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Introduction | Dermatitis is the inflammation of the skin. Irritant contact dermatitis is due to the activated innate immune response to various external agents that involves skin barrier disruption, cellular changes, transepidermal water loss, [10] and release of proinflammatory mediators [4] in response to a chemical damage. [5] Depending on the irritant and its exposure pattern irritant contact dermatitis can be subdivided into three categories as subjective irritancy, acute irritant contact dermatitis and chronic irritant contact dermatitis. |
History of exposure to a cutaneous irritant | Idiosyncratic stinging and smarting reactions occur usually following exposure to cosmetic or sunscreen constituents. [1] Acute irritant contact dermatitis is the result of exposure to concentrated acids, e.g. sulphuric, nitric, hydrochloric, chromic, hydrofluoric acids, strong alkali, e.g. calcium, sodium, potassium hydroxide, wet concrete, sodium and potassium cyanide, organic and inorganic salts, e.g. dichromates, arsenic salts, solvents/gases, e.g. acrylonitrile, ethylene oxide, carbon disulphide, mustine etc. [1] Chronic irritant contact dermatitis is associated with irritants such as detergents, organic solvents, [5] soaps, weak acids, and alkalis, low humidity air, heat, powders, and dusts. [1] Not only the type of irritant, [4] but also the exposure volume, concentration, duration, repetition, and the presence of further environmental and mechanical factors will influence the severity of the disease. [4] |
Frequency of exposure | Subjective irritancy may occur within minutes of contact. [1] Acute irritant contact dermatitis will also result after single overwhelming exposure to an irritant. Chronic irritant contact dermatitis occurs following repetitive exposure to contact. [1] |
Site | Irritant contact dermatitis usually involve the dorsum of the hands and fingers and the finger webs, rather than the palms. Idiosyncratic stinging and smarting reactions may occur usually on the face. Chronic ICD is presenting with dry, scaly fissuring, and eczematous lesions on the fingers and hands. [1] |
Occupation | Nearly 30% of all cases of occupational illness in industrialised countries are due to dermatological problems. [1] Certain occupations such as wet work, e.g. chefs, bakers, bar tenders, caterers, cleaners, hairdressers, metalworkers, nurses, solderers, fisherman, and construction workers are at high risk of getting irritant contact dermatitis. |
Pain | Vesiculation and disruption of the skin [4] with fissuring [1] may be responsible for the pain by some individuals. [7] |
Itching | IL-1 and TNF-α are the primary cytokines involved in the pathogenesis of irritant contact dermatitis that will initiate activation of cascade of secondary cytokines/chemokines such as IL-2, IL-6, GM-CSF, IFN-γ, VEGF, CXCL8, CCL2, CCL5, and CCL20. [4] Itching may one of the earliest presenting features. [3] |
Secondary infections | Loss of skin integrity as a result of dermatitis will favour the skin infections particularly with organisms like Staphylococcus aureus. [6] |
Skin darkening ans scring | Skin barrier impairment in these patients include xerosis, scaling, hyperkeratosis, and inflammation. [8] Postinflammatory hyperpigmentation or hypopigmentation [9] is seen in areas involvedby irritant contact dermatitis. Inflammatry response may be followed healing which may be complicated with scaring. |
History of diabetes mellitus | Risk of getting secondary complications like bacterial infections are more in patients with diabetes mellitus. [6] |
History of asthma, hay fever and bronchial asthma | Patient may have coexisting allergic contact dermatitis which may be associated with other atopic diseases. [2] Atopy is an intrinsic factor that influence the susceptibility to irritant contact dermatitis. [4] |
Fact | Explanation |
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Site | Irritant contact dermatitis usually involve the dorsum of the hands and fingers and the finger webs, rather than the palms. Idiosyncratic stinging and smarting reactions may occur usually on the face. Chronic irritant contact dermatitis involves the fingers and hands. [1] |
Appearance of lesion | There can be erythematous lesions with intense itching in the acute phase. [1] Usually there are no vesicles. [2] Gradually they will become erythematous-scaly as the condition progresses to the subacute phase and will become papular-hyperkeratotic in the chronic phase. [1] Irregular erosions may be surrounded by grouped vesicles on a sharply demarcated, erythematous, and edematous base. [3] Sometimes there can oedema of the area of involvement. [4] |
Fissures | Chronic irritant contact dermatitis is presenting with dry, scaly fissuring, and eczematous lesions on the fingers and hands. [1] |
Scratch marks | Itching is a common feature of the disease. [3] |
Lichenification | Continuous rubbing of a site initially affected by irritant contact dermatitis will develop lichenification. It may be associated with papulous lesions with peculiar lilac-red gradation. [1] |
Hyperpigmentation or hypopigmentation | Skin barrier impairment in these patients include xerosis, scaling, hyperkeratosis, and inflammation. [5] Postinflammatory hyperpigmentation or hypopigmentation is seen in areas involved by irritant contact dermatitis. [6] |
Features of secondary infections | Skin lesions may be secondarily infected [2] with organisms like Staphylococcus aureus and may cause discharge, erythema and tenderness. |
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Allergic contact dermatitis | Allergic contact dermatitis is a common cutaneous eczematous disorder due to a contact with various types of environmental substances. There is a classic eczematous form, and less common noneczematous form. [1] Both innate and adaptive immunologic mechanisms play a role in pathogenesis of allergic dermatitis. [1] Woods and plants, topical medicaments, nickel and cobalt are some common factors triggering the dermatitis. [1] Area of involvement in the body may bge simple guide to evaluate the aetiology of the disease. Irritant contact dermatitis tend to affect the dorsa of the hands, fingers and the finger webs,with no vesicles where as eczema tend to have vesicular lesions on the palms and sides of the fingers. [2] Eyelid swelling is also indicative of allergic contact dermatitis rather than irritant contact dermatitis. [2] Irritant dermatitis may be a non pruritic when compared to allergic dermatitis. [3] |
Erysipelas | Erysipelas is an infectious condition of the skin or subcutaneous tissue which is commonly caused by streptococci sp. Local factors such as disruption of the cutaneous barrier, lymphoedema, venous insufficiency or general factors such as diabetes mellitus, overweight, alcohol misuse may be the risk factors for erysipelas. [4] Swelling, tenderness, warmth on palpation is associated with well demarcrated erythematous margin. Commonly lower limbs are involved. [5] CRP like inflammatory markers will be elevated. [5] |
Lichen Simplex Chronicus | Lichen simplex chronicus is thickening of the skin with variable scaling secondary to repetitive scratching or rubbing. Erythema and pruritus [6] may occur in areas of scalp, neck, extensor forearms and elbows, vulva and scrotum, upper medial thighs, knees, lower legs, and ankles. There are erythematous, scaly, well-demarcated, lichenified, firm, rough plaques seen in the affected areas. [6] Dermatitis due to various causes such as atopic dermatitis and irritant contact dermatitis lead to lichenification. [6] It wil also be associated with diseases like psoriasis. On examination there is a chronic dry thickening of the skin associated with scaling and pigmentation. [7] Lesions may be single or multiple with a characteristic margin. [7] |
Impetigo | This is a common condition in children. [8] Localized red rash where skin may appear red or brown with blisters and pus will be evident, there may be associated lymphadenopathy. This is usually caused by either group A β-hemolytic streptococci or Staphylococcus aureus. [8] A bacterial culture of the skin is the investigation to diagnose the condition. Secondary bacterial infections complicating the irritant contact dermatitis may look similar to impetigo. |
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Patch test | This is the mainstay of diagnosis for allergic contact dermatitis and indirectly used to diagnose the irritant contact dermatitis in an individual sensitised to a particular antigen(s). [1] Standardized concentrations of antigen is applied to the skin commonly using Finn chambers. Differentiation between allergic and irritant contact dermatitis may possible as reactions occur early and fade quickly in irritant dermatitis , whereas allergic reactions have crescendo pattern over many days. [6] Exposure pattern to irritants and negative patch tests to potential allergens aids the diagnosis of irritant contact dermatitis. [1] |
Full blood count | Secondary bacterial infections are a potential complication of irritant contact dermatitis. [1] Neutrophil count will be elevated in case of secondary bacterial infections. [2] |
Bacterial/Fungal testing | Staphylococcus aureus can be cultured from both involved and uninvolved skin in majority of patients with dermatitis. [3] Malassezia and Candida like fungi may also complicate the picture of dermatits and therefore need testing on suspicion. [3] Potassium hydroxide (KOH) examination of scrapings is needed to diagnose candida and other fungal sp. Malassezia folliculitis is a chronic disease with pruritic follicular papules and pustules that affects the upper trunk, neck, and upper arms. [3] |
Direct Microscopy | Viral infections, like herpes simplex virus, may aggravate the dermatitis and need to be excluded. [3] Scabies exclusion needs skin scrapings of cutaneous lesions. [4] |
Skin Biopsy | Skin biopsy is helpful in excluding other disorders, (tinea, psoriasis, or cutaneous T-cell lymphoma) [5] |
Fact | Explanation |
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Serum IgE level | Irritant contact dermatitis has shown increase the risk of developing allergic contact dermatitis in latter course of the disease. [1] May be important in follow up of patients with irritant contact dermatitis associated with allergic contact dermatitis. |
Fact | Explanation |
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Serum immunoglobulin E | Elevated serum immunoglobulin E may be found in individuals with atopy. It is helpful in differentiating irritant contact dermatitis from eczema. [1] |
Mathias criteria | Mathias criteria has a framework of seven objectives to aid the diagnosis of contact dermetitis particularly due to the occupational irritants. [2] Clinical appearance compatible with contact dermatits, history of exposure to cutaneous irritants, anatomical distribution compatible with irritant exposure related to job, temporal relationship of exposure to onset of contact dermatitis, exclusion of other non occupational causes, removal of exposure leading to clinical improvement and patch test indicating specific work place exposur are the seven above mentioned criteria. [2] |
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Identification of risk factors for irritant contact dermatitis and prevention | Understanding of the aetiology of a disease is important to introduce preventive strategies. [2] Prevention is the key to monimize the episodes of irritant contact dermatitis. Safe working methods, personal protective equipments, pre-employment screening, elimination or replacement of harmful substances, [2] technical measures are important in reducing the irritant contact dermatitis in the occupational setting. [1] |
Patient education | This is vital in managing the patients with irritant dermatitis as prevention needs a proper understanding about the disease process and its triggering factors. Employers should receive training on safety measures and occupational hazards of particular substance to which they are exposed to. [1] |
Elimination or replacement of harmul exposures | Replacement of the responsible irritant with less irritative substances may be beneficial. eg:- adding ferrous sulphate to cement to inhibit sensitisation to chromium, [1] use of alcohol-based hand rubs containing emollients rather than various irritating soaps |
Technical control measures | This can be considered depending on the route of exposure. eg:- ventilatory controls for mist, dust, fume, or vapour [1] |
Personal protection | Correct use of gloves, barrier creams, after-work creams, soaps etc are beneficial in preventing the attacks. [1] |
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Immediate management | Topical soaks with cool tap water, Burow solution, saline etc can be used for the immediate management. Acute, oozy lesions are initially treated with saline or Burow solution thin wet dressings to dry up the exudate, and latter a potent corticosteroid cream or lotion is applied. [8] Offending agent has to be removed by washing with a gentle soap and water where possible. [2] Large vesicles particularly if they are infected may need therapeutic drainage and antibiotics. Sometimes chemical burns,may require the intensive treatment or surgical intervention during the follow-up. [6] |
Emollients | Emolients are used to protect the skin from environmental and chemical aggressors, soften and soothe dry skin and to reduce itching sensation and irritation signs. [4] Emollients are available as creams, ointments, gels, pastes, or liquid preparations [4] and may be beneficial specifically in chronic cases. They will contain a combination of emollient lipids (e.g., mineral oils, waxes, fatty acids, and glycerides), humectants (e.g., alpha-hydroxy acids, urea, and glycerin), emulsifiers, and antipruritics (e.g., glycine), and inactive components. [4] |
Barrier creams | Barrier creams are important to prevent contact with irritants. [1] Apart from the barrier protection properties, the addition of ingredients in the cream will support barrier repair. [3] |
Topical corticosteroids and immunomodulators | There is no proven benefit from the steroids and immunomodulators. [2] But extensive dermatitis will have some benefit from a short course of systemic corticosteroids. [8] Chronic, fissured, and scaly dermatitis may also be treated with midstrength to potent topical corticosteroids. [8] |
Oral antihistamines | These may be useful for treatment of any associated pruritis. [2,8] |
Management of complications | Secondary complications like bacterial infections need specific antibacterial therapy. [5] Management of post inflammatory hyperpigmentation & scarring may be done with topical depigmenting agents, such as hydroquinone, azelaic acid, kojic acid, licorice extract, and retinoids, used alone or in combination with other agents. [7] Procedures such as chemexfoliation and laser therapy are also effective strategies. [7] |