Why does thrombocytopenia cause bleeding

Chronic alcohol abuse, congenital syndromes, ITP, liver disease, myelodysplastic syndrome. The physical examination should include the eyes e. Bleeding e. Thrombocytopenia can be classified as emergent usually requires inpatient management or nonemergent outpatient management. Some syndromes may fall in either category based on the severity of thrombocytopenia. A peripheral blood smear can provide diagnostic information on a variety of white blood cell disorders, hemolytic anemias, and thrombocytopenia.

Table 4 lists common findings on peripheral blood smear and their associated diagnoses. Ribosomal precipitate appears as blue granules throughout the cytoplasm of the red blood cell. Cryoglobulinemia, mycoplasma pneumonia, multiple myeloma, some autoimmune disorders. Caused by increased platelet turnover or release of immature forms into the circulation. Thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, disseminated intravascular coagulation, defective prosthetic heart valve.

The findings of isolated thrombocytopenia in an outpatient setting have prognostic implications. A prospective study evaluated the long-term outcomes of patients with incidental thrombocytopenia. In 64 percent of patients, platelet counts normalized or remained stable. The probability of developing immune thrombocytopenic purpura or an autoimmune disorder was approximately 7 and 12 percent, respectively.

Four cases of myelodysplastic syndrome were diagnosed 2 percent , all of which were in older patients. Pseudothrombocytopenia is secondary to platelet clumping and has no clinical significance. It occurs in one in 1, persons in the general population, and can be confirmed by a peripheral blood smear. If the complete blood count still shows thrombocytopenia, other causes should be investigated.

Immune thrombocytopenic purpura is an acquired immune-mediated disorder characterized by isolated thrombocytopenia and the absence of other conditions or agents known to induce thrombocytopenia.

The incidence is cases per 1 million persons annually, and approximately 50 percent of cases occur in children. The risk of bleeding correlates to the severity of thrombocytopenia.

Patients may present without symptoms, with minimal bleeding, or with serious hemorrhage e. Older patients, patients on antiplatelet therapy, and patients with comorbid conditions may have more severe bleeding manifestations. Secondary immune thrombocytopenic purpura is associated with other underlying conditions, such as autoimmune disorders e. Testing to rule out other causes should be performed as clinically indicated. Forty percent of patients with immune thrombocytopenic purpura test positive for antinuclear or antiphospholipid antibodies without having an underlying autoimmune syndrome.

Corticosteroids are considered first-line treatment and increase platelet counts usually within one week of initiation.

Second-line treatment includes thrombopoietin-receptor agonists and splenectomy. Any patient older than 60 years presenting with isolated thrombocytopenia should be evaluated for myelodysplastic syndrome and lympho-proliferative disorders. Heparin-induced thrombocytopenia should be suspected in patients recently treated with heparin.

Platelet counts decline within five to 10 days in patients with no previous exposure to heparin and may decline precipitously within hours in patients with recent heparin exposure. This life-threatening disorder is characterized by the presence of platelet-activating antibodies recognizing multimolecular complexes bound to unfractionated heparin or low-molecular-weight heparin.

Patients with heparin-induced thrombocytopenia present with mild thrombocytopenia or a 50 percent decrease in platelet count from baseline. Thrombosis complications termed heparin-induced thrombocytopenia with thrombosis develop in 20 to 50 percent of patients and may affect arterial and venous systems, even after heparin is discontinued.

Characteristic features are erythematous or necrotizing skin reactions at the site of injection or severe manifestations, such as deep venous thrombosis, pulmonary emboli, stroke, or myocardial infarction. This test has a high sensitivity greater than 97 percent but a lower specificity 74 to 86 percent because of the presence of platelet factor 4 antibodies in patients without heparin-induced thrombocytopenia.

One study showed that patients who developed heparin-induced thrombocytopenia had a 20 percent in-hospital mortality rate, regardless of thrombosis development. Patients presenting with thrombocytopenia and microangiopathic hemolytic anemia should be admitted to the hospital with a presumptive diagnosis of thrombotic thrombocytopenic purpura.

Renal manifestations, neurologic changes, and fever also may be present. Severity is reflected by the extent of microvascular aggregation of platelets resulting in ischemia and necrosis of tissue cells. The incidence of thrombotic thrombocytopenic purpura is four to 11 patients per 1 million annually in the United States. Thrombotic thrombocytopenic purpura occurs primarily in adults. Shiga toxin-producing Escherichia coli is the most common causative organism in hemolytic uremic syndrome.

Pregnant patients beyond 20 weeks' gestation with thrombocytopenia or signs and symptoms such as headache, visual disturbances, right upper quadrant abdominal pain, or elevated blood pressure should be evaluated for preeclampsia and HELLP syndrome. Laboratory abnormalities may include anemia, elevated liver enzymes, elevated lactate dehydrogenase, and proteinuria. Aplastic anemia, chemotherapy, irradiation, acute leukemias, and myelodysplastic disorders may result in severe or symptomatic thrombocytopenia.

Paroxysmal nocturnal hemoglobinuria is associated with hemolysis, renal disease, and thrombosis complications. Hospitalized patients with comorbid conditions, such as sepsis, trauma, burns, or malignancy, can develop disseminated intravascular coagulation with resultant thrombocytopenia.

One of the most common types of thrombocytopenia in the outpatient setting is drug-induced thrombocytopenia. An epidemiologic study from Europe and the United States showed an annual incidence of 10 cases per 1 million persons, but numbers could be higher in older persons and in hospitalized patients.

Quinine is a common cause of drug-induced thrombocytopenia and often is missed in the patient history. Table 5 lists common medications that may cause thrombocytopenia.

Drug-induced thrombocytopenia typically occurs within five to seven days of exposure to the causative agent and usually resolves within seven to 14 days after discontinuation. Adapted with permission from Kenney B, Stack G. Drug-induced thrombocytopenia. Arch Pathol Lab Med. Copyright College of American Pathologists. Infections may cause thrombocytopenia by direct bone marrow suppression or increased peripheral platelet consumption. Common viruses include hepatitis B and C, human immunodeficiency virus, Epstein-Barr, cytomegalovirus, parvovirus B19, varicellazoster, rubella, and mumps.

Recent studies found thrombocytopenia in 14 percent of hospitalized patients with influenza A H1N1 virus. If the patient has a recent travel history, especially to South America or Mexico, dengue fever and malaria should be considered. Other travel-associated infections, such as typhoid fever , can cause thrombocytopenia.

Chronic liver disease usually causes persistent thrombocytopenia, and manifests as cirrhosis, fibrosis, and portal hypertension. The most common cause is chronic alcohol abuse; however, other etiologies include infectious hepatitis, drug-induced liver disease, nonalcoholic liver disease, and metabolic disorders.

Patients who consume excessive amounts of alcohol can present with varying degrees of liver impairment ranging from asymptomatic fatty liver to end-stage liver disease. Thrombocytopenia results from direct toxic marrow suppression and splenic sequestration. Folic acid deficiency related to malnutrition often coexists with alcohol abuse. Abstinence and nutritional replacement often lead to platelet normalization in three to four weeks in the absence of chronic liver disease.

Gestational thrombocytopenia is the most common diagnosis of thrombocytopenia in pregnancy, occurring in 8 percent of pregnancies. Gestational thrombocytopenia is characterized by mild thrombocytopenia, no history of thrombocytopenia, no association of fetal thrombocytopenia, and spontaneous resolution after delivery.

Recommendations for the initial evaluation of thrombocytopenia in pregnancy include a complete blood count and peripheral blood smear. A suggested algorithm for the management of thrombocytopenia is shown in Figure 1. Patients with incidental thrombocytopenia i.

Additional laboratory evaluation should be performed as clinically indicated, and a trial of discontinuing agents known to decrease platelet counts is recommended. Patients with chronic alcohol abuse or known nutritional deficiencies with stable thrombocytopenia can be treated by a primary care physician. Rickettsial diseases and most viral infections causing transient thrombocytopenia also can be managed by a primary care physician. Patients with unexplained severe thrombocytopenia, decreasing platelet counts, additional hematologic abnormalities, or associated bleeding complications should be referred to a hematologist.

Algorithm for the management of thrombocytopenia. Information from reference 4. General recommendations for activity participation have been based on historical data from patients with chronic severe thrombocytopenia. Patients with a platelet count greater than this level can engage in most activities, but should use caution if participating in contact sports. Key words included: thrombocytopenia, review, treatment, idiopathic immune thrombocytopenic purpura, thrombocytopenia in pregnancy, thrombotic thrombocytopenic purpura, heparin-induced thrombocytopenia, hemolytic uremic syndrome, preeclampsia, HELLP syndrome, gestational thrombocytopenia, pseudothrombocytopenia, myelodysplastic syndrome, microangiopathic hemoglobinopathies, drug-induced thrombocytopenia, platelet transfusion, inherited thrombocytopenias, antiphospholipid antibodies, and viral infections.

Information published between and June was included. Original search dates: April 5 and June 16, Final search date: November 23, Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. Address correspondence to Robert L. Reprints are not available from the authors. The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U.

Army Medical Department or the U. Army at large. A novel approach to the assessment of variations in the human platelet count. Thromb Haemost. Immune thrombocytopenic purpura. N Engl J Med. Thrombocytopenias: a clinical point of view. Blood Transfus. Helsinki, Finland: Wiley Interscience.

April 27, Accessed November 25, Approach to the adult patient with thrombocytopenia [subscription required]. Accessed November 28, Inherited thrombocytopenias: a proposed diagnostic algorithm from the Italian Gruppo di Studio delle Piastrine. George JN. Clinical practice. Thombotic thrombocytopenic purpura.

Kenney B, Stack G. Platelet count at term pregnancy: a reappraisal of the threshold. Obstet Gynecol. ACOG practice bulletin: Thrombocytopenia in pregnancy. Number 6, September Clinical management guidelines for obstetrician-gynecologists. American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet.

Risk of immune thrombocytopenic purpura after measles-mumps-rubella immunization in children. Bratton RL, Corey R. If a doctor finds one of these substances to be the cause of a low platelet count, stopping intake of the substance can return the platelet count to normal.

If the cause is a drug being taken for a different condition, the prescribing doctor might change the medication. Symptoms of a low platelet count only occur at severely low levels.

A slightly lower-than-normal count may not produce symptoms. If the count is low enough to cause spontaneous bleeding, an individual may notice small bleeds that create small, round, dark red spots on the skin called petechiae.

ITP can also cause the gums or nose to bleed without reason and the presence of blood in the urine or stools. Platelets form a crucial part of the composition of blood. They are responsible for repairing tissue damage and play a vital role in the blood-clotting system, which helps to stop bleeding and heal wounds. Blood clotting is also known as hemostasis. Platelets are not invisible to the naked eye. The bone marrow produces them, and they travel in the blood for an average of 10 days before being destroyed.

When a blood vessel wall is damaged, it exposes a substance that activates platelets. Activated platelets trigger further events that bring in more platelets, and a blood clot starts to form. This serves to plug any leak. Activated platelets also release sticky proteins to help form the clot.

A protein known as fibrin forms a mesh of threads that holds the plug together. A platelet count measures the concentration of platelets in the blood.

A technician would carry this test out in a laboratory. When the number of platelets is low, this concentration reduces. Women normally experience a platelet count that varies slightly during the menstrual cycle and can fall near the end of pregnancy.

A doctor will ask some questions and perform a physical examination. The questions might cover symptoms, family history, and medications. The examination will assess for skin rashes and bruising.

A laboratory platelet count will confirm the diagnosis, showing the exact concentration of platelets in the blood. The doctor is likely to perform other blood tests at the same time. These may include :. Because each platelet lives only about 10 days, your body normally renews your platelet supply continually by producing new platelets in your bone marrow.

Thrombocytopenia rarely is inherited; or it can be caused by a number of medications or conditions. Whatever the cause, circulating platelets are reduced by one or more of the following processes: trapping of platelets in the spleen, decreased platelet production or increased destruction of platelets. The spleen is a small organ about the size of your fist situated just below your rib cage on the left side of your abdomen.

Normally, your spleen works to fight infection and filter unwanted material from your blood. An enlarged spleen — which can be caused by a number of disorders — can harbor too many platelets, which decreases the number of platelets in circulation. Platelets are produced in your bone marrow. Factors that can decrease platelet production include:. Some conditions can cause your body to use up or destroy platelets faster than they're produced, leading to a shortage of platelets in your bloodstream.

Examples of such conditions include:. Dangerous internal bleeding can occur when your platelet count falls below 10, platelets per microliter. Though rare, severe thrombocytopenia can cause bleeding into the brain, which can be fatal. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. This content does not have an English version.

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