The diagnostic testing for vasculitis should be guided by the patient's history and physical exam. The clinician should ask about the duration, onset, and presence any associated symptoms such as weight loss or fatigue (that would indicate a systemic cause). It is important to distinguish between IgA and non-IgA vasculitis. IgA vasculitis is more likely to present with abdominal pain, bloody urine, and joint pain. In the case that the cause is not obvious, a reasonable initial workup would include a complete blood count, urinalysis, basic metabolic panel, fecal occult blood testing, erythrocyte sedimentation rate (ESR), and C-reactive protein level. Small vessel cutaneous vasculitis is a diagnosis of exclusion and requires ruling out systemic causes of the skin findings. Skin biopsy (punch or excisional) is the most definitive diagnostic test and should be performed with 48 hours of appearance of the vasculitis. A skin biopsy will be able to determine if the clinical findings are truly due to a vasculitis or due to some other cause.

A detailed history is important to elicit any recent medications, any risk of hepatitis infection, or any recent diagnosis with a connective tissue disorder such as systemic lupus erythematosus (SLE). A thorough physical exam is needed as usual.

- Lab tests. Basic lab tests may include a CBC, chem-7 (look for creatinine), muscle enzyme, liver function tests, ESR, hepatitis seroloties, urinalysis, CXR, and EKG. Additional, more specific tests include:

- Antinuclear antibody (ANA) test can detect an underlying connective tissue disorder, especially SLE

- Complement levels that are low can suggest mixed cryoglobulinemia, hepatitis C infection, and SLE, but not most other vasculitides.

- Antineutrophil cytoplasmic antibody (ANCA) may highly suggest granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis, or drug-induced vasculitis, but is not diagnostic.

- Electromyography. It is useful if a systemic vasculitis is suspected and neuromuscular symptoms are present.

- Arteriography. Arteriograms are helpful in vasculitis affecting the large and medium vessels but not helpful in small vessel vasculitis. Angiograms of mesenteri or renal arteries in polyarteritis nodosa may show aneurysms, occlusions, and vascular wall abnormalities. Arteriography are not diagnostic in itself if other accessible areas for biopsy are present. However, in Takayasu's arteritis, where the aorta may be involved, it is unlikely a biopsy will be successful and angiography can be diagnostic.

- Tissue biopsy. This is the gold standard of diagnosis when biopsy is taken from the most involved area.

Multiple standards exist for defining Henoch–Schönlein purpura, including the 1990 American College of Rheumatology (ACR) classification and the 1994 Chapel Hill Consensus Conference (CHCC). Some have reported the ACR criteria to be more sensitive than those of the CHCC.

More recent classifications, the 2006 European League Against Rheumatism (EULAR) and Pediatric Rheumatology Society (PReS) classification, include palpable purpura as a mandatory criterion, together with at least one of the following findings: diffuse abdominal pain, predominant IgA deposition (confirmed on skin biopsy), acute arthritis in any joint, and renal involvement (as evidenced by the presence of blood and/or protein in the urine).

Henoch–Schönlein purpura may present with an atypical manifestation, which can be confused with papular urticaria, systemic lupus erythematosus, meningococcemia, dermatitis herpetiformis, and acute hemorrhagic edema of infancy.

Schamberg's disease can only be properly diagnosed by a healthcare provider. While reviewing medical history is important to diagnose this condition, it is essential that the purpuric lesions are physically examined. A skin biopsy will be taken to determine capillaritis of dermal vessels. Capillaritis or pigmented purpura is skin condition that has brown-reddish patches on the skin, which is caused by leaky capillaries. The skin biopsy is sent to a laboratory for a pathological examination, where the biopsy is observed under a microscope. In addition to the skin biopsy, dermatologists will perform a dermatoscopy. With the results from the biopsy and from the dermatoscopy, a doctor will be able to identify that the skin lesions are in fact due Schamberg's disease. To ensure that the skin lesions are not caused by other skin conditions or infections, doctors will order a complete blood count (CBC) and other blood tests. Blood tests are usually normal and they are only performed to rule out other bleeding disorders that cause purpura. Since Schamberg's disease is usually asymptomatic, there is not a lot of other tests that can be performed. This condition is easy to diagnose because the appearance of skin lesions on the skin is the first indicator that the lesions are due to Schamberg's disease.

The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans may lead to complications of fluid overload and death, especially in neonates, such as transfusion-related acute lung injury. Exposure to multiple plasma donors over time increases the cumulative risk for transfusion-associated viral infection and allergic reaction to donor proteins found in fresh frozen plasma.

Allergic reactions and alloantibody formation are also potential complications, as with any protein replacement therapy.

Concomitant warfarin therapy in subjects with congenital protein C deficiency is associated with an increased risk of warfarin skin necrosis.

Drug-induced purpura is a skin condition that may be related to platelet destruction, vessel fragility, interference with platelet function, or vasculitis.

The cardinal features of purpura investigations are the same as those of disseminated intravascular coagulation: prolonged plasma clotting times, thrombocytopenia, reduced plasma fibrinogen concentration, increased plasma fibrin-degradation products and occasionally microangiopathic haemolysis.

Amyloid purpura affects a minority of individuals with amyloidosis. For example, purpura is present early in the disease in approximately 15% of patients with primary systemic amyloidosis.

Treat the underlying disease . Eg for wegner's treatment is steroids and cyclophosphamide.

Schamberg's disease is caused by leaky blood vessels near the surface of the skin, capillaries, which allow red blood cells to slip through into the skin. The red blood cells in the skin then fall apart and release their iron, which is released from hemoglobin. The iron causes a rust color and this accounts for the orange tint of the rash that can be seen on the skin. The underlying cause of the leaky blood vessels is not known, but researchers are suggesting that there could be some potential triggers. Some possible triggers include viral infection, a hypersensitivity to some agent, and interaction of some medications, such as thiamine and aspirin. Even though there is no correlation with genetics, there have been a few cases where few people in a family had this condition.

Although the cause of capillary inflammation is unknown, certain preventive measures can be taken. Doctors may prescribe medications that enhance the circulation of blood, which can keep blood vessels strong and healthy. Daily intake of vitamin C has proven to be a natural home remedy that can prevent the onsite of any disease or infection. Doctors always recommend that their patients monitor what they eat because their diet could be a possible factor that contributes to this condition. A healthy body that receives nutritious meals is more likely to have a healthy life that does not revolve around a lot of health problems.

Treatment should be directed towards the specific underlying cause of the vasculitis. If no underlying cause is found and the vasculitis is truly limited to the skin then treatment is primarily supportive. Such treatment involves measures such as leg elevation, stockings, and topical steroids to relieve itching/burning. If the vasculitis does not self-resolve within 3–4 weeks, more aggressive treatment may be warranted. Oral colchicine or dapsone are often used for this purpose. If rapid control of symptoms is needed, a short course of high-dose oral steroids may be given. Immunosuppressive agents such as methotrexate and azathioprine may be used in truly refractory cases not responsive to colchicine or dapsone.

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.

Waldenström hyperglobulinemic purpura (also known as "Purpura hyperglobulinemica") is a skin condition that presents with episodic showers of petechiae (small red or purple spots) occurring on all parts of the body, most profusely on the lower extremities.

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.

Diagnosis is done by the help of symptoms and only blood count abnormality is thrombocytopenia.

CBC and blood film: decreased platelets and schistocytes PT, aPTT, fibrinogen: normal Markers of hemolysis: increased unconjugated bilirubin, increased LDH, decreased haptoglobin Negative Coombs test

Creatinine, urea, to follow renal function ADAMSTS-13 gene, activity or inhibitor testing (TTP)

Solar purpura (also known as "Actinic purpura," and "Senile purpura") is a skin condition characterized by large, sharply outlined, 1- to 5-cm, dark purplish-red ecchymoses appearing on the dorsa of the forearms and less often the hands.

The condition is most common in elderly people of European descent. It is caused by sun-induced damage to the connective tissue of the skin.

No treatment is necessary. The lesions typically fade over a period of up to 3 weeks.

Nonthrombocytopenic purpura is a type of purpura (red or purple skin discoloration) not associated with thrombocytopenia.

Examples/causes include:

- Henoch–Schönlein purpura.

- Hereditary hemorrhagic telangiectasia

- Congenital cytomegalovirus

- Meningococcemia

Cryoglobulinemic purpura is a skin condition characterized by purpura and occurring most frequently in multiple myeloma and macroglobulinemia.

Purpura hemorrhagica may be prevented by proper management during an outbreak of strangles. This includes isolation of infected horses, disinfection of fomites, and good hygiene by caretakers. Affected horses should be isolated at least one month following infection. Exposed horses should have their temperature taken daily and should be quarantined if it becomes elevated. Prophylactic antimicrobial treatment is not recommended.

Vaccination can reduce the incidence and severity of the disease. However, horses with high SeM antibody titers are more likely to develop purpura hemorrhagica following vaccination and so these horses should not be vaccinated. Titers may be measured by ELISA.

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.

Amyloid purpura usually occurs above the nipple-line and is found in the webbing of the neck and in the face and eyelids.

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.

Treatment is targeted to the underlying cause. However, most vasculitis in general are treated with steroids (e.g. methylprednisolone) because the underlying cause of the vasculitis is due to hyperactive immunological damage. Immunosuppressants such as cyclophosphamide and azathioprine may also be given.

A systematic review of antineutrophil cytoplasmic antibody (ANCA) positive vasculitis identified best treatments depending on whether the goal is to induce remission or maintenance and depending on severity of the vasculitis.