Thrombocytopenia (Low Platelet Count) (cont.)
Charles Patrick Davis, MD, PhD
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
Siamak N. Nabili, MD, MPH
Dr. Nabili received his undergraduate degree from the University of California, San Diego (UCSD), majoring in chemistry and biochemistry. He then completed his graduate degree at the University of California, Los Angeles (UCLA). His graduate training included a specialized fellowship in public health where his research focused on environmental health and health-care delivery and management.
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
In this Article
- Thrombocytopenia (low platelet count) definition and facts
- What is thrombocytopenia (low platelet count)?
- What are the symptoms of thrombocytopenia?
- What causes thrombocytopenia?
- Decreased platelet production
- Increased platelet destruction or consumption
- Splenic sequestration
- When should I seek medical care for thrombocytopenia?
- Which specialties of doctors treat thrombycytopenia (low platelet count)?
- How is thrombocytopenia diagnosed?
- What is the treatment for thrombocytopenia (low platelet count)?
- What are the complications of thrombocytopenia?
- Can thrombocytopenia be prevented?
- What is the prognosis for a person with thrombocytopenia (low platelet count)?
- Find a local Hematologist in your town
Increased platelet destruction or consumption
Increased platelet destruction or consumption can be seen a number of medical conditions. They can be divided into immune related and non-immune related causes.
Many medications can cause low platelet count by causing immunologic reaction against platelets, called drug-induced thrombocytopenia. Some examples may include:
- sulfonamide antibiotics,
- carbamazepine [(Tegretol, Tegretol XR , Equetro, Carbatrol) anti-seizure drug],
- digoxin (Lanoxin),
- quinine (Quinerva, Quinite, QM-260),
- quinidine (Quinaglute, Quinidex),
- acetaminophen (Tylenol and others), and
- Heparin, a commonly used blood thinner, and similar medications [low molecular weight heparins like enoxaparin (Lovenox) can occasionally induce an immune response against platelets resulting in rapid and severe destruction of platelets. This condition is termed heparin-induced thrombocytopenia or HIT. HIT develops about 1 to 2 days in HIT type 1 and is a non-immune disorder that occurs because of the direct effect of heparin platelet activation. However, HIT type 2 is an immune mediated disorder that occurs about 4 to10 days after exposure to heparin and can develop into life- and limb-threatening complications. HIT is usually not marked by bleeding problems, but by DVT and pulmonary embolism. Diagnosis is based on clinical findings and supported by laboratory findings such as 30% drop platelet count acute thrombotic event like DVT, presence of heparin-PF4 antibodies and the resolution of thrombocytopenia after stopping heparin. Guidelines for treating HIT are too detailed to cover in this article, but can be found in reference 2.
- Idiopathic thrombocytopenic purpura (ITP) is a condition where the immune system attacks platelets. In severe conditions, ITP can result in very low platelet counts. In adults, this is often a chronic (long standing) condition, whereas, in children, it can be caused acutely after a viral infection. This is usually a diagnosis of exclusion, meaning other causes need to be ruled out.
- Some rheumatologic condition, such as systemic lupus erythematosus (SLE) or other autoimmune conditions (connective tissue diseases), can cause platelet destruction.
- Transfusion of blood products and organ transplantation can sometimes cause immunologic disturbances resulting in thrombocytopenia.
- Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are related conditions that can cause non-immune consumptive thrombocytopenia resulting from some infection bacteria in the blood), pregnancy, some metastatic cancers, or chemotherapy. Other manifestations of these conditions include kidney insufficiency, confusion, anemia (hemolytic), and fever. Classic HUS is largely seen in children and is generally thought of as an aftermath of an infection with a certain strain of Escherichia coli bacteria (E. coli O157:H7) which causes infectious diarrhea.
- HELLP syndrome (hemolysis, elevated liver tests, low platelets) is another non-immune thrombocytopenia that may occur during pregnancy and can include elevation of liver enzymes and anemia (specifically, hemolytic anemia or rupturing of red blood cells).
- Disseminated intravascular coagulopathy (DIC) is a rare but severe condition that may be a complication of overwhelming infections, traumas, burns, or pregnancy.
- Injury to or inflammation of blood vessels (vasculitis) and, sometimes, artificial heart valves can cause increased destruction of platelets.
- Severe infections (sepsis) or trauma can sometimes cause consumptive thrombocytopenia (without DIC).
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