Background

Irritant contact dermatitis (ICD) is inflammation of the skin typically manifested by erythema, mild edema, and scaling. Irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage that releases mediators of inflammation predominately from epidermal cells. A corrosive agent causes the immediate death of epidermal cells, manifested by chemical burns and cutaneous ulcers. Note the image belo .

Chronic irritant contact dermatitis of the hands in an older resulted in early retirement.

orker! the condition

"he hands are the most important sites of irritant contact dermatitis. Irritant contact dermatitis from repeated orkplace e#posure of the hands to soaps, cleansers, and solvents is the source of most occupational skin disorders. Irritant contact dermatitis remains understudied compared ith allergic contact dermatitis. $ost articles on contact dermatitis concern allergic contact dermatitis. "his largely reflects the fact that ith history and patch testing, a specific hypersensitivity and a probable cause of dermatitis can be identified in most cases of allergic contact dermatitis. No diagnostic test e#ists for irritant contact dermatitis. "he diagnosis rests on the e#clusion of other cutaneous diseases (especially allergic contact dermatitis) and on the clinical appearance of dermatitis at a site sufficiently e#posed to a kno n cutaneous irritant. %aboratory studies may be of value in eliminating some disorders from the differential diagnosis. (&ee 'orkup). "he definitive treatment of irritant contact dermatitis is the identification and removal of any potential causal agents. Advise individuals to use ceramide creams or bland emollients after ashing hands ith soap and before sleep. (&ee "reatment.) Although the term hypoallergenic is used idely in the marketing of consumer products, no (ood and Drug Administration)approved definition of *hypoallergenic* e#ists. Individuals ith susceptible skin (eg, atopic dermatitis, facial skin of individuals ith rosacea) ould benefit greatly from hypoirritating cleansers, cosmetics, moisturi+ers, and protectants, but there is no standard method for identifying such products. ,o to Allergic Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact Dermatitis for complete information on these topics.

Pathophysiology
Irritant contact dermatitis is the clinical result of sufficient inflammation arising from the release of proinflammatory cytokines from skin cells (principally keratinocytes), usually in response to chemical stimuli. Different clinical forms may arise. "he . main pathophysiological changes are skin barrier disruption, epidermal cellular changes, and cytokine release. 'ith sufficient concentration or duration of e#posures, a ide range of chemicals can act as cutaneous irritants. Common cutaneous irritants include solvents, microtrauma, and mechanical irritants. Cumulative irritant contact dermatitis from repeated mild skin irritation from soap and ater is common. (or e#ample, hand/ ashing fre0uency of more than .1 times per shift as associated strongly ith occupational hand dermatitis in intensive care unit orkers (odds ratio 2 3.4.). &imilarly, most cases of

*homemaker5s* ec+ema are irritant contact dermatitis resulting from repeated skin e#posure to lo /grade cutaneous irritants, particularly soaps, ater, and detergents. &olvents cause cutaneous irritation because they remove essential fats and oils from the skin, hich increases transepidermal ater loss and renders the skin susceptible to the increased direct to#ic effects of other previously ell/tolerated cutaneous e#posures. "he alcohol propanol is less irritating to the skin than the detergent sodium lauryl sulfate. p Ka, an acid dissociation constant, is a 0uantitative measure of the strength of an acid in solution. p Ka has been sho n to be highly predictive of acute skin irritation for acids and bases6 acids ith a p Ka of less than 3 and bases ith a p Ka of less than 7 are highly irritative.849 $icrotrauma may produce skin irritation. A common e#ample is fiberglass, hich may produce pruritus ith minimal visible inflammation in susceptible individuals. $any plant leaves and stems bear small spicules and barbs that produce direct skin trauma. -hysical irritants (eg, friction, abrasive grains, occlusion) and detergents such as sodium lauryl sulfate produce more irritant contact dermatitis in combination than singly. 8:9 -ropanol and sodium lauryl sulfate are not additive irritants, ho ever. &kin irritation predisposes the skin to develop sensiti+ation to topical agents. &kin irritation by both nonallergenic and allergenic compounds induces %angerhans cell migration and maturation. 8.9 An e#acerbation of irritant contact dermatitis may reflect development of allergic contact dermatitis to topical creams, medications, or rubber gloves. "he pathogenesis of irritant contact dermatitis involves resident epidermal cells, dermal fibroblasts, endothelial cells, and various leukocytes interacting ith each other under the control of a net ork of cytokines and lipid mediators. ;eratinocytes play an important role in the initiation and perpetuation of skin inflammatory reactions through the release of and responses to cytokines. <esting keratinocytes produce some cytokines constitutively. A variety of environmental stimuli (eg, ultraviolet light, chemical agents) can induce epidermal keratinocytes to release the follo ing cytokines6 Inflammatory cytokines (interleukin 4, tumor necrosis factor/alpha) Chemotactic cytokines (interleukin 7, interleukin 4=) ,ro th/promoting cytokines (interleukin >, interleukin ?, interleukin 41, granulocyte/macrophage colony/stimulating factor, transforming gro th factor)alpha) Cytokines regulating humoral versus cellular immunity (interleukin 4=, interleukin 4:, interleukin 47) Intercellular adhesion molecule 4 promotes the infiltration of leukocytes into the epidermis in cutaneous inflammatory reactions, including irritant contact dermatitis. &ignificantly increased numbers of dividing keratinocytes are present 37 and @> hours after e#posure to the anionic emulsifying agent sodium lauryl sulfate (used in shampoos, skin cleansers, acne treatments, and toothpastes and in laboratories as an e#perimental irritant). Ao ever, Aeinemann et al found that repeated occlusive application of =.1B sodium lauryl sulfate over . eeks often resulted in adaptation (the so/called hardening phenomenon), ith an increase in ceramide 4 in the lipid composition of the stratum corneum.839 All irritants provoke a similar pattern of cellular infiltration in the dermis! the densities of most of the cell types rise in proportion to the intensity of inflammation. 'ithin the epidermis, marked differences e#ist in the patterns of cellular infiltration among different irritants. Individuals ith a history of atopic dermatitis are prone to develop irritant contact dermatitis of the hands. -olymorphisms in the filaggrin (FLG) gene, hich result in loss of filaggrin production, may alter the skin barrier and are a predisposing factor for atopic dermatitis. FLG null alleles are associated ith increased susceptibility to chronic irritant contact dermatitis.819

Etiology
Almost any material may be a cutaneous irritant, if the e#posure is sufficiently prolonged andCor the concentration of the substance sufficiently high. Dnvironmental factors may enhance the effect of other irritants.

Dry air and temperature variation

Dry air renders the skin more susceptible to cutaneous irritants. &ufficiently dry air alone may provoke irritant contact dermatitis. $ost cases of inter itch are a result of dry skin from the drier air found during sustained periods of cold eather. An increase in temperature (up to 3.EC from :=EC) increases the cutaneous effect of an irritant. 8>9

Water
Continual e#posure to ater may produce maceration or repeated evaporation of ater from the skin may produce cutaneous irritation by desiccation of the skin. Dven distilled ater e#perimentally provokes increased CD44cF cells and neutrophils in the epidermis.

Solvents
$any individuals are e#posed to solvents, particularly at ork. &olvents such as alcohol or #ylene remove lipids from the skin, producing direct irritant contact dermatitis and rendering the skin more susceptible to other cutaneous irritants, such as soap and ater. Irritant contact dermatitis from alcohol most often is cumulative. $anual orkers may ash their hands inappropriately ith solvents to remove oil, grease, paints, or other materials! thus, they develop irritant contact dermatitis. Inappropriate skin cleansing is a primary cause of irritant contact dermatitis in the orkplace. 'ashing facilities and methods must be inspected hen investigating the orkplace for 4 or more cases of occupational irritant contact dermatitis. "he irritating agents include aromatic, aliphatic, and chlorinated solvents, as ell as solvents such as turpentine, alcohol, esters, and ketones. &ome organic solvents produce an immediate erythematous reaction on the skin and remove lipids from the stratum corneum.

Metalworking fluids
Neat oils most commonly produce folliculitis and acne. "hey may cause irritant contact dermatitis (as ell as allergic dermatitis). 'ater/based metal orking fluids often cause irritant contact dermatitis in e#posed orkers! surfactants in these fluids are the main culprit.

Cumulative irritant contact dermatitis

"his is common in many occupations that often are termed * et ork.* Aealthcare orkers ash their hands :=/3= times a day, producing cumulative irritant contact dermatitis. &imilar e#posures occur among individuals ho ash hair repeatedly or in cleaners or kitchen orkers. $ultiple skin irritants may be additive or synergistic in their effects. Alcohol/based hand/cleansing gels cause less skin irritation than hand ashing and therefore are preferred for hand hygiene from the dermatological point of vie . An alcohol/based hand/cleansing gel may even decrease, rather than increase, skin irritation after a hand ash, o ing to a mechanical partial elimination of the detergent. 8?9

Microtrauma
(iberglass produces direct damage to the skin, usually manifested by pruritus that may result in e#coriation and secondary skin damage. Cutaneous irritation primarily is caused by fiberglass ith diameters e#ceeding 3.1 Gm. Controversy surrounds hether individuals ith dermatographism are more susceptible to fiberglass dermatitis.

$ost orkers ith irritant contact dermatitis resulting from fiberglass develop hardening, in hich they tolerate further cutaneous e#posure to fiberglass. $any plant leaves and stems bear small spicules and barbs that produce direct skin trauma

Mechanical trauma
-ressure produces callus formation. -ounding produces petechia or ecchymosis. &udden trauma or friction produces blistering in the epidermis. <epeated rubbing or scratching produces lichenification. & eating and friction appear to be the main cause of dermatitis that appears under soccer shin guards in children.879

Ru

er gloves

&ome rubber gloves may provoke direct cutaneous irritation. $any orkers complain of irritation from the po der in rubber gloves. <emember that gloves compromised by a hole may allo an irritant to enter! occlusion dramatically increases skin damage from the irritant. Hcclusion accentuates the effects, good or bad, of topical agents. ;erosene may produce skin changes similar to that of to#ic epidermal necrolysis follo ing occluded cutaneous e#posure. D#cessive amounts of ethylene o#ide in surgical sheets also may produce similar changes.

Sodium lauryl sulfate

"his chemical is found in some topical medications, particularly acne medications, as ell as a range of soaps and shampoos. It is also a classic e#perimental cutaneous irritant.

!ydrofluoric acid
A hydrofluoric acid burn is a medical emergency. <emember that onset of clinical manifestations may be delayed after the acute e#posure (this is crucial to diagnosis). Infortunately, hydrofluoric acid burns are most fre0uent on the digits, here the pain is most severe and management is most difficult (see Aydrofluoric Acid Jurns).

"lkalies
&kin surfaces normally have an acidic pA, and alkalies (eg, many soaps) produce more irritation than many acids. "he *acid mantle* of the stratum corneum seems to be important for both permeability barrier formation and cutaneous antimicrobial defense. Ise of skin cleansing agents, especially synthetic detergents ith a pA of appro#imately 1.1 rather than alkaline pA, may help prevent skin disease. 8@9 -atofisiologi Dermatitis kontak iritan adalah hasil klinis peradangan yang cukup timbul dari pelepasan sitokin proinflamasi dari sel kulit (terutama keratinosit), biasanya dalam menanggapi rangsangan kimia. Jentuk klinis yang berbeda mungkin timbul. . perubahan patofisiologi utama adalah gangguan kulit penghalang, perubahan seluler epidermis, dan pelepasan sitokin. Dengan konsentrasi yang cukup atau durasi eksposur, berbagai bahan kimia dapat bertindak sebagai iritasi kulit. Iritasi kulit yang umum termasuk pelarut, microtrauma, dan iritasi mekanik. Dermatitis kontak iritan kumulatif dari berulang iritasi kulit ringan dari sabun dan air adalah umum. &ebagai contoh, frekuensi mencuci tangan lebih dari .1 kali per shift dikaitkan kuat dengan dermatitis tangan kerKa pada pekerKa unit pera atan intensif (rasio odds 2 3,4.). Demikian pula, sebagian besar kasus *ibu itu* eksim dermatitis kontak iritan yang dihasilkan dari paparan berulang kulit kelas rendah kulit iritasi, terutama sabun, air, deterKen dan.

-elarut menyebabkan iritasi kulit karena mereka menghilangkan lemak esensial dan minyak dari kulit, yang meningkatkan kehilangan air transepidermal dan membuat kulit rentan terhadap peningkatan efek toksik langsung dari sebelumnya ditoleransi eksposur kulit lainnya. Alkohol propanol kurang mengiritasi kulit daripada deterKen natrium lauril sulfat. p ;a, disosiasi asam konstan, adalah ukuran kuantitatif kekuatan asam dalam larutan. p ;a telah terbukti sangat prediktif iritasi kulit akut untuk asam dan basa6 asam dengan ap ;a kurang dari 3 dan basa dengan ap ;a kurang dari 7 sangat iritasi 849. $icrotrauma dapat menghasilkan iritasi kulit. &ebuah contoh umum adalah fiberglass, yang dapat menghasilkan pruritus dengan peradangan terlihat minim pada individu yang rentan. Janyak daun tanaman dan batang beruang spikula kecil dan duri yang menghasilkan trauma kulit langsung. Iritasi fisik (misalnya, gesekan, butir kasar, oklusi) dan deterKen seperti sodium lauryl sulfate menghasilkan lebih dermatitis kontak iritan dalam kombinasi daripada sendiri/sendiri 8:9 -ropanol dan natrium lauril sulfat tidak iritasi aditif, namun.. Iritasi kulit predisposisi kulit untuk mengembangkan sensitisasi terhadap agen topikal. Iritasi kulit oleh kedua nonallergenic dan alergi senya a menginduksi migrasi sel %angerhans dan pematangan 8.9 &ebuah eksaserbasi dermatitis kontak iritan mungkin mencerminkan perkembangan dermatitis kontak alergi terhadap krim topikal, obat/obatan, atau sarung tangan karet.. -atogenesis dermatitis kontak iritan melibatkan sel/sel epidermis penduduk, fibroblas dermal, sel endotel, dan berbagai leukosit berinteraksi satu sama lain di ba ah kendali Karingan sitokin dan mediator lipid. ;eratinosit memainkan peran penting dalam inisiasi dan pelestarian kulit reaksi inflamasi melalui pelepasan dan tanggapan terhadap sitokin. ;eratinosit Istirahat menghasilkan beberapa sitokin konstitutif. Jerbagai rangsangan lingkungan (misalnya, sinar ultraviolet, bahan kimia) dapat menginduksi keratinosit epidermis untuk melepaskan sitokin berikut6 L sitokin inflamasi (interleukin 4, tumor necrosis factor/alpha) L sitokin chemotactic (interleukin 7, interleukin 4=) L -ertumbuhan mempromosikan sitokin (interleukin >, interleukin ?, interleukin 41, granulosit/makrofag colony/stimulating factor, transforming gro th factor/alpha) L &itokin mengatur humoral dibandingkan seluler imunitas (interleukin 4=, interleukin 4:, interleukin 47) Antar molekul adhesi 4 mempromosikan infiltrasi leukosit ke dalam epidermis dalam reaksi peradangan kulit, termasuk dermatitis kontak iritan. &ecara signifikan meningkatkan Kumlah keratinosit membagi hadir 37 dan @> Kam setelah terpapar agen pengemulsi anionik natrium lauril sulfat (digunakan dalam shampoo, pembersih kulit, pera atan Kera at, dan pasta gigi dan laboratorium sebagai iritan eksperimental). Namun, Aeinemann et al menemukan bah a aplikasi oklusif berulang dari =,1B natrium lauril sulfat lebih dari . minggu sering mengakibatkan adaptasi (yang disebut fenomena pengerasan), dengan peningkatan ceramide 4 dalam komposisi lipid dari stratum corneum. 839 &emua iritasi memprovokasi pola yang sama infiltrasi seluler di dermis, kepadatan sebagian besar Kenis sel meningkat secara proporsional dengan intensitas peradangan. Dalam epidermis, perbedaan ditandai ada di pola infiltrasi seluler antara iritasi yang berbeda.

Individu dengan ri ayat dermatitis atopik rentan untuk mengembangkan dermatitis kontak iritan dari tangan. -olimorfisme dalam filaggrin ((%,) gen, yang mengakibatkan hilangnya produksi filaggrin, dapat mengubah penghalang kulit dan merupakan faktor predisposisi untuk dermatitis atopik. (%, alel null dikaitkan dengan peningkatan kerentanan terhadap dermatitis kontak iritan kronis. 819 Dtiologi Aampir semua bahan bisa merupakan iritan kulit, Kika paparan yang cukup lama dan C atau konsentrasi substansi cukup tinggi. (aktor/faktor lingkungan dapat meningkatkan efek iritasi lainnya. Idara kering dan variasi suhu Idara kering membuat kulit lebih rentan terhadap iritasi kulit. Idara cukup kering saKa dapat menimbulkan dermatitis kontak iritan. &ebagian besar kasus gatal musim dingin adalah hasil dari kulit kering dari udara kering yang ditemukan selama periode berkelanKutan cuaca dingin. -eningkatan suhu (hingga 3. E C dari := E C) meningkatkan efek kulit dari iritasi. 8>9 Air -aparan terus/menerus untuk dapat menghasilkan air maserasi atau penguapan berulang air dari kulit dapat menghasilkan iritasi kulit oleh pengeringan kulit. Jahkan air suling eksperimental memprovokasi peningkatan sel F CD44c dan neutrofil pada epidermis. -elarut Janyak orang yang terkena pelarut, terutama di tempat kerKa. -elarut seperti alkohol atau #ilena menghapus lipid dari kulit, memproduksi langsung dermatitis kontak iritan dan rendering kulit lebih rentan terhadap iritasi kulit lainnya, seperti sabun dan air. Dermatitis kontak iritan dari alkohol paling sering adalah kumulatif. -ekerKa manual dapat mencuci tangan mereka dengan tidak dengan pelarut untuk menghilangkan minyak, lemak, cat, atau bahan lainnya, dengan demikian, mereka mengembangkan dermatitis kontak iritan. -embersih kulit yang tidak tepat adalah penyebab utama dari dermatitis kontak iritan di tempat kerKa. $encuci fasilitas dan metode harus diperiksa ketika menyelidiki tempat kerKa untuk 4 atau lebih kasus kerKa dermatitis kontak iritan. -ara agen menKengkelkan termasuk aromatik, alifatik, dan pelarut diklorinasi, serta pelarut seperti terpentin, alkohol, ester, dan keton. Jeberapa pelarut organik menghasilkan reaksi eritematosa langsung pada kulit dan menghilangkan lipid dari stratum korneum. Cairan $etal orking $inyak rapi paling sering menghasilkan folikulitis dan Kera at. $ereka dapat menyebabkan dermatitis kontak iritan (serta dermatitis alergi). $etal orking cairan berbasis air sering menyebabkan dermatitis kontak iritan pada pekerKa yang terpapar, surfaktan dalam cairan ini adalah penyebab utama. Dermatitis kontak iritan kumulatif Aal ini biasa terKadi di banyak pekerKaan yang sering disebut sebagai *pekerKaan basah.* -etugas kesehatan mencuci tangan mereka :=/3= kali sehari, menghasilkan kumulatif dermatitis kontak iritan. Dksposur serupa terKadi di antara individu/individu yang mencuci rambut berulang/ulang atau dalam pembersih atau pekerKa dapur.

Jeberapa iritasi kulit mungkin aditif atau sinergis dalam efek mereka. ,el tangan pembersihan berbasis alkohol menyebabkan iritasi kulit kurang dari mencuci tangan dan oleh karena itu lebih disukai untuk kebersihan tangan dari sudut pandang dermatologis. &ebuah tangan/cleansing gel berbasis alkohol bahkan mungkin menurun, bukan meningkat, iritasi kulit setelah mencuci tangan, karena untuk penghapusan parsial mekanik deterKen. 8?9 $icrotrauma (iberglass menghasilkan kerusakan langsung pada kulit, biasanya dimanifestasikan oleh pruritus yang dapat mengakibatkan celaan dan kerusakan kulit sekunder. Iritasi kulit terutama disebabkan oleh fiberglass dengan diameter melebihi 3,1 m. ;ontroversi seputar apakah individu dengan dermatographism lebih rentan terhadap dermatitis fiberglass. ;ebanyakan pekerKa dengan dermatitis kontak iritan yang dihasilkan dari fiberglass mengembangkan pengerasan, di mana mereka mentolerir paparan lebih lanKut untuk kulit fiberglass. Janyak daun tanaman dan batang beruang spikula kecil dan duri yang menghasilkan trauma kulit langsung "rauma mekanis "ekanan menghasilkan pembentukan kalus. Jerdebar menghasilkan petechia atau ekimosis. "rauma tiba/tiba atau gesekan menghasilkan terik di epidermis. Jerulang menggosok atau menggaruk menghasilkan lichenification. Jerkeringat dan gesekan tampaknya menKadi penyebab utama dermatitis yang muncul di ba ah sepak bola pelindung tulang kering pada anak/anak. 879 &arung tangan karet Jeberapa sarung tangan karet dapat menimbulkan iritasi kulit langsung. Janyak pekerKa mengeluhkan iritasi dari bubuk dalam sarung tangan karet. Ingat bah a sarung tangan dikompromikan oleh lubang dapat memungkinkan seorang iritasi untuk masuk, oklusi dramatis meningkatkan kerusakan kulit dari iritasi. Hklusi menonKolkan efek, baik atau buruk, agen topikal. $inyak tanah dapat menghasilkan perubahan kulit yang mirip dengan "DN berikut paparan kulit tersumbat. Jerlebihan etilen oksida dalam lembaran bedah Kuga dapat menghasilkan perubahan serupa. &odium lauril sulfat ;imia ini ditemukan dalam beberapa obat topikal, obat Kera at khususnya, serta berbagai sabun dan sampo. Ini Kuga merupakan iritan kulit klasik eksperimental. Asam fluorida &ebuah membakar asam fluorida adalah keadaan darurat medis. Ingat bah a timbulnya manifestasi klinis mungkin tertunda setelah akut (ini penting untuk diagnosis). &ayangnya, luka bakar asam fluorida yang paling sering di digit, di mana rasa sakit yang paling parah dan manaKemen yang paling sulit (lihat %uka bakar Asam fluorida). Alkali

-ermukaan kulit biasanya memiliki pA asam, dan alkali (misalnya, banyak sabun) menghasilkan iritasi lebih dari banyak asam. "he *mantel asam* dari stratum korneum tampaknya menKadi penting bagi pembentukan penghalang permeabilitas dan pertahanan antimikroba kulit. -enggunaan agen pembersih kulit, deterKen sintetik terutama dengan pA sekitar 1,1 daripada pA basa, dapat membantu mencegah penyakit kulit. 8@9

Epidemiology
#nited States statistics
Irritant contact dermatitis is common in occupations that involve repeated hand ashing or repeated e#posure of the skin to ater, food materials, and other irritants. Aigh/risk occupations include cleaning, hospital care, food preparation, and hairdressing. "he prevalence of occupational hand dermatitis as found to be 11.>B in : intensive care units and as >@.?B in the most highly e#posed orkers. Aand/ ashing fre0uency of more than .1 times per shift as associated strongly ith occupational hand dermatitis.84=9

$nternational statistics
In Denmark, cleaners comprise the greatest number of affected orkers, but culinary orkers have the highest incidence. A higher proportion of prolonged sick leave is seen among those in food/related occupations compared ith those in et occupations.8449 "he incidence rates of contact dermatitis in ,ermany ere 3.1 per 4=,=== orkers for irritant contact dermatitis, compared ith 3.4 per 4=,=== orkers for allergic contact dermatitis. "he highest irritant contact dermatitis annual incidence rates ere found in hairdressers (3>.@ cases per 4=,=== orkers per year), bakers (:..1 cases per 4=,=== orkers per year), and pastry cooks (4>.@ cases per 4=,=== orkers per year.84:9

Se%ual differences in incidence

Irritant contact dermatitis is significantly more common in omen than in men. "he high fre0uency of hand ec+ema in omen in comparison ith men is caused by environmental factors, not genetic factors. Hccupational irritant contact dermatitis affects omen almost t ice as often as men, in contrast to other occupational diseases that predominantly affect men. 'omen are e#posed more highly to cutaneous irritants from their disproportionately greater role in housecleaning and the care of small children at home. In addition, omen predominantly perform many occupations at high risk for irritant contact dermatitis (eg, hairdressing, nursing).

"ge&related differences in incidence

Irritant contact dermatitis may occur at any age. $any cases of diaper dermatitis are irritant contact dermatitis resulting from direct skin irritants present in urine and, especially, feces. Hlder persons have drier and thinner skin that does not tolerate soaps and solvents as ell as younger individuals. Hccupational hand ec+ema often is associated ith persistent dermatitis and prolonged sick leave, ith substantially greater severity among those ith occupational irritant contact dermatitis and atopic dermatitis and age older than 1= years.

Prognosis
-rognosis is good for nonatopic individuals in hom irritant contact dermatitis is diagnosed and managed promptly. Individuals ith atopic dermatitis remain highly susceptible to irritant contact dermatitis and may find that the tasks of many common occupations (eg, nursing, hairdressing) produce too much direct skin inflammation to continue ith these careers. Aardening may be specific to the irritant inducing the hardening phenomenon and does not occur in all persons e#posed long term to an irritant.849 Aardened skin may also have a thickened stratum granulosum, ith changes in the e#pression of various inflammatory mediators and markers. 849 An induction of an

increase in the stratum corneum lipid ceramide 4 may play a key role as a protection mechanism against irritation by repeated application of sodium lauryl sulfate. 8:, 39 Activities of daily living and ork may be reduced by severe irritant contact dermatitis. Acute irritant contact dermatitis reactions to potent irritants (eg, acids, alkaline solutions) are comparable to a chemical burn and can be graded like thermal burns (ie, first/, second/, or third/degree burns). 'ith appropriate symptomatic management, the prognosis for this type of irritant contact dermatitis is usually good, and, unless the dermis is damaged, no permanent scarring should occur. &ee Chemical Jurns for more information.

Mortality
Aydrofluoric acid is a potent cutaneous irritant used in lo /technology and high/technology industries and at home in rust removal.84.9 Death from hypocalcemia may ensue if as little as 4B of the skin5s surface area is e#posed sufficiently to this strong inorganic acid and if complications are not managed optimally (seeAydrofluoric Acid Jurns).

Patient Education
<emind individuals that they must continue to avoid cutaneous irritants! they ill redevelop or aggravate dermatitis if they continue to have the same skin care e#posures that resulted in irritant contact dermatitis. "he possibility of secondary or complicating allergic contact dermatitis al ays must be borne in mind. (or patient education information, see the &kin, Aair, and Nails Center, as ell asContact Dermatitis.

!istory
A detailed history is re0uired because the diagnosis of irritant contact dermatitis rests on the history of e#posure of the affected body site to the cutaneous irritant. -atch testing also is used in severe or persistent cases to e#clude allergic contact dermatitis as a component of the individual5s cutaneous manifestations. Hnset of symptoms occurs ithin minutes to hours of e#posure in simple acute irritant contact dermatitis. Acute delayed irritant contact dermatitis is characteristic of certain irritants, such as ben+alkonium chloride (eg, +ephiran, a preservative and disinfectant), hich elicits a deferred (7/:3 h after e#posure) inflammatory reaction.8439 "he onset of signs and symptoms may be delayed by eeks in cumulative irritant contact dermatitis. Cumulative irritant contact dermatitis is a conse0uence of multiple incidents of subthreshold damage to the skin, ith the time bet een e#posures being too short for a full resolution of skin barrier function. -atients ith sensitive skin (ie, atopic individuals) have a decreased irritant threshold or a prolonged restoration time, making them more vulnerable to clinical irritant contact dermatitis. Cumulative irritant contact dermatitis typically occurs ith e#posure to eak irritants rather than strong ones. Hften, the e#posure (eg, ater) is not only at ork but also at home. "hese patients report both itching and pain caused by fissuring of the hyperkeratotic skin (chapping). -ain, burning, stinging, or discomfort e#ceeding pruritus occur early in the clinical course. %ess important subKective criteria for irritant contact dermatitis include the onset of dermatitis ithin : eeks of e#posure, and reports of many other co orkers or family members affected.

'ccupational history
Irritant contact dermatitis is a maKor occupational disease! skin disorders comprise up to 3=B of occupational illnesses. "he physician needs to take an occupational history from adults ith suspect irritant contact dermatitis.

Hccupational irritant contact dermatitis typically affects orkers ho are ne to a Kob, ho are constitutionally more susceptible to irritant contact dermatitis, or ho have not learned to protect their skin from cutaneous irritants. Individuals ith history of atopic dermatitis (especially of the hands) are more susceptible to irritant contact dermatitis, particularly of the hands. $ost affected orkers have a degree of permanent inKury that is lo er than that of other occupational diseases! ho ever, the compensation pay as higher for skin diseases than for diseases of the respiratory system or musculoskeletal disorders, according to a study in Denmark.

Physical E%amination
<ietschel and (o ler proposed the follo ing as primary diagnostic criteria for irritant contact dermatitis 8419 6 $acular erythema, hyperkeratosis, or fissuring predominating over vesiculation ,la+ed, parched, or scalded appearance of the epidermis Aealing process beginning promptly on ithdra al of e#posure to the offending agent Negative results on patch testing that includes all possible allergens $inor obKective criteria for irritant contact dermatitis include the follo ing6 &harp circumscription of the dermatitis Dvidence of gravitational influence such as a dripping effect %o er tendency for the dermatitis to spread than in cases of allergic contact dermatitis $orphologic changes suggesting small differences in concentration or contact time producing large differences in skin damage Individuals may develop a habit of continuing to rub a site initially affected by irritant contact dermatitis and may develop secondary neurodermatitis or lichen simple# chronicus (lichenification). "his may be accepted as a se0uela of an occupational inKury.

Complications
&kin lesions may become coloni+ed secondarily andCor infected, particularly by Staphylococcus aureus. &econdary neurodermatitis (lichen simple# chronicus) may develop in individuals ith irritant contact dermatitis, particularly in those ith orkplace e#posures or under psychological stress. -ostinflammatory hyperpigmentation or hypopigmentation may occur in areas affected by irritant contact dermatitis or persist after resolution of irritant contact dermatitis in individuals ith more pigmented skin. &carring may occur after corrosive agent e#posure, e#coriation, or artifact, causing ulceration. Irritant contact dermatitis increases the risk of sensiti+ation to topical medications.

"pproach Considerations
No diagnostic test e#ists for irritant contact dermatitis. "he diagnosis rests on the e#clusion of other cutaneous diseases (especially allergic contact dermatitis) and on the clinical appearance of dermatitis at a site sufficiently e#posed to a kno n cutaneous irritant. %aboratory studies are generally of little value in proving a diagnosis of contact dermatitis. Ao ever, they may be of value in eliminating some disorders from the differential diagnosis. (indings of significantly elevated serum immunoglobulin D occasionally are useful to substantiate an atopic diathesis in the absence of a personal or family history of atopy. ,o to Allergic Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact Dermatitis for complete information on these topics.

Bacterial and (ungal Studies

A bacterial culture can be obtained in cases complicated by secondary bacterial infection. A potassium hydro#ide (;HA) e#amination of scrapings may be performed and samples for mycology may be obtained to e#clude superficial tinea infections or candidal infections, depending on site and morphology of lesions.

Patch )esting
-atch testing can be performed to diagnose contact allergies, but no patch test e#ists that proves that a cutaneous irritant is responsible for a particular case of irritant contact dermatitis. Diagnosis rests on e#clusion of allergic contact dermatitis and history of sufficient e#posure to a cutaneous irritant. Also see the follo ing summaries of clinical guidelines from the Moint Council of Allergy, Asthma and Immunology6 Allergy diagnostic testing6 an updated practice parameter. -art 4 84>9 Allergy diagnostic testing6 an updated practice parameter. -art : 84?9

Skin Biopsy
&kin biopsy can help e#clude other disorders, such as tinea, psoriasis, or cutaneous "/cell lymphoma. All clinical cases of dermatitis are similar histologically. &kin biopsy of skin lesions of the palms and soles has several potential pitfalls. "he stratum corneum and epidermis are particularly thick there, hich makes the histologic diagnosis of psoriasis more difficult and increases the possibility that the specimen lacks sufficient dermis for optimal diagnosis. In the thenar area, an overly deep biopsy can cut the recurrent branch of the median nerve. A biopsy from the sole may leave a chronic painful scar on hich the patient must alk. A sauceri+ed shave biopsy is usually the most suitable method.

Direct Microscopy
&kin scrapings of cutaneous lesions may help e#clude scabies or may reveal fiberglass fibers as a cause of a patient5s pruritus.

!istologic (indings
"he histopathology of acute e#perimental irritant contact dermatitis has been studied to a greater e#tent than chronic irritant contact dermatitis, hich is the primary clinical complaint. Cellular changes seen in the skin vary according to the chemical nature and concentration of the irritant applied, duration of e#posure, severity of ensuing response, and time of sampling for acute irritant contact dermatitis. $any primary irritants cause overt necrosis if applied in a sufficiently high concentration for sufficient time. $ost histologic e#aminations of irritant contact dermatitis reveal some degree of intercellular edema or spongiosis in the epidermis. &pongiosis usually is less pronounced than that seen in allergic contact dermatitis reactions. -arakeratosis also is observed idely in irritant contact dermatitis reactions. "he histology of chronic irritant contact dermatitis is one of hyperkeratosis ith areas of parakeratosis, moderate/to/marked epidermal hyperplasia (acanthosis), and elongation of the rete ridges.

Emergency Department Care

Dmergency department treatment may include the follo ing6 "opical soaks ith cool tap ater, Juro solution (463= dilution), saline (4 tspCpint) %uke arm ater baths (antipruritic) Aveeno (oatmeal) luke arm baths Dmollients (eg, hite petrolatum, Ducerin) may be beneficial chronic cases. %arge vesicles may benefit from therapeutic drainage (but not removing the vesicle tops). 849 "hese lesions should then be covered ith antibiotic dressing or a dressing soaked in Juro solution.

Aospital admission is re0uired only in severe cutaneous irritant contact dermatitis, ie, chemical burns from hydrofluoric acid or, occasionally, from freshly mi#ed -ortland cement.

Barrier Creams
Creams containing ceramides (eg, Impruv, Cerave) may be particularly helpful in restoring the epidermal barrier in persons ith irritant contact dermatitis and atopic dermatitis. Creams containing dimethicone (eg, Cetaphil cream) can be helpful in restoring the epidermal barrier in persons ith et ork)related irritant contact dermatitis.

Cleansers
$ost soaps and detergents are alkaline and induce an increase in cutaneous pA, hich affects the physiologic protective acid mantle of the skin by decreasing the fat content. Disruption of stratum corneum and changes in pA are key elements in the induction of irritant contact dermatitis and pruritus by soaps. "hese conditions are e#acerbated in the inter months in patients ith dry, sensitive skin. &yndets, ith a pA appro#imately 1.1, do not modify skin pA. $ost bar soaps and li0uid detergents available on the market are a mi#ture of soap and syndet. A study found that Dove and Cetaphil had a lo er irritant effect than the other soaps tested. Interestingly, no significant correlation as made bet een the price of the products and their irritation potential. Irritant contact dermatitis is a fre0uent problem in health care orkers, due to fre0uent hand ashing. "he best antimicrobial efficacy can be achieved ith ethanol (>=/71B), isopropanol (>=/7=B), and N / propanol (>=/7=B). "he antimicrobial efficacy of chlorhe#idine (:/3B) and triclosan (4/:B) is both lo er and slo er and carries a potential risk of bacterial resistance. "he use of alcohol/based hand rubs containing various emollients instead of irritating soaps and detergents is one strategy to reduce skin damage, dryness, and irritation in health care orkers. Irritant contact dermatitis occurs most fre0uently ith preparations containing 3B chlorhe#idine gluconate, less fre0uently ith nonantimicrobial soaps and preparations containing lo er concentrations of chlorhe#idine gluconate, and least fre0uently ith ell/formulated alcohol/based hand rubs containing emollients and other skin conditioners.

"pproach Considerations
"he definitive treatment of irritant contact dermatitis is the identification and removal of any potential causal agents. An inflammatory reaction from acute delayed irritant contact dermatitis to an agent such as ben+alkonium chloride (eg, +ephiran) rarely needs treatment and usually resolves ith cessation of e#posure. (urther symptomatic therapy depends on the degree of involvement and the presence or absence of secondary infection. Advise individuals to use ceramides creams or bland emollients after ashing hands ith soap and before sleep. Cleansers may be ranked by their irritancy.8479<ecommend mild skin cleansers (eg, A0uanil, Cetaphil cleanser, Hilatum AD, Neutrogena cleanser) in place of soap on affected areas. Instruct individuals to refrain from the use of inappropriate solvents (eg, gasoline) or abrasives (eg, pumice stone) to cleanse hands! these directly defat or traumati+e the skin. A clinical guideline summary from the American Academy of Allergy, Asthma and Immunology, Contact Dermatitis6 A -ractice -arameter, may be helpful.84@9 A summary of the Danish Contact Dermatitis ,roup guideline for hand ec+ema includes a diagrammed se0uence of general treatment principles and notes that moisturi+ing cream should be given in combination ith all treatments. If hand ec+ema does not resolve ithin 4 month, the guideline recommends physicians refer the patient to a dermatologist! longer delays are associated ith a poorer prognosis.8:=9 ,o to Allergic Contact Dermatitis, -ediatric Contact Dermatitis, and -rotein Contact Dermatitis for complete information on these topics.

Steroids and $mmunomodulators

"opical corticosteroids and immunomodulators are of unproven use in treating irritant contact dermatitis. Corticosteroids ere found ineffective in treating the surfactant/induced irritant dermatitis hen compared ith the vehicle and ith the untreated control.8:49 Ao ever, topical steroids may be helpful for superimposed ec+ematous features. -otential complications center on the use of steroids, particularly around the eye. "he avoidance of long/ term steroid use is essential, because such use may cause cataracts, glaucoma, corneal thinningCperforation, and loss of the eye, as ell as other problems. "opical tacrolimus is an irritant that may produce further stinging and irritation in persons ith irritant contact dermatitis.8::9

Consultations
$ultidisciplinary consultations may be re0uired hen many orkers become affected ith irritant contact dermatitis in a orkplace. Identifying and remediating the causes of idespread irritant contact dermatitis interfering ith orkplace productivity and orker 0uality of life is important. Any patient ith hydrofluoric acid burn should be evaluated as a medical emergency by a physician e#perienced in the management of hydrofluoric e#posures and burns. Consider regional intravenous infusion of calcium gluconate as a therapeutic option in hydrofluoric acid burns to forearm, hand, or digits hen topical therapy fails.

Medication Summary
After the identification and removal of any potential causal agents, the use of ceramides creams or bland emollients and bland barrier creams such as those containing dimethicone are the mainstays of medical treatment for irritant contact dermatitis. A number of agents commonly found in therapeutic products for the skin (eg, propylene glycol, lactic acid, urea, salicylic acid) may produce further skin inflammation and may need to be avoided in these individuals. "opical corticosteroids play a limited role in the treatment of irritant contact dermatitis. "hey do not address the process directly, but they may be helpful for superimposed ec+ematous features.

Corticosteroids* topical
Class Summary
Corticosteroids are immunosuppressives ith anti/inflammatory properties that modify the body5s immune response to diverse stimuli. Hther actions include vasoconstriction and antiproliferation. "hese agents have limited use in the treatment of irritant contact dermatitis.
Nie full drug information

"mcinonide
A highly potent, fluorinated corticosteroid (class :/.), amcinonide suppresses mitotic activity and causes vasoconstriction. It stimulates synthesis of en+ymes needed to decrease inflammation and may suppress histamine release associated ith pruritus.
Nie full drug information

(luocinolone +Cape%* Derma&Smoothe,(S(luocinolone is a fluorinated corticosteroid of mid potency at the =.=:1B concentration (class 3/1) and mild potency at the =.=4B concentration (class >).