Case Report

IRRITANT CONTACT DERMATITIS

by: RIDZA WISDA ARVIKA 0807101010111

Supervisor: dr. Nanda Earlia, Sp.KK

DERMATOLOGY AND VENEROLOGY DEPARTMENT SCHOOL OF MEDICINE SYIAH KUALA UNIVERSITY BLUD RSUZA BANDA ACEH 2012

INTRODUCTION
Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions to substances that come in contact with the skin1. This also is a common problem that can be encountered in many settings. The majority of cases are irritant-induced, with 20% being attribute to an allergic etiology2. Irritant contact dermatitis (ICD) is a cutaneous response to contact with an external chemical, physical, or biological agent; endogenous response such as skin barrier function and pre-existing dermatitis also play role3. ICD account for 80 percent of all cases of contact dermatitis, and is often occupation-related. Contact dermatitis is especially common in the work-place, accounting for 90% of occupational skin disease or 7% of all occupational disease4. ICD is a multi-factorial disease where both exogenous (irritant and environmental) and endogenous (host) factors play a role. Irritant contact dermatitis has a spectrum of clinical features which can be divided into several different categories, depending on the irritant, exposure pattern, mechanical, thermal, climatic, and constitutional factors. At least 10 clinical types of ICD have been described such as Acute ICD, Delayed acute ICD, Irritant reaction, Chronic reaction, Traumatic ICD, Acneiform ICD,

Nonerythematous (suberythematous irritation), Subjective (sensory) irritation, Friction dermatitis, Asteatotic irritant eczema, and other clinical subtypes of acute and chronic ICD.1 Pathogenesis Four interrelated mechanisms have been associated with ICD: (1) removal of surface lipids and water-holding substances, (2) damage to cell membranes, (3) epidermal keratin denaturation, and (4) direct cytotoxic effects1. There is a clearly demonstrated immunologic-like component to the irritant response, which is characterized by the release of pro-inflammatory mediators, particularly cytokines, from non immune cutaneous cells (keratinocytes) in response to chemical stimuli. This is a process that does not require previous sensitization5. Mechanisms involved in acute and chronic phases of ICD are fundamentally different. Acute reactions involve direct cytotoxic damage to keratinocytes.

Chronic ICD results from repeated exposures to solvents and surfactants that cause slow damage to cell membranes, disrupting the skin barrier and leading to protein denaturation and cellular toxicity.2 Skin Findings May occur minutes after exposure or may be delayed up to 24 hoursmmmmm. The spectrum of changes ranges from erythema to vesiculation and caustic burn with necrosis. Acute ICD represents sharply demarcated erythema and superficial edema, corresponding to the application site of the toxic substance. Lesions do not spread beyond the site of contact. In more severe reactions vesicles and blisters arise within the erythematous lesions, followed by erosions and/or even frank necrosis, as with acids or alkaline solutions. No papules. Configuration often bizarre or linear ("outside job" or dripping effect).2 Diagnosis and Differential Diagnosis Diagnosis is by history and clinical examination (lesions, pattern, site). Rietschel6 has proposed criteria with subjective and objective features, each with major and minor findings for the diagnosis of ICD in the table 1 below. Table 1. Differential Diagnosis of ICD (Major types) Most likely Localized - Seborrheic dermatitis - Statis dermatitis - Atopic eczema - Tinea - Asteatosis Consider Localized - Lichen Simplex chronicus - Herpes simplex - Herpes zoster - Steroid acne - Rosacea - Factitial dermatitis Always Rule Out Localized - Allergic contact dermatitis - Bowen disease Diseminated - Atopic eczema - Asteatosis - Autoeczematization - Tinea corporis

Diseminated - Psoriasis - Polymorphous light eruption - Nummular eczema - Parapsoriasis - Lyme disease - Drug eruption - Secondary syphilis Diseminated - Allergic contact dermatitis - Secondary syphilis - Cutaneous T-cell lymphoma

CASE REPORT
Identity of Patient Name Sex : Mrs. FY : Female

Registration Number : 0-89-96-79 Age Address Career Hospitalized Examination Day : 47 years old : Lambaro Skep, Banda Aceh : Trader : September 14th, 2012 : September 14th, 2012

Anamnese 1. The Chief Complaint: Redish rash are itchy on the left foot sole since 4 days ago 2. History of Present Illness : Patient comes to hospital with chief complaint of red rashes which is very itchy on the left foot sole since 4 days ago. At the beginning the lesion was small and only one. The patient feel very itch in that area so she scrapes it again and again, and next the lesion increase so much than before. Beside that, the patient also felt that the area of lesion swell up and getting warm. At the day she comes to the hospital, the lesion was flatting back but still itched 3. History of Past Illness 4. Family History 5. Social History 6. History of medicine : Diabetic Mellitus : Denied : bad hygiene : drug of Diabetic mellitus, some powder to soothe the itch, and Mikonazole zalf. Dermatologic Status: Location: a/r dorsum pedis sinistra Patch erythematous, plaque size, with irregular margin, sharply demarcated, and in its surface there are vesicles and papules lesion spread localized at the region.

Differential Diagnosis: 1. Irritant Contact Dermatitis 2. Atopic Dermatitis 3. Sebhorrheic Dermatitis 4. Tinea Pedis Supporting Examination: Patch testing Clinical Diagnosis Irritant Contact Dermatitis Treatment Systemic: Anti allergic, Mebhidrolin napadisilat (ex. Interhistin) Topical: Thyamicin 2% / Inerson oint and Asam fusidat (ex. Fuson cream) Education Avoid yourself from any irritant materials and Do not scratch the lesion. Prognose: Quo ad vitam Quo ad functionam Quo ad sanctionam : dubia ad bonam : dubia ad bonam : dubia ad bonam

DISCUSSION

ICD can occur in anyone being exposed to a substance irritant or toxic to the skin1. It may occur minutes after exposure or may be delayed up to 24 hours2. These are some etiologic agents that caused irritant contact dermatitis based on table 3. Table 3 Most Common Irritant/Toxic Agents

Soaps, detergents, waterless hand cleaners Acids and alkalis*: hydrofluoric acid, cement, chromic acid, phosphorus, ethylene oxide, phenol, metal salts. Industrial solvents: coal tar solvents, petroleum, chlorinated hydrocarbons, alcohol solvents, ethylene glycol ether, turpentine, ethyl ether, acetone, carbon dioxide, dioxane, styrene. Plants: Euphorbiaceae (spurges, crotons, poinsettias, machneel tree). Racunculaceae (buttercup), Cruciferae (black mustard), Urticaceae (nettles), Solanaceae (pepper, capsaicin), Opuntia (prickly pear). Others: fiberglass, wool, rough synthetic clothing, fire-retardant fabrics, "NCR" paper. * Lead to chemical burns and necrosis, if concentrated. In this case the patient said that four days ago the lesion was only small, soliter, as a vesicle, then she scratch it (because it felt so itchy), so next day the lesion were multiple and swelling. But on the day the patient comes to hospital, the lesion had been flattened but it still multiple. The lesion occur after exposure. ICD is often diagnosed by excluding other cause for the dermatitis, including ACD. A detailed inquiry, including occupational, recreational (hobbies) and past medical histories, and a meticulous clinical examination are important for making diagnosis. When an allergic component is considered, diagnostic patch testing should be performed.1 If the reaction after this test decreased, that is an

ICD, but if the reaction increased that will be clue for ACD. The standard method involves the application of antigen to the skin at standardized concentration in appropriate vehicle and under occlusion. Back is commonly used principally for convenience. The optimum timing of the patch test readings is probably days 2 and 4. In this case patient comes to hospital with chief complaint of redish rash which is very itchy at the left foot sole since 4 days ago. She said that was the first time she got the rash. It is similar to the theory which is that ICD does not require previous sensitization5. Bourke (2011) also explained the reaction types of contact dermatitis such as acute irritant contact dermatitis that often the result of a single overwhelming exposure or a few brief exposures to strong irritants or caustic agents and chronic (cumulative) irritant contact dermatitis that occurs following repetitive exposure to weaker irritants that may be either wet such as detergens, organic, solvents, soaps, weak acids and alkalis, or dry, such as low humidity air, heat, powders, and dusts. 4 Patient felt the area of lesion was very itchy, no painful. But many theories explain that Irritant contact dermatitis usually more painful than itchy4. I think it just individual perception which is so subjective. The patient did not try patch testing. But if she did, we will see irritant patch test reaction which is present as erythema with or without papules and often remain confined to the test site and are sharply demarcated. The margin and site are sharp, strictly confined to site of exposure.1 The images of irritant contact dermatitis between case report and theory

(An erythema, oedema, bullae and necrosis, leading to a burning and stinging senzation7,9.)

Allergic and irritant contact dermatitis can be difficult to distinguish, because the resulting rashes are very similar. The pattern and location of the rash on the skin help distinguish whether it was caused by an allergen or irritant. Table 2 Differences Between Irritant and Allergic Contact Dermatitis* Irritant CD Symptoms Acute Stinging, smarting itching Erythema vesicle erosion crust scaling Allergic CD Itching pain Itching/pain Erythema papules vesicles erosions crust scaling

Chronic Itching/pain Lesions Acute

Chronic Papules, plaques, fissures, Papules, plaques, scaling, scaling, crusts crusts Margination Acute and site Sharp, strictly confined Sharp, confined to site of to site of exposure exposure but spreading in the periphery; usually tiny papules; may become generalized Ill-defined, spreads Not so rapid (12 to 72 hours after exposure) Months or longer; exacerbation after every reexposure Relatively independent of amount applied, usually very low concentrations sufficient but depends on degree of sensitization Rapid (few hours after exposure)

Chronic Ill-defined Evolution Acute

Chronic Months to years of repeated exposure Causative agents Dependent on concentration of agent and state of skin barrier; occurs only above threshold level

May occur in practically Occurs only in the everyone sensitized * Differences are printed in bold.

Incidence

Management The management of ICD principally involves the protection of the skin from irritants or avoid caustic chemical(s) by wearing protective clothing (i.e., goggles, shields, gloves). If contact does occur, wash with water or weak neutralizing solution.

Beside that we can use barrier creams to protect skin from irritants. There are controlled clinical showing benefit in the use of soap substitutes and afterwork creams in reducing the incidence and prevalence of contact dermatitis. They should be encouraged and made readily available in the workplace. In occupational ICD that persists in spite of adherence to the above measures, change of job may be necessary. Course and Prognosis Healing usually occurs within 2 weeks of removal of noxious stimuli; in more chronic cases, 6 weeks or longer may be required. In the setting of occupational ICD, only one-third of individuals have complete remission and may require allocation to another job. Several studies have confirmed that the longterm prognosis for occupational contact dermatitis is often very poor.7 Atopic individuals have a worse prognosis too. In cases of chronic subcritical levels or irritant, some workers develop tolerance or "hardening."2 The point is if the patient can avoid the cause of contact dermatitis then dermatitis will clear.
7

REFERENCES
1. Wolff, K., Johnson, Richard A, Suurmond, Dick. 2007. Fitzpatricks Color Atlas & Synopsis of Clinical Dermatology. New York: Mc Graw Hill Companies. 2. Amrol, D., Keitel, D., Hagaman, D., Murray, J. 2003. Topical pimecrolimus in the treatment of human allergic dermatitis. Annals of Allergic, Asthma, & Immunology, Volume 91, 563-6. 3. Wolff, K., Goldsmith, L., Katz, S. I., Gilchrest, B., Paller, A., & Leffeell, D. J. 2008. Fitzpatrick's Dermatology in General Medicine. New York: Mc Craw Hill Companies. 4. Jennifer, E. C; Philip, R.C. 2012. Fiddlers neck: Chin res-associated irritant contact dermatitis and allergic contact dermatitis in a violin player. Texas: Dermatology Online Journal.

http://dermatology.cdlib.org/1809/05_vgn/10_12-00157/article.html [Retrieved on September 16th, 2012] 5. Smith H. R., Basketter, D. A., McFadden J. P. 2002. Irritant dermatitis, irritancy and its role in allergic contact dermatitis. Clin Exp Dermatol, Volume 27, 138. 6. Rietschel, R. L., 2004. Clues to an accurate diagnosis of contact dermatitis. Dermatol Ther, Volume 17, 224.\ 7. Bourke I, Coulson I, English I. Guidelines for Care of Contact Dermatitis. British Journal of Dermatology. 2001: 877-85. 8. Little, Frederic F. 2009. Contact Dermatitis. Chicago: Boston University. http://health.rush.edu/HealthInformation/Pediatric%20Center/28/000011.aspx [Retrieved on September 16th,2012].

9. http://eczema.dermis.net/content/e03typesof/e02irritant/e419/f_zoomImage?k
ey=imghires&lang=eng&manage_lang=eng