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.

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.

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.

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.

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.

Most cases are well managed with topical treatments and ultraviolet light. About 2% of cases are not. In more than 60% of young children, the condition subsides by adolescence.

During diagnosis it is important to determine the type of hand eczema and plan specific treatment accordingly. An additional diagnosis of allergies will indicate whether contact allergies or atopy diathesis are the cause of the hand eczema. Discussion concerning frequency of contact with water, irritants, and allergens in private and professional environments will also help evaluate individual stresses on the patient's skin. The hands may also exhibit various other skin illnesses and potential fungal infection or psoriasis must be ruled out. Usually, taking the patient’s personal history into account will help provide an accurate diagnosis.

Patch testing has been found to be helpful in the diagnosis of hand eczema.

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

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.

In adults, the prevalence of IgE sensitization to allergens from house dust mite and cat, but not grass, seem to decrease over time as people age. However, the biological reasons for these changes are not fully understood.

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.

A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects.

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.

Corticosteroids: For years, there was no treatment for atopic eczema. Atopy was believed to be allergic in origin due to the patients’ extremely high serum IgE levels, but standard therapies at the time did not help. Oral prednisone was sometimes prescribed for severe cases. Wet wraps (covering the patients with gauze) were sometimes used in hospitals to control itching. However, the discovery of corticosteroids in the 1950s, and their subsequent incorporation in topical creams and ointments, provided a significant advancement in the treatment of atopic eczema and other conditions. Thus, the use of topical steroids avoided many of the undesirable side-effects of systemic administration of corticosteroids. Topical steroids control the itching and the rash that accompany atopic eczema. Side-effects of topical steroid use are plentiful, and the patient is advised to use topical steroids in moderation and only as needed.

Immune modulators: Pimecrolimus and tacrolimus creams and ointments became available in the 1980s and are sometimes prescribed for atopic eczema. They act by interfering with T cells but have been linked to the development of cancer.

Avoiding dry skin: Dry skin is a common feature of patients with atopic eczema (see also eczema for information) and can exacerbate atopic eczema.

Avoiding allergens and irritants: See eczema for information.

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.

Treatment consists of two phases: stopping the urushiol contact that is causing the reaction (this must be done within minutes) and, later, reducing the pain and/or itching.

Primary treatment involves washing exposed skin thoroughly with soap, water, and friction as soon as possible after exposure is discovered. Soap or detergent is necessary because urushiol is an oil; friction, with a washcloth or something similar, is necessary because urushiol adheres strongly to the skin. Commercial removal preparations, which are available in areas where poison ivy grows, usually contain surfactants, such as the nonionic detergent Triton X-100, to solubilize urushiol; some products also contain abrasives.

The U.S. Food and Drug Administration recommends applying a wet compress or soaking the affected area in cool water; topical corticosteroids (available over-the-counter) or oral corticosteroids (available by prescription); and topical skin protectants, such as zinc acetate, zinc carbonate, zinc oxide, and calamine. Baking soda or colloidal oatmeal can relieve minor irritation and itching. Aluminium acetate, sometimes known as Burow's solution, can also ease the rash.

Showers or compresses using hot (but not scalding) water can relieve itching for up to several hours, though this "also taxes the skin's integrity, opening pores and generally making it more vulnerable", and is only useful for secondary treatment (not for cleaning urushiol from the skin, which should be done with cold water). People who have had a prior systemic reaction may be able to prevent subsequent exposure from turning systemic by avoiding heat and excitation of the circulatory system and applying moderate cold to any infected skin with biting pain.

Antihistamine and hydrocortisone creams, or oral antihistamines in severe cases, can alleviate the symptoms of a developed rash. Nonprescription oral diphenhydramine (U.S. trade name Benadryl) is the most commonly suggested antihistamine. Topical formulations containing diphenhydramine are also available but may further irritate the skin.

In cases of extreme symptoms, steroids such as prednisone or triamcinolone are sometimes administered to attenuate the immune response and prevent long-term skin damage, especially if the eyes are involved. Prednisone is the most commonly prescribed systemic treatment but can cause serious adrenal suppression, so it must be taken carefully and tapered off slowly. If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.

Scrubbing with plain soap and cold water will remove urushiol from skin if it is done within a few minutes of exposure. Many home remedies and commercial products (e.g., Tecnu, Zanfel) also claim to prevent urushiol rashes after exposure. A study that compared Tecnu ($1.25/oz.) with Goop Hand Cleaner or Dial Ultra Dishwashing Soap ($0.07/oz.) found that differences among the three—in the range of 56–70% improvement over no treatment—were nonsignificant ("P" > 0.05), but that improvement over no treatment was significant at the same level of confidence.

Further observations:

- Ordinary laundering with laundry detergent will remove urushiol from most clothing but not from leather or suede.

- The fluid from the resulting blisters does "not" spread urushiol to others.

- Blisters should be left unbroken during healing.

- Poison ivy and poison oak are still harmful when the leaves have fallen off, as the toxic residue is persistent, and exposure to any parts of plants containing urushiol can cause a rash at any time of the year.

- Ice, cold water, cooling lotions, and cold air do "not" help cure poison ivy rashes, but cooling can reduce inflammation and soothe the itch.

- Results for jewelweed as a natural agent for treatment are conflicting. Some studies indicate that it "failed to decrease symptoms of poison ivy dermatitis" [1980] and had "no prophylactic effect" [1997]. The juice of the leaves and stems of Impatiens capensis is a traditional Native American remedy for skin rashes, including poison ivy and such use has been supported by at least one peer-reviewed study, as recently as 2012.

Independent of the triggering cause or the prevailing signs of skin illness, the selection and planning of treatment options is important, since different types of illness also differ in terms of their degree of severity and the course of the illness.

While light hand eczema heals relatively quickly following dermatological therapy and patient participation, more pronounced hand eczema may persist over several weeks. Severe hand eczema is characterised by consistent or recurring, extended inflammation of the skin that severely affects the patient. Hand eczema is described as chronic if it lasts at least 3 months in spite of dermatological treatment, or if it recurs at least twice within a period of 12 months (relapsed) . Severe and chronic patterns of hand eczema are often resilient to treatment, making the condition extremely stressful for those affected.

Dyshidrosis is diagnosed clinically, by gathering a patient's history and making careful observations (see signs and symptoms section). Severity of symptoms can also be assessed using the dyshidrotic eczema area and severity index (DASI). The DASI has been designed for clinical trials and is not typically used in practice.

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.

Prevention includes avoiding exposure to the sun and wearing sun block on the affected area.

- Cover up: wear long sleeves, slacks, and a wide-brimmed hat whenever harsh exposure is probable

- Avoid chemicals that may trigger a reaction

- Wear sunscreen at least factor 30 with a high UVA protection level

- Wear gloves and/or remain indoors after handling fruits or plants which increase sensitivity to light

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 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.

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.

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.

Once a nickel allergy is detected, the best treatment is avoidance of nickel-releasing items. It is important to know the main items that can cause nickel allergy, which may be remembered using the mnemonic "BE NICKEL AWARE". The top 13 categories that contain nickel include beauty accessories, eyeglasses, money, cigarettes, clothes, kitchen and household, electronics and office equipment, metal utensils, aliment, jewelry, batteries, orthodontic and dental appliances, and medical equipment. Other than strict avoidance of items that release free nickel, there are other treatment options for reduction of exposure. The first step is to limit friction between skin and metallic items. Susceptible people may try to limit sweating while wearing nickel items, to reduce nickel release and thus decrease chances for developing sensitization and/or allergy. Another option is to shield electronics, metal devices, and tools with fabric, plastic, or acrylic coverings. Dermatological application tests has shown that barrier creams effectively prevent the symptoms of nickel allergy, such as the Nidiesque™.

There are test kits that can be very helpful to check for nickel release from items prior to purchasing. The ACDS providers can give a guidance list of safe items. In addition to avoidance, healthcare providers may prescribe additional creams or medications to help relieve the skin reaction.