A skin biopsy can be performed to test for EAC; tests should be performed to rule out other possible diseases such as: pityriasis rosea, tinea corporis, psoriasis, nummular eczema, atopic dermatitis, drug reaction, erythema migrans and other rashes.

No treatment is usually needed as they usually go away anywhere from months to years. The lesions may last from anywhere between 4 weeks to 34 years with an average duration of 11 months. If caused by an underlying disease or malignancy, then treating and removing the disease or malignancy will stop the lesions. It usually doesn't require treatment, but topical corticosteroids may be helpful in reducing redness, swelling and itchiness.

Some supported and not supported methods of having an effect on EAC include:

- Photosensitive so it can be moved/reduced with appropriate sunlight.

- Vitamin D

- Immune system - hence it will increase in size/number when the immune system is low or overloaded.

- Hormone Drugs

- Disulone

- Stress reduction

- Topical calcipotriol - a topical vitamin D derivative has been known to be beneficial

Erythema nodosum is diagnosed clinically. A biopsy can be taken and examined microscopically to confirm an uncertain diagnosis. Microscopic examination usually reveals a neutrophilic infiltrate surrounding capillaries that results in septal thickening, with fibrotic changes in the fat around blood vessels. A characteristic microscopic finding is radial granulomas, well-defined nodular aggregates of histiocytes surrounding a stellate cleft.

Additional evaluation should be performed to determine the underlying cause of erythema nodosum. This may include a full blood count, erythrocyte sedimentation rate (ESR), antistreptolysin-O (ASO) titer and throat culture, urinalysis, intradermal tuberculin test, and a chest x-ray. The ESR is typically high, the C-reactive protein elevated, and the blood showing an increase in white blood cells.

The ESR is initially very high, and falls as the nodules of erythema nodosum. The ASO titer is high in cases associated with a streptococcal throat infection. A chest X-ray should be performed to rule out pulmonary diseases, in particular sarcoidosis and Löfgren syndrome.

Discontinuing contact with the heat source is the initial treatment of erythema ab igne. If the area is only mildly affected with slight redness, the condition may resolve itself in a few months. If the condition is severe and the skin pigmented and atrophic, resolution is unlikely. In this case, there is a possibility that a squamous cell carcinoma or a neuroendocrine carcinoma such as a Merkel cell carcinoma may form. If there is a persistent sore that does not heal or a growing lump within the rash, a skin biopsy should be performed to rule out the possibility of skin cancer. If the erythema ab igne lesions demonstrate pre-cancerous changes, the use of 5-fluorouracil cream has been recommended. Abnormally pigmented skin may persist for years. Treatment with topical tretinoin or laser may improve the appearance.

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.

In all cases of suspected NEH, a skin biopsy should be performed, because the clinical symptoms are non specific, but the histopathological findings on the biopsy are specific. The biopsy shows characteristic changes of the eccrine glands, the major sweat glands of the body.

In NEH, eccrine gland necrosis, and neutrophils surroundings the eccrine glands, are typical findings on biopsy. If the chemotherapy has recently been administered, chemotherapy induced neutropenia may be present, and, as a result, the neutrophils may be absent. But the other characteristic finding, i.e. eccrine gland necrosis, can still be seen. A vacuolar interface dermatitis also is visible in glands and ducts, along with necrosis of the lining cells.

In addition, in patients receiving chemotherapy, keratinocyte atypia can be seen.

Painful red swelling of the hands and feet in a patient receiving chemotherapy is usually enough to make the diagnosis. The problem can also arise in patients after bone marrow transplants, as the clinical and histologic features of PPE can be similar to cutaneous manifestations of acute (first 3 weeks) graft-versus-host disease. It is important to differentiate PPE, which is benign, from the more dangerous graft-versus-host disease. As time progresses, patients with graft-versus-host disease progress to have other body parts affected, while PPE is limited to hands and feet. Serial biopsies every 3 to 5 days can also be helpful in differentiating the two disorders (Crider et al., 1986).

Whilst usually a straightforward diagnosis at times the appearance can raise concern that the rash could be due to herpes simplex; however, the latter generally has a more clustered and vesicular appearance.

In uncertain cases, a scraping of a lesion can be taken and the fluid examined under the microscope. Herpes lesions will have a positive direct fluorescent antibody test. The fluid from erythema toxicum lesions will show many eosinophils. If blood samples are taken, they may show a high level of circulating eosinophils; however, this is not usually required.

Differential diagnosis may include Herpes simplex virus, Impetigo, neonatal sepsis, Listeria and Varicella (chicken pox).

Because the eruption is transient and self-limiting, no treatment is indicated.

Erythema ab igne was once commonly seen in the elderly who stood or sat closely to open fires or electric heaters; however, erythema ab igne has been reported in both young and elderly individuals. Women have a higher incidence of erythema ab igne than men. Although wide use of central heating has reduced the overall incidence of erythema ab igne, it is still sometimes found in people exposed to heat from other sources such as heating pads, space heaters, hot water bottles, and electronic devices.

The cooling of hands and feet during chemotherapy may help prevent PPE (Baack and Burgdorf, 1991; Zimmerman et al., 1995). Support for this and a variety of other approaches to treat or prevent acral erythema comes from small clinical studies, although none has been proven in a randomised controlled clinical trial of sufficient size.

A single case report suggested that oral dapsone may be useful for prevention. However, the efficacy of oral dapsone as prevention has not been demonstrated very clearly until now.

Erythema nodosum is self-limiting and usually resolves itself within 3–6 weeks. A recurring form does exist, and in children it is attributed to repeated infections with streptococcus. Treatment should focus on the underlying cause. Symptoms can be treated with bedrest, leg elevation, compressive bandages, wet dressings, and nonsteroidal anti-inflammatory agents (NSAIDs). NSAIDs are usually more effective at the onset of EN versus with chronic disease.

Potassium iodide can be used for persistent lesions whose cause remains unknown. Corticosteroids and colchicine can be used in severe refractory cases. Thalidomide has been used successfully in the treatment of Erythema nodosum leprosum, and it was approved by the U.S. FDA for this use in July 1998.

Localised discoid lupus erythematosus typically presents with skin lesions localised above the neck, with favoured sites being the scalp, bridge of the nose, cheeks, above the lips and ears as well as the arms hair scratching glasses touching name="Andrews1"/> Another form of discoid lupus erythematosus includes oral discoid. Oral discoid lupus erythematosus results in oral lesions which present themselves as white spots, ulcers and central erythema lesions. Oral discoid lesions most commonly occur on the labial mucosa, vermillion border and buccal mucosa. Atrophy may be observed in some cases. Dentists may be important in establishing the diagnosis before the cutaneous lesions become apparent.

Discoid lupus erythematosus (DLE) is a chronic skin condition of sores with inflammation and scarring favouring the face, ears, and scalp and at times on other body areas. These lesions develop as a red, inflamed patch with a scaling and crusty appearance. The centre areas may appear lighter in colour with a rim darker than the normal skin.

Discoid lupus erythematosus can be divided into localised, generalised, and childhood discoid lupus erythematosus.

The differential diagnoses are: acrodermatitis enteropathica, erythema infectiosum, erythema multiforme, hand-foot-and-mouth disease, Henoch–Schönlein purpura, Kawasaki disease, lichen planus, papular urticaria, papular purpuric gloves and socks syndrome, and scabies.

Palmar erythema has no specific treatment. Management is based on the underlying cause. When its cause is treated then patients get relief. If it is attributable to a particular drug then the drug should be withdrawn.

The medieval "Bald's Leechbook" recommended treating chilblains with a mix of eggs, wine, and fennel root.

A common tradition of Hispanic America recommends warm garlic on the chilblains.

Many suspected aetiologic factors have been reported to cause EM.

- Infections: Bacterial (including Bacillus Calmette-Guérin (BCG) vaccination, haemolytic "Streptococci", legionellosis, leprosy, "Neisseria meningitidis, Mycobacterium, "Pneumococcus, "Salmonella" species, "Staphylococcus" species, "Mycoplasma pneumoniae), "Chlamydial.

- Fungal (Coccidioides immitis)

- Parasitic ("Trichomonas" species, "Toxoplasma gondii), "

- Viral (especially Herpes simplex)

- Drug reactions, most commonly to: antibiotics (including, sulphonamides, penicillin), anticonvulsants (phenytoin, barbiturates), aspirin, antituberculoids, and allopurinol and many others.

- Physical factors: radiotherapy, cold, sunlight

- Others: collagen diseases, vasculitides, non-Hodgkin lymphoma, leukaemia, multiple myeloma, myeloid metaplasia, polycythemia

EM minor is regarded as being triggered by HSV in almost all cases. A herpetic aetiology also accounts for 55% of cases of EM major. Among the other infections, "Mycoplasma" infection appears to be a common cause.

Herpes simplex virus suppression and even prophylaxis (with acyclovir) has been shown to prevent recurrent erythema multiforme eruption.

The differential diagnosis includes oral lichen planus, erythematous candidiasis, leukoplakia, lupus erythematosus, glossitis, and chemical burns. Atrophic glossitis is usually distinguished from benign migratory glossitis on the basis of the migrating pattern of the lesions and the presence of a whitish border, features which are not present in atrophic glossitis, which instead shows lesions which enlarge rather than migrate. Rarely, blood tests may be required to distinguish from glossitis associated with anemia or other nutritional deficiencies. Since the appearance and the history of the condition (i.e. migrating areas of depapillation) are so striking, there is rarely any need for biopsy. When biopsy is taken, the histopathologic appearance is quite similar to psoriasis:

- Hyperparakeratosis.

- Acanthosis.

- Subepithelial T lymphocyte inflammatory infiltrate.

- Migration of neutrophilic granulocytes into the epithelial layer, which may create superficial microabscesses, similar to the Munro's microabscesses described in pustular psoriasis.

Lucio's phenomenon is treated by anti-leprosy therapy (dapsone, rifampin, and clofazimine), optimal wound care, and treatment for bacteremia including antibiotics. In severe cases exchange transfusion may be helpful.

Baboon syndrome affects both sexes equally, and can occur at any age, but seems to be more common in childhood than in adulthood.

The diagnosis of Gianotti–Crosti syndrome is clinical. A validated diagnostic criteria is as follows:

A patient is diagnosed as having Gianotti–Crosti syndrome if:

1. On at least one occasion or clinical encounter, he/she exhibits all the positive clinical features,

2. On all occasions or clinical encounters related to the rash, he/she does not exhibit any of the negative clinical features,

3. None of the differential diagnoses is considered to be more likely than Gianotti–Crosti syndrome on clinical judgment, and

4. If lesional biopsy is performed, the histopathological findings are consistent with Gianotti–Crosti syndrome.

The positive clinical features are:

- Monomorphous, flat-topped, pink-brown papules or papulovesicles 1-10mm in diameter.

- At least three of the following four sites involved – (1) cheeks, (2) buttocks, (3) extensor surfaces of forearms, and (4) extensor surfaces of legs.

- Being symmetrical, and

- Lasting for at least ten days.

The negative clinical features are:

- Extensive truncal lesions, and

- Scaly lesions.

Urticarial erythema multiforme is an unusual reaction virtually always associated with antibiotic ingestions, characterized by skin lesions that consist of urticarial papules and plaques, some of which clear centrally forming annular lesions, but with no true urticarial lesions.

Erythema multiforme major (also known as "erythema multiforme majus") is a form of rash with skin loss or epidermal detachment.

The term "erythema multiforme majus" is sometimes used to imply a bullous (blistering) presentation.

According to some sources, there are two conditions included on a spectrum of this same disease process:

- Stevens–Johnson syndrome (SJS)

- Toxic epidermal necrolysis (TEN) which described by Alan Lyell and previously called Lyell syndrome[5].

In this view, EM major, SJS and TEN are considered a single condition, distinguished by degree of epidermal detachment.

However, a consensus classification separates erythema multiforme minor, erythema multiforme major, and SJS/TEN as three separate entities.