Since contact dermatitis relies on an irritant or an allergen to initiate the reaction, it is important for the patient to identify the responsible agent and avoid it. This can be accomplished by having patch tests, one of various methods commonly known as allergy testing. The top three allergens found in patch tests from 2005–06 were: nickel sulfate (19.0%), Myroxylon pereirae (Balsam of Peru, 11.9%), and fragrance mix I (11.5%).

The patient must know where the irritant or allergen is found to be able to avoid it. It is important to also note that chemicals sometimes have several different names, and do not always appear on labels.

The distinction between the various types of contact dermatitis is based on a number of factors. The morphology of the tissues, the histology, and immunologic findings are all used in diagnosis of the form of the condition. However, as suggested previously, there is some confusion in the distinction of the different forms of contact dermatitis. Using histology on its own is insufficient, as these findings have been acknowledged not to distinguish, and even positive patch testing does not rule out the existence of an irritant form of dermatitis as well as an immunological one.

Diagnosing allergic contact dermatitis is primarily based on physical exam and medical history. In some cases doctors can establish an accurate diagnosis based on the symptoms that the patient experiences and on the rash's appearance. In the case of a single episode of allergic contact dermatitis, this is all that is necessary. Chronic and/or intermittent rashes which are not readily explained by history and physical exam often will benefit from further testing.

A patch test (contact delayed hypersensitivity allergy test) is a commonly used examination to determine the exact cause of an allergic contact dermatitis. According to the American Academy of Allergy, Asthma, and Immunology, "patch testing is the gold standard for contact allergen identification".

The patch test consists of applying small quantities of potential allergens to small patches and which are then placed on the skin. After two days, they are removed and if a skin reaction occurred to one of the substances applied, a raised bump will be noticeable underneath the patch. The tests are again read at 72 or 96 hours after application.

Patch testing is used for patients who have chronic, recurring contact dermatitis. Other tests that may be used to diagnose contact dermatitis and rule out other potential causes of the symptoms include a skin biopsy and culture of the skin lesion.

Atopic dermatitis is typically diagnosed clinically, meaning it is diagnosed based on signs and symptoms alone, without special testing. Several different forms of criteria developed for research have also been validated to aid in diagnosis. Of these, the UK Diagnostic Criteria, based on the work of Hanifin and Rajka, has been the most widely validated.

Diagnosis of eczema is based mostly on the history and physical examination. In uncertain cases, skin biopsy may be useful. Those with eczema may be especially prone to misdiagnosis of food allergies.

Patch tests are used in the diagnosis of allergic contact dermatitis.

In an industrial setting the employer has a duty of care to its worker to provide the correct level of safety equipment to mitigate exposure to harmful irritants. This can take the form of protective clothing, gloves, or barrier cream, depending on the working environment.

Topical antibiotics should not be used to prevent infection in wounds after surgery. When they are used, it is inappropriate, and the person recovering from surgery is at significantly increased risk of developing contact dermatitis.

There is no good evidence that a mother's diet during pregnancy, the formula used, or breastfeeding changes the risk. There is tentative evidence that probiotics in infancy may reduce rates but it is insufficient to recommend its use.

People with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

The pathophysiology may involve a mixture of type I and type IV-like hypersensitivity reactions.

A diagnosis of perioral dermatitis is typically made based on the characteristics of the rash. A skin biopsy is usually not required to make the diagnosis but can be helpful to rule out other skin diseases which may resemble perioral dermatitis. Extended patch testing maybe useful to also rule out allergic contact causes.

Nickel allergy can be confirmed by a properly trained health care provider based on the medical history, physical exam and a painless specialized patch test— when necessary. A significant number of people may self-diagnose, and not contact medical professionals, which could result in massive underreporting of the problem by scientific researchers.

Confirming the diagnosis of Ni-ACD specifically involves inducing the skin to demonstrate a rash where the chemicals are applied (a delayed type hypersensitivity reaction), evidence that the patient is exposed to nickel, and establishing that the reaction and the exposure explain the current rash/symptoms under question. The patch test plays a significant role in diagnosing ACD.

The patch test evokes a delayed, Type IV hypersensitivity reaction, which is a cell-mediated, antibody independent, immune response. Patch testing is the "gold standard" diagnostic tool for Ni-ACD. In this sense, a positive patch test to nickel establishes that the subject has been previously exposed and is therefore sensitized to nickel. It does not necessarily indicate that the patch reaction is the cause of the current clinical disease. A negative test demonstrates that the patient is sub-threshold, either minimally or not sensitized. Cumulatively, clinical reasoning and a patch test help determine if nickel could be the cause of a current dermatitis reaction.

The clinical expression of the dermatitis can be mitigated by avoidance of the allergen. Through compliance with avoidance measures, the immune system can become less stimulated. The key to avoidance is proper evaluation and detection of the inciting allergen. However, once the immune system registers the allergen, the recognition is permanent.

The first step in treating the condition is appropriate recognition of the clinical problem, followed by identification of the culprit chemical and the source of that chemical. Corticosteroid creams should be used carefully and according to the prescribed directions because when overused over longer periods of time they can cause thinning of the skin. Also, in some instances such as poison ivy dermatitis calamine lotion and cool oatmeal baths may relieve itching.

Usually, severe cases are treated with systemic corticosteroids which may be tapered gradually, with various dosing schedules ranging from a total of 12 – 20 days to prevent the recurrence of the rash (while the chemical allergen is still in the skin, up to 3 weeks, as well as a topical corticosteroid. Tacrolimus ointment or pimecrolimus cream can also be used additionally to the corticosteroid creams or instead of these. Oral antihistamines such as diphenhydramine or hydroxyzine may also be used in more severe cases to relieve the intense itching. Topical antihistamines are not advised as there might be a second skin reaction (treatment associated contact dermatitis) from the lotion itself.

The other symptoms caused by allergic contact dermatitis may be eased with cool compresses to stop the itching. It is vital for treatment success that the trigger be identified and avoided. The discomfort caused by the symptoms may be relieved by wearing smooth-textured cotton clothing to avoid frictional skin irritation or by avoiding soaps with perfumes and dyes.

Commonly, the symptoms may resolve without treatment in 2 to 4 weeks but specific medication may hasten the healing as long as the trigger is avoided. Also, the condition might become chronic if the allergen is not detected and avoided.

Other rashes that occur in a widespread distribution can look like an id reaction. These include atopic dermatitis, contact dermatitis, dyshidrosis, photodermatitis, scabies and drug eruptions.

The prevalence of nummular dermatitis in the United States is approximately 2 per 1,000. It is considered a disease of adulthood, for it is rare in children.

The aim of treatment is to relieve the allergy-induced itch and to remove the fleas from the pet and its home environment. In some cases, secondary bacterial or yeast infections will also need treatment before the itching subsides. Environmental flea control includes using flea foggers or bombs, vacuuming, and treating pet bedding by washing on a hot cycle (over 60 degrees Celsius) in the washing machine. The current on-pet treatment recommended by veterinary dermatologists is spinosad (Comfortis) monthly and nitenpyram (Capstar or generics) every 48 hours until improvement.

Many pets with FAD may also have other allergies, such as allergies to food, contact allergies, and atopic dermatitis.

Diagnosis of nummular dermatitis largely clinical. Biopsies are typically not necessary, and cannot be used to rule out other atopic dermatitis or other eczemas. However, patch testing may be employed to rule out irritants (contact dermatitis) as a cause. In children, nummular dermatitis is commonly confused with tinea corporis.

Prevention measures include avoidance of the irritant through its removal from the workplace or through technical shielding by the use of potent irritants in closed systems or automation, irritant replacement or removal and personal protection of the workers.

Nickel has wide utility of application in manufactured metals, because it is both strong and malleable, leading to ubiquitous presence and the potential for consumers to be in contact with it daily. However, for those that have the rash of allergic contact dermatitis (ACD) due to a nickel allergy, it can be a challenge to avoid. Foods, common kitchen utensils, cell phones, jewelry and many other items may contain nickel and be a source of irritation due to the allergic reaction caused by the absorption of free released nickel through direct and prolonged contact. The most appropriate measure for nickel allergic persons is to prevent contact with the allergen.

In 2011, researchers showed that applying a thin layer of glycerine emollient containing nanoparticles of either calcium carbonate or calcium phosphate on an isolated piece of pig skin (in vitro) and on the skin of mice (in vivo) prevents the penetration of nickel ions into the skin. The nanoparticles capture nickel ions by cation exchange, and remain on the surface of the skin, allowing them to be removed by simple washing with water. Approximately 11-fold fewer nanoparticles by mass are required to achieve the same efficacy as the chelating agent ethylenediamine tetraacetic acid. Using nanoparticles with diameters smaller than 500 nm in topical creams may be an effective way to limit the exposure to metal ions that can cause skin irritation'.

Pre-emptive avoidance strategies (PEAS) might ultimately lower the sensitization rates of children who would suffer from ACD In an expert review of clinical immunology from "Taylor & Francis Online", it is theorized that prevention of exposure to nickel early on could reduce the number of those that are sensitive to nickel by one-quarter to one-third. Identification of the many sources of nickel is vital to understanding the nickel sensitization story, food like chocolate and fish, zippers, buttons, cells phones and even orthodontic braces and eyeglass frames might contain nickel. Items that contain sentimental value (heirlooms, wedding rings) could be treated with an enamel or rhodium plating.

Sensitized individuals may check product labels or contact the manufacturer or retailer regarding possible nickel content. The Dermatitis Academy has created an educational website to provide more information about nickel, including information about prevention, exposure, sources, and general information about nickel allergy. These resources provide guidance in a prevention initiative for children worldwide.

The diagnosis of flea allergy dermatitis is complicated by the grooming habits of pets. Cats in particular are very efficient at grooming out fleas, often removing any evidence of infestation. Fleas begin biting within 5 minutes of finding a host, and there are no flea treatments that kill fleas before biting occurs.

Perioral dermatitis is likely to fully resolve with short courses of antibiotics but if left untreated it can persist for years and take a chronic form.

Improvement with tetracyclines is usually seen after 4 days and significantly so after 2 weeks.

Possible treatments include minimizing diaper use, barrier creams, mild topical cortisones, and antifungal agents. A variety of other inflammatory and infectious processes can occur in the diaper area and an awareness of these secondary types of diaper dermatitis aids in the accurate diagnosis and treatment of patients.

Dermatitis herpetiformis is often misdiagnosed, being confused with drug eruptions, contact dermatitis, dishydrotic eczema (dyshidrosis), and even scabies.

The diagnosis can be confirmed by a simple blood test for IgA antibodies against tissue transglutaminase (which cross-react with epidermal transglutaminase), and by a skin biopsy in which the pattern of IgA deposits in the dermal papillae, revealed by direct immunofluorescence, distinguishes it from linear IgA bullous dermatosis and other forms of dermatitis. These tests should be done before the patient starts on a gluten-free diet, otherwise they might produce false negatives. Like in ordinary celiac disease, IgA against transglutaminase disappears (often within months) when patients eliminate gluten from their diet. Thus, for both groups of patients, it may be necessary to restart gluten for several weeks before testing can be done reliably. In 2010, "Cutis" reported an eruption labelled "gluten-sensitive dermatitis" which is clinically indistinguishable from dermatitis herpetiformis but lacks the IgA connection, similar to gastrointestinal symptoms mimicking coeliac disease but without the diagnostic immunological markers.

The most effective treatment, although not the most practical one, is to discontinue use of diapers, allowing the affected skin to air out. Another option is simply to increase the frequency of diaper changing. Thorough drying of the skin before diapering is a good preventive measure because it is the excess moisture, either from urine and feces or from sweating, that sets the conditions for a diaper rash to occur.

Intertrigo can be diagnosed clinically by a medical professional after taking a thorough history and performing a detailed physical examination. Many other skin conditions can mimic intertrigo's appearance including erythrasmascabies, pyoderma, atopic dermatitis, candidiasis, and seborrheic dermatitis, and fungal infections of the superficial skin caused by "Tinea versicolor" or "Tinea corporis".

The classification of exfoliative dermatitis into Wilson-Brocq (chronic relapsing), Hebra or pityriasis rubra (progressive), and Savill (self-limited) types may have had historical value, but it currently lacks pathophysiologic or clinical utility.

Once pederin is on the skin from the initial beetle contact, it may also be spread elsewhere on the skin. "Kissing" or "mirror-image" lesions where two skin areas come in contact (for example, the elbow flexure) are often seen. Washing the hands and skin with soap and water is strongly recommended, if contact with a rove beetle has occurred.

Initial skin contact with pederin shows no immediate result. Within 12–36 hours, however, a reddish rash (erythema) appears, which develops into blisters. Irritation, including crusting and scaling, may last from two to three weeks.

One study reported best results with a treatment regimen that combined topical steroids with oral antihistamines and antibiotics. The authors hypothesized that antibiotics were helpful because of the possible contamination of skin by pederin-producing bacteria.