The first element of treatment is usually to discontinue the offending drug, although there have been reports describing how the eruption evolved little after it had established in spite of continuing the medication. Vitamin K1 can be used to reverse the effects of warfarin, and heparin or its low molecular weight heparin (LMWH) can be used in an attempt to prevent further clotting. None of these suggested therapies have been studied in clinical trials.

Heparin and LMWH act by a different mechanism than warfarin, so these drugs can also be used to prevent clotting during the first few days of warfarin therapy and thus prevent warfarin necrosis (this is called 'bridging').

Based on the assumption that low levels of protein C are involved in the underlying mechanism, common treatments in this setting include fresh frozen plasma or pure activated protein C.

Since the clot-promoting effects of starting administration of 4-hydroxycoumarins are transitory, patients with protein C deficiency or previous warfarin necrosis can still be restarted on these drugs if appropriate measures are taken. These include gradual increase starting from low doses and supplemental administration of protein C (pure or from fresh frozen plasma).

The necrotic skin areas are treated as in other conditions, sometimes healing spontaneously with or without scarring, sometimes going on to require surgical debridement or skin grafting.

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

Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin usually secondary to vasculitis or dietary deficiency of vitamin C (scurvy). They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.

Purpura is common with typhus and can be present with meningitis caused by meningococci or septicaemia. In particular, meningococcus ("Neisseria meningitidis"), a Gram-negative diplococcus organism, releases endotoxin when it lyses. Endotoxin activates the Hageman factor (clotting factor XII), which causes disseminated intravascular coagulation (DIC). The DIC is what appears as a rash on the affected individual.

Purpura are a common and nonspecific medical sign; however, the underlying mechanism commonly involves one of:

- Platelet disorders (thrombocytopenic purpura)

- Primary thrombocytopenic purpura

- Secondary thrombocytopenic purpura

- Post-transfusion purpura

- Vascular disorders (nonthrombocytopenic purpura)

- Microvascular injury, as seen in senile (old age) purpura, when blood vessels are more easily damaged

- Hypertensive states

- Deficient vascular support

- Vasculitis, as in the case of Henoch–Schönlein purpura

- Coagulation disorders

- Disseminated intravascular coagulation (DIC)

- Scurvy (vitamin C deficiency) - defect in collagen synthesis due to lack of hydroxylation of procollagen results in weakened capillary walls and cells

- Meningococcemia

- Cocaine use with concomitant use of the one-time chemotherapy drug and now veterinary deworming agent levamisole can cause purpura of the ears, face, trunk, or extremities, sometimes needing reconstructive surgery. Levamisole is purportedly a common cutting agent.

- Decomposition of blood vessels including purpura is a symptom of acute radiation poisoning in excess of 2 Grays of radiation exposure. This is an uncommon cause in general, but is commonly seen in victims of nuclear disaster.

Cases of psychogenic purpura are also described in the medical literature, some claimed to be due to "autoerythrocyte sensitization". Other studies suggest the local (cutaneous) activity of tissue plasminogen activator can be increased in psychogenic purpura, leading to substantial amounts of localized plasmin activity, rapid degradation of fibrin clots, and resultant bleeding. Petechial rash is also characteristic of a rickettsial infection.

Treatment differs according to what rash a patient has been diagnosed with. Common rashes can be easily remedied using steroid topical creams (such as hydrocortisone) or non-steroidal treatments. Many of the medications are available over the counter in the United States.

The problem with steroid topical creams i.e. hydrocortisone; is their inability to penetrate the skin through absorption and therefore not be effective in clearing up the affected area, thus rendering the hydrocortisone almost completely ineffective in all except the most mild of cases.

Gianotti-Crosti disease is a harmless and self-limiting condition, so no treatment may be required. Treatment is mainly focused on controlling itching, symptomatic relief and to avoid any further complications. For symptomatic relief from itching, oral antihistamines or any soothing lotions like calamine lotion or zinc oxide may be used. If there are any associated conditions like streptococcal infections, antibiotics may be required.

Treatment is often with a steroids. This can be either applied as a cream or taken by mouth. As the condition tends to get better on its own taking steroids by mouth should generally only be tried if the rash covers a large area and it does not get better with other measures.

The condition usually resolves on its own, and treatment is not required. Oral antihistamines or topical steroids may be used to decrease itching. Steroids do provide relief from itching, and improve the appearance of the rash, but they also cause the new skin that forms (after the rash subsides) to take longer to match the surrounding skin color. While no scarring has been found to be associated with the rash, scratching should be avoided. It's possible that scratching can make itching worse and an itch-scratch cycle may develop with regular scratching (that is, you itch more because you scratch, so you scratch more because you itch, and so on). Irritants such as soaps with fragrances, hot water, wool, and synthetic fabrics should be avoided. Lotions that help stop or prevent itching may also be helpful.

Direct sunlight makes the lesions resolve more quickly. According to this principle, medical treatment with ultraviolet light has been used to hasten resolution, though studies disagree whether it decreases itching or not. UV therapy is most beneficial in the first week of the eruption.

Oral erythromycin was effective in treating patients in one early trial, but a later study could not confirm these results. Since Human Herpes Virus 6 or Human Herpes Virus 7 has been hypothesized to be the cause, the antiviral drug Acyclovir may reduce length of duration and severity.

Once a diagnosis of JDMS is made, the treatment is often a 3-day course of Intravenous ("pulse") steroids (methylprednisolone, Solu-Medrol), followed by a high dose of oral prednisone (usually 1–2 mg/kg of body weight) for several weeks. This action usually brings the disease under control, lowering most lab tests to or near normal values. Some minor improvement in muscle symptoms may also be seen in this time, but normally it takes a long time for full muscle strength to be regained.

Once the disease process is under control, oral steroids are tapered gradually to minimize their side effects. Often, steroid-sparing drugs, such as methotrexate (a chemotherapy drug) or other DMARDs, are given to compensate for the reduction in oral steroids. Once the oral steroids are reduced to a less toxic level, the sparing agents can also be gradually withdrawn. Lab results are closely monitored during the tapering process to ensure that the disease does not recur.

In the cases where steroids or second-line drugs are not tolerated or are ineffective, there are other treatments that can be tried. These include other chemotherapy drugs, such as ciclosporin, infliximab, or other DMARDs. Another is intravenous immunoglobulin (IVIg), a blood product that has been shown to be very effective against JDMS.

To treat the skin rash, anti-malarial drugs, such as hydroxychloroquine (Plaquenil) are usually given. Topical steroid creams (hydrocortisone) may help some patients, and anti-inflammatory creams (such as tacrolimus) are proving to be very effective. Dry skin caused by the rash can be combated by regular application of sunscreen or any moisturizing cream. Most JDM patients are very sensitive to sun exposure, and sunburn may be a disease activity trigger in some, so daily application of high-SPF sunscreen is often recommended.

Many conditions mimic or may be mistaken for warfarin necrosis, including pyoderma gangrenosum or necrotizing fasciitis. Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome, which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in the immediate postpartum period in patients with protein S deficiency.

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.

The culprit can be both a prescription drug or an over-the-counter medication.

Examples of common drugs causing drug eruptions are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), fixed drug eruption due to acetaminophen or NSAIDs (Ibuprofen), and the rash following ampicillin in cases of mononucleosis.

Certain drugs are less likely to cause drug eruptions (rates estimated to be ≤3 per 1000 patients exposed). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.

Soothing mild cases during pregnancy consists mainly of the application of topical moisturising creams or aqueous/emollient ointments. Class I or II corticosteroid creams and ointments are used in more aggressive cases, and oral (systemic) corticosteroids can be used to treat very severe cases—although the benefits of a pregnant woman's ingesting high-potency corticosteroids must be weighed carefully against possible (and mostly unknown) risks to the developing fetus or fetuses. Rarely, in unusually persistent and distressing cases, some women have had their labor induced as soon as they are considered to be at term (37 weeks).

Antihistamine tablets may be prescribed to provide relief from the itch, although they are generally considered much less effective than corticosteroid treatments, and may act as little more than a sleep aid.

Pine tar soap/body wash can bring relief as can keeping the skin chilled such as through a cold shower or iced cloths.

In the majority of cases, PUPPP resolves spontaneously within a week of delivery. However, a few women continue to experience symptoms long into the postpartum period.

If symptoms are well controlled with moisturizers, steroids may only be required when flares occur. Corticosteroids are effective in controlling and suppressing symptoms in most cases. Once daily use is generally enough. For mild-moderate eczema a weak steroid may be used (e.g., hydrocortisone), while in more severe cases a higher-potency steroid (e.g., clobetasol propionate) may be used. In severe cases, oral or injectable corticosteroids may be used. While these usually bring about rapid improvements, they have greater side effects.

Long term use of topical steroids may result in skin atrophy, stria, telangiectasia. Their use on delicate skin (face or groin) is therefore typically with caution. They are, however, generally well tolerated. Red burning skin, where the skin turns red upon stopping steroid use, has been reported among adults who use topical steroids at least daily for more than a year.

Topical immunosuppressants like pimecrolimus and tacrolimus may be better in the short term and appear equal to steroids after a year of use. Their use is reasonable in those who do not respond to or are not tolerant of steroids. Treatments are typically recommended for short or fixed periods of time rather than indefinitely. Tacrolimus 0.1% has generally proved more effective than pimecrolimus, and equal in effect to mid-potency topical steroids. There is no link to increased risk of cancer from topical use of 1% pimecrolimus cream.

When eczema is severe and does not respond to other forms of treatment, systemic immunosuppressants are sometimes used. Immunosuppressants can cause significant side effects and some require regular blood tests. The most commonly used are ciclosporin, azathioprine, and methotrexate.

Fulminant infection from meningococci bacteria in the bloodstream is a medical emergency and requires emergent treatment with adequate antibiotics. Benzylpenicillin was once the drug of choice with chloramphenicol as a good alternative in allergic patients. Ceftriaxone is an antibiotic commonly employed today. Hydrocortisone can sometimes reverse the adrenal insufficiency. Plastic surgery and tissue grafting are sometimes needed to treat tissue necrosis resulting from the infection.

A number of medications speed up recovery including: tetracycline, doxycycline, and erythromycin. Erythromycin may be used as a cream. Doxycycline is most often the first antibiotic drug choice, given at a daily dosage of 100 mg for upto a month before considering tapering off or stopping. Sometimes, longer duration of low doses of doxycycline are required.

Metronidazole is less effective, is available in a gel and can be applied twice daily. If the perioral dermatitis was triggered by a topical steroid then pimecrolimus cream has been suggested as effective in improving symptoms. However, this has also been documented to cause the condition.

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

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.

Multiple treatment regimes are available and treatment algorithms have been proposed.

Perioral dermatitis will usually resolve within a few months without medication and by limiting the use of cosmetics. This is called zero treatment. Topical corticosteroids should be stopped entirely if possible. If the flare proves intolerable, temporary use of a less potent topical corticosteroid can often be helpful.

In persistent or especially bad rashes, an antifungal cream often has to be used. In cases that the rash is more of an irritation, a "mild" topical corticosteroid preparation, e.g. hydrocortisone cream, is used. As it is often difficult to tell a fungal infection apart from a mere skin irritation, many physicians prefer an corticosteroid-and-antifungal combination cream such as hydrocortisone/miconazole.

Antiviral treatment has been tried with some success in a small number of patients.

If the rash does not improve or continues to spread after 2–3 of days of self-care, or if the itching and/or pain is severe, the patient should contact a dermatologist or other physician. Medical treatment usually consists of lotions, creams, or oral medications.

- Corticosteroids. A corticosteroid medication similar to hydrocortisone may be prescribed to combat inflammation in a localized area. It may be applied to the skin as a cream or ointment. If the reaction covers a relatively large portion of the skin or is severe, a corticosteroid in pill or injection form may be prescribed.

In severe cases, a stronger medicine like halobetasol may be prescribed by a dermatologist.

- Antihistamines. Prescription antihistamines may be given if non-prescription strengths are inadequate.

Various moisture-absorbing powders, such as talcum or starch, reduce moisture but may introduce other complications. Airborne powders of any sort can irritate lung tissue, and powders made from starchy plants (corn, arrowroot) provide food for fungi and are not recommended by the American Academy of Dermatology.

Treatment with either glucocorticoids, methotrexate, anakinra, or tocilizumab has been examined. Anakinra has been shown to resolve the clinical features of the disease in 87% of patients. It also induces remission in half of corticosteroid-resistant patients. The results of another study were similar, with half of the patients responding to treatment with Anakinra. Canakinumab, an antibody to

interleukin-1 beta, is indicated for treatment in patients who respond poorly to other treatments.