There is increasing use of immunosuppressants such as mycophenolate mofetil and azathioprine because of their effectiveness. In chronic refractory cases, where immune pathogenesis has been confirmed, the off-label use of the "vinca" alkaloid and chemotherapy agent vincristine may be attempted. However, vincristine has significant side effects and its use in treating ITP must be approached with caution, especially in children.

Intravenous immunoglobulin (IVIg) may be infused in some cases in order to decrease the rate at which macrophages consume antibody-tagged platelets. However, while sometimes effective, it is costly and produces improvement that generally lasts less than a month. Nevertheless, in the case of an ITP patient already scheduled for surgery who has a dangerously low platelet count and has experienced a poor response to other treatments, IVIg can rapidly increase platelet counts, and can also help reduce the risk of major bleeding by transiently increasing platelet counts.

Discontinuation of heparin is critical in a case of heparin-induced thrombocytopenia (HIT). Beyond that, however, clinicians generally treat to avoid a thrombosis, often by starting patients directly on warfarin. For this reason, patients are usually treated with a direct thrombin inhibitor, such as lepirudin or argatroban, which are approved by the FDA for this use. Other blood thinners sometimes used in this setting that are not FDA-approved for treatment of HIT include bivalirudin and fondaparinux. Platelet transfusions are not routinely used to treat HIT because thrombosis, not bleeding, is the primary problem.

Treatment is guided by the severity and specific cause of the disease. Treatment focuses on eliminating the underlying problem, whether that means discontinuing drugs suspected to cause it or treating underlying sepsis. Diagnosis and treatment of serious thrombocytopenia is usually directed by a hematologist. Corticosteroids may be used to increase platelet production. Lithium carbonate or folate may also be used to stimulate platelet production in the bone marrow.

Due to the high mortality of untreated TTP, a presumptive diagnosis of TTP is made even when only microangiopathic hemolytic anemia and thrombocytopenia are seen, and therapy is started. Transfusion is contraindicated in thrombotic TTP, as it fuels the coagulopathy. Since the early 1990s, plasmapheresis has become the treatment of choice for TTP. This is an exchange transfusion involving removal of the patient's blood plasma through apheresis and replacement with donor plasma (fresh frozen plasma or cryosupernatant); the procedure must be repeated daily to eliminate the inhibitor and abate the symptoms. If apheresis is not available, fresh frozen plasma can be infused, but the volume that can be given safely is limited due to the danger of fluid overload. Plasma infusion alone is not as beneficial as plasma exchange. Corticosteroids (prednisone or prednisolone) are usually given. Rituximab, a monoclonal antibody aimed at the CD20 molecule on B lymphocytes, may be used on diagnosis; this is thought to kill the B cells and thereby reduce the production of the inhibitor. A stronger recommendation for rituximab exists where TTP does not respond to corticosteroids and plasmapheresis.

Caplacizumab is an alternative option in treating TTP as it has been shown that it induces a faster disease resolution compared with those patient who were on placebo. However, the use of caplacizumab was associated with increase bleeding tendencies in the studied subjects.

Most patients with refractory or relapsing TTP receive additional immunosuppressive therapy, e.g. vincristine, cyclophosphamide, splenectomy or a combination of the above.

Children with Upshaw-Schülman syndrome receive prophylactic plasma every two to three weeks; this maintains adequate levels of functioning ADAMTS13. Some tolerate longer intervals between plasma infusions. Additional plasma infusions may necessary for triggering events, such as surgery; alternatively, the platelet count may be monitored closely around these events with plasma being administered if the count drops.

Measurements of blood levels of lactate dehydrogenase, platelets, and schistocytes are used to monitor disease progression or remission. ADAMTS13 activity and inhibitor levels may be measured during follow-up, but in those without symptoms the use of rituximab is not recommended.

Treatment is directed at the prevention of haemorrhagic shock. Standard dose prednisolone does not increase the platelet count. High-dose methylprednisolone therapy in children with Onyalai has been shown to improve platelet count and reduce the requirement for transfusions. Vincristine sulphate may be of benefit to some patients. Splenectomy is indicated in patients with severe uncontrollable haemorrhage. High-dose intravenous gammaglobulin may help in increasing the platelet count and cessation of haemorrhage.

For people who have severe congenital protein C deficiency, protein C replacement therapies are available, which is indicated and approved for use in the United States and Europe for the prevention of purpura fulminans. Protein C replacement is often in combination with anticoagulation therapy of injectable low molecular weight heparin or oral warfarin. Before initiating warfarin therapy, a few days of therapeutic heparin may be administered to prevent warfarin skin necrosis and other progressive or recurrent thrombotic complications.

The course of treatment and the success rate is dependent on the type of TMA. Some patients with atypical HUS and TTP have responded to plasma infusions or exchanges, a procedure which replaces proteins necessary for the complement cascade that the patient does not have; however, this is not a permanent solution or treatment, especially for patients with congenital predispositions.

The mortality rate is around 95% for untreated cases, but the prognosis is reasonably favorable (80–90% survival) for patients with idiopathic TTP diagnosed and treated early with plasmapheresis.

Early stage sepsis-associated purpura fulminans may be reversible with quick therapeutic intervention. Treatment is mainly removing the underlying cause and degree of clotting abnormalities and with supportive treatment (antibiotics, volume expansion, tissue oxygenation, etc.). Thus, treatment includes aggressive management of the septic state.

Purpura fulminans with disseminated intravascular coagulation should be urgently treated with fresh frozen plasma (10–20 mL/kg every 8–12 hours) and/or protein C concentrate to replace pro-coagulant and anticoagulant plasma proteins that have been depleted by the disseminated intravascular coagulation process.

Protein C in plasma in the steady state has a half life of 6- to 10-hour, therefore, patients with severe protein C deficiency and presenting with purpura fulminans can be treated acutely with an initial bolus of protein C concentrate 100 IU/kg followed by 50 IU /kg every 6 hours. A total of 1 IU/kg of protein C concentrate or 1 mL/kg of fresh frozen plasma will increase the plasma concentration of protein C by 1 IU/dL. Cases with comorbid pathological bleeding may require additional transfusions with platelet concentrate (10–15 mL/kg) or cryoprecipitate (5 mL/kg).

Established soft tissue necrosis may require surgical removal of the dead tissue, fasciotomy, amputation or reconstructive surgery.

Initial treatment is with glucocorticoid corticosteroids or intravenous immunoglobulin, a procedure that is also used in ITP cases. In children, good response to a short steroid course is achieved in approximately 80 percent of cases. Although the majority of cases initially respond well to treatment, relapses are not uncommon and immunosuppressive drugs (e.g. ciclosporin, mycophenolate mofetil, vincristine and danazol) are subsequently used, or combinations of these.

The off-label use of rituximab (trade name Rituxan) has produced some good results in acute and refractory cases, although further relapse may occur within a year. Splenectomy is effective in some cases, but relapses are not uncommon.

The only prospect for a permanent cure is the high-risk option of an allogeneic hematopoietic stem cell transplantation (SCT).

Treatment of DIC is centered around treating the underlying condition. Transfusions of platelets or fresh frozen plasma can be considered in cases of significant bleeding, or those with a planned invasive procedure. The target goal of such transfusion depends on the clinical situation. Cryoprecipitate can be considered in those with a low fibrinogen level.

Treatment of thrombosis with anticoagulants such as heparin is rarely used due to the risk of bleeding.

Recombinant human activated protein C was previously recommended in those with severe sepsis and DIC, but drotrecogin alfa has been shown to confer no benefit and was withdrawn from the market in 2011.

Recombinant factor VII has been proposed as a "last resort" in those with severe hemorrhage due to obstetric or other causes, but conclusions about its use are still insufficient.

Cordocentesis can be performed in utero to determine the platelet count of the fetus. This procedure is only performed if a "prior" pregnancy was affected by . Intrauterine transfusions can be performed during cordocentesis for primary prevention of intracerebral hemorrhage. Any administered cellular blood products must be irradiated to reduce the risk of graft-versus-host disease in the fetus. Additionally, all administered blood products should be reduced-risk ( seronegative and leukoreduced are considered essentially equivalent for the purposes of risk reduction).

If intrauterine platelet transfusions are performed, they are generally repeated weekly (platelet lifespan after transfusion is approximately 8 to 10 days). Platelets administered to the fetus must be negative for the culprit antigen (often -1a, as stated above). Many blood suppliers (such as American Red Cross and United Blood Services) have identified -1a negative donors. An alternative donor is the mother who is, of course, negative for the culprit antigen. However, she must meet general criteria for donation and platelets received from the mother must be washed to remove the offending alloantibody and irradiated to reduce the risk of graft-versus-host disease. If platlet transfusions are needed urgently, incompatible platelets may be used, with the understanding that they may be less effective and that the administration of any blood product carries risk.

The use of Intravenous immunoglobulin () during pregnancy and immediately after birth has been shown to help reduce or alleviate the effects of in infants and reduce the severity of thrombocytopenia. The most common treatment is weekly infusions at a dosage of 1 g/kg beginning at 16 to 28 weeks of pregnancy, depending on the severity of the disease in the previous affected child, and continuing until the birth of the child. In some cases this dosage is increased to 2 g/kg and/or combined with a course of prednisone depending on the exact circumstances of the case. Although this treatment has not been shown to be effective in all cases it has been shown to reduce the severity of thrombocytopenia in some. Also, it is suspected that (though not understood why) provides some added protection from intercranial haemorrhage () to the fetus. Even with treatment, the fetal platelet count may need to be monitored and platelet transfusions may still be required.

The goal of both and platelet transfusion is to avoid hemorrhage. Ultrasound monitoring to detect hemorrhage is not recommended as detection of intracranial hemorrhage generally indicates permanent brain damage (there is no intervention that can be performed to reverse the damage once it has occurred).

Before delivery, the fetal platelet count should be determined. A count of >50,000 μL is recommended for vaginal delivery and the count should be kept above 20,000 μL after birth.

Analgesics may be needed for the abdominal and joint pains. It is uncertain as to whether HSP needs treatment beyond controlling the symptoms. Most patients do not receive therapy because of the high spontaneous recovery rate. Steroids are generally avoided. However, if they are given early in the disease episode, the duration of symptoms may be shortened, and abdominal pain can improve significantly. Moreover, the chance of severe kidney problems may be reduced. A systematic review of randomized clinical trials did not find any evidence that steroid treatment (prednisone) is effective at decreasing the likelihood of developing long-term kidney disease.

Evidence of worsening kidney damage would normally prompt a kidney biopsy. Treatment may be indicated on the basis of the appearance of the biopsy sample; various treatments may be used, ranging from oral steroids to a combination of intravenous methylprednisolone (steroid), cyclophosphamide and dipyridamole followed by prednisone. Other regimens include steroids/azathioprine, and steroids/cyclophosphamide (with or without heparin and warfarin). Intravenous immunoglobulin (IVIG) is occasionally used.

There is no evidence from randomized clinical trials that treating children who have HSP with antiplatelet agent prevents persistent kidney disease. There is also no evidence from randomized clinical trials that treating children or adults with cyclophosphamide prevents severe kidney disease. Heparin treatment is not justified.

There has been no general recommendation for treatment of patients with Giant Platelet Disorders, as there are many different specific classifications to further categorize this disorder which each need differing treatments. Platelet transfusion is the main treatment for people presenting with bleeding symptoms. There have been experiments with DDAVP (1-deamino-8-arginine vasopressin) and splenectomy on people with Giant platelet disorders with mixed results, making this type of treatment contentious.

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

Immune thrombocytopenic purpura (), sometimes called idiopathic thrombocytopenic purpura is a condition in which autoantibodies are directed against a patient's own platelets, causing platelet destruction and thrombocytopenia. Anti-platelet autoantibodies in a pregnant woman with immune thrombocytopenic purpura will attack the patient's own platelets and will also cross the placenta and react against fetal platelets. Therefore, is a significant cause of fetal and neonatal immune thrombocytopenia. Approximately 10% of newborns affected by will have platelet counts <50,000 μL and 1% to 2% will have a risk of intracerebral hemorrhage comparable to infants with .

Mothers with thrombocytopenia or a previous diagnosis of should be tested for serum antiplatelet antibodies. A woman with symptomatic thrombocytopenia and an identifiable antiplatelet antibody should be started on therapy for their which may include steroids or . Fetal blood analysis to determine the platelet count is not generally performed as -induced thrombocytopenia in the fetus is generally less severe than . Platelet transfusions may be performed in newborns, depending on the degree of thrombocytopenia.

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.

The therapy of an acute TTP episode has to be started as early as possible. The standard treatment is the daily replacement of the missing ADAMTS13 protease in form of plasma infusions or in more severe episodes by plasma exchange. In the latter the patients plasma is replaced by donated plasma. The most common sources of ADAMTS13 is platelet-poor fresh frozen plasma (FFP) or solvent-detergent plasma.

The benefit of plasma exchange compared to plasma infusions alone may result from the additional removal of ULVWF. In general both plasma therapies are well tolerated, several mostly minor complications may be observed. The number of infusion/exchange sessions needed to overcome a TTP episode are variable but usually take less than a week in USS. The intensive plasma-therapy is generally stopped when platelet count increases to normal levels and is stable over several days.

By tradition, the term idiopathic thrombocytopenic purpura is used when the cause is idiopathic. However, most cases are now considered to be immune-mediated.

Another form is thrombotic thrombocytopenic purpura.

Not all affected patients seem to need a regular preventive plasma infusion therapy, especially as some reach longterm remission without it. Regular plasma infusions are necessary in patients with frequent relapses and in general situations with increased risk to develop an acute episode (as seen above) such as pregnancy. Plasma infusions are given usually every two to three weeks to prevent acute episodes of USS but are often individually adapted.

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.

Treatment usually involves high doses of steroids such as dexamethasone. While high doses of steroids may risk laminitis, low doses are associated with refractory cases. Antibiotics are used to treat any residual nidus of "S. equi". Non-steroidal anti-inflammatory drugs (NSAIDs), such as phenylbutazone or flunixin, may be useful to reduce fever and relieve pain. Intravenous DMSO is sometimes used as a free-radical scavenger and anti-inflammatory. Additionally, wrapping the legs may reduce edema and skin sloughing. Supportive care with oral or IV fluids may also be required.

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.

Prognosis is good with early, aggressive treatment (92% survival in one study).