Dermatitis, Contact

Article Author:
Pragya Nair
Article Editor:
Amber Atwater
Updated:
10/4/2017 11:26:54 AM
PubMed Link:
Dermatitis, Contact

Introduction

Contact dermatitis is an inflammatory eczematous skin disease. It is caused by chemicals or metal ions that exert toxic effects without inducing a T-cell response (contact irritants) or by small reactive chemicals that modify proteins and induce innate and adaptive immune responses (contact allergens).

Contact dermatitis is divided into irritant contact dermatitis and allergic contact dermatitis. Irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage that releases mediators of inflammation predominantly from epidermal cells while allergic contact dermatitis is a delayed (type 4) hypersensitivity reaction to exogenous contact antigens. Immunological responses are due to the interaction of cytokines and T cells. In photo contact, allergic dermatitis lesions are confined to sun-exposed areas even though the allergen is in contact with covered areas.

Etiology

Irritant contact dermatitis 

The likelihood of developing irritant contact dermatitis (irritant contact dermatitis ) increases with the duration, intensity, and concentration of the substance. Chemical or physical agents and microtrauma may produce skin irritation thus causing Irritant contact dermatitis. Physical irritants like friction, abrasions, occlusion, and detergents like sodium lauryl sulfate produce more irritant contact dermatitis in combination than alone.

The factors which determine the severity of irritant contact dermatitis include quantity and concentration of the irritant, duration, and frequency of exposure. It also depends on the type of skin if it is thick, thin, oily, dry, very fair, previously damaged skin, or having a pre-existing atopic tendency. Environmental factors like high or low temperature and humidity also determine the severity.

Allergic contact dermatitis

Common etiological allergens for allergic contact dermatitis are nickel,  balsam of Peru, chromium, neomycin, formaldehyde, thiomersal, fragrance mix, cobalt, and parthenium.

Epidemiology

Females, infants, elderly, and individuals with atopic tendency are more susceptible to irritant contact dermatitis.  It is reported that up to 80% of cases of occupational dermatitis are irritant contact dermatitis.

All individuals are at risk of developing allergic contact dermatitis.  Risk factors for allergic contact dermatitis include age, occupation, and history of atopic dermatitis.

Pathophysiology

Irritant contact dermatitis 

It is due to sufficient inflammation arising from the release of proinflammatory cytokines from keratinocytes, usually in response to chemical stimuli. It mainly causes skin barrier disruption, epidermal cellular changes, and cytokine release.

Irritants can be classified as cumulatively toxic (e.g., hand soap causing irritant dermatitis in a hospital employee), subtoxic, degenerative, or toxic (e.g., hydrofluoric acid exposure at a chemical plant).

Allergic contact dermatitis

It is T-cell mediated inflammation of the skin caused by repeated skin exposure to haptens in a sensitized individual.

Allergic contact dermatitis has two phases. The sensitization phase in which antigen-specific effector T cells are induced in the draining lymph nodes by antigen captured cutaneous dendritic cells that migrate from the skin. The elicitation phase includes effector T cells that are activated in the skin by antigen captured cutaneous dendritic cells and produce various chemical mediators, which create antigen-specific inflammation.

Histopathology

Contact irritant dermatitis presents with mild spongiosis, epidermal cell necrosis, and neutrophilic infiltration of the epidermis, while in allergic contact dermatitis dermal inflammatory infiltrates predominately contains lymphocytes and other mononuclear cells.

History and Physical

Symptoms of irritant contact dermatitis may include burning, itching, stinging, soreness, and pain, particularly at the beginning of the clinical course, while pruritus is more common in allergic contact dermatitis. Patients with a history are at increased risk for developing nonspecific hand dermatitis and irritant contact dermatitis.

Both irritant contact dermatitis and allergic contact dermatitis can present with three morphological patterns.

  • Acute phase: erythema, edema, oozing,  crusting, tenderness, vesicles or pustules
  • Subacute phase: crusts, scales, and hyperpigmentation
  • Chronic phase: Lichenification. 

Hands are the common site of contact allergic dermatitis.

No pathognomonic clinical signs and symptoms can differentiate between allergic contact dermatitis and irritant contact dermatitis.

The acute irritant reaction usually reaches its peak quickly, within minutes to few hours after exposure, and then starts to heal, while in allergic contact dermatitis, the elicitation time depends on the characteristics of the sensitizer, the intensity of exposure, and degree of sensitivity. Lesions usually appear 24 to 72 hours after the exposure to the causative agent and reach their peak at approximately 72 to 96  hours. Allergic contact dermatitis improves more slowly than irritant contact dermatitis when exposure ends, and then recurs faster (in a few days) when exposure is re-established.

Common allergens causing allergic contact dermatitis includes following -

  1. Paraphenylenediamine (PPD) present in hair dye is the most common cause of allergic contact dermatitis over ears and face rather than the scalp
  2. Neomycin and bacitracin applied to the areas of stasis dermatitis and leg ulcers are the cause of allergic contact dermatitis over legs and feet
  3. Topical neomycin and corticosteroids can lead to allergic contact dermatitis in patients with otitis externa
  4. In women with lichen sclerosus et atrophicus, benzocaine applied in pruritus ani and pruritus vulvae frequently develop allergic contact dermatitis which also complicates chronic vulvar dermatosis
  5. Nickel is the most common metal present in artificial jewelry which is the cause of allergic contact dermatitis.

Different clinical patterns of allergic contact dermatitis include erythema multiforme, urticarial papular plaques, lichen-planus, lichenoid eruptions, purpuric petechial reactions, dermal reactions, lymphomatoid contact dermititis, granulomatous and pustular reactions, pigmentation disturbances, or pemphigoid.

Evaluation

History regarding occupation, hobbies and any topical or oral medications is important in diagnosing contact dermatitis. Patch testing is considered to be the gold standard in diagnosing contact allergic dermatitis and is used to determine the exact cause. A patch test mainly relies on the principle of a. The chemicals included in the patch test kit are chemicals present in metals (e.g., nickel), rubber, leather, formaldehyde, lanolin, fragrance, toiletries, hair dyes, medicine, pharmaceutical items, food, drink, preservative, and other additives. They are the offenders in approximately 85% to 90% of contact allergic eczema. Patch testing helps identify which substances may be causing a delayed-type allergic reaction in a patient and may identify allergens which are not identified by blood testing or skin prick testing. It produces a local allergic reaction on a small area of the patient's back, where the diluted chemicals are  applied.

Patch testing is done after a week of subsidence of active eczema.Allergens are put in Finn chambers and applied over the back of the patient. Results are read on 2 and three days. Grading of the reactions is  done based on the International Contact Dermatitis Research Group guidelines.

Negative (-)

Irritant reaction (IR)

Equivocal / uncertain (+/-)

Weak positive (+)

Strong positive (++)

Extreme reaction (+++)

Treatment / Management

Compliance with avoidance is important. The key to avoidance is proper evaluation and detection of causative allergen. Wear appropriate clothing to protect against irritants at home and in a work environment.

A topical steroid is used to reduce the inflammation. Antihistamines such as hydroxyzine and cetirizine are recommended for controlling the pruritus. Cool compresses with calamine can also be given to stop itching. Systemic steroids are advised in severe cases but should be tapered gradually to prevent recurrences. Friction should be avoided as well as the use of soaps, perfumes, and dyes. Emollients are used for hydrating the skin. Tacrolimus and pimecrolimus ointment are immunomodulating drugs that inhibit calcineurin and is helpful in allergic contact dermatitis. Azathioprine, cyclosporine are immunosuppressive drugs which are used in chronic and resistant cases.