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.

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.

Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of its development. Heparin-induced necrosis can develop both at sites of local injection and - when infused intravenously - in a widespread pattern.

In warfarin's initial stages of action, inhibition of protein C and Factor VII is stronger than inhibition of the other vitamin K-dependent coagulation factors II, IX and X. This results from the fact that these proteins have different half-lives: 1.5 to six hours for factor VII and eight hours for protein C, versus one day for factor IX, two days for factor X and two to five days for factor II. The larger the initial dose of vitamin K-antagonist, the more pronounced these differences are. This coagulation factor imbalance leads to paradoxical activation of coagulation, resulting in a hypercoagulable state and thrombosis. The blood clots interrupt the blood supply to the skin, causing necrosis. Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis with necrosis and gangrene of limbs.

Notably, the prothrombin time (or international normalized ratio, INR) used to test the effect of warfarin is highly dependent on factor VII, which explains why patients can have a therapeutic INR (indicating good anticoagulant effect) but still be in a hypercoagulable state.

In one third of cases, warfarin necrosis occurs in patients with an underlying, innate and previously unknown deficiency of protein C. The condition is related to purpura fulminans, a complication in infants with sepsis (blood stream infection) which also involves skin necrosis. These infants often have protein C deficiency as well. There have also been cases in patients with other deficiency, including protein S deficiency, activated protein C resistance (Factor V Leiden) and antithrombin III deficiency.

Although the above theory is the most commonly accepted theory, others believe that it is a hypersensitivity reaction or a direct toxic effect.

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 cause of erythema toxicum is thought to be an activation of the immune system. Some neonates are more sensitive than others and develop erythematous spots all over the body. Another theory is hypersensitivity to detergents in bedsheets and clothing is sometimes suspected, but the connection remains unproven.

It is thought to be a benign condition that causes no discomfort to the infant. The rash will generally disappear spontaneously in about 2 weeks.

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

Common causes of rashes include:

- Food allergy

- Medication side effects

- Anxiety

- Allergies, for example to food, dyes, medicines, insect stings, metals such as zinc or nickel; such rashes are often called hives.

- Skin contact with an irritant

- Fungal infection, such as ringworm

- Balsam of Peru

- Reaction to vaccination

- Skin diseases such as eczema or acne

- Exposure to sun (sunburn) or heat

- Friction due to chafing of the skin

- Irritation such as caused by abrasives impregnated in clothing rubbing the skin. The cloth itself may be abrasive enough for some people

- Secondary syphilis

- Poor personal hygiene

Uncommon causes:

- Autoimmune disorders such as psoriasis

- Lead poisoning

- Pregnancy

- Repeated scratching on a particular spot

- Lyme Disease

- Scarlet fever

Non-blanching rash (NBR) is a medical term used to describe a skin rash that does not fade when pressed with, and viewed through, a glass.

It is a characteristic of both purpuric and petechial rashes. Individual purpura measure 3–10 mm (0.3–1 cm, - in), whereas petechiae measure less than 3 mm.

A non-blanching rash can be a symptom of bacterial meningitis, but this is not the exclusive cause.

A maculopapular rash is a type of rash characterized by a flat, red area on the skin that is covered with small confluent bumps. It may only appear red in lighter-skinned people. The term "maculopapular" is a compound: "macules" are small, flat discolored spots on the surface of the skin; and "papules" are small, raised bumps. It is also described as erythematous, or red.

This type of rash is common in several diseases and medical conditions, including scarlet fever, measles, Ebola virus disease, rubella, secondary syphilis (Congenital syphilis, which is asymptomatic, the newborn may present this type of rash), erythrovirus (parvovirus B19), chikungunya (alphavirus), zika, and heat rash. It is also a common manifestation of a skin reaction to the antibiotic amoxicillin or chemotherapy drugs. Cutaneous infiltration of leukemic cells may also have this appearance. Maculopapular rash is seen in graft-versus-host disease (GVHD) developed after a hematopoietic stem cell transplant (bone marrow transplant), which can be seen within one week or several weeks after the transplant. In the case of GVHD, the maculopapular rash may progress to a condition similar to toxic epidermal necrolysis. In addition, this is the type of rash that some patients presenting with Ebola virus hemorrhagic (EBO-Z) fever will reveal but can be hard to see on dark skin people. It is also seen in patients with Marburg hemorrhagic fever, a filovirus not unlike Ebola.

This type of rash can be as a result of large doses of niacin or no-flush niacin (2000 – 2500 mg), used for the management of low HDL cholesterol.

This type of rash can also be a symptom of Sea bather's eruption. This stinging, pruritic, maculopapular rash affects swimmers in some Atlantic locales (e.g., Florida, Caribbean, Long Island). It is caused by hypersensitivity to stings from the larvae of the sea anemone (e.g., "Edwardsiella lineate") or the thimble jellyfish ("Linuche unguiculata"). The rash appears where the bathing suit contacts the skin.

This type of rash can also be a symptom of acute arsenic intoxication, appearing 2 weeks later.

The term morbilliform refers to a rash that looks like measles. The rash consists of macular lesions that are red and usually 2–10 mm in diameter but may be confluent in places.

Patients with measles will have the rash but there are other syndromes and infections that will display the same symptom such as patients with Kawasaki disease, meningococcal petechiae or Waterhouse-Friderichsen syndrome, Dengue, congenital syphilis, rubella, Echovirus 9, drug hypersensitivity reactions (in particular with certain classes of antiretroviral drugs, such as abacavir and nevirapine, and also the antiepileptic drug phenytoin), or other conditions may also have a morbilliform rash.

One cause of morbilliform rash is an allergic reaction to transfused blood/blood components. In such a case, the skin lesions would develop within a few hours (Approx. 4hours) of transfusion along with pruritus. The condition may even present with other symptoms, such as conjunctival oedema, oedema in the lips and tongue, and even localised angioedema. On rare occasions, the condition may even escalate to anaphylactic shock where pulmonary restrictions are seen. The associated cause for this is a reaction against an allergen that is seldom identified during testing. Transfusing products with anti-IgA antibodies to IgA-deficient patients has also been a suspected cause for such reactions. Management usually relates to the stoppage of transfusion for around 30minutes, until given antihistamines take effect. Transfusion may even be continued after, if no further progression is seen.

"Rickettsia aeschlimannii" infection is a condition characterized by a rash of maculopapules.

Symmetrical drug-related intertriginous and flexural exanthema (SDRIFE), more popularly known as Baboon syndrome because of its resemblance to the distinctive red buttocks displayed by female baboons, is a systemic contact dermatitis characterized by well-demarcated patches of erythema distributed symmetrically on the buttocks.

The cause of the syndrome may be drug-related, i.e. induced by systemic administration of hydroxyzine penicillin, iodinated radio contrast media and others.

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

It is estimated that 2—3 percent of hospitalised patients are affected by a drug eruption, and that serious drug eruptions occur in around 1 in 1000 patients.

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.

Acute cutaneous lupus erythematosus is a cutaneous condition characterized by a bilateral malar rash (also known as a "butterfly rash") and lesions that tend to be transient, and that follow sun exposure.

A rash is a change of the human skin which affects its color, appearance, or .

A rash may be localized in one part of the body, or affect all the skin. Rashes may cause the skin to change color, itch, become warm, bumpy, chapped, dry, cracked or blistered, swell, and may be painful.

The causes, and therefore treatments for rashes, vary widely. Diagnosis must take into account such things as the appearance of the rash, other symptoms, what the patient may have been exposed to, occupation, and occurrence in family members. Rash can last 5 to 20 days, the diagnosis may confirm any number of conditions.

The presence of a rash may aid diagnosis; associated signs and symptoms are diagnostic of certain diseases. For example, the rash in measles is an erythematous, morbilliform, maculopapular rash that begins a few days after the fever starts. It classically starts at the head, and spreads downwards.

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

Eosinophilic cellulitis, also known as Wells' syndrome, is a skin disease that presents with painful, red, raised, and warm patches of skin. The rash comes on suddenly, lasts for a few weeks, and often repeatedly comes back. Scar formation does not typically occur.

Eosinophilic cellulitis is of unknown cause. It is suspected to be an autoimmune disorder. It may be triggered by bites from insects such as spiders, fleas, or ticks, or from medications or surgery. Diagnosis is made after other potential cases are ruled out. Skin biopsy of the affected areas may show an increased number of eosinophils. Other conditions that may appear similar include cellulitis, contact dermatitis, and severe allergic reactions such as anaphylaxis.

Treatment is often with a corticosteroids. Steroids applied as a cream is generally recommended over the use of steroids by mouth. Antihistamines may be used to help with itchiness. Many times the condition goes away after a few weeks without treatment. The condition is uncommon with about 200 described cases. It affects both sexes with the same frequency. It was first described by George Crichton Wells in 1971.

Eosinophilic cellulitis is of unknown cause. It is suspected to be an autoimmune disorder. It may be triggered by bites from insects such as spiders, fleas, or ticks, or from medications or surgery.

In most patients, the condition lasts only a matter of weeks; in some cases it can last longer (up to six months). The disease resolves completely without long-term effects. Two percent of patients have recurrence.

Gianotti–Crosti syndrome ( ), also known as infantile papular acrodermatitis, papular acrodermatitis of childhood, and papulovesicular acrolocated syndrome, is a reaction of the skin to a viral infection. Hepatitis B virus and Epstein–Barr virus are the most frequently reported pathogens. Other incriminated viruses are hepatitis A virus, hepatitis C virus, cytomegalovirus, coxsackievirus, adenovirus, enterovirus, rotavirus, rubella virus, HIV, and parainfluenza virus.

It is named for Ferdinando Gianotti and Agostino Crosti.

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.

The cause of the condition is generally unknown. There is a correlation between the PUPPP rash and dairy. When some women stop drinking dairy the rash has been known to go away. This skin condition occurs mostly in first pregnancies (primigravida), in the third trimester and is more likely with multiple pregnancies (more so with triplets than twins or singletons).

Other than additional associations with hypertension and induction of labour, there are no observed difference in the outcome of the pregnancy for mothers or babies.

Multiple species of bacteria can be associated with the condition:

- Meningococcus is another term for the bacterial species "Neisseria meningitidis"; blood infection with said species usually underlies WFS. While many infectious agents can infect the adrenals, an acute, selective infection is usually meningococcus.

- "Pseudomonas aeruginosa" can also cause WFS.

- WFS can also be caused by "Streptococcus pneumoniae" infections, a common bacterial pathogen typically associated with meningitis in the adult and elderly population.

- "Mycobacterium tuberculosis" could also cause WFS. Tubercular invasion of the adrenal glands could cause hemorrhagic destruction of the glands and cause mineralocorticoid deficiency.

- "Staphylococcus aureus" has recently also been implicated in pediatric WFS.

- It can also be associated with "Haemophilus influenzae".

Viruses may also be implicated in adrenal problems:

- Cytomegalovirus can cause adrenal insufficiency, especially in the immunocompromised.

- Ebola virus infection may also cause similar acute adrenal failure.