epidermal keratinocytes to release the follo"ing cytokines:
Infammatory cytokines (interlekin 8, tmor necrosis factor3alpha)
Chemotactic cytokines (interlekin ;, interlekin 8A)
0ro"th3promoting cytokines (interlekin B, interlekin C, interlekin 85,
granlocyte3macrophage colony3stimlating factor, transforming
gro"th factor-alpha)
Cytokines reglating hmoral verss celllar immnity (interlekin 8A,
interlekin 8>, interlekin 8;)
Intercelllar adhesion molecle 8 promotes the infltration of lekocytes into
the epidermis in ctaneos infammatory reactions, inclding irritant
contact dermatitis.
*ignifcantly increased nmbers of dividing keratinocytes are present 7;
and DB hors after e%posre to the anionic emlsifying agent sodim laryl
slfate (sed in shampoos, skin cleansers, acne treatments, and
toothpastes and in laboratories as an e%perimental irritant). Eo"ever,
Eeinemann et al fond that repeated occlsive application of A.5F sodim
laryl slfate over 2 "eeks often reslted in adaptation (the so3called
hardening phenomenon), "ith an increase in ceramide 8 in the lipid
composition of the stratm cornem.<7=
All irritants provoke a similar pattern of celllar infltration in the dermis# the
densities of most of the cell types rise in proportion to the intensity of
infammation. +ithin the epidermis, marked di)erences e%ist in the
patterns of celllar infltration among di)erent irritants.
Individals "ith a history of atopic dermatitis are prone to develop irritant
contact dermatitis of the hands. 1olymorphisms in the flaggrin (FLG) gene,
"hich reslt in loss of flaggrin prodction, may alter the skin barrier and
are a predisposing factor for atopic dermatitis. FLG nll alleles are
associated "ith increased ssceptibility to chronic irritant contact
dermatitis.<5=
Etiology
Almost any material may be a ctaneos irritant, if the e%posre is
s'ciently prolonged andGor the concentration of the sbstance s'ciently
high. Hnvironmental factors may enhance the e)ect of other irritants.
Dry air and temperature variation
Dry air renders the skin more ssceptible to ctaneos irritants. *'ciently
dry air alone may provoke irritant contact dermatitis. &ost cases of "inter
itch are a reslt of dry skin from the drier air fond dring sstained periods
of cold "eather.
An increase in temperatre (p to 72IC from >AIC) increases the ctaneos
e)ect of an irritant.<B=
Water
Continal e%posre to "ater may prodce maceration or repeated
evaporation of "ater from the skin may prodce ctaneos irritation by
desiccation of the skin. Hven distilled "ater e%perimentally provokes
increased CD88c
J
cells and netrophils in the epidermis.
Solvents
&any individals are e%posed to solvents, particlarly at "ork. *olvents
sch as alcohol or %ylene remove lipids from the skin, prodcing direct
irritant contact dermatitis and rendering the skin more ssceptible to other
ctaneos irritants, sch as soap and "ater.
Irritant contact dermatitis from alcohol most often is cmlative. &anal
"orkers may "ash their hands inappropriately "ith solvents to remove oil,
grease, paints, or other materials# ths, they develop irritant contact
dermatitis.
Inappropriate skin cleansing is a primary case of irritant contact dermatitis
in the "orkplace. +ashing facilities and methods mst be inspected "hen
investigating the "orkplace for 8 or more cases of occpational irritant
contact dermatitis. $he irritating agents inclde aromatic, aliphatic, and
chlorinated solvents, as "ell as solvents sch as trpentine, alcohol, esters,
and ketones. *ome organic solvents prodce an immediate erythematos
reaction on the skin and remove lipids from the stratm cornem.
Metalworking fuids
!eat oils most commonly prodce folliclitis and acne. $hey may case
irritant contact dermatitis (as "ell as allergic dermatitis). +ater3based
metal"orking fids often case irritant contact dermatitis in e%posed
"orkers# srfactants in these fids are the main clprit.
Cumulative irritant contact dermatitis
$his is common in many occpations that often are termed ."et "ork..
Eealthcare "orkers "ash their hands >A37A times a day, prodcing
cmlative irritant contact dermatitis. *imilar e%posres occr among
individals "ho "ash hair repeatedly or in cleaners or kitchen "orkers.
&ltiple skin irritants may be additive or synergistic in their e)ects. Alcohol3
based hand3cleansing gels case less skin irritation than hand "ashing and
therefore are preferred for hand hygiene from the dermatological point of
vie". An alcohol3based hand3cleansing gel may even decrease, rather than
increase, skin irritation after a hand "ash, o"ing to a mechanical partial
elimination of the detergent.<C=
Microtrauma
,iberglass prodces direct damage to the skin, sally manifested by
prrits that may reslt in e%coriation and secondary skin damage.
Ctaneos irritation primarily is cased by fberglass "ith diameters
e%ceeding 7.5 Km.
Controversy srronds "hether individals "ith dermatographism are more
ssceptible to fberglass dermatitis.
&ost "orkers "ith irritant contact dermatitis reslting from fberglass
develop hardening, in "hich they tolerate frther ctaneos e%posre to
fberglass.
&any plant leaves and stems bear small spicles and barbs that prodce
direct skin trama
Mechanical trauma
1ressre prodces calls formation. 1onding prodces petechia or
ecchymosis. *dden trama or friction prodces blistering in the epidermis.
@epeated rbbing or scratching prodces lichenifcation. *"eating and
friction appear to be the main case of dermatitis that appears nder
soccer shin gards in children.<;=
Ruer gloves
*ome rbber gloves may provoke direct ctaneos irritation. &any "orkers
complain of irritation from the po"der in rbber gloves.
@emember that gloves compromised by a hole may allo" an irritant to
enter# occlsion dramatically increases skin damage from the irritant.
Lcclsion accentates the e)ects, good or bad, of topical agents. ?erosene
may prodce skin changes similar to that of to%ic epidermal necrolysis
follo"ing occlded ctaneos e%posre. H%cessive amonts of ethylene
o%ide in srgical sheets also may prodce similar changes.
Sodium lauryl sul!ate
$his chemical is fond in some topical medications, particlarly acne
medications, as "ell as a range of soaps and shampoos. It is also a classic
e%perimental ctaneos irritant.
"ydrofuoric acid
A hydroforic acid brn is a medical emergency. @emember that onset of
clinical manifestations may be delayed after the acte e%posre (this is
crcial to diagnosis). Mnfortnately, hydroforic acid brns are most
fre4ent on the digits, "here the pain is most severe and management is
most di'clt (see Eydroforic Acid Nrns).
#lkalies
*kin srfaces normally have an acidic pE, and alkalies (eg, many soaps)
prodce more irritation than many acids. $he .acid mantle. of the stratm
cornem seems to be important for both permeability barrier formation and
ctaneos antimicrobial defense. Mse of skin cleansing agents, especially
synthetic detergents "ith a pE of appro%imately 5.5 rather than alkaline pE,
may help prevent skin disease.<D=
Epidemiology
$nited States statistics
Irritant contact dermatitis is common in occpations that involve repeated
hand "ashing or repeated e%posre of the skin to "ater, food materials,
and other irritants. Eigh3risk occpations inclde cleaning, hospital care,
food preparation, and hairdressing.
$he prevalence of occpational hand dermatitis "as fond to be 55.BF in >
intensive care nits and "as BD.CF in the most highly e%posed "orkers.
Eand3"ashing fre4ency of more than 25 times per shift "as associated
strongly "ith occpational hand dermatitis.<8A=
%nternational statistics
In Denmark, cleaners comprise the greatest nmber of a)ected "orkers,
bt clinary "orkers have the highest incidence. A higher proportion of
prolonged sick leave is seen among those in food3related occpations
compared "ith those in "et occpations.<88=
$he incidence rates of contact dermatitis in 0ermany "ere 7.5 per 8A,AAA
"orkers for irritant contact dermatitis, compared "ith 7.8 per 8A,AAA
"orkers for allergic contact dermatitis. $he highest irritant contact
dermatitis annal incidence rates "ere fond in hairdressers (7B.D cases
per 8A,AAA "orkers per year), bakers (>2.5 cases per 8A,AAA "orkers per
year), and pastry cooks (8B.D cases per 8A,AAA "orkers per year.<8>=
Se&ual di'erences in incidence
Irritant contact dermatitis is signifcantly more common in "omen than in
men. $he high fre4ency of hand ec/ema in "omen in comparison "ith
men is cased by environmental factors, not genetic factors.
Lccpational irritant contact dermatitis a)ects "omen almost t"ice as
often as men, in contrast to other occpational diseases that predominantly
a)ect men. +omen are e%posed more highly to ctaneos irritants from
their disproportionately greater role in hosecleaning and the care of small
children at home. In addition, "omen predominantly perform many
occpations at high risk for irritant contact dermatitis (eg, hairdressing,
nrsing).
#ge(related di'erences in incidence
Irritant contact dermatitis may occr at any age. &any cases of diaper
dermatitis are irritant contact dermatitis reslting from direct skin irritants
present in rine and, especially, feces. Llder persons have drier and thinner
skin that does not tolerate soaps and solvents as "ell as yonger
individals. Lccpational hand ec/ema often is associated "ith persistent
dermatitis and prolonged sick leave, "ith sbstantially greater severity
among those "ith occpational irritant contact dermatitis and atopic
dermatitis and age older than 5A years.
Prognosis
1rognosis is good for nonatopic individals in "hom irritant contact
dermatitis is diagnosed and managed promptly. Individals "ith atopic
dermatitis remain highly ssceptible to irritant contact dermatitis and may
fnd that the tasks of many common occpations (eg, nrsing, hairdressing)
prodce too mch direct skin infammation to contine "ith these careers.
Eardening may be specifc to the irritant indcing the hardening
phenomenon and does not occr in all persons e%posed long term to an
irritant.<8= Eardened skin may also have a thickened stratm granlosm,
"ith changes in the e%pression of varios infammatory mediators and
markers.<8= An indction of an increase in the stratm cornem lipid
ceramide 8 may play a key role as a protection mechanism against irritation
by repeated application of sodim laryl slfate.<>, 7=
Activities of daily living and "ork may be redced by severe irritant contact
dermatitis.
Acte irritant contact dermatitis reactions to potent irritants (eg, acids,
alkaline soltions) are comparable to a chemical brn and can be graded
like thermal brns (ie, frst3, second3, or third3degree brns). +ith
appropriate symptomatic management, the prognosis for this type of
irritant contact dermatitis is sally good, and, nless the dermis is
damaged, no permanent scarring shold occr. *ee Chemical Nrns for
more information.
Mortality
Eydroforic acid is a potent ctaneos irritant sed in lo"3technology and
high3technology indstries and at home in rst removal.<82= Death from
hypocalcemia may ense if as little as 8F of the skin9s srface area is
e%posed s'ciently to this strong inorganic acid and if complications are
not managed optimally (see Eydroforic Acid Nrns).
Patient Education
@emind individals that they mst contine to avoid ctaneos irritants#
they "ill redevelop or aggravate dermatitis if they contine to have the
same skin care e%posres that reslted in irritant contact dermatitis. $he
possibility of secondary or complicating allergic contact dermatitis al"ays
mst be borne in mind.
,or patient edcation information, see the *kin, Eair, and !ails Center, as
"ell as Contact Dermatitis.
Proceed to Clinical Presentation"istory
A detailed history is re4ired becase the diagnosis of irritant contact
dermatitis rests on the history of e%posre of the a)ected body site to the
ctaneos irritant. 1atch testing also is sed in severe or persistent cases to
e%clde allergic contact dermatitis as a component of the individal9s
ctaneos manifestations.
Lnset of symptoms occrs "ithin mintes to hors of e%posre in simple
acte irritant contact dermatitis. Acte delayed irritant contact dermatitis is
characteristic of certain irritants, sch as ben/alkonim chloride (eg,
/ephiran, a preservative and disinfectant), "hich elicits a deferred (;3>7 h
after e%posre) infammatory reaction.<87=
$he onset of signs and symptoms may be delayed by "eeks in cmlative
irritant contact dermatitis. Cmlative irritant contact dermatitis is a
conse4ence of mltiple incidents of sbthreshold damage to the skin, "ith
the time bet"een e%posres being too short for a fll resoltion of skin
barrier fnction. 1atients "ith sensitive skin (ie, atopic individals) have a
decreased irritant threshold or a prolonged restoration time, making them
more vlnerable to clinical irritant contact dermatitis.
Cmlative irritant contact dermatitis typically occrs "ith e%posre to
"eak irritants rather than strong ones. Lften, the e%posre (eg, "ater) is
not only at "ork bt also at home.
$hese patients report both itching and pain cased by fssring of the
hyperkeratotic skin (chapping). 1ain, brning, stinging, or discomfort
e%ceeding prrits occr early in the clinical corse.
(ess important sbOective criteria for irritant contact dermatitis inclde the
onset of dermatitis "ithin > "eeks of e%posre, and reports of many other
co"orkers or family members a)ected.
)ccupational history
Irritant contact dermatitis is a maOor occpational disease# skin disorders
comprise p to 7AF of occpational illnesses. $he physician needs to take
an occpational history from adlts "ith sspect irritant contact dermatitis.
Lccpational irritant contact dermatitis typically a)ects "orkers "ho are
ne" to a Oob, "ho are constittionally more ssceptible to irritant contact
dermatitis, or "ho have not learned to protect their skin from ctaneos
irritants. Individals "ith history of atopic dermatitis (especially of the
hands) are more ssceptible to irritant contact dermatitis, particlarly of the
hands.
&ost a)ected "orkers have a degree of permanent inOry that is lo"er than
that of other occpational diseases# ho"ever, the compensation pay "as
higher for skin diseases than for diseases of the respiratory system or
mscloskeletal disorders, according to a stdy in Denmark.
Physical E&amination
@ietschel and ,o"ler proposed the follo"ing as primary diagnostic criteria
for irritant contact dermatitis<85= :
&aclar erythema, hyperkeratosis, or fssring predominating over
vesiclation
0la/ed, parched, or scalded appearance of the epidermis
Eealing process beginning promptly on "ithdra"al of e%posre to the
o)ending agent
!egative reslts on patch testing that incldes all possible allergens
&inor obOective criteria for irritant contact dermatitis inclde the follo"ing:
*harp circmscription of the dermatitis
Hvidence of gravitational infence sch as a dripping e)ect
(o"er tendency for the dermatitis to spread than in cases of allergic contact
dermatitis
&orphologic changes sggesting small di)erences in concentration or
contact time prodcing large di)erences in skin damage
Individals may develop a habit of contining to rb a site initially a)ected
by irritant contact dermatitis and may develop secondary nerodermatitis
or lichen simple% chronics (lichenifcation). $his may be accepted as a
se4ela of an occpational inOry.
Complications
*kin lesions may become coloni/ed secondarily andGor infected, particlarly
by Staphylococcus aureus. *econdary nerodermatitis (lichen simple%
chronics) may develop in individals "ith irritant contact dermatitis,
particlarly in those "ith "orkplace e%posres or nder psychological
stress.
1ostinfammatory hyperpigmentation or hypopigmentation may occr in
areas a)ected by irritant contact dermatitis or persist after resoltion of
irritant contact dermatitis in individals "ith more pigmented skin.
*carring may occr after corrosive agent e%posre, e%coriation, or artifact,
casing lceration.
Irritant contact dermatitis increases the risk of sensiti/ation to topical
medications.
Proceed to Di'erential Diagnoses
Diagnostic Considerations
Lther cases of contact dermatitis mst be e%clded. Hlements of the
history andGor patch testing to relevant allergens can identify allergic
contact dermatitis. *cabies may resemble fberglass dermatitis.
Di'erential Diagnoses
Atopic Dermatitis
Dermatologic &anifestations of @enal Disease
Dermatologic &anifestations of *cabies
Drg Hrptions
Hrysipelas
Hrythema Infectiosm (,ifth Disease)
Id @eaction (Atoec/emati/ation)
(ichen *imple% Chronics
1erioral Dermatitis
1hytophotodermatitis
*eborrheic Dermatitis
#pproach Considerations
!o diagnostic test e%ists for irritant contact dermatitis. $he diagnosis rests
on the e%clsion of other ctaneos diseases (especially allergic contact
dermatitis) and on the clinical appearance of dermatitis at a site s'ciently
e%posed to a kno"n ctaneos irritant. (aboratory stdies are generally of
little vale in proving a diagnosis of contact dermatitis. Eo"ever, they may
be of vale in eliminating some disorders from the di)erential diagnosis.
,indings of signifcantly elevated serm immnogloblin H occasionally are
sefl to sbstantiate an atopic diathesis in the absence of a personal or
family history of atopy.
0o to Allergic Contact Dermatitis, 1ediatric Contact Dermatitis, and 1rotein
Contact Dermatitis for complete information on these topics.
Bacterial and *ungal Studies
A bacterial cltre can be obtained in cases complicated by secondary
bacterial infection. A potassim hydro%ide (?LE) e%amination of scrapings
may be performed and samples for mycology may be obtained to e%clde
sperfcial tinea infections or candidal infections, depending on site and
morphology of lesions.
Patch +esting
1atch testing can be performed to diagnose contact allergies, bt no patch
test e%ists that proves that a ctaneos irritant is responsible for a
particlar case of irritant contact dermatitis. Diagnosis rests on e%clsion of
allergic contact dermatitis and history of s'cient e%posre to a ctaneos
irritant. Also see the follo"ing smmaries of clinical gidelines from the
Point Concil of Allergy, Asthma and Immnology:
Allergy diagnostic testing: an pdated practice parameter. 1art 8 <8B=
Allergy diagnostic testing: an pdated practice parameter. 1art > <8C=
Skin Biopsy
*kin biopsy can help e%clde other disorders, sch as tinea, psoriasis, or
ctaneos $3cell lymphoma. All clinical cases of dermatitis are similar
histologically.
*kin biopsy of skin lesions of the palms and soles has several potential
pitfalls. $he stratm cornem and epidermis are particlarly thick there,
"hich makes the histologic diagnosis of psoriasis more di'clt and
increases the possibility that the specimen lacks s'cient dermis for
optimal diagnosis. In the thenar area, an overly deep biopsy can ct the
recrrent branch of the median nerve. A biopsy from the sole may leave a
chronic painfl scar on "hich the patient mst "alk. A saceri/ed shave
biopsy is sally the most sitable method.
Direct Microscopy
*kin scrapings of ctaneos lesions may help e%clde scabies or may reveal
fberglass fbers as a case of a patient9s prrits.
"istologic *indings
$he histopathology of acte e%perimental irritant contact dermatitis has
been stdied to a greater e%tent than chronic irritant contact dermatitis,
"hich is the primary clinical complaint. Celllar changes seen in the skin
vary according to the chemical natre and concentration of the irritant
applied, dration of e%posre, severity of ensing response, and time of
sampling for acte irritant contact dermatitis. &any primary irritants case
overt necrosis if applied in a s'ciently high concentration for s'cient
time.
&ost histologic e%aminations of irritant contact dermatitis reveal some
degree of intercelllar edema or spongiosis in the epidermis. *pongiosis
sally is less prononced than that seen in allergic contact dermatitis
reactions.
1arakeratosis also is observed "idely in irritant contact dermatitis reactions.
$he histology of chronic irritant contact dermatitis is one of hyperkeratosis
"ith areas of parakeratosis, moderate3to3marked epidermal hyperplasia
(acanthosis), and elongation of the rete ridges.
Proceed to +reatment , Management
Emergency Department Care
Hmergency department treatment may inclde the follo"ing:
$opical soaks "ith cool tap "ater, Nro" soltion (8:7A diltion), saline (8
tspGpint)
(ke"arm "ater baths (antiprritic)
Aveeno (oatmeal) lke"arm baths
Hmollients (eg, "hite petrolatm, Hcerin) may be benefcial chronic cases.
(arge vesicles may beneft from therapetic drainage (bt not removing the
vesicle tops).<8= $hese lesions shold then be covered "ith antibiotic
dressing or a dressing soaked in Nro" soltion.
Eospital admission is re4ired only in severe ctaneos irritant contact
dermatitis, ie, chemical brns from hydroforic acid or, occasionally, from
freshly mi%ed 1ortland cement.
Barrier Creams
Creams containing ceramides (eg, Imprv, Cerave) may be particlarly
helpfl in restoring the epidermal barrier in persons "ith irritant contact
dermatitis and atopic dermatitis. Creams containing dimethicone (eg,
Cetaphil cream) can be helpfl in restoring the epidermal barrier in persons
"ith "et "ork-related irritant contact dermatitis.
Cleansers
&ost soaps and detergents are alkaline and indce an increase in
ctaneos pE, "hich a)ects the physiologic protective acid mantle of the
skin by decreasing the fat content. Disrption of stratm cornem and
changes in pE are key elements in the indction of irritant contact
dermatitis and prrits by soaps. $hese conditions are e%acerbated in the
"inter months in patients "ith dry, sensitive skin.
*yndets, "ith a pE appro%imately 5.5, do not modify skin pE. &ost bar
soaps and li4id detergents available on the market are a mi%tre of soap
and syndet. A stdy fond that Dove and Cetaphil had a lo"er irritant e)ect
than the other soaps tested. Interestingly, no signifcant correlation "as
made bet"een the price of the prodcts and their irritation potential.
Irritant contact dermatitis is a fre4ent problem in health care "orkers, de
to fre4ent hand "ashing. $he best antimicrobial e'cacy can be achieved
"ith ethanol (BA3;5F), isopropanol (BA3;AF), and N 3propanol (BA3;AF).
$he antimicrobial e'cacy of chlorhe%idine (>37F) and triclosan (83>F) is
both lo"er and slo"er and carries a potential risk of bacterial resistance.
$he se of alcohol3based hand rbs containing varios emollients instead of
irritating soaps and detergents is one strategy to redce skin damage,
dryness, and irritation in health care "orkers. Irritant contact dermatitis
occrs most fre4ently "ith preparations containing 7F chlorhe%idine
glconate, less fre4ently "ith nonantimicrobial soaps and preparations
containing lo"er concentrations of chlorhe%idine glconate, and least
fre4ently "ith "ell3formlated alcohol3based hand rbs containing
emollients and other skin conditioners.
#pproach Considerations
$he defnitive treatment of irritant contact dermatitis is the identifcation
and removal of any potential casal agents. An infammatory reaction from
acte delayed irritant contact dermatitis to an agent sch as ben/alkonim
chloride (eg, /ephiran) rarely needs treatment and sally resolves "ith
cessation of e%posre. ,rther symptomatic therapy depends on the degree
of involvement and the presence or absence of secondary infection.
Advise individals to se ceramides creams or bland emollients after
"ashing hands "ith soap and before sleep. Cleansers may be ranked by
their irritancy.<8;= @ecommend mild skin cleansers (eg, A4anil, Cetaphil
cleanser, Lilatm AD, !etrogena cleanser) in place of soap on a)ected
areas. Instrct individals to refrain from the se of inappropriate solvents
(eg, gasoline) or abrasives (eg, pmice stone) to cleanse hands# these
directly defat or tramati/e the skin.
A clinical gideline smmary from the American Academy of Allergy,
Asthma and Immnology, Contact Dermatitis: A 1ractice 1arameter, may be
helpfl.<8D=
0o to Allergic Contact Dermatitis, 1ediatric Contact Dermatitis, and 1rotein
Contact Dermatitis for complete information on these topics.
Steroids and %mmunomodulators
$opical corticosteroids and immnomodlators are of nproven se in
treating irritant contact dermatitis. Corticosteroids "ere fond ine)ective in
treating the srfactant3indced irritant dermatitis "hen compared "ith the
vehicle and "ith the ntreated control.<>A= Eo"ever, topical steroids may be
helpfl for sperimposed ec/ematos featres.
1otential complications center on the se of steroids, particlarly arond
the eye. $he avoidance of long3term steroid se is essential, becase sch
se may case cataracts, glacoma, corneal thinningGperforation, and loss
of the eye, as "ell as other problems.
$opical tacrolims is an irritant that may prodce frther stinging and
irritation in persons "ith irritant contact dermatitis.<>8=
Consultations
&ltidisciplinary consltations may be re4ired "hen many "orkers
become a)ected "ith irritant contact dermatitis in a "orkplace. Identifying
and remediating the cases of "idespread irritant contact dermatitis
interfering "ith "orkplace prodctivity and "orker 4ality of life is
important.
Any patient "ith hydroforic acid brn shold be evalated as a medical
emergency by a physician e%perienced in the management of hydroforic
e%posres and brns. Consider regional intravenos infsion of calcim
glconate as a therapetic option in hydroforic acid brns to forearm,
hand, or digits "hen topical therapy fails.
Proceed to Medication
Medication Summary
After the identifcation and removal of any potential casal agents, the se
of ceramides creams or bland emollients and bland barrier creams sch as
those containing dimethicone are the mainstays of medical treatment for
irritant contact dermatitis.
A nmber of agents commonly fond in therapetic prodcts for the skin
(eg, propylene glycol, lactic acid, rea, salicylic acid) may prodce frther
skin infammation and may need to be avoided in these individals. $opical
corticosteroids play a limited role in the treatment of irritant contact
dermatitis. $hey do not address the process directly, bt they may be
helpfl for sperimposed ec/ematos featres.
Corticosteroids- topical
Class Summary
Corticosteroids are immnosppressives "ith anti3infammatory properties
that modify the body9s immne response to diverse stimli. Lther actions
inclde vasoconstriction and antiproliferation. $hese agents have limited
se in the treatment of irritant contact dermatitis.
Qie" fll drg information
#mcinonide

A highly potent, forinated corticosteroid (class >32), amcinonide
sppresses mitotic activity and cases vasoconstriction. It stimlates
synthesis of en/ymes needed to decrease infammation and may sppress
histamine release associated "ith prrits.
Qie" fll drg information
*luocinolone .Cape&- Derma(Smoothe/*S0

,locinolone is a forinated corticosteroid of mid potency at the A.A>5F
concentration (class 735) and mild potency at the A.A8F concentration
(class B).
Practice Essentials
Individals "ith allergic contact dermatitis may have persistent or relapsing
dermatitis, particlarly if the material(s) to "hich they are allergic is not
identifed or if they practice inappropriate skin care. $he longer an
individal has severe dermatitis, the longer, it is believed, that the
dermatitis "ill take to resolve once the case is identifed.
Essential update1 #llergic contact dermatitis caused y non(late&
ruer gloves
In a stdy of srgery personnel in *"eden "ith occpational allergic contact
dermatitis, 1ontRn et al fond evidence that the condition "as cased by
8,23diphenylganidine (8,23D10) in non3late% rbber gloves.<8= Msing patch
tests, the investigators fond that 8> of 8B patients reacted to 8,23D10. $he
8,23D10 "as present in the gloves "orn by the patients in the stdy, "ith a
higher concentration on the inside of the gloves than on the otside. In C of
; patients, contact allergy to cetylpyridinim chloride "as also fond<8=
Signs and symptoms
Acte allergic contact dermatitis is characteri/ed by prritic paples and
vesicles on an erythematos base. (ichenifed prritic pla4es may indicate
a chronic form of the condition.
Individals "ith allergic contact dermatitis typically develop the condition
"ithin a fe" days of e%posre, in areas that "ere e%posed directly to the
allergen. Certain allergens (eg, neomycin), ho"ever, penetrate intact skin
poorly# in sch cases, the onset of dermatitis may be delayed for p to a
"eek follo"ing e%posre.
Individals may develop "idespread dermatitis from topical medications
applied to leg lcers or from cross3reacting systemic medications
administered intravenosly.
Intraoral metal contact allergy may reslt in mcositis that mimics lichen
plans, "hich has an association "ith intraoral s4amos cell carcinoma.
*ee Clinical 1resentation for more detail.
Diagnosis
Diagnostic stdies for allergic contact dermatitis inclde the follo"ing:
1otassim hydro%ide preparation andGor fngal cltre: $o e%clde tinea#
these tests are often indicated for dermatitis of the hands and feet
1atch testing: $o identify e%ternal chemicals to "hich the person is allergic
@epeat open application test (@LA$): $o determine "hether a reaction is
signifcant in individals "ho develop "eak or 8J positive reactions to
a chemical
Dimethylglo%ime test: $o determine "hether a metallic obOect contains
enogh nickel to provoke allergic dermatitis
*kin biopsy: &ay help to e%clde other disorders, particlarly tinea,
psoriasis, and ctaneos lymphoma
*ee +orkp for more detail.
Management
$he defnitive treatment for allergic contact dermatitis is the identifcation
and removal of any potential casal agents# other"ise, the patient is at
increased risk for chronic or recrrent dermatitis. $reatments also inclde
the follo"ing:
Corticosteroids: $opical corticosteroids are the mainstay of treatment,
althogh acte, severe allergic contact dermatitis, sch as from
poison ivy, often needs to be treated "ith a >3"eek corse of systemic
corticosteroids
$opical immnomodlators ($I&s): Approved for atopic dermatitis, bt they
are also prescribed for cases of allergic contact dermatitis "hen they
o)er safety advantages over topical corticosteroids
1hototherapy: Administered to individals "ith chronic allergic contact
dermatitis that is not controlled "ell by topical corticosteroids# these
patients may beneft from treatment "ith a combination of psoralen (a
photosensiti/er) and ltraviolet3A (1MQA)
Immnosppressive agents: Chronic immnosppressive agents are, in rare
instances, sed 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
Dislfram: Lccasionally, an individal "ho is highly allergic to nickel and
has severe vesiclar hand dermatitis "ill beneft from treatment "ith
dislfram (Antabse)# the drg has a chelating e)ect
*ee $reatment and &edication for more detail.
%mage lirary
Chronic stasis dermatitis "ith allergic contact dermatitis to 4aternim385, a preservative
in moistri/er. Allergic contact dermatitis prodces areas of erythema in areas of atrophie
blanche and varicose veins.
Background
Allergic contact dermatitis (ACD) is a delayed type of indced sensitivity
(allergy) reslting from ctaneos contact "ith a specifc allergen to "hich
the patient has developed a specifc sensitivity. $his allergic reaction cases
infammation of the skin manifested by varying degrees of erythema,
edema, and vesiclation.
$he term contact dermatitis sometimes is sed incorrectly as a synonym for
allergic contact dermatitis. Contact dermatitis is infammation of the skin
indced by chemicals that directly damage the skin (see Irritant Contact
Dermatitis) and by specifc sensitivity in the case of allergic contact
dermatitis.
Padassohn frst described allergic contact dermatitis in 8;D5. Ee developed
the patch test to identify the chemicals to "hich the patient "as allergic.
*l/berger poplari/ed patch testing in the Mnited *tates in the 8D2As. $he
,inn chamber method for patch testing "as designed in the 8DCAs# these
chambers consist of small metal cps, typically attached to strips of tape,
flled "ith allergens dispersed in either petrolatm or "ater. $he thin3layer
rapid se epictaneos ($@MH) test for patch testing became available in
the Mnited *tates in the 8DDAs.
$he importance of specifc sbstances as cases of allergic contact
dermatitis varies "ith the prevalence of that sbstance in the environment.
&ercry componds once "ere signifcant cases of allergic contact
dermatitis bt rarely are sed as topical medications and, crrently, are
ncommon as a case of allergic contact dermatitis. Hthylenediamine,
"hich "as present in the original &ycolog cream, declined as a primary
case of allergic contact dermatitis once &ycolog cream "as reformlated
to no longer contain this allergen.
A detailed history, both before and after patch testing, is crcial in
evalating individals "ith allergic contact dermatitis. Nefore patch testing,
the history identifes potential cases of allergic contact dermatitis and the
materials to "hich individals are e%posed that shold be inclded in patch
testing. After patch testing, the history determines the clinical signifcance
of the fndings. (*ee Clinical.)
$opical corticosteroids are the mainstay of treatment, "hile a variety of
symptomatic treatments can provide short3term relief of prrits. Eo"ever,
the defnitive treatment of allergic contact dermatitis is the identifcation
and removal of any potential casal agents# other"ise, the patient is at
increased risk for chronic or recrrent dermatitis. (*ee $reatment.)
0o to Irritant Contact Dermatitis, 1ediatric Contact Dermatitis, and 1rotein
Contact Dermatitis for complete information on these topics.
Pathophysiology
Appro%imately 2AAA chemicals are "ell docmented as specifc cases of
allergic contact dermatitis. &ost of the chemicals able to provoke allergic
contact dermatitis are small molecles (S 5AA d). $hese molecles mst
bind to carrier proteins on (angerhans cells, "hich are sitated "ithin the
sprabasilar layer of the epidermis.
(angerhans cells are the antigen3presenting cells "ithin the skin.
(angerhans cells interact "ith CD7
J
$ cells (helper $ cells). *kin irritation by
both nonallergenic and allergenic componds indces (angerhans cell
migration and matration. In contrast, only allergenic componds indce
CD8a
J
CD;2
J
(angerhans cell migration "ith partial matration at sbto%ic
concentrations.<>=
Cytokines also play an important role in allergic contact dermatitis becase
they reglate accessory3adhesion molecles, sch as intercelllar adhesion
molecle 8. Interlekin ; 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 re4ires intact lymphatic
path"ays.
$he initial sensiti/ation typically takes 8A387 days from initial e%posre to a
strong contact allergen sch as poison ivy. *ome individals develop
specifc sensitivity to allergens follo"ing years of chronic lo"3grade
e%posre# for e%ample, sensitivity to chromate in cement can eventally
develop in individals "ith chronic irritant contact dermatitis reslting from
the alkaline natre of cement. Lnce an individal is sensiti/ed to a
chemical, allergic contact dermatitis develops "ithin hors to several days
of e%posre.
CD7
J
CC@8A
J
memory $ cells persist in the dermis after clinical resoltion
of allergic contact dermatitis.
,ilaggrin barrier defects that predispose individals to atopic dermatitis
might also predispose them to allergic contact dermatitis by allo"ing
greater penetration of chemical haptens.<2=
Etiology
Appro%imately >5 chemicals appear to be responsible for as many as one
half of all cases of allergic contact dermatitis. $hese inclde nickel,
preservatives, dyes, and fragrances.
Poison ivy
1oison ivy (Toxicodendron radicans) is the classic e%ample of acte allergic
contact dermatitis in !orth America. Allergic contact dermatitis from poison
ivy is characteri/ed by linear streaks of acte dermatitis that develop "here
plant parts have been in direct contact "ith the skin.
2ickel
!ickel is the leading case of allergic contact dermatitis in the "orld. $he
incidence of nickel allergic contact dermatitis in !orth America is
increasing# in contrast, ne" reglations in Hrope have reslted in a
decreasing prevalence of nickel allergy in yong and middle3aged "omen.
<7, 5=
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 obOects (inclding the keypads of some cell
phones<B= ) containing nickel are in contact "ith the skin.
!ickel may be considered a possible occpational allergen. +orkers in
"hom nickel may be an occpational allergen primarily inclde
hairdressers, retail clerks, caterers, domestic cleaners, and metal"orkers.
Individals allergic to nickel occasionally may develop vesicles on the sides
of the fngers (dyshidrotic hand ec/ema or pompholy%) from nickel in the
diet.
Allergic contact dermatitis to nickel in a necklace.
Ruer gloves
Allergy to 8 or more chemicals in rbber gloves is sggested in any
individal "ith chronic hand dermatitis "ho "ears them, nless patch
testing demonstrates other"ise. Allergic contact dermatitis to chemicals in
rbber gloves typically occrs ma%imally on the dorsal aspects of the hand.
Msally, a cto) of dermatitis occrs on the forearms "here skin is no
longer in contact "ith the gloves. Individals allergic to chemicals in rbber
gloves may develop dermatitis from other e%posres to the chemicals (eg,
nder elastic "aistbands).
"air dye and temporary tattoos
p31henylenediamine (11D) is a fre4ent component of and sensiti/er in
permanent hair dye prodcts and temporary henna tattoos<C= # e%posre in
to it in hair dye prodcts may case acte dermatitis "ith severe facial
edema. *evere local reactions from 11D may occr in black henna tattoos
in adlts and children. Hpidemiologic data indicate that the median
prevalence of positive patch test reactions to 11D among dermatitis
patients is 7.2F (increasing) in Asia, 7F (platea) in Hrope, and B.>F
(decreasing) in !orth America.<;=
+e&tiles
Individals allergic to dyes and permanent press and "ash3and3"ear
chemicals added to te%tiles typically develop dermatitis on the trnk, "hich
occrs ma%imally on the lateral sides of the trnk bt spares the valt of
the a%illae. 1rimary lesions may be small folliclar paples or may be
e%tensive pla4es.
Individals in "hom this allergic contact dermatitis is sspected shold be
tested "ith a series of te%tile chemicals, particlarly if rotine patch testing
reveals no allergy to formaldehyde. !e" clothing is most likely to provoke
allergic contact dermatitis, since most allergens decrease in concentration
in clothing follo"ing repeated "ashings.
Preservatives
1reservative chemicals added to cosmetics, moistri/ers, and topical
medications are maOor cases of allergic contact dermatitis (see the image
belo"). $he risk of allergic contact dermatitis appears to be highest to
4aternim385, follo"ed by allergic contact dermatitis to isothia/olinones
(?athon C0). Althogh parabens are among the most "idely sed
preservatives, they are not a fre4ent case of allergic contact dermatitis.
*evere allergic contact dermatitis reslting from preservatives in snscreen. 1atch testing
"as negative to the active ingredients in the snscreen.
*chnch et al estimated that preservatives fond in leave3on topical
prodcts varied over > orders of magnitde in relative sensiti/ation risk.<D=
,ormaldehyde is a maOor case of allergic contact dermatitis (see the image
belo"). Certain preservative chemicals "idely sed in shampoos, lotions,
other moistri/ers, and cosmetics are termed formaldehyde releasers (ie,
4aternim385 <Do"icil >AA=, imida/olidinyl rea <0ermall 885=, and
isothia/olinones<D= ).
Lnycholysis developing from allergic contact dermatitis to formaldehyde sed to harden
nails.
*ragrances
Individals may develop allergy to fragrances. ,ragrances are fond not
only in perfmes, colognes, aftershaves, deodorants, and soaps, bt also in
nmeros other prodcts, often as a mask to camofage an npleasant
odor. Mnscented prodcts may contain fragrance chemicals sed as a
component of the prodct and not labeled as fragrance.
Individals allergic to fragrances shold se fragrance3free prodcts.
Mnfortnately, the e%act chemicals responsible for a fragrance in a prodct
are not labeled. ,or thosand di)erent fragrance molecles are available
to formlate perfmes. $he fragrance indstry is not re4ired to release the
names of ingredients sed to compose a fragrance in the Mnited *tates,
even "hen individals develop allergic contact dermatitis to fragrances
fond in topical medications.
Deodorants may be the most common case of allergic contact dermatitis
to fragrances becase they are applied to occlde skin that is often
abraded by shaving in "omen.
&assage and physical therapists and geriatric nrses are at higher risk of
occpational allergic contact dermatitis to fragrances.
Corticosteroids
In the last decade, it has become clear that some individals "ith chronic
dermatitis develop allergy to topical corticosteroids. &ost a)ected
individals can be treated "ith some topical corticosteroids, bt an
individal can be allergic to all topical and systemic corticosteroids.
Ndesonide and ti%ocortol pivalate are sefl patch test corticosteroids for
identifying individals allergic to topical corticosteroids.
2eomycin
$he risk of allergy to neomycin is related directly to the e%tent of its se in
a poplation. $he risk of allergy to neomycin is mch higher "hen it is sed
to treat chronic stasis dermatitis and venos lcers than "hen it is sed as
a topical antibiotic on cts and abrasions in children. Assme that
individals allergic to neomycin are allergic to chemically related
aminoglycoside antibiotics (eg, gentamicin, tobramycin).<8A= Avoid these
drgs both topically and systemically in individals allergic to neomycin.
Ben3ocaine
Avoid topical se of ben/ocaine. Nen/ocaine is inclded in most standard
patch test trays. Individals allergic to ben/ocaine may safely se or be
inOected "ith lidocaine (Tylocaine), "hich does not cross3react "ith
ben/ocaine.
&any individals complain of adverse reactions to snscreens, bt many of
these individals are not allergic to the snscreen materials. $hey may be
allergic to preservatives in these prodcts or may have nonspecifc
ctaneos irritation from these prodcts.
Photoallergy
Lccasionally, individals develop photoallergic contact dermatitis. Allergic
contact dermatitis may be accentated by ltraviolet (MQ) light, or patients
may develop an allergic reaction only "hen a chemical is present on the
skin and "hen the skin is e%posed s'ciently to ltraviolet light A (MQ3A#
2>A37AA nm).
Epidemiology
$nited States statistics
$he !ational Eealth and !trition H%amination *rvey (!EA!H*) estimated
the prevalence of contact dermatitis to be 82.B cases per 8AAA poplation,
sing physical e%aminations by dermatologists of a selected sample of
patients. !EA!H* nderreported the prevalence compared "ith the
physical e%amination fndings.
$he !ational Amblatory &edical Care *rvey condcted in 8DD5 estimated
;.7 million otpatient visits to American physicians for contact dermatitis.
$his "as the second most fre4ent dermatologic diagnosis. Lf o'ce visits
to dermatologists, DF are for dermatitis. At a stdent health center
dermatology clinic, 2.8F of patients presented for allergic contact
dermatitis, and >.2F presented for irritant contact dermatitis.
$he $@MH test +eb site can provide accrate basic information on common
allergens. $he Contact Allergen &anagement 1rogram is provided as a
service to the American Contact Dermatitis *ociety (ACD*) members and is
particlarly valable for allergens fond in topical skin care prodcts. $he
Contact Allergen @eplacement Database (CA@D) contains more than ;8AA
kno"n ingredients cataloged in more than 55AA commercial skincare
prodcts and is available as a *martphone application.
%nternational statistics
A *"edish stdy fond that prevalence of allergic contact dermatitis of the
hands "as >.C cases per 8AAA poplation. A Dtch stdy fond that
prevalence of allergic contact dermatitis of the hands "as 8> cases per
8AAA poplation.
Race- se&- and age(related demographics
!o racial predilection e%ists for allergic contact dermatitis. Allergic contact
dermatitis is more common in "omen than in men. $his predominantly is a
reslt of allergy to nickel, "hich is mch more common in "omen than in
men in most contries.
Allergic contact dermatitis may occr in neonates. In elderly individals, the
development of allergic contact dermatitis may be delayed some"hat, bt
the dermatitis may be more persistent once developed. Contact allergy to
topical medicaments is more common in persons older than CA years.<88=
Prognosis
Individals "ith allergic contact dermatitis may have persistent or relapsing
dermatitis, particlarly if the material(s) to "hich they are allergic is not
identifed or if they contine to practice skin care that is no longer
appropriate (ie, they contine to se harsh chemicals to "ash their skin,
they do not apply creams "ith ceramides or bland emollients to protect
their skin).
$he longer an individal has severe dermatitis, the longer it is believed it
"ill take the dermatitis to resolve once the case is identifed.
*ome individals have persistent dermatitis follo"ing allergic contact
dermatitis, "hich appears to be tre especially in individals allergic to
chrome.
A particlar problem is nerodermatitis (lichen simple% chronics), in "hich
individals repeatedly rb or scratch an area initially a)ected by allergic
contact dermatitis.
Mortality
Death from allergic contact dermatitis is rare in the Mnited *tates. Allergic
contact dermatitis to the "eed "ild feverfe" cased deaths in India "hen
the seeds contaminated "heat shipments to India. $his plant then became
"idespread and a primary case of severe airborne allergic contact
dermatitis.
Patient Education
1atients have the best prognosis "hen they are able to remember the
materials to "hich they are allergic and ho" to avoid frther e%posres.
1rovide patients "ith as mch information as possible concerning the
chemical to "hich they are allergic, inclding all kno"n names of the
chemical. +eb sites, *martphone applications, standard te%tbooks, and the
$@MH test kit contain basic information abot the chemicals.
*sceptible individals need to read the list of ingredients before applying
cosmetic prodcts to their skin, since preservative chemicals are sed
"idely in consmer, medical, and "orkplace prodcts. $he same chemical
may have di)erent names "hen sed for consmer or indstrial prposes.
1rovide pamphlets "ith color pictres of poison ivy to individals allergic to
the plant. $he American Academy of Dermatology also has pamphlets on
allergic contact dermatitis and hand ec/ema.
,or patient edcation information, see the *kin, Eair, and !ails Center, as
"ell as Contact Dermatitis.
Proceed to Clinical Presentation
"istory
A detailed history, both before and after patch testing, is crcial in
evalating individals "ith allergic contact dermatitis. 1otential cases of
allergic contact dermatitis and the materials to "hich individals are
e%posed shold be inclded in patch testing. Hvalation of allergic contact
dermatitis re4ires a mch more detailed history than most other
dermatologic disorders.
Eistory is e4ally important after patch testing. Lnly history and
4estioning can determine "hether the materials to "hich a patient is
allergic are partly or "holly responsible for the crrent dermatitis. A positive
patch reaction may indicate only a sensitivity and not the case of crrent
dermatitis.
Pree&isting skin diseases
Individals "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 lcers. !eomycin is an important case of allergic
contact dermatitis in these individals becase it is sed fre4ently despite
the lack of docmentation of its e'cacy in the treatment of stasis lcers.
Individals "ith otitis e%terna fre4ently are allergic to topical neomycin
and topical corticosteroids.
Individals "ith prrits ani and prrits vlvae may become sensiti/ed to
ben/ocaine and other medications applied to chronic prritic processes.
+omen "ith lichen scleross et atrophics fre4ently develop allergic
contact dermatitis, complicating the severe chronic vlvar dermatosis.
1atch testing these patients may provide important information that can
help in the management of recalcitrant and di'clt3to3manage dermatosis.
#topic dermatitis
1atients "ith a history of atopic dermatitis are at increased risk for
developing nonspecifc hand dermatitis and irritant contact dermatitis.
Eo"ever, they do not appear to be at an increased risk for allergic contact
dermatitis, despite the "ide range of topical medications and moistri/ers
sed by individals "ith chronic atopic dermatitis. $hey are at lo"er risk of
allergic contact dermatitis to poison ivy. *ome Hropean stdies indicate
that patients "ith atopic dermatitis may have increased incidence of
allergic contact dermatitis to nickel.
)nset o! symptoms
Individals "ith allergic contact dermatitis typically develop dermatitis,
"ithin a fe" days of e%posre, 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 p to a "eek follo"ing e%posre.
A minimm of 8A days is re4ired for individals to develop specifc
sensitivity to a ne" contactant. ,or e%ample, an individal "ho never has
been sensiti/ed to poison ivy may develop only a mild dermatitis > "eeks
follo"ing the initial e%posre bt typically develops severe dermatitis "ithin
83> days of the second and sbse4ent e%posres.
@emember that removing the poison ivy allergen from the skin is di'clt,
and nless an individal "ashes e%posed skin "ithin 2A mintes of
e%posre, allergic contact dermatitis "ill develop. $he hallmark of the
diagnosis of poison ivy is linear dermatitic lesions. $he possibility of an
e%ternal case of dermatitis al"ays mst be considered if the dermatitis is
linear or sharply defned.
$he immediate onset of dermatitis follo"ing initial e%posre to material
sggests either a cross3sensiti/ation reaction, prior forgotten e%posre to
the sbstance, or nonspecifc irritant contact dermatitis provoked by the
agent in 4estion.
Eyelid dermatitis
Individals may develop dermatitis on eyelids and other e%posed skin
follo"ing e%posre to airborne allergens or allergens transferred to that site
by the fngers. Contact dermatitis may also reslt from allergy to eyelid
makep.
Contact urticaria
Immediate reactions, ie, visible lesions developing less than 2A mintes
after e%posre, indicate contact rticaria (not allergic contact dermatitis).
$his is particlarly tre if the lesions are rticarial in appearance and if the
skin reaction is associated "ith other symptoms, sch as distant rticaria,
"hee/ing, ophthalmedema, rhinorrhea, or anaphyla%is.
4ate&
@bber late% crrently is the most important sorce of allergic contact
rticaria (see (ate% Allergy). $he term hypoallergenic may refer to gloves
that do not contain sensiti/ing chemicals added to rbber late% bt may not
indicate "hether the gloves are rbber late% free.
*ome individals may have delayed specifc contact sensitivity to rbber
late%, bt contact rticaria to rbber late% is mch more common than
allergic contact dermatitis to late%. Individals "ith hand dermatitis,
hospital "orkers, children "ith spina bifda, and atopic individals are at
increased risk of developing contact rticaria to rbber late%. Individals
may have allergic contact dermatitis to chemicals added to rbber gloves
and have contact rticaria to late%. Individals "earing rbber gloves
shold be evalated careflly for both possibilities.
@are reports e%ist of immediate anaphylactic reactions to topical antibiotics
(eg, bacitracin).
)ccupational dermatitis
Contact dermatitis is 8 of the 8A leading occpational illnesses. It may
prevent individals 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 dring holidays, bt individals "ith chronic
dermatitis may not demonstrate the classic history of "eekend and holiday
improvement.
Irritant contact dermatitis is more likely if mltiple "orkers are a)ected in
the "orkplace. &ost allergens rarely sensiti/e a high percentage of the
poplation.
"oies
Eobbies may be the sorce of allergic contact dermatitis. H%amples inclde
"ood"orking "ith e%otic tropical "oods or processing flm sing color3
developing chemicals that may provoke ctaneos lesions of lichen plans
from direct skin e%posre.
Medications
&edications (both self3prescribed and physician3prescribed) are important
cases of allergic contact dermatitis. $he "orkplace nrse may dispense
ine)ective and sensiti/ing topical preparations, sch as thimerosal
(&erthiolate), "hich may change a simple abrasion into a severe case of
allergic contact dermatitis. Individals may develop allergy to preservatives
in medications andGor to the active ingredients in topical medications,
especially neomycin and topical corticosteroids.<8>, 82=
1atients "ith dermatitis that did not clear "ith topical corticosteroid
treatment shold be considered for patch testing "ith a corticosteroid
series and the commercial preparations of corticosteroids and their
vehicles.
Physical E&amination
Acte allergic contact dermatitis is characteri/ed by prritic paples and
vesicles on an erythematos base. (ichenifed prritic pla4es may indicate
chronic allergic contact dermatitis. Lccasionally, allergic contact dermatitis
may a)ect the entire integment (ie, erythroderma, e%foliative dermatitis).
$he initial site of dermatitis often provides the best cle regarding the
potential case of allergic contact dermatitis. !ote the follo"ing.
"ands
Eands are an important site of allergic contact dermatitis, particlarly in the
"orkplace. Common cases of allergic dermatitis on the hands inclde the
chemicals in rbber gloves.
+opical medication sites
Allergic contact dermatitis is fre4ent in the perianal area as a reslt of the
se of sensiti/ing medications and remedies (eg, topical ben/ocaine).
$opical medications are also important cases of allergic contact dermatitis
in cases of otitis e%terna. Allergy to chemicals in ophthalmologic
preparations may provoke dermatitis arond the eyes.
#irorne allergic contact dermatitis
Chemicals in the air may prodce airborne allergic contact dermatitis. $his
dermatitis sally occrs ma%imally on the eyelids, bt it may a)ect other
areas e%posed to chemicals in the air, particlarly the head and the neck.
"air dyes
Eair dyeUin particlar, the component p3phenylenediamine (11D)Umay
trigger allergic contact dermatitis. Individals allergic to hair dyes typically
develop the most severe dermatitis on the ears and adOoining face rather
than on the scalp.
Stasis dermatitis and stasis ulcers
Individals "ith stasis dermatitis and stasis lcers are at high risk for
developing allergic contact dermatitis to topical medications applied to
infamed or lcerated skin (see the image belo"). $he chronicity of this
condition and the fre4ent occlsion of applied medications contribte to
the high risk of allergic contact dermatitis to medicament (eg, neomycin) in
these patients.
Individals may develop "idespread dermatitis from topical medications
applied to leg lcers or from cross3reacting systemic medications
administered intravenosly. ,or e%ample, a patient allergic to neomycin
may develop systemic contact dermatitis if treated "ith intravenos
gentamicin.
Chronic stasis dermatitis "ith allergic contact dermatitis to 4aternim385, a preservative
in moistri/er. Allergic contact dermatitis prodces areas of erythema in areas of atrophie
blanche and varicose veins.
Erythema multi!orme
Hrythema mltiforme (H&) is a severe ctaneos reaction "ith targetoid
lesions that occrs primarily after e%posre to certain medications or is
triggered by infection, most commonly by herpes simple% virs. @are cases
of H& have been reported after allergic contact dermatitis reslting from
e%posre to poison ivy,<87= tropical "oods, nickel, and hair dye (see the
image belo").
Hrythema mltiformelike reaction that developed actely follo"ing hair dying.
Intraoral metal contact allergy may reslt in mcositis that mimics lichen
plans, "hich has an association "ith intraoral s4amos cell carcinoma.
Intraoral s4amos cell carcinoma adOacent to a dental restoration
containing a metal to "hich the patient "as allergic has been reported.<85=
Allergic contact dermatitis may be a direct trigger for skin lceration in
patients "ith venos ins'ciency. Harly diagnosis and treatment of allergic
contact dermatitis may prevent the development of venos lcers.
Complications
Darkly pigmented individals may develop areas of hyperpigmentation or
hypopigmentation from allergic contact dermatitis. Lccasionally, they may
develop depigmentation at sites of allergic contact dermatitis to certain
chemicals.
Lccasionally, allergic contact dermatitis is complicated by secondary
bacterial infection, "hich may be treated by the appropriate systemic
antibiotic.
Proceed to Di'erential Diagnoses
Diagnostic Considerations
Contact dermatitis from allergy mst be di)erentiated from contact
dermatitis de to irritation, as "ell as other forms of dermatitis. In addition,
the specifc sbstance to "hich the patient is sensitive needs to be
identifed.
Di'erential Diagnoses
Asteatotic Hc/ema
Contact Dermatitis, Irritant
Drg3Indced Nllos Disorders
Drg3Indced 1hotosensitivity
!mmlar Dermatitis
Lnycholysis
1erioral Dermatitis
1hytophotodermatitis
1rrigo !odlaris
*eborrheic Dermatitis
$inea Corporis
$ransient Acantholytic Dermatosis
Mrticaria, Contact *yndrome
Proceed to Workup
#pproach Considerations
0ideline smmaries are available as follo"s:
American Academy of Allergy, Asthma and Immnology, American College
of Allergy, Asthma and Immnology 3Allergy diagnostic testing: an
pdated practice parameter. 1art 8 <8B=
American Academy of Allergy, Asthma and Immnology, American College
of Allergy, Asthma and Immnology 3Allergy diagnostic testing: an
pdated practice parameter. 1art > <8C=
0o to Irritant Contact Dermatitis, 1ediatric Contact Dermatitis, and 1rotein
Contact Dermatitis for complete information on these topics.
4a Studies
1otassim hydro%ide preparation andGor fngal cltre to e%clde tinea are
often indicated for dermatitis of the hands and feet. $his "ill identify
disorders sch as tinea pedis.
Patch +esting
1atch testing<8;, 8D, >A= is re4ired to identify the e%ternal chemicals to
"hich the person is allergic. $he greatest 4ality3of3life benefts from patch
testing occr in patients "ith recrrent or chronic allergic contact dermatitis
(ACD). 1atch testing is most cost3e)ective and redces the cost of therapy
in patients "ith severe allergic contact dermatitis.
1atch testing mst be performed by health care providers trained in the
proper techni4e. &ost dermatologists can perform patch testing sing the
$@MH test, "hich can identify relevant allergies in as many as one half of
a)ected patients. &ore e%tensive patch testing is indicated to identify
allergies to chemicals not fond in the $@MH test. *ch testing typically is
available only in a limited nmber of dermatology o'ces and clinics.
$he patch testing procedre is as follo"s:
*mall amonts of appropriate labeled diltions of chemicals are applied to
the skin and occlded for > days
1atch tests may be left on for 2 days before removal
,or reasons of schedling, a chemical mst remain nder a skin patch for a
minimm of 8 day to prodce a positive patch test reaction >3C days
follo"ing initial application
$he patch test mst be read not only at 7; hors, "hen the patch tests
cstomarily are removed, bt again bet"een C> hors and 8 "eek
follo"ing initial application
Individals "ith sspected allergic contact dermatitis "ithot positive
reactions on the $@MH test or "ith chronic dermatitis or relapsing
dermatitis, despite avoiding chemicals to "hich they are allergic (identifed
on $@MH test), need additional patch testing. &any individals have more
than 8 contact allergy and may be allergic to 8 or more chemicals fond on
the $@MH test and on special allergen trays or series.
$esting reactions to more allergens increases accracy of the diagnosis of
allergic contact dermatitis. *election of allergens for testing re4ires
consideration of the patient9s history and access to appropriate
environmental contactants.
Certain chemicals (eg, neomycin) typically prodce delayed positive patch
test reactions at 7 days or later follo"ing initial application. A tendency
e%ists for elderly patients to manifest positive patch test reactions later
than yonger patients. Do not perform patch testing on patients taking
more than 85 mgGd of prednisone. Lral antihistamines may be sed dring
the patch test period if re4ired.
Angry back syndrome or e%cited skin syndrome may occr. If a patient has
a large nmber of positive patch test reactions, retesting the patient
se4entially to a small series of these allergens may be necessary to
e%clde nonspecifc false3positive reactions. $he syndrome most likely
occrs in individals "ho have active dermatitis at the time of patch testing
or "ho have a strong positive patch test reaction, both of "hich may indce
local skin hyperreactivity in the area "here patches "ere applied.
Additional patch test series or sets inclde the follo"ing:
Corticosteroids, particlarly ti%ocortol pivalate and bdesonide
Ingredients in cosmetics not fond in the $@MH test
Chemicals sed in dentistry that may prodce mcosal and lip dermatitis in
dental clients or that may prodce chronic dermatitis of the hands in
dentists and dental team members
Chemicals sed in hairdressing that may prodce facial, ear, and neck
dermatitis in clients or chronic hand dermatitis or eyelid dermatitis in
hairdressers
,ragrances fond in cosmetics and a "ide range of consmer prodcts
Important allergens not fond in the $@MH test that are fre4ent cases of
allergic contact dermatitis are as follo"s:
Nacitracin
Acrylates sed in dentistry, artifcial nails, and printing
Chemicals sed in baking
1esticides (many cases of dermatitis attribted to pesticides reslt from
other cases, particlarly from plants sch as poison ivy)
Chemicals sed in machining, eg, ctting oils and fids
1hotographic chemicals sed by photographers and photographic
developers
1lants e%clding poison ivy
Chemicals in plastics and gles
Chemicals fond in rbber prodcts not inclded in the $@MH test
Chemicals in shoes and clothing
Mltraviolet (MQ) protective ingredients in snscreens
Lther chemicals prodcing photo allergic contact dermatitis
&iscellaneos allergens
$he chemicals listed above are tested nder ,inn chambers, allergHAVH
chambers, or the IW Chamber patch test. In photopatch testing, the
chemicals are applied in dplicate sets. Lne set receives 8A PGcm
>
of MQ3A
(or 8 PGcm
>
less than the minimm erythema dose, "hichever is lo"est) >7
hors after application of the allergens. $he other series is protected from
MQ e%posre to di)erentiate allergic contact dermatitis and photo3
accentated allergic contact dermatitis from photo3allergic contact
dermatitis. Noth sets are read at 7; hors after application, as "ell as at an
additional time point as in rotine patch testing.
$he safety of patch testing in pregnancy has not been stdied# ho"ever,
the minte amonts of allergens applied appear nlikely to be absorbed in
s'cient amonts to harm the fets. !onetheless, as "ith all treatments in
pregnant "omen, the benefts of testing shold be "eighed against any
potential, albeit ndocmented, risk.
Repeat )pen #pplication +est
,or individals "ho develop "eak or 8J positive reactions to a chemical,
the repeat open application test (@LA$) is sefl in determining "hether
the reaction is signifcant. @LA$ is most sefl "hen an individal has a 8J
reaction to a chemical fond in a leave3on consmer prodct.
,or e%ample, an individal "ith a "eak reaction to a preservative fond in a
moistri/er may apply the moistri/er t"ice a day for a "eek to the side of
the neck or behind an ear# if clinical dermatitis does not develop, the 8J
reaction likely "as not meaningfl. Conversely, if dermatitis develops after
a fe" days of repeated application of the sspected prodct, then the "eak
patch test reaction is highly relevant.
Dimethylglo&ime +est
$he dimethylglo%ime test is a sefl and practical "ay to identify metallic
obOects that contain enogh nickel to provoke allergic dermatitis in
individals allergic to nickel. Dermatology sta) may test sspected metal
prodcts in the o'ce, or the individal may prchase a test kit and test
obOects at home or at "ork, particlarly Oe"elry or metallic srfaces.
Lther chemical tests are available for other sspected allergens (eg,
formaldehyde, cobalt, chromate). Lccasionally, chemical analyses may be
necessary to determine "hether a material contains a sspected allergen
or to identify ne" nkno"n allergens.
Skin Biopsy
*kin biopsy may help e%clde other disorders, particlarly tinea, psoriasis,
and ctaneos lymphoma. *kin biopsy of skin lesions of the palms and
soles has several potential pitfalls, ho"ever.
$he stratm cornem and epidermis are particlarly thick on the palms and
soles. $his makes the histologic diagnosis of psoriasis more di'clt and
increases the possibility that the biopsy specimen "ill lack s'cient dermis
for optimal diagnosis.
An overly deep skin biopsy of the thenar area can ct the motor nerve,
"hich is the recrrent branch of the median nerve. A biopsy from the sole
may leave a chronic painfl scar on "hich the patient mst "alk.
"istologic *indings
$he histology of allergic contact dermatitis is similar to that fond in other
forms of ec/ematos dermatitis. A pattern of sbacte chronic dermatitis or
acte dermatitis may be seen. $he infammatory infltrate in the dermis
predominately contains lymphocytes and other mononclear cells.
Hpidermal edema (ie, spongiosis and microvesicle formation) may be seen,
bt these changes may be absent in long3standing dermatitis in "hich
thickening of the epidermis (acanthosis) "ith hyperkeratosis and
parakeratosis may be seen in the epidermis and stratm cornem. Allergic
contact dermatitis may provoke atypical $3cell infltrates, simlating
mycosis fngoides.
Proceed to +reatment , Management
Background
(eprosy is a chronic infection cased by the acid3fast, rod3shaped bacills
Mycobacterium leprae. (eprosy can be considered > connected diseases
that primarily a)ect sperfcial tisses, especially the skin and peripheral
nerves. Initially, a mycobacterial infection cases a "ide array of celllar
immne responses. $hese immnologic events then elicit the second part
of the disease, a peripheral neropathy "ith potentially long3term
conse4ences.
$he social and psychological e)ects of leprosy, as "ell as its highly visible
debilities and se4elae (as seen in the image belo"), have reslted in a
historical stigma associated "ith leprosy. $o minimi/e the preOdice against
those "ith leprosy, the condition is also kno"n as Eansen disease, named
after 0.A. Eansen, "ho is credited "ith the 8;C2 discovery of M leprae. $his
mycobacterim gro"s e%tremely slo"ly and has not been sccessflly
cltred in vitro.
Eands "ith V3thmbs, cla"ing, contractres, and shortening of fngers de to repetitive
inOry and healing. Eo Chi &inh City, Qietnam. (Cortesy of D. *cott *mith, &D)
In the 8DDAs, the +orld Eealth Lrgani/ation (+EL) lanched a campaign to
eliminate leprosy as a pblic health problem by >AAA. Hlimination, as
defned by the +EL, "as defned as a redction of patients "ith leprosy
re4iring mltidrg therapy to fe"er than 8 per 8A,AAA poplation. $his
goal "as achieved in terms of global prevalence by >AA>, bt 85 of the 8>>
contries "here leprosy "as endemic in 8D;5 still have prevalence rates of
greater than 8 per 8A,AAA poplation.<8=
Althogh mltidrg regimens have been sed globally to cre nearly 87
million patients "ith leprosy since 8D;5, the nmber of ne" leprosy cases
remained relatively nchanged from 8D;A to >AAA, ranging from 5AA,AAA3
CAA,AAA "orld"ide per year.<>= Access and delivery of antibiotics contines
to be a problem in the most endemic nations. +ith the precise transmission
mechanism of leprosy still nkno"n and a lack of an e)ective vaccine,
leprosy "ill probably contine to pose an ongoing pblic health problem in
the coming decades.
Pathophysiology
(eprosy can manifest in di)erent forms, depending on the host response to
the organism.
Individals "ho have a vigoros celllar immne response to M leprae have
the tbercloid form of the disease that sally involves the skin and
peripheral nerves. $he nmber of skin lesions is limited, and they tend to
be dry and hypoesthetic. !erve involvement is sally asymmetric. $his
form of the disease is also referred to as pacibacillary leprosy becase of
the lo" nmber of bacteria in the skin lesions (ie, S 5 skin lesions, "ith
absence of organisms on smear). @eslts of skin tests "ith antigen from
killed organisms are positive in these individals.
Individals "ith minimal celllar immne response have the lepromatos
form of the disease, "hich is characteri/ed by e%tensive skin involvement.
*kin lesions are often described as infltrated nodles and pla4es, and
nerve involvement tends to be symmetric in distribtion. $he organism
gro"s best at >C32AIC# 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 mltibacillary leprosy becase of the large
nmber of bacteria fond in the lesions (ie, XB lesions, "ith possible
visali/ation of bacilli on smear). @eslts of skin tests "ith antigen from
killed organisms are nonreactive.
1atients may also present "ith featres of both categories# ho"ever, over
time, they sally evolve to one or the other (indeterminate or borderline
leprosy). Interestingly, most individals "ho are e%posed to leprosy never
develop the disease.
Classifcation of leprosy: (eprosy has > classifcation schemas: the 53
category @idley3Popling system and the simpler and more commonly sed
+EL standard.
@idley3Popling: Depending on the host response to the organism, leprosy
can manifest clinically along a spectrm bonded by the tbercloid
and lepromatos forms of the disease. &ost patients fall into the
intermediate classifcations, "hich inclde borderline tbercloid
leprosy, midborderline leprosy, and borderline lepromatos leprosy.
$he classifcation of the disease typically changes as it evolves dring
its progression or management. $he @idley3Popling system is sed
globally and forms the basis of clinical stdies of leprosy. It may also
be more sefl in giding treatment regimens and assessing risk of
acte complications. 1hysical fndings in each sbtype are presented
in the Clinical section.
+EL system: $he +EL recommends classifying leprosy according to the
nmber of lesions and the presence of bacilli on a skin smear. $his
method is sefl in contries "here biopsy analysis in navailable.
1acibacillary leprosy is characteri/ed by 5 or fe"er lesions "ith absence of
organisms on smear. 1acibacillary leprosy generally incldes
the tbercloid and borderline lepromatos categories from the
@idley3Popling system.
&ltibacillary leprosy is marked by B or more lesions "ith possible
visali/ation of bacilli on smear. (epromatos leprosy, borderline
lepromatos leprosy, and midborderline leprosy on the @idley3
Popling scale are inclded in the mltibacillary leprosy category.
Epidemiology
*re5uency
$nited States
In the Mnited *tates, an average of 85A cases are diagnosed each year. In
>AA7, BD ne" cases of leprosy "ere detected and 828 total persons "ere
reported to have the disease, according to the +EL. &ost cases of leprosy
in the Mnited *tates are fond in immigrants, althogh endemic foci e%ist in
parts of (oisiana, ,lorida, and $e%as along the 0lf of &e%ico# in &e%ican
and Asian California poplations# and in *panish Americans in !e" York
City. Arond ;5F of these detected leprosy cases involve patients "ho have
lived in foreign contries, primarily Asia, Africa, and (atin America.<2=
Nased on genetic analysis stdies, "ild armadillos and many patients "ith
leprosy in the sothern Mnited *tates are infected "ith the same strain of M
leprae.<7= (eprosy may be a /oonosis in the sothern Mnited *tates becase
armadillos are a large reservoir for this disease.
%nternational
According to +EL fgres, the global registered prevalence of leprosy at the
start of >AA5 "as >;B,AB2 cases. 0lobal annal detection rates have
declined from >AA8 to >AA7, "hen CB2,>B> and 7AC,CD8 ne" cases "ere
reported, respectively. (eprosy is still deemed a pblic health problem in D
contries: Angola, Nra/il, Central African @epblic, Democratic @epblic of
the Congo, India, &adagascar, &o/ambi4e, !epal, and the Mnited @epblic
of $an/ania. $hese contries accont for ;7F of reported cases.
,rthermore, more than D7F of ne" cases of leprosy in (atin America are
reported in Nra/il.<8=
Mortality/Moridity
(eprosy is rarely fatal, and the primary conse4ence of infection is nerve
impairment and debilitating se4elae. According to one stdy, 2235BF of
ne"ly diagnosed patients already displayed signs of impaired nerve
fnction.<5= According to estimates, 2 million people "ho have completed
mltidrg therapy for leprosy have sstained disability de to nerve
damage. Althogh both lepromatos leprosy and tbercloid leprosy
involve the skin and peripheral nerves, tbercloid leprosy has more severe
manifestations. !erve involvement reslts in loss of sensory and motor
fnction, "hich may lead to fre4ent trama and amptation. $he lnar
nerve is most commonly involved.
Damage in the follo"ing nerves is associated "ith characteristic
impairments in leprosy:
Mlnar and median 3 Cla"ed hand
1osterior tibial 3 1lantar insensitivity and cla"ed toes
Common peroneal 3,oot drop
@adial ctaneos, facial, and greater ariclar nerves (may also be
involved# as seen in the image belo")
1atient "ith facial nerve palsy and contractres of the hand. Daloa, Ivory
Coast. (Cortesy of D. *cott *mith, &D)
Infltration by bacteria may lead to destrction of nasal cartilage
(lepromatos leprosy), oclar involvement, and di)se thickening of
the skin. Advanced cases of leprosy involve the loss of eyebro"s and
lashes, bt these deformities are less common today.
+orld"ide, leprosy is considered the most common case of crippling of the
hand, "hich is cased by lnar nerve involvement.<B= 1eroneal nerve
involvement can lead to foot drop, posterior tibial nerve involvement,
and cla"ed toes.
Race
(eprosy "as once endemic "orld"ide, and no racial predilection is kno"n.
In the late 8;AAs, the incidence of leprosy in northern Hrope and !orth
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 male3
to3female ratio of 8.5:8. In some areas in Africa, the prevalence of leprosy
among females is e4al to or greater than that in males.<>=
#ge
(eprosy can occr at any age, bt, in developing contries, the age3specifc
incidence of leprosy peaks in children yonger than 8A years, "ho accont
for >AF of leprosy cases. (eprosy is very rare in infants# ho"ever, they are
at a relatively high risk of ac4iring leprosy from the mother, especially in
cases of lepromatos leprosy or midborderline leprosy."istory
*ymptoms
1ainless skin patch accompanied by loss of sensation bt not itchiness ((oss
of sensation is a featre of tbercloid leprosy, nlike
lepromatos leprosy, in "hich sensation is preserved.) Chronic
insensate patch is seen in the mage belo".
Chronic insensate patch de to leprosy infection. Eo Chi &inh City, Qietnam.
(Cortesy of D. *cott *mith, &D)
(oss of sensation or paresthesias "here the a)ected peripheral nerves are
distribted
+asting and mscle "eakness
,oot drop or cla"ed hands (may reslt from neritic pain and rapid
peripheral nerve damage# as seen in the image belo")
Characteristic cla"ed hand deformity cased by lnar involvement in
leprosy. Daloa, Ivory Coast. (Cortesy of D. *cott *mith, &D)
Mlcerations on hands or feet (lcer at the metatarsal head is seen in the
image belo")
Chronic nonhealing lcer at the metatarsal head reslting from loss of
sensation in the feet. ?arigiri, $amil !ad, India. (Cortesy of $ara
@amachandra)
(agophthalmos, iridocyclitis, corneal lceration, andGor secondary cataract
de to nerve damage and direct bacillary skin or eye invasion<C=
*ymptoms in reactions
$ype 8 (reversal) 3 *dden onset of skin redness and ne" lesions
$ype > (erythema nodosm leprosm <H!(=# as seen in the image belo") 3
&any skin nodles, fever, redness of eyes, mscle pain, and Ooint
pain
1atient "ith erythema nodosm leprosm type > reaction several "eeks
after initiation of drg therapy. $his photograph "as taken after tendon
release. @ed"ood City, California. (Cortesy of D. *cott *mith, &D)
$ravel: (eprosy shold be considered in anyone "ho has lived in the
tropics or "ho has traveled for prolonged periods to endemic areas.
H%posre: $he incbation period of leprosy is long, ranging from a fe"
months to >A35A years. $he mean incbation time is estimated to be
8A years for lepromatos leprosy and 7 years for tbercloid leprosy.
$he organism9s slo" dividing time (once every > "k) contribtes to
the challenge of epidemiologically linking e%posres to the
development of disease.
Necase of immnologic reasons, only arond 538AF of the poplation
is estimated to be ssceptible to infection.
Physical
$he cardinal signs of leprosy inclde hypoesthesia, skin lesions, and
peripheral neropathy. $he frst physical signs of leprosy are sally
ctaneos. $he sbtype of leprosy often determines the degree of skin
involvement.
1hysical e%amination shold inclde the follo"ing:
Hvalation of skin lesions
Carefl sensory and motor e%amination
1alpation of peripheral nerves for pain or enlargement, "ith particlar
attention paid to the follo"ing locations:
Hlbo"s 3 Mlnar nerve
+rist 3 *perfcial radial ctaneos and median nerves
1opliteal fossa 3 Common peroneal nerve
!eck 3 0reat ariclar nerve
1hysical fndings in specifc leprosy sbtypes inclde the follo"ing:
$bercloid leprosy
$he initial lesion is often a sharply demarcated hypopigmented macle that
is ovoid, circlar, or serpiginos. $he lesions may be
some"hat elevated "ith a dry scaly center and
erythematos borders.
Common lesion sites inclde the bttocks, face, and e%tensor srfaces of
limbs. $he perinem, scalp, and a%illa are not normally
involved becase of the temperatre di)erential in these
/ones, as predilection is to"ard cooler /ones.
As the disease progresses, lesions tend to destroy the normal skin organs
sch as s"eat glands and hair follicles.
*perfcial nerves that lead from the lesions tend to enlarge and are
sometimes palpable. $he patient may e%perience severe
neropathic pain. !erve involvement can also lead to
trama and mscle atrophy.
(epromatos leprosy
$his form is characteri/ed by e%tensive bilaterally symmetric ctaneos
involvement, "hich can inclde macles, nodles, pla4es,
or paples. &ltiple fat hypopigmented lesions are seen in
the image belo".
&ltiple fat hypopigmented lesions on sholder and neck, sggestive
of mltibacillary leprosy. !ote lceration of hypothenar area of hand,
indicative of lnar neropathy. @ed"ood City, California, Mnited
*tates. (Cortesy of D. *cott *mith, &D)
Mnlike lesions in tbercloid leprosy, those in lepromatos leprosy have
poorly defned borders and raised and indrated centers.
As in all forms of leprosy, lepromatos lesions are "orst on
cooler parts of the body. Common areas of involvement
inclde the face, ears, "rists, elbo"s, bttocks, and knees.
Eoarseness, loss of eyebro"s and eyelashes, and nasal collapse secondary
to septa perforation may occr in advanced cases of
disease. Involvement of the eye may inclde keratitis,
glacoma, or iridocyclitis as seen in the image belo".
&an "ith advanced deformities cased by nmanaged leprosy.
?eratitis, loss of eyebro", thickened skin, and typical hand
impairments. Eo Chi &inh City, Qietnam. (Cortesy of D. *cott *mith,
&D)
$he leonine facies associated "ith leprosy develop as the disease
progresses, and the facial skin becomes thickened and
corrgated.
A%illary and inginal adenopathy may develop, in addition to scarring of the
testes and sbse4ent gynecomastia and sterility.
!erve involvement in lepromatos leprosy is not as severe as in tbercloid
leprosy, since nerves, althogh visibly thickened and highly
infected, still fnction reasonably "ell in early stages of the
disease.
Norderline tbercloid leprosy: $he lesions are fe" or moderate and
asymmetric "ith almost complete anesthesia. 1eripheral nerves
are often involved and thickened asymmetrically, and ctaneos
nerves are sometimes enlarged.
&idborderline leprosy: $he nmber of skin lesions is moderate, and they are
asymmetrical and some"hat anesthetic. 1eripheral nerves may
be some"hat symmetrically enlarged, bt ctaneos nerves are
not.
Norderline lepromatos leprosy: &oderate to nmeros slightly
asymmetrical skin lesions appear "ith minor or no anesthesia.
1eripheral nerves are often enlarged symmetrically, bt
ctaneos nerves are not.
Indeterminate leprosy: *kin lesions are typically either hypopigmented or
hyperpigmented macles or pla4es. 1atients may note that
these lesions are anesthetic or paresthetic.
Causes
M leprae is the casative agent associated "ith leprosy, "hich has
been recogni/ed as an infectios disease for the last > millennia. M
leprae "as discovered as the casative agent in 8;C2. $he acid fast,
gram3positive bacills is an obligate intracelllar organism "ith a
predilection for *ch"ann cells and macrophages. M leprae has not
been sccessflly gro"n sing artifcial media.
$he rote of transmission has not been defnitively established,
althogh hman3to3hman aerosol spread of nasal secretions is
thoght to be the most likely mode of transmission in most cases.
(eprosy is not spread by toch, since the mycobacteria are incapable
of crossing intact skin. (iving near people "ith leprosy is associated
"ith increased transmission. Among hosehold contacts, the relative
risk for leprosy is increased ;3 to 8A3fold in mltibacillary and >3 to 73
fold in pacibacillary forms. Animal reservoirs do e%ist (armadillos,
certain nonhman primates), and cases of sspected /oonotic
transmission have been reported.
Proceed to Workup
4aoratory Studies
$he +EL case defnition of leprosy is M leprae infection in an individal
"ho has not completed a corse of treatment and has one or more of the
follo"ing:
Eypopigmented 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 acid3fast bacilli
(aboratory stdies inclde the follo"ing:
*kin biopsy, nasal smears, or both are sed to assess for acid3fast bacilli
sing ,ite stain. Niopsies shold be fll dermal thickness taken from
an edge of the lesion that appears most active.<;=
*erologic assays can be sed to detect phenolic glycolipid38 (specifc for M
leprae) and lipoarabinomannan (commonly seen in mycobacteria).<;=
&oleclar probes detect 7A35AF of cases missed on prior histologic
evalation. *ince probes re4ire a minimm amont of genetic
material (ie, 8A
7
D!A copies), they can fail to identify pacibacillary
leprosy.
(aboratory tests related to drg treatment follo"3p inclde the follo"ing:
CNC cont
Creatinine level
(iver fnction tests
)ther +ests
Immnologic tests inclde the follo"ing:
(epromin skin test (not available in the Mnited *tates): Althogh not
diagnostic of e%posre to or infection "ith M leprae, this test
assesses a patient9s ability to mont a granlomatos response
against a skin inOection of killed M leprae. 1atients "ith
tbercloid leprosy or borderline lepromatos leprosy typically
have a positive response (X5 mm). 1atients "ith lepromatos
leprosy typically have no response.
1henolic glycolipid38: $his is a specifc serologic test based on the detection
of antibodies to phenolic glycolipid38. $his test yields a
sensitivity of D5F for the detection of lepromatos leprosy bt
only 2AF for tbercloid leprosy.
1olymerase chain reaction (1C@): 1C@ and recombinant D!A technology
have allo"ed for the development of gene probes "ith M leprae
-specifc se4ences. $his technology can be sed to identify the
mycobacterim in biopsy samples, skin and nasal smears, and
blood and tisse sections.
(ymphocyte migration inhibition test ((&I$): As determined by a
lymphocyte transformation and (&I$, cell3mediated immnity to
M leprae is absent in patients "ith lepromatos leprosy bt
present in those "ith tbercloid leprosy.
Contact or family screening for history of leprosy
Procedures
*kin biopsy samples stained "ith hemato%ylin3eosin and ,ite3,araco
are the primary basis for laboratory diagnosis and categori/ation. A
fll3thickness skin biopsy sample shold be taken from an advancing
border of an active lesion and shold inclde dermis and epidermis.
*kin smears that demonstrate acid3fast bacilli strongly sggest a
diagnosis of leprosy, bt the bacilli may not be demonstrable in
tbercloid (pacibacillary) leprosy.
A nerve biopsy can be benefcial in rling ot diseases sch as
hereditary neropathies or polyarteritis nodosa. !erve biopsies may
also help identify abnormalities in patients "ith sbclinical leprosy and
may be the only "ay to defnitively diagnose completely neropathic
forms of leprosy. If a nerve biopsy is needed to confrm diagnosis, a
prely sensory nerve (eg, sral or radial ctaneos nerve) shold be
sed. $his procedre is rarely necessary.<C=
"istologic *indings
,indings vary bt can inclde dermatitis, giant cells, infltration of nerve
bndles "ith mononclear cells, and granlomas. (epromatos lesions
generally contain nmeros acid3fast bacilli and fat3laden macrophages
"ith a pacity of lymphocytes. Eistopathology of leprosy is seen in the
image belo".
Eistopathology of leprosy: (arge nmbers of acid3fast bacilli (in clsters) in histiocytes
and "ithin nerves. ,ite3,araco stain 5AA T. (Cortesy of $ara @amachandra and D. *cott
*mith, &D)
In contrast, tbercloid lesions contain fe"3to3no acid3fast bacilli bt
manifest granlomatos changes "ith epithelial cells and lymphocytes. $he
immnopathologic spectrm of leprosy has been delineated in the
!erologic &anifestations of (eprosy topic in &edscape @eference9s
!erology volme.
Staging
(eprosy is staged or graded based on microscopy fndings to classify cases
as pacibacillary or mltibacillary so that dration and type of drg therapy
can be determined.
Proceed to +reatment , ManagementMedical Care
In response to the increased incidence of dapsone resistance, the +EL
introdced a mltidrg regimen in 8D;8 that incldes rifampicin, dapsone,
and clofa/imine. *ome clinical stdies have also sho"n that certain
4inolones, minocycline, and a/ithromycin have activity against M leprae.
$he +EL recently recommended single3dose treatment "ith rifampin,
minocycline, or ofo%acin in patients "ith pacibacillary leprosy "ho have a
single skin lesion. Eo"ever, the +EL still recommends the se of the long3
term mltidrg regimens "henever possible becase they have been fond
to be more e'cacios.
$able. &ltidrg $herapy 1lan @ecommended by the +EL (Lpen $able in a
ne" "indo")
+ype o! 4eprosy
Daily- Sel!(
#dministered
Monthly
Supervised
Months o!
+reatment
1acibacillary Dapsone 8AA mg @ifampicin BAA mg B38>
&ltibacillary Dapsone 8AA mg, @ifampicin BAA mg, >7
Clofa/imine 5A mg Clofa/imine 2AA mg
1ediatric Dapsone > mgGkg,
Clofa/imine 8 mgGkg
@ifampicin 8A mgGkg,
Clofa/imine B mgGkg
*ame as in adlts
M* regimens emphasi/e the se of rifampin, "hich is the most bactericidal
drg sed to treat leprosy. Althogh a single dose of BAA mg once monthly
(the +EL standard) is considered bactericidal, treatment plans in the
Mnited *tates may inclde doses of BAA mgGday.
1acibacillary leprosy shold be treated for B38> months "ith dapsone 8AA
mgGday nspervised pls rifampin BAA mgGmonth spervised. $his
regimen shold be follo"ed by treatment "ith dapsone as
monotherapy for 2 years in patients "ith tbercloid leprosy or 5
years in patients "ith borderline lepromatos leprosy.
&ltibacillary leprosy shold be treated for >7 months "ith dapsone 8AA
mgGday nspervised, clofa/imine 5A mgGday nspervised, and
rifampin BAA mg pls clofa/imine 2AA mgGmonth spervised.
Corticosteroids have been sed to treat nerve damage associated "ith
leprosy, bt a recent revie" of 2 randomi/ed controlled trials sho"s
no signifcant long3term e)ect.<D= 1rednisolone is believed to minimi/e
pain and acte infammation. $he recommended initial dose is
prednisolone 7A mg daily.
Lbservations of increasing resistance in patients treated for leprosy have
been reported in *otheast Asia, notably in Qietnam.<8A= $he drg
most commonly fond to be resistant is dapsone, often in the conte%t
of prior e%posre or treatment attempts "ith monotherapy. Althogh
drg resistance is an ongoing concern, it is di'clt to assess in this
slo"3gro"ing organism. In a stdy of M leprae strains from *oth
America, fe" of >2A strains sbOected to moleclar drg3ssceptibility
analysis "ere drg3resistant. Lf the >2A strains, 2 "ere identifed as
clinically relapsing and "ere fond to be resistant by genetic testing#
> of the 2 "ere dapsone3resistant# and 8 "as dapsone3resistant and
rifampin3resistant sing genetic testing for point mtation.<88=
Surgical Care
$he goals of srgical treatment in patients "ith leprosy are to prevent
frther deterioration, to improve motor fnction, and, in some cases,
to improve sensation.
1reoperative re4irements: ,irst, a fll sensory and motor appraisal
"ith fnctional and occpational assessment mst be completed to
determine the e%tent of damage. Additionally, patients mst have
completed the mltidrg therapy and shold have negative skin
smear reslts. $he patient shold not se steroids a fe" months
before srgery, and acte neritis shold not be evident. *ti)ness of
hands and feet shold be minimi/ed "ith preoperative therapy.
!eral srgery
Attempts to restore atonomic fnction and sensation are rarely ndertaken
since little evidence sho"s that fnction is signifcantly regained.
Draining of acte nerve abscesses and fasciclar dissection can
redce the pressre on nerves and may improve sensation. In
some cases, longitdinal epinerotomy may relieve some
sensory loss. Considerable nerve fnction can be regained in the
posterior tibial nerve "ith nerovasclar decompression via
release of the fe%or retinaclm. Calcaneal bands can be slit to
relieve distal compression of branches on the sole of the foot.
!erve grafts may be of some beneft in patients "ith locali/ed lesions.
!eral srgery may also be indicated in patients "ith
nremitting nerve pain.
@econstrction and fnctional restoration<B=
In leprosy management, the goal of most srgical procedres is to remedy
motor paralysis de to primary nerve impairment. Cla" fngers
and V3thmbs cased by lnar nerve paralysis are among the
most common deformities. Cla"ed hands are repaired "ith
arthrodesis or "ith a tendon transfer to 8 of 7 insertion sites on
the fnger: interosses tendons, pro%imal phalan%, dorsal
e%tensor e%pansion, or fe%or sheath annlar plleys. $he
palmaris longs, fe%or digitorm sperfcialis, e%tensor carpi
radialis longs, and e%tensor indices are tendons that can be
sed for transfer. $endon transfers are also sed to repair
abdction and opposition of the thmb, dorsife%ion of the foot,
and fe%ion and e%tension of the metacarpophalangeal and
pro%imal interphalangeal Ooints, respectively.
Contractres of the hand, sch as the thmb "eb contractre, can be
repaired "ith V3plasty, and Ooint stability can be improved "ith
tenodesis.
$he constrictions cased by repetitive inOry and healing in patients "ith
leprosy can be treated "ith several methods. 1ossible treatment
options inclde removal of the carpal tnnel roof, lnar nerve
transposition anteriorly, and epicondylectomy.
1rocedres that limit hypere%tension of the metacarpophalangeal Ooint or
keep it in fe%ion are not indicated in the insensate hands of
patients "ith leprosy, "ho s)er from contined "eakness.
Amptation is a last resort and is reserved for cases of e%tremely diseased
tisse.
Hye procedres: (oss of eyelid fnction may be treated "ith passing a
strip from the temporalis mscle throgh the eyelid and connecting it
to the inner canths. $arsorrhaphy may help narro" the opening of
the eyelid, and canthoplasty redces sagging of the eyelids.
Cosmetic srgery: After the disease is controlled medically, the
follo"ing cosmetic procedres may also be considered:
!asal reconstrction
@emoval of e%cess skin
@eplacement of eyebro"s sing transplants of scalp hair
@emoval of breast tisse formation de to gynecomastia
Consultations
Consltations may inclde an orthopedic srgeon, dermatologist,
nerologist, and physical therapist, based on the needs of the individal
patient.

Medication Summary
$he goals of pharmacotherapy are to eradicate the infection, to prevent
complications, and to redce morbidity.
$he mltidrg therapy plan recommended by the +EL can be sed to plan
therapy based on the type of leprosy (pacibacillary or mltibacillary) and
"hether it is spervised monthly or self3administered daily (see &edical
Care).
#ntimycoacterial #gents
Class Summary
$hese agents have bactericidal and bacteriostatic activity against
mycobacteria.
Qie" fll drg information
Dapsone .#vlosul!on0

Nactericidal and bacteriostatic against mycobacteria# mechanism of action
is similar to that of slfonamides, in "hich competitive antagonists of 1ANA
prevent formation of folic acid, inhibiting bacterial gro"th. 1art of a >3drg
regimen for treatment of pacibacillary leprosy# part of a 23drg regimen
for treatment of mltibacillary leprosy.
Qie" fll drg information
Ri!ampin .Ri!adin- Rimactane0

,or se in combination "ith at least 8 other antitberclos drg# inhibits
D!A3dependent bacterial bt not mammalian @!A polymerase. &ost
bactericidal drg sed against M leprae. Cross3resistance may occr.
$reat for B3D mo or ntil B mo have elapsed from conversion to sptm3
cltre negativity.
1art of >3drg regimen for treatment of pacibacillary leprosy# part of 23
drg regimen for treatment of mltibacillary leprosy.
Qie" fll drg information
Clo!a3imine .4amprene0

Inhibits mycobacterial gro"th, binds preferentially to mycobacterial D!A.
Eas antimicrobial properties, bt mechanism of action is nkno"n. 1art of
23drg regimen for treatment of mltibacillary leprosy.
Qie" fll drg information
Minocycline

Msed to treat leprosy in patients "ho cannot tolerate clofa/imine.
Proceed to *ollow(up
*urther )utpatient Care
$he +EL recommends that the monthly doses of rifampin be
administered nder direct observation dring the visit.
&onthly otpatient follo"3p is recommended dring treatment,
althogh "eekly visits may be necessary if the patient e%periences a
leprosy reaction.
,ollo"3p laboratory stdies dring treatment inclde the follo"ing:
Mrinalyses
CNC cont
Creatinine
(iver fnction tests
Yearly skin scrapings taken from the 2 or 7 most active lesions are
recommended.
@esponse to treatment
*ccessfl treatment can reslt in fattening and elimination of nodles,
paples, and pla4es, as "ell as improved nerve fnction.
Nacillary load is rarely a convenient method of assessing
response to treatment. !oncompliance or drg resistance shold
be sspected if intact organisms are present after several
months of treatment.
Lnce treatment is completed, the patient shold be monitored for the ne%t
538A years to evalate for signs of relapse. $o date, the relapse
rate follo"ing completion of mltidrg therapy has been 8F for
both types of leprosy. In sch cases, ne" bacills3positive lesions
may develop and shold be treated "ith a thorogh M* regimen
that incorporates once3daily rifampin (see $reatment).
1atients "ho have been sccessflly treated occasionally develop reversal
reactions and frther neropathy. If skin biopsy samples are
bacills3negative, these patients are deemed to have a reversal
reaction (see Complications).
Complications
Carefl attention to the development of reversal reactions dring treatment
and prompt and proper management "ill minimi/e long3term nerologic
se4elae.
$ype 8 reaction
@eversal reaction, or lepra type 8 reaction, is a delayed3type
hypersensitivity reaction that arises "hen borderline leprosy
shifts to"ard borderline lepromatos leprosy "ith treatment.
$hese types of reactions refect the development of an
appropriate immne response and the local generation of tmor
necrosis factor3alpha and interferon3gamma. $he reaction is
characteri/ed by edema and erythema of e%isting skin lesions,
formation of ne" skin lesions, neritis, and additional sensory
and motor loss.
$he likelihood of a type 8 reaction in patients "ith borderline leprosy is
2AF.<C=
$reatment incldes nonsteroidal anti3infammatory drgs (!*AIDs) and
high3dose steroids. 1rednisone is given at a dose of 7A3BA
mgGday "ith a decreasing taper of 5 mg every >37 "eeks after
improvement is demonstrated.
$ype > reaction
Hrythema nodosm leprosm (H!(), also kno"n as lepra type > reaction, is
a complication of lepromatos leprosy. It is characteri/ed by the
development of infamed sbctaneos nodles accompanied at
times by fever, lymphadenopathy, and arthralgias. Eigh levels of
tmor necrosis factor3alpha and immne comple% deposition are
associated "ith H!(.<C= $reatment incldes prednisolone,
clofa/imine, or thalidomide. Hrythema nodosm leprosm
reaction is seen in the image belo".
1atient "ith mltibacillary leprosy sho"ing sbse4ent erythema nodosm
leprosm reaction. *anta Clara, California. (Cortesy of D. *cott *mith, &D)
&ild H!( reactions are treated "ith aspirin BAA38>AA mgGday in 73B doses
per day.
*evere H!( reactions are treated "ith prednisone BA3;A mgGday "ith a slo"
taper, redcing by 538A mg every >37 "eeks, depending on
response and severity, to prevent residal deformity and nerve
damage.
Alternatively, thalidomide 8AA mg 1L 7 times per day (if available and in
the absence of contraindications) can be sed in cases that
involve large sbctaneos pla4es, arthritis, and temperatre
that e%ceeds 2;.;IC.
(cio phenomenon is a severe complication of mltibacillary leprosy that is
marked by ble hemorrhagic pla4es and necrotic lcerations. $he
bacilli may e%tend to the endothelial cells along "ith the appearance
of necrotic epidermis and vasclitis "ith thrombs formation and
endothelial proliferation.
Prognosis
@ecovery from nerologic impairment is limited, bt skin lesions
generally clear "ithin the frst year of therapy. Discoloration and skin
damage typically persist.
1hysical therapy, reconstrctive srgery, nerve and tendon
transplants, and srgical release of contractres have all contribted
to increasing the fnctional ability in patients "ith leprosy. A common
residal deformity is insensitive feet, as seen in persons "ith diabetes.
Patient Education
@egional amblatory clinics: $he !ational Eansen9s Disease 1rograms
(!ED1) provide otpatient services and medical care to patients "ith
leprosy in the Mnited *tates and 1erto @ico. +ith the goals of
prevention and early detection, the program spports delivery of
services in areas "ith considerable poplations of patients "ith
leprosy. ,or additional information abot these free services, contact
the !ED1 directly at 83;AA3B7>3>7CC. $he !ED1 Center in Naton
@oge, (a, provides free histopathologic services to facilitate
diagnosis. Hleven otpatient ED clinics are located at hospitals,
niversities, and pblic health departments in Ari/ona, California,
,lorida, Illinois, &assachsetts, !e" York, 1erto @ico, $e%as, and
+ashington. $hese clinics provide the follo"ing services:
*kin biopsy diagnostic confrmation
Additional medical care
Eospitali/ation for treatment complications
Consltations
&aterials for professional and patient edcation
1atients "ith leprosy shold be advised abot the importance of
contining long3term therapy ntil the corse of antibiotics is
completed. $he +EL recommends that the monthly administration of
rifampin be directly observed.
In patient "ith leprosy "ho have advanced nerve damage, self3care
techni4es are of tmost importance in maintaining fnction and
preventing frther disability. $he se of visal inpt to reglate
activity, self3inspection, hygiene, and proper foot"ear can help
prevent lcer formation and tisse damage.
$he +EL recommends e%amination of all hosehold contacts of
patients "ith leprosy, "ith carefl instrctions to seek medical care if
signs and symptoms of leprosy appear.
1regnancy in patients "ith leprosy can reslt in hormonal
changes that lead to sppression of cell3mediated immnity, "hich may
e%acerbate symptoms of leprosy. ,rthermore, pregnant "omen "ith
leprosy are at greater risk of developing reactions and relapses. $ype 8
reactions are more likely dring the frst fe" months follo"ing childbirth,
"hereas type > reactions typically occr dring the third trimester of
pregnancy and dring lactation.<C=