Symptoms for both types of contact dermatitis are essentially the same and they present as a red rash to begin with. This reaction is immediate in case of irritant dermatitis and delayed for few hours or days in case of allergic dermatitis [2] [7]. This is followed by formation of pustules, blisters or even urticaria of that specific part. The area involved in case of irritant dermatitis is confined to area where the trigger has touched the skin but is widely distributed in case of allergic dermatitis.

This progresses to itching, burning and increased sensitivity of the skin. The skin looks rough, dry, parched. In case of systemic contact dermatitis, pre-sensitized individuals may produce a reaction to the allergen entering via any route - oral, inhalant, contact, etc. The commonest manifestation of this is the Baboon syndrome characterized by widespread erythema over inner thighs, buttocks and axillae [8].

The appearance of the skin clinically confirms the diagnosis. Blood tests show an elevated erythrocyte sedimentation rate (ESR) and immunoglobulin E (IgE) levels [9]. History of allergic substances and contact with irritant chemicals or solvents helps in identifying the type of dermatitis.

Patch testing is one of the most reliable tests done which identifies the specific irritant or allergen to which the individual is sensitive. In this test an appropriate chemical is applied to the affected skin and is allowed to remain on skin for at least a day. The test results are read after 48 hours. In individuals with negative testing results, despite of suspected allergic tendency, a repeat testing is done. A delayed positive reaction is observed due to certain chemicals especially neomycin [10].

Topical steroids are used as the primary line of treatment. The use of long term steroids is known to cause local atrophy of skin along with systemic complications. In patients not responding to corticosteroids and with severe allergic dermatitis, are benefited with phototherapy.

Symptomatically, large vesicles are treated by drainage. Then they are covered through dressing containing antibiotics or containing Burrow’s solution to avoid further bacterial infection. For pruritis, oral and topical antihistaminic agents are used. Doxepin cream is a common antihistaminic used. For acute vesicular lesions cool soaks in Burrow’s solution or saline are helpful [11].

For irritant contact dermatitis, local application of restoraderm cream or impruv cream are useful. They act by preserving the epidermal layer of skin from the irritant exposed. Alcohol based hand cleansers are used to reduce further skin damage and irritation. Emollients such as white petroleum jelly are useful for long term chronic disorder.

Rarely, immunosuppressants are utilized. In cases of severe dermatitis caused due to chemical burns, hospital admission might be indicated [12].

Contact dermatitis results in more of morbidity than mortality. Very few deaths have been reported in the US. Morbidity is due to the chronicity of the disease. The disease persists for many years, and older the disease, more amount of time is taken to overcome it. Also, this condition has a strong relapsing tendency.

Irritant contact dermatitis is a result of direct local contact of the irritant on the skin. A significant amount of exposure with respect to its concentration and duration is considered to result in such an inflammation. The agents can be chemicals such as chromic acid, nitric acid, sulfuric acid or strong alkalis like calcium oxide, sodium hydroxide, potassium cyanide, bromine etc.

Dermatitis also results due to local friction from tight undergarments, use of diapers, prosthetic limbs or dressing materials used. Other causes are handling certain plants such as cactus, plastic/rubber materials etc. [3] [4].

Allergic dermatitis generally results after exposure to an allergen that the person has been previously exposed to. Exposures to nickel are one of the frequent causes seen in allergic dermatitis. It is seen in metal workers, clerks, cleaners etc. Certain preservatives used in skin moisturizers, cosmetics leads to an allergic reaction too.

The prevalence of occupational dermatitis is very high and about 1,700 cases are observed every 100,000 individuals. Highest amount of people affected are hairdressers, cooks and people employed in baking industry. It accounts to 95% of all skin disorders. Annually, about 10-20 cases are noted per 10,000 employees.

It affects all age group people. Statistics show that hand eczema is most frequently seen and is more common in females than males. Allergic dermatitis is frequently seen in infants more than in an adult age group [5].

Allergic contact dermatitis is induced through sensitization of haptens which activate the innate immunity. Haptens are self proteins that are identified by the immune system under the skin. These then activate the inflammatory mechanism resulting in the activation of the dendrite cells. The cells then acquire the antigens and settle in the lymph nodes [2] [5] [6]. Here, the antigens are presented to the memory cells. Finally on exposure to antigens, these T cells release cytokines and interferons- gamma to kill the hapten cells, resulting in an inflammatory response in the form of an inflammatory rash on the skin. The initial response occurs after few days of exposure to the allergen, but once the sensitization takes place, individuals develop a reaction within hours of exposure.

There are mainly three pathological changes occurring in case of irritant contact dermatitis. These are epidermal changes, destruction of the skin barrier and release of the cytokines. Keratinocytes play a major role in initiation of the inflammatory response by releasing cytokines. Skin irritation is mainly due to significant irritation caused by using harsh soaps repeatedly especially in individuals who are involved in repeated hand washing multiple times in a day. This leads to loss of essential fats and skin’s protective oils.

Patients must discontinue the use of irritants that produce a skin reaction. They must read about the product or the cosmetic to be used before application. The allergen must be known to them. In diet they should refrain from allergens that would cause an adverse reaction, use of nickel is avoided [7] [13]. A patch test should be done before trying out any new toiletry or cosmetic.

Contact dermatitis is the result of an inflammatory reaction of the skin due to direct exposure to either allergens, called allergic dermatitis, or to an irritant, called irritant contact dermatitis [1]. The substances leading to dermatitis are hapten-specific T cells which are non protein chemical cells. These activate the immune system leading to a delayed type of hypersensitive reaction.

The immune reaction can be innate or acquired depending on the substance for which the skin is exposed. Irritant contact dermatitis generally results due to destruction of the external layer of the skin after a significant exposure. In children, it results in the form of napkin irritation on the genitals, or on thumb due to thumb sucking. In adults hands are commonly affected due to continued contact with detergents commonly called as housewife’s dermatitis.

Allergic contact dermatitis is an antigen-antibody reaction occurring within 48 to 72 hours of contact [1] [2].

Contact dermatitis is a chronic, intermittent, skin inflammatory disease in which there is intense swelling, vesicles, redness and itching caused after the exposure to the irritant. In cases of allergic contact dermatitis, the response can be delayed by few hours or days. The dermatitis caused by irritant products such as detergents, soaps, alkalis etc leads to superficial skin disruption. This is seen in employees working in a chemical industry or those who are involved with domestic work, cleansers etc. repeated and prolong exposure results in irritant dermatitis.

The approach to such a condition is firstly abstinence from the prolonged exposure. The individual must avoid the contact with the substance known to cause dermatitis. Secondly, certain medications such as antihistaminics are used to reduce irritation and itching. In cases of severe allergy steroidal applications are used. After this certain barrier creams are used for long term protection. Cleansers that are alcohol based are recommended as they can help in skin protection and renewal. In severe cases immune modulator drugs, immune suppressants are used.

1. Shaffer MP, Belsito DV. Allergic contact dermatitis from glutaraldehyde in health-care workers. Contact Dermatitis. 2000 Sep;43(3):150-6.
2. Bråred Christensson J, Andersen KE, Bruze M, et al. Air-oxidized linalool: a frequent cause of fragrance contact allergy. Contact Dermatitis. 2012 Nov;67(5):247-59.
3. Kaplan DH, Igyártó BZ, Gaspari AA. Early immune events in the induction of allergic contact dermatitis. Nat Rev Immunol. 2012 Jan 13;12(2):114-24.
4. Niklasson IB, Delaine T, Islam MN, Karlsson R, et al. Cinnamyl alcohol oxidizes rapidly upon air exposure. Contact Dermatitis. 2013 Mar;68(3):129-38.
5. Pontén A, Hamnerius N, Bruze M, Hansson C, et al. Occupational allergic contact dermatitis caused by sterile non-latex protective gloves: clinical investigation and chemical analyses. Contact Dermatitis. 2013 Feb;68(2):103-10.
6. Pot LM, Scheitza SM, Coenraads PJ, Blömeke B. Penetration and haptenation of p-phenylenediamine.Contact Dermatitis. 2013 Apr;68(4):193-207.
7. Schlosser BJ. Systemic contact dermatitis. Dermatol Clin. 2010 Oct 1; 28(4): 697-706
8. Kulberg A, Schliemann S, Elsner P. Contact dermatitis as a systemic disease. Clin Dermatol. 2014 May-Jun;32(3):414-9.
9. Watkins SA, Maibach HI. The hardening phenomenon in irritant contact dermatitis: an interpretative update. Contact Dermatitis. 2009 Mar;60(3):123-30.
10. Fluhr JW, Akengin A, Bornkessel A, Fuchs S, et al. Additive impairment of the barrier function by mechanical irritation, occlusion and sodium lauryl sulphate in vivo. Br J Dermatol. 2005 Jul;153(1):125-31.
11. Jacobs JJ, Lehé CL, Hasegawa H, Elliott GR, Das PK. Skin irritants and contact sensitizers induce Langerhans cell migration and maturation at irritant concentration. Exp Dermatol. 2006 Jun;15(6):432-40.
12. Heinemann C, Paschold C, Fluhr J, Wigger-Alberti W, et al. Induction of a hardening phenomenon by repeated application of SLS: analysis of lipid changes in the stratum corneum. Acta Derm Venereol. 2005;85(4):290-5.
13. de Jongh CM, Khrenova L, Verberk MM, Calkoen F, et al. Loss-of-function polymorphisms in the filaggrin gene are associated with an increased susceptibility to chronic irritant contact dermatitis: a case-control study. Br J Dermatol. 2008 Sep;159(3):621-7.
14. Kartono F, Maibach HI. Irritants in combination with a synergistic or additive effect on the skin response: an overview of tandem irritation studies. Contact Dermatitis. 2006 Jun;54(6):303-12