This is an acute or chronic inflammation of the skin, often sharply demarcated in a particular area, caused by skin contact with certain substances. There are two distinct types of contact dermatitis: allergic contact dermatitis and irritant contact dermatitis. Due to the different ways in which these diseases develop, allergic contact dermatitis is specific to an individual, while irritant contact dermatitis will develop in all people with sufficient exposure to the substance in question.
This type of dermatitis may be caused by a delayed hypersensitivity reaction (allergic contact dermatitis) or it may be caused by a primary chemical irritant. The former occurs when someone is exposed to a substance to which they develop sensitivity. Instead of reacting immediately, the immune system usually reacts some time later, and signs of this reaction occur only when the person is re-exposed to the allergen. This reaction can take between six and 10 days in the case of strong sensitisers, such as poison ivy, or it may take years with weaker sensitisers. On re-exposure, itching and dermatitis may appear within four to 12 hours.
Certain drugs used on the skin contain ingredients that are a major cause of allergic contact dermatitis. These include antibiotics, antihistamines, anaesthetics and antiseptics.
Plants are another frequent cause of contact dermatitis, and there are many potential sensitisers used in the manufacture of shoes and clothing. Metal compounds such as nickel, chromates and mercury, as well as dyes and cosmetics can also cause allergic contact dermatitis. It is important to remember that we are exposed to hundreds of substances on a daily basis that could potentially cause these reactions.
Irritants may damage normal skin or aggravate existing dermatitis. Weak or marginal irritants, such as soap, detergents, acetone or even water, may need several days of exposure to cause signs of damage. Strong irritants, such as acids, alkalis and phenol, cause skin damage within minutes. Irritant contact dermatitis is more common in climates that are dry and warm, most likely due to a reduction in the efficiency of our natural skin barrier. Frequent and prolonged exposure to water may also contribute to this.
Photoallergic or phototoxic contact dermatitis requires exposure to light following the application of certain chemicals to the skin. These appear as an exaggerated response to sunlight. Agents that commonly cause this problem include aftershave lotions, sunscreens and sulphonamide antibiotics in creams or ointments and certain soaps. Medications, taken per mouth, may also cause this form of dermatitis, such as sulphonamide antibiotics and certain diuretics.
Symptoms and signs
Signs of contact dermatitis range from transient redness to severe swelling, with the formation of large blisters, weeping and crusting. Itching is common. The skin findings may mimic other diseases of the skin, or be non-specific, making the initial diagnosis of this condition extremely challenging.
Any exposed skin that comes into contact with a sensitising or irritating substance may be affected. Typically, dermatitis is initially limited to the site of contact, and this may be a useful clue in diagnosing this condition. Certain forms of exposure have very characteristic patterns, e.g. patients exposed to sprayed chemicals may have sparing of protected areas, and individuals working without gloves may have primary involvement of the hands. In some severe cases, contact dermatitis may become widespread.
Diagnosis can be difficult since this type of dermatitis may simulate many other skin conditions. Typical skin changes, pattern of involvement and a history of exposure to a particular substance may help, but identifying the specific substance may require careful questioning about previous exposure.
Patch testing with a standardised group of contact sensitisers may be useful if careful questioning does not provide the information. A specialist should select the test concentrations, particularly for industrial substances.
Patch testing is often done after the eruption has subsided, as the results may not be conclusive during the acute phase of the condition.
A negative patch test may not rule out contact dermatitis. It may merely mean that the offending agent was not tested. There are hundreds of potential culprits.
Skin biopsy may confirm the presence of dermatitis, and rule out other conditions.
The main treatment is to remove the offending agent. Without this, the dermatitis may promptly recur and any treatment is unlikely to be effective. Avoidance can be extremely challenging, e.g. an allergy to nickel may require avoidance not only of jewellery and clothing accessories (e.g. buttons) containing nickel, but also avoidance of nickel containing foods (e.g. canned foods, cocoa and legumes). Other contact sensitisers with potential for significant dietary exposure include chromate, cobalt and balsam of Peru.
Do not initiate an avoidance diet without discussing first this with your doctor.
Avoidance may be further facilitated by use of barrier creams when working with aggravating substances, as well as use of gloves and other protective equipment.
During the acute phase, applying thin gauze cloths soaked in saline or tap water to the lesion can be soothing and cooling. In severe and extensive cases oral corticosteroids can be helpful, particularly when there is facial inflammation.
Cortisone creams and ointments are not useful if there are blisters present, but they can be used once the dermatitis has settled somewhat.
Antihistamines and allergen desensitisation are not effective in contact dermatitis.
The course varies. If the source is removed, the redness disappears within a few days and the blisters dry up. As the inflammation subsides, there may be some scaling or temporary thickening of the skin. Continuing exposure to the causative substance can be expected to perpetuate the dermatitis. Once the skin is damaged by the dermatitis, the chance of developing infections in that area increases. This is an extremely challenging condition for both doctors and patients.
Previously reviewed by Dr D.G.C. Presbury, dermatologist
Updated by Dr Bianca Tod, MBBCh (Wits), dermatology registrar (Tygerberg Hospital), August 2011