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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 likelyLocalized
- Seborrheic dermatitis- Statis dermatitis- Atopic eczema- Tinea- Asteatosis
Diseminated- Atopic eczema- Asteatosis- Autoeczematization- Tinea corporis
ConsiderLocalized
- Lichen Simplex chronicus- Herpes simplex- Herpes zoster- Steroid acne- Rosacea- Factitial dermatitis
Diseminated- Psoriasis- Polymorphous light eruption- Nummular eczema- Parapsoriasis- Lyme disease- Drug eruption- Secondary syphilis
Always Rule OutLocalized
- Allergic contact dermatitis- Bowen disease
Diseminated- Allergic contact dermatitis- Secondary syphilis- Cutaneous T-cell lymphoma
CASE REPORT
Identity of Patient
Name : Mrs. FY
Sex : Female
Registration Number : 0-89-96-79
Age : 47 years old
Address : Lambaro Skep, Banda Aceh
Career : Trader
Hospitalized : September 14th, 2012
Examination Day : 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 : Diabetic Mellitus
4. Family History : Denied
5. Social History : bad hygiene
6. History of medicine : 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 it’s 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 : dubia ad bonam
- Quo ad functionam : dubia ad bonam
- Quo ad sanctionam : 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 Allergic CD
Symptoms Acute Stinging, smarting ⇛ itching
Itching ⇛ pain
Chronic Itching/pain Itching/pain
Lesions Acute Erythema ⇛ vesicle ⇛ erosion ⇛ crust ⇛ scaling
Erythema ⇛ papules ⇛ vesicles ⇛ erosions ⇛ crust ⇛ scaling
Chronic Papules, plaques, fissures, scaling, crusts
Papules, plaques, scaling, crusts
Margination and site
Acute Sharp, strictly confined to site of exposure
Sharp, confined to site of exposure but spreading in the periphery; usually tiny papules; may become generalized
Chronic Ill-defined Ill-defined, spreads
Evolution Acute Rapid (few hours after exposure)
Not so rapid (12 to 72 hours after exposure)
Chronic Months to years of repeated exposure
Months or longer; exacerbation after every re-exposure
Causative agents
Dependent on concentration of agent and state of skin barrier; occurs only above threshold level
Relatively independent of amount applied, usually very low concentrations sufficient but depends on degree of sensitization
Incidence May occur in practically everyone
Occurs only in the sensitized
* Differences are printed in bold.
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 after-
work 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 long-
term 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. Fitzpatrick’s 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. Fiddler’s 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?
key=imghires&lang=eng&manage_lang=eng