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.

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).

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.

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.

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

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.

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.

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

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.

Erythema marginatum is a type of erythema (redness of the skin or mucous membranes) involving pink rings on the torso and inner surfaces of the limbs which come and go for as long as several months. It is found primarily on extensor surfaces.

An association with bradykinin has been proposed in the case of hereditary angioedema.

It occurs in less than 5% of patients with rheumatic fever, but is considered a major Jones criterion when it does occur. The four other major criteria include carditis, polyarthritis, Sydenham's Chorea, and subcutaneous nodules. In this case, it is often associated with Group A streptococcal infection, otherwise known as "Streptococcus pyogenes" infection, which can be detected with an ASO titer.

It is an early feature of rheumatic fever and not pathognomonic of it. It may be associated with mild myocarditis (inflammation of heart muscle). It is also seen in conditions like allergic drug reactions, sepsis and glomerulonephritis.

It often occurs as a harbinger of attacks in hereditary angioedema. In this case it may occur several hours or up to a day before an attack.

A full recovery is expected with treatment. Recurrent id reactions are frequently due to inadequate treatment of the primary infection or dermatitis and often the cause of recurrence is unknown.

Because granuloma annulare is usually asymptomatic and self-limiting with a course of about 2 years, initial treatment is generally topical steroid creams, followed by oral steroids and finally intradermal injections at the site of each ring. Treatment success varies widely, with most patients finding only brief success with the above-mentioned treatments. New research out of India suggests that the combination of rifampin (600 mg), ofloxacin (400 mg), and minocycline hydrochloride (100 mg) once monthly, or ROM therapy, produces promising results. Most lesions of granuloma annulare disappear in pre-pubertal patients with no treatment within two years while older patients (50+) have rings for upwards of 20 years. The appearance of new rings years later is not uncommon.

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.

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

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.

Granuloma annulare, microscopically, consists of dermal epithelioid histiocytes around a central zone of mucin - a so-called palisaded granuloma.

Both lyme disease and STARI can be treated with antibiotics, particularly doxycyclin.

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.

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 (redness) multiforme (EM) is usually a reaction of the skin and mucous membranes that occurs suddenly. It appears as a symmetrical rash and may include the mucous membrane lesions. This means that the body is sensitive to something that causes the skin and mucous membranes to react. The more common mild form is refer to as EM minor. It consists of a skin rash that involve no more than one mucosal surface. The sudden onset will progress rapidly as symmetrical lesions with circular color changes in some or all of the lesions. Rash will spread towards center or trunk of the body. Evenly distributed bumps on the skin become classic iris or target lesions. They have bright red borders and small white bumps in the center.

The cause of EM appears to be a highly sensitive reaction that can be triggered by a variety of causes. The causes can include bacterial, viral or chemical products, such as antibiotics – specifically penicillins or cephalosporins. This reaction is an allergic reaction and is in no way contagious.

Erythema multiforme minus is sometimes divided into papular and vesiulobullous forms.

Southern tick-associated rash illness (STARI) produces a similar rash pattern although it develops more quickly and is smaller. This erythema is also sometimes called erythema migrans or EM. The associated infectious agent has not been determined. Antibiotic treatment resolves the illness quickly.

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.

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.

NL is diagnosed by a skin biopsy, demonstrating superficial and deep perivascular and interstitial mixed inflammatory cell infiltrate (including lymphocytes, plasma cells, mononucleated and multinucleated histiocytes, and eosinophils) in the dermis and subcutis, as well as necrotising vasculitis with adjacent necrobiosis and necrosis of adnexal structures. Areas of necrobiosis are often more extensive and less well defined than in granuloma annulare. Presence of lipid in necrobiotic areas may be demonstrated by Sudan stains. Cholesterol clefts, fibrin, and mucin may also be present in areas of necrobiosis. Depending on the severity of the necrobiosis, certain cell types may be more predominant. When a lesion is in its early stages, neutrophils may be present, whereas in later stages of development lymphocytes and histiocytes may be more predominant.