Thrombocytopenia is a general term for blood disorders that cause low levels of platelets in the blood. A platelet is a type of blood cell that helps the blood clot. These cells clump together at the site of a blood vessel injury in order to prevent blood loss.
Therefore, thrombocytopenia is often associated with abnormal bleeding.
Healthy individuals have anywhere from 150,000 to 450,000 platelets per microliter of circulating blood in the body. The bone marrow continually produces new platelets because they only live about 10 days. Thrombocytopenia occurs when the platelet count falls below 20,000 per microliter of blood. The risk of bleeding increases as the number of platelets decreases. When there are less than 10,000 platelets per microliter of circulating blood, the condition is considered severe, and internal bleeding may occur.
Thrombocytopenia can occur by itself, or it can develop as a complication of another disease, such as cancer or a viral infection. Drug-induced thrombocytopenia may occur in response to medication (such as heparin). In some cases, thrombocytopenia is a chronic (long-lasting) condition that persists for years. However, it may develop suddenly and dramatically in some individuals.
Thrombocytopenia usually improves after treating the underlying cause. In some cases, medications or surgery can help treat chronic thrombocytopenia. If bleeding is severe, some patients may require a blood transfusion.
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types of thrombocytopenia
Disseminated intravascular coagulation (DIC)
Disseminated intravascular coagulation (DIC) occurs when the blood coagulates through the entire body, which causes a depletion of platelets. This disorder has variable effects, and can result in either clotting symptoms or, more often, bleeding. Bleeding can be severe. DIC may be stimulated by many factors, including bacterial or fungal infections in the blood, severe tissue injury (like burns or head trauma), cancer, reactions to blood transfusions and obstetrical complications (like retained placenta after delivery).
Individuals suffering from this condition are at an increased risk of hemorrhage (internal bleeding). This disorder is most common among critically ill patients.
Drug-induced, non-immune thrombocytopenia
Certain drugs can reduce the number of healthy platelets in the blood, resulting in drug-induced non-immune thrombocytopenia. Medications, such as heparin, quinidine, quinine, sulfa-containing antibiotics, some oral hypoglycemia agents (drugs that treat diabetes) like diazoxide, gold salts and rifampin, may destroy platelets. This is not an allergic reaction because the immune system is not involved. Instead, the drugs either destroy the platelets or damage the bone marrow where platelets are produced.
Type I Heparin-induced thrombocytopenia (HIT): Heparin is used to treat and prevent abnormal blood clotting. Heparin can induce thrombocytopenia in some patients. Type I Heparin-induced thrombocytopenia, also called heparin-associated thrombocytopenia (HAT), causes a transient decrease in platelet count without any further symptoms.
The cause of type I HIT may be mediated by a direct interaction between heparin and circulating platelets, which causes platelet clumping or sequestration. This type of thrombocytopenia may occur in patients who are receiving heparin in the presence of other comorbid factors, such as other medications or sepsis, which may complicate the diagnosis. Type I HIT usually occurs within the first 48 to 72 hours after initiation of heparin therapy. The platelet count usually rarely falls below 100 X 103/mm.3 Platelet levels often return to normal within four days, even if heparin is still administered. No laboratory tests are necessary to diagnose type I HIT, and it is not associated with an increased risk of thrombosis.
Type I HIT occurs in about 10-20% of all patients on heparin. It is not due to an immune reaction and antibodies are not present.
Drug-induced immune thrombocytopenia
Certain medications may lead to the formation of antibodies against platelets. Some medications may cause the immune system to mistake the platelets for an invading substance, and the antibodies set out to destroy the cells. As a result of this autoimmune response, platelets are removed rapidly from the blood circulation. Quinidine and quinine have been most commonly implicated but, recently, both heparin and heroin have been indicated in an increasing number of reports.
Type II Heparin-induced thrombocytopenia (HIT): Heparin is used to treat and prevent abnormal blood clotting. Heparin can induce thrombocytopenia in some patients. Type II Heparin-induced thrombocytopenia, also called heparin-associated thrombocytopenia (HAT), is immune-mediated. This condition occurs when the antibodies also activate platelets and cause a hypercoagulable state. Type II Heparin-induced thrombocytopenia can range from mild to severe. In some cases, heparin-induced thrombocytopenia can cause excessive blood clotting instead of bleeding, which increases the risk of clot formation in a deep blood vessel in the leg. Such clots may also be transported to the lungs, which can be life threatening.
The condition may develop one to ten days after initiation of heparin therapy. Type II occurs in about 1-3% of patients receiving heparin.
Hypersplenism, also called splenomegaly (enlarged spleen), occurs when the spleen, which fights infection and filters the blood, is overactive. When hypersplenism occurs, the spleen starts to automatically remove cells that may still be normal in function. This is often the result of tumors, anemia, malaria, tuberculosis or various connective tissue and inflammatory diseases. The spleen becomes enlarged, which often results in a low level of one or more types of blood cells. Individuals who have an enlarged spleen are at risk for developing thrombocytopenia because the spleen may harbor up to 90% of the body's platelets, causing a decrease in the number of platelets in circulation.
Idiopathic thrombocytopenic purpura (ITP)
When the immune system destroys platelets for an unknown reason, the condition is referred to as idiopathic thrombocytopenic purpura (or immune thrombocytopenic purpura). The lymphocytes (immune system cells) produce antibodies to fight off the platelets, which are then destroyed in the spleen. When the immune system mistakenly attacks part of a person's own body, the condition is called an autoimmune disease.
Acute ITP generally lasts less than six months. It mainly occurs in children, and it is the most common type of ITP. It typically occurs after a viral infection. This type of ITP often goes away on its own within a few weeks or months and does not return. Treatment may not be needed. Chronic ITP (lasting six months or longer) mainly affects adults. However, some teenagers and even younger children acquire this type of ITP. Chronic ITP affects women two to three times more often than men. Treatment depends on how severe the bleeding symptoms are and on the platelet count. In mild cases, treatment may not be needed.
Thrombotic thrombocytopenic purpura (TTP)
Thrombotic thrombocytopenic purpura (TTP) is a rare disorder that is characterized by low levels of platelets, low levels of red blood cells, as well as abnormalities in the kidneys and nervous system. Most cases of TTP are the result of a deficiency of the ADAMTS13 enzymes, which are responsible for cleaving ultra large multimers of the von Willebrand factor. This result in hemolysis and organ damage. The condition is considered a medical emergency.
With the development of plasmapheresis, a process that involves removing plasma from blood, about 80-90% of individuals with TTP are able to recover. During plasmapheresis, plasma (which contains platelets) from a blood donor is transfused into the TTP patient's blood. Plasmapheresis is continued until the platelet count normalizes and there is minimal hemolysis.