Friction blisters, caused by rubbing against the skin, can be prevented by reducing the friction to a level where blisters will not form. This can be accomplished in a variety of ways.

Blisters on the feet can be prevented by wearing comfortable, well-fitting shoes and clean socks. Inherently ill-fitting or stiffer shoes, such as high heels and dress shoes, present a larger risk of blistering. Blisters are more likely to develop on skin that is moist, so socks that manage moisture or frequent sock changes will aid those with particularly sweaty feet. While exercising or playing sports, special sports socks can help keep feet drier and reduce the chance of blisters. Before going for a long walk, it is also important to ensure that shoes or hiking boots have been properly broken in.

Even before a "hot" or irritated area on the foot is felt, taping a protective layer of padding or a friction-reducing interface between the affected area and the footwear can prevent the formation of a blister. Bandages, moleskin and tapes generally must be applied to the foot daily, and most have a very high coefficient of friction (COF), but a friction-management patch applied to the shoe will remain in place much longer, throughout many changes of socks and insoles. This type of intervention may be used with footwear that is worn daily, with specialty shoes and boots like hockey skates, ice skates, inline skates, ski boots and cleats, or even with orthotic braces and splints. For periods of sustained use such as hiking and trail running, especially where water ingress or moisture build up in the shoe or boot can occur, moisture wicking liner socks can provide the required friction protection.

To avoid friction blisters on the hands, gloves should be worn when using tools such as a shovel or pickaxe, doing manual work such as gardening, or using sports equipment like golf clubs or baseball bats. Oars used for competitive rowing are known for causing frequent blisters on the hands of oarsmen. Weightlifters are also prone to blisters as are gymnasts from the friction developed by the rubbing against the bars. To further reduce the occurrence one can tape the hands, and there are also a number of products on the market that claim to reduce the occurrence of blisters. These are all intended to be worn as a liner underneath a glove. The majority of these offerings simply add padding and create a layer that reduces the coefficient of friction between the skin and the glove.

A lubricant, typically talcum powder, can be used to reduce friction between skin and apparel in the short term. People put talcum powder inside gloves or shoes for this purpose, although this type of lubricant will increase the friction in the long term, as it absorbs moisture. Increased friction makes blisters more likely.

Sunscreen and protective clothing should also be used during the hottest part of the day to avoid blisters from sunburn. Avoiding sunlight during midday is the best way to avoid blisters from sunburn. Protective gloves should be worn when handling detergents, cleaning products, solvents and other chemicals.

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.

Dempster-Shafer Theory is used for detecting skin infection and displaying the result of the detection process.

Prickly heat can be prevented by avoiding activities that induce sweating, using air conditioning to cool the environment, wearing light clothing and in general, avoiding hot and humid weather. Frequent cool showers or cool baths with mild soap can help to prevent heat rash.

The primary remedy for miliaria is to wear lighter clothing, move to a cooler climate, or otherwise avoid overheating one's body. The immediate treatment of the involved skin areas involves the use of a soothing ointment such as calamine lotion.

Medical assistance should be sought for the first episode of a rash with the appearance of miliaria. The differential diagnosis includes several conditions that an experienced practitioner should be able to recognise and may require treatment distinct from the usual measures taken for miliaria. In most cases the rash of miliaria will resolve without intervention. However, severe cases can last for weeks and cause significant disability. General measures should be recommended for all patients, including moving to an air-conditioned environment if possible, avoiding sweat-provoking activities and occlusive clothing, and taking frequent cool showers.

It has been suggested that the use of topical antibacterials (including antibacterial soaps) may shorten the duration of symptoms in miliaria rubra even in the absence of obvious superinfection. Other topical agents that may reduce the severity of symptoms include anti-itch preparations such as calamine or menthol- or camphor-based preparations, and topical steroid creams. However, caution should be used with oil-based preparations (ointments and oily creams as opposed to water-based or aqueous lotions) that may increase blockage to the sweat glands and prolong duration of illness. Other agents have been investigated including supplemental vitamin A and C and vitamin A based medications, but it is worth noting that there is little scientific evidence supporting any of the above treatments in reducing the duration of symptoms or frequency of complications.

In most cases, doctors will recommend that any pimple-like blisters that may form should have the fluid drained out of them (either through in-office procedure or at home in a sterile environment) to avoid the rash from spreading underneath the skin, leading to an increased state of dermatitis. Left untreated, the blisters may spread and take on an increased red appearance, with the fluid inside increasing in viscosity. It is recommended by physicians to sanitize the infected area and then drain the blisters with a sterilized needle or lancet.

In most tropical areas the local dispensaries sell prickly heat powder, a talc admixture containing drying milk proteins (Labilin) and Triclosan to fight the infection. These include cooling menthol to help alleviate difficulty getting to sleep. This is an effective treatment—the powder stays on the skin longer and treats bacteria dispersed into bed linens, providing a reasonably dry refuge area for healing. Miliaria often covers large areas, and generous use of Cortisone may be contraindicated for reasons stated on package warnings. Regular talcum powder will not reduce the rash but can alleviate burning and itching.

In cases where the rash has developed into open blisters or pustular lesions a doctor should be consulted since more aggressive, medically monitored treatment may be required.

Other conditions that can result in symptoms similar to the common form include contact dermatitis, herpes simplex virus, discoid lupus, and scabies.

Other conditions that can result in symptoms similar to the blistering form include other bullous skin diseases, burns, and necrotizing fasciitis.

In most cases exfoliation resolves spontaneously and no lasting damage is seen. On the other hand, some patients experience cracking and even bleeding in extreme cases.

Erythema multiforme is frequently self-limiting and requires no treatment. The appropriateness of glucocorticoid therapy can be uncertain, because it is difficult to determine if the course will be a resolving one.

Normally, exfoliation is restricted to a particular area and normal skin will replace the exfoliated parts, so no treatment is needed. Since keratolysis exfoliativa is caused by friction, detergents, and solvents, these factors should be avoided. Creams, especially those with silicone and lactic acid are also helpful. In severe cases, photochemotherapy is an option.

There are several methods of healing blood blisters, including elevation of the wound, application of a cold pack, and application of padded dressings or splints.

Impetigo is usually diagnosed based on its appearance. It generally appears as honey-colored scabs formed from dried serum, and is often found on the arms, legs, or face. If a visual diagnosis is unclear a culture may be done to test for resistant bacteria.

Some of the investigations done for ulcer are:

- Study of discharging fluid: Culture and sensitivity

- Edge biopsy: Edge contains multiplying cells

- Radiograph of affected area to look for periostitis or osteomyelitis

- FNAC of lymph node

- Chest X-ray and Mantoux test in suspected tuberculous ulcer

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.

Pemphigus is a group of autoimmune blistering diseases that may be classified into the following types:

Because it is a rare disease, diagnosis is often complicated and takes a long time. Early in the disease patients may have erosions in the mouth or blisters on the skin. These blisters can be itchy or painful. Theoretically, the blisters should demonstrate a positive Nikolsky's sign, in which the skin sloughs off from slight rubbing, but this is not always reliable. The gold standard for diagnosis is a punch biopsy from the area around the lesion that is examined by direct immunofluorescent staining, in which cells are acantholytic, that is, lacking the normal intercellular connections that hold them together. These can also be seen on a Tzanck smear. These cells are basically rounded, nucleated keratinocytes formed due to antibody mediated damage to cell adhesion protein desmoglein.

Pemphigus vulgaris is easily confused with impetigo and candidiasis. IgG4 is considered pathogenic. The diagnosis can be confirmed by testing for the infections that cause these other conditions, and by a lack of response to antibiotic treatment.

While the term pemphigus typically refers to "a rare group of blistering autoimmune diseases" affecting "the skin and mucous membranes", Hailey–Hailey disease is not an autoimmune disorder and there are no autoantibodies. According to Pemphigus Pemphigoid Foundation (IPPF), "familial benign chronic pemphigus, or Hailey-Hailey disease, is a different condition from Pemphigus".

There are many treatments available for dyshidrosis. However, few of them have been developed or tested specifically on the condition.

- Barriers to moisture and irritants, including barrier creams and gloves.

- Topical steroids - while useful, can be dangerous long-term due to the skin-thinning side-effects, which are particularly troublesome in the context of hand dyshidrosis, due to the amount of toxins and bacteria the hands typically come in contact with.

- Potassium permanganate dilute solution soaks - also popular, and used to 'dry out' the vesicles, and kill off superficial "Staphylococcus aureus", but it can also be very painful. Undiluted it may cause significant burning.

- Dapsone (diamino-diphenyl sulfone), an antibacterial, has been recommended for the treatment of dyshidrosis in some chronic cases.

- Antihistamines: Fexofenadine up to 180 mg per day.

- Alitretinoin (9-cis-retinoic acid) has been approved for prescription in the UK. It is specifically used for chronic hand and foot eczema. It is made by Basilea of Switzerland (BAL 4079).

- Systemic steroids can be taken orally to treat especially acute and severe cases of dyshidrosis.

When visiting a doctor, the basic diagnosis procedure applies. This includes checking the patient's medical history and medical record for risk factors, a medical interview during which the doctor asks questions (such as about itching and scratching), and a physical examination. Athlete's foot can usually be diagnosed by visual inspection of the skin and by identifying less obvious symptoms such as itching of the affected area.

If the diagnosis is uncertain, direct microscopy of a potassium hydroxide preparation of a skin scraping (known as a KOH test) can confirm the diagnosis of athlete's foot and help rule out other possible causes, such as candidiasis, pitted keratolysis, erythrasma, contact dermatitis, eczema, or psoriasis. Dermatophytes known to cause athlete's foot will demonstrate multiple septate branching hyphae on microscopy.

A Wood's lamp (black light), although useful in diagnosing fungal infections of the scalp (tinea capitis), is not usually helpful in diagnosing athlete's foot, since the common dermatophytes that cause this disease do not fluoresce under ultraviolet light.

Epidermolysis bullosa can be diagnosed either by a skin (punch) biopsy at the edge of a wound with immunofluorescent mapping, or via blood sample and genetic testing.

Pemphigus defines a group of autoimmune interepithelial blistering diseases that are characterized by loss of normal cell-cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug induced pemphigus, Senear Usher syndrome and endemic pemphigus foliaceus exist;recognized by a dermatologist from the appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head and neck surgery, periodontists, oral and maxillofacial surgeons and eye doctors, as lesions can affect the eyes and mucous membrane of the oral cavity. Intraorally it resembles the more common diseases lichen planus and mucous membrane pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister. This bottom layer of cells is said to have a "tombstone appearance".

Definitive diagnosis also requires the demonstration of anti-desmoglein autoantibodies by direct immunofluorescence on the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern reminiscent of chicken wire. Anti-desmoglein antibodies can also be detected in a blood sample using the ELISA technique.

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.

A 2014 study classified cases into three types—epidermolysis bullosa simplex (EBS), junctional epidermolysis bullosa (JEB), and dystrophic epidermolysis bullosa (DEB) -- and reviewed their times of death. The first two types tended to die in infancy and the last in early adulthood.

Phytophotodermatitis can be prevented by staying indoors after handling the above substances. However, the primary triggering mechanism is UV-A radiation (320–380 nm) which windows are not guaranteed to filter out.

Many different topical and oral medications can be used to treat the inflammatory reaction of phytophotodermatitis. A dermatologist may also prescribe a bleaching cream to help treat the hyperpigmentation and return the skin pigmentation back to normal. If they do not receive treatment, the affected sites may develop permanent hyperpigmentation or hypopigmentation.

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.