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mcatmemoranda · 1 year ago

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●Definition – Thrombocytopenia (ie, platelet count <150,000/microL [150 x 109/L]) may be associated with a variety of conditions, with associated risks that range from life-threatening to none. We are most concerned about spontaneous bleeding with counts <10,000/microL, and surgical bleeding with counts <50,000/microL. Rarely, thrombocytopenia is associated with a risk of thrombosis rather than, or in addition to, bleeding. (See 'Definitions and areas of concern' above.)

●Causes – The potential causes of thrombocytopenia differ depending on the clinical setting in which it occurs (table 6). (See 'Causes of thrombocytopenia' above and 'Overview of our approach' above.)

•Severe thrombocytopenia with bleeding and certain causes of thrombocytopenia (suspected heparin-induced thrombocytopenia [HIT], thrombotic thrombocytopenic purpura [TTP], hemolytic uremic syndrome [HUS], drug-induced thrombotic microangiopathy [DITMA], or bone marrow failure syndrome with severe pancytopenia) are medical emergencies that require immediate action. (See 'Thrombocytopenic emergencies requiring immediate action' above.)

•In asymptomatic outpatients with thrombocytopenia, common diagnoses include immune thrombocytopenia (ITP), occult liver disease, HIV infection, and myelodysplastic syndromes. Congenital thrombocytopenias (sometimes misdiagnosed as ITP) may also occur (table 2). (See 'Asymptomatic, incidental finding, mild thrombocytopenia' above.)

•In patients with bleeding who lack signs of systemic illness or other abnormalities of the complete blood count (CBC), drug-induced immune thrombocytopenia (table 3) or primary ITP are likely diagnoses. (See 'Thrombocytopenia with bleeding or other symptoms' above.)

•In patients with other clinical findings, causes of thrombocytopenia include infection, sepsis, disseminated intravascular coagulation (DIC), drug-induced thrombocytopenia, HIT, liver disease, lymphoma, other malignancies, nutrient deficiencies (vitamin B12, folate, copper), TTP or HUS, antiphospholipid syndrome (APS), and paroxysmal nocturnal hemoglobinuria (PNH). (See 'Thrombocytopenia with bleeding or other symptoms' above.)

•In acutely ill patients, common causes of new-onset thrombocytopenia include sepsis, DIC, and drug-induced thrombocytopenia (table 1). Many patients in the intensive care unit with thrombocytopenia have more than one cause. (See 'Acutely ill/intensive care unit' above.)

●Evaluation – We confirm thrombocytopenia by repeating the CBC and reviewing the peripheral blood smear; obtain prior platelet counts, if available, and assess other hematologic abnormalities. The pace of the subsequent evaluation, further testing, and hematologist consultation depends on the clinical presentation, which can range from asymptomatic to acutely ill. (See 'Overview of our approach' above and 'Initial questions and pace of the evaluation' above.)

•History and examination – The history should focus on prior platelet counts, family history, bleeding, medications (table 3), over-the-counter remedies (table 4), infectious exposures, dietary practices, and other medical conditions (eg, hematologic disorders, rheumatologic conditions, surgery, transfusion). The physical examination should evaluate bleeding, lymphadenopathy, hepatosplenomegaly, thrombosis, and organ involvement. (See 'History' above and 'Physical examination' above.)

•Laboratory testing – No additional laboratory testing besides the CBC and peripheral blood smear is absolutely required in a patient with isolated thrombocytopenia. Adults with new thrombocytopenia should have HIV and HCV testing if not done recently. Additional laboratory testing may be warranted in patients with other findings. (See 'Laboratory testing' above.)

●Referral – Hematologist consultation is appropriate to confirm a new diagnosis or if the cause of thrombocytopenia is unclear. The urgency of referral depends on the degree of thrombocytopenia and other abnormalities, and the stability of the findings. In hospitalized patients, early hematology involvement is appropriate for individuals with suspected TTP, HUS, HIT, and some hematologic malignancies (eg, acute leukemia). (See 'Hematologist referral/consultation' above.)

●Bone marrow – Bone marrow evaluation is not required in all patients with thrombocytopenia; however, it may be helpful in some patients if the cause of thrombocytopenia is unclear, or if a primary hematologic disorder is suspected. (See 'Bone marrow evaluation' above.)

●Management – Management of patients with thrombocytopenia depends on the underlying diagnosis. General principles that apply to all patients include a review of medications that may interfere with normal hemostasis and a decision regarding whether they should be continued, coordination with anesthesiologists and surgeons before invasive procedures, and correction of coagulation abnormalities. Activity restrictions are often not needed. (See 'General management principles' above and "Platelet transfusion: Indications, ordering, and associated risks".)

●Other populations – Thrombocytopenia in neonates and children, and thrombocytopenia during pregnancy are discussed separately. (See "Neonatal thrombocytopenia: Etiology" and "Causes of thrombocytopenia in children" and "Thrombocytopenia in pregnancy".)

#thrombocytopenia #low platelets

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mcatmemoranda · 2 years ago

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When to worry about thrombosis — Rarely, patients with thrombocytopenia are at risk for thrombosis rather than, or in addition to, bleeding. While most of the implicated disorders are rare, it is important to consider them because urgent treatment may be needed to prevent life-threatening thrombotic events.

Examples include the following:

●Heparin-induced thrombocytopenia – A small percentage of patients exposed to heparin (less than 5 percent) will develop heparin-induced thrombocytopenia (HIT) in which antibodies to a platelet factor 4 epitope induced by heparin can cause thrombocytopenia and platelet activation, leading to life-threatening venous and/or arterial thrombosis. This diagnosis should be considered in a patient recently exposed to heparin who develops thrombocytopenia, thrombosis, anaphylaxis, or skin reactions. Treatment involves immediate discontinuation of heparin and administration of a non-heparin anticoagulant (e.g., dabigatran or bivalirudin).

●Vaccine-induced immune thrombotic thrombocytopenia (VITT) – VITT is a rare syndrome that occurs after vaccination with coronavirus disease 2019 (COVID-19) adenoviral vector vaccines (AstraZeneca and Janssen [Johnson & Johnson]). It resembles spontaneous HIT in that there is no prior heparin exposure, and it is associated with life-threatening venous and/or arterial thrombosis. Individuals with thrombosis and/or thrombocytopenia should be evaluated for recent administration of a COVID-19 vaccine within the preceding 5 to 30 days, and for which specific type of vaccine they received.

●Antiphospholipid syndrome – The antiphospholipid syndrome (APS) can develop in individuals with systemic lupus erythematosus, other medical conditions (eg, infection, medications, cancer), or in individuals without an underlying condition. Patients may have venous and/or arterial thrombosis. Treatment involves anticoagulation or aspirin, and treatment of any underlying condition.

●Disseminated intravascular coagulation – Patients with disseminated intravascular coagulation (DIC) are at risk of bleeding or thrombosis, usually venous. DIC is commonly seen in acutely ill patients with sepsis or malignancy, but it can also be seen in a variety of other conditions.

●Thrombotic microangiopathy – Thrombotic microangiopathies (TMAs) such as thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or drug-induced TMA (DITMA) are associated with small-vessel platelet-rich thrombi. These microthrombi can occur in any organ and can be life-threatening. Plasma exchange for TTP may be life-saving and should be initiated immediately when TTP is suspected.

●Paroxysmal nocturnal hemoglobinuria – Paroxysmal nocturnal hemoglobinuria (PNH) is a rare condition caused by loss of glycosyl phosphatidylinositol from cell membranes. Thrombosis (often involving unusual locations such as intraabdominal or cerebral veins) can occur, along with hemolytic anemia and/or bone marrow failure. Treatment depends on the degree of cytopenias and the presence of thrombosis.

●ITP with a concomitant thrombotic disorder – Certain conditions can occur in patients with ITP increasing their risk of thrombosis such as atrial fibrillation or recent or previous deep vein thrombosis. Management of anticoagulation in that population can be challenging; however, it is important to note that the low platelet count is not protective against thrombosis, and anticoagulation is often indicated.

Work up:

Peripheral blood smear — Review of the peripheral blood smear is used to exclude pseudothrombocytopenia (eg, falsely low platelet count due to platelet clumping) and to evaluate morphologic abnormalities of blood cells that could be useful in determining the cause of thrombocytopenia. As an example, giant platelets may suggest a congenital platelet disorder (eg, MYH-9-related disorders, Bernard Soulier syndrome [BSS]); these may be counted as red blood cells by some automated counters.

Pseudothrombocytopenia — The possibility of pseudothrombocytopenia (ie, falsely low platelet count) should be eliminated before any further evaluation is undertaken. Pseudothrombocytopenia can occur in a number of settings, all of which can be identified by review of the peripheral blood smear and/or repeating the CBC using a non-EDTA anticoagulant:

●Incompletely mixed or inadequately anticoagulated samples may form a clot that traps platelets in the collection tube and prevents them from being counted.

●In approximately 0.1 percent of individuals, exposure of patient samples to the EDTA anticoagulant in the collection tube can induce platelet clumps or platelet rosettes around white blood cells (WBCs). These may be counted by automated counters as leukocytes rather than platelets. The mechanism is "naturally occurring" platelet autoantibodies directed against a concealed epitope on platelet membrane glycoprotein (GP) IIb/IIIa that becomes exposed by EDTA-induced dissociation of GPIIb/IIIa [45-52].

If platelet clumping is observed, the platelet count is repeated using heparin or sodium citrate as an anticoagulant in the collection tube. If citrate is used, the platelet count should be corrected for dilution caused by the amount of citrate solution; no such correction is needed for heparin. Alternatively, fresh, non-anticoagulated blood can be pipetted directly into platelet-counting diluent fluid.

RBC and WBC abnormalities — Abnormal RBC and WBC morphologies may suggest a specific condition.

Examples include the following:

●Schistocytes suggest a microangiopathic process (eg, DIC, TTP, HUS, DITMA).

●Nucleated RBCs, and Howell-Jolly bodies, may be seen post-splenectomy or occasionally in patients with poor splenic function.

●Spherocytes suggest immune-mediated hemolytic anemia or hereditary spherocytosis.

●Leukoerythroblastic findings, teardrop cells, nucleated RBCs, or immature granulocytes suggest an infiltrative process in the bone marrow.

●Leukocytosis with a predominance of bands and/or toxic granulations suggests infection.

●Immature WBCs (eg, myeloblasts) or dysplastic WBCs suggest leukemia or myelodysplasia.

●Multi-lobed/hypersegmented neutrophils (ie, more than 5 lobes) suggest a megaloblastic process (eg, B12/folate/copper deficiency).

HIV and HCV testing — Thrombocytopenia has been identified as an important "indicator condition" for HIV infection. Thus, adults with new thrombocytopenia should have HIV testing if not done recently.

Thrombocytopenia may also be seen with hepatitis C virus (HCV) infection; testing is appropriate for adults with thrombocytopenia if not done recently. Other laboratory testing — Aside from the testing mentioned above (CBC, review of peripheral smear, HIV and HCV testing), no additional laboratory testing is absolutely required in a patient with isolated thrombocytopenia. However, additional testing may be warranted in patients with other findings.

Examples of findings that may trigger other laboratory testing include the following:

●Symptoms or findings of systemic autoimmune disorders (eg, systemic lupus erythematosus [SLE], anti-phospholipid syndrome [APS]) may prompt testing for anti-nuclear antibodies or anti-phospholipid antibodies, respectively. We do not test for these in patients with isolated thrombocytopenia and no signs or symptoms suggestive of SLE or APS.

●Findings of liver disease should prompt measurements of hepatic enzymes and possibly tests of liver synthetic function (eg, albumin, coagulation testing), depending on the severity of the liver disease.

●Thrombosis should prompt consideration of DIC, heparin-induced thrombocytopenia (HIT) and related syndromes, and APS. Depending on the site of thrombosis and other hematologic findings, paroxysmal nocturnal hemoglobinuria (PNH) may also be a consideration.

●Microangiopathic changes on the peripheral smear should prompt coagulation testing (eg, PT, aPTT, fibrinogen) and measurement of serum lactate dehydrogenase (LDH) and renal function to evaluate for DIC, TTP, or HUS; with subsequent evaluation based on the results.

ADDITIONAL EVALUATION

Hematologist referral/consultation — Referral to a hematologist is appropriate to confirm any new diagnosis of a thrombocytopenic condition or to determine the cause of any unexplained thrombocytopenia. The urgency of referral depends on the degree of thrombocytopenia and other abnormalities, and the stability of the findings.

In hospitalized patients, some conditions are medical emergencies that require immediate action. Immediate hematologist involvement in diagnosis and management is appropriate for the following:

●Suspected thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS).

●Suspected heparin-induced thrombocytopenia (HIT).

●Suspected COVID-19 vaccine-induced immune thrombotic thrombocytopenia (VITT).

●Suspected hematologic malignancy (eg, acute leukemia), aplastic anemia, or other bone marrow failure syndrome.

The consulting hematologist can also assist in diagnosis and management of patients with severe thrombocytopenia (ie, platelet count less than 50,000/microL) who have serious bleeding or require an urgent invasive procedure, and in pregnant women with severe thrombocytopenia, regardless of the cause.

Bone marrow evaluation — Bone marrow evaluation (aspirate and biopsy) is not required in all patients with thrombocytopenia. However, it may be helpful in some patients if the cause of thrombocytopenia is unclear, or if a primary hematologic disorder is suspected. A possible exception may be a clinical picture consistent with a nutrient deficiency in which a bone marrow would only be needed if a deficiency could not be documented, or if the hematologic findings did not resolve upon nutrient repletion.

The following bone marrow findings may be helpful:

●Normal or increased numbers of megakaryocytes suggests that the thrombocytopenia is due, at least in part, to a condition associated with platelet destruction (eg, ITP, drug-induced immune thrombocytopenia).

●Decreased megakaryocyte numbers, along with overall decreased or absent cellularity (picture 18 and picture 19), is consistent with decreased bone marrow production of platelets, as in aplastic anemia.

●In rare cases, severe reduction or absence of megakaryocytes with no other abnormalities (also called acquired amegakaryocytic thrombocytopenia or acquired pure megakaryocytic aplasia) may occur. This finding is most often reported in patients with SLE, and is typically due to an autoantibody directed against the thrombopoietin receptor.

●Megaloblastic changes in the RBC and granulocytic series suggest a nutrient deficiency (eg, vitamin B12, folate, copper) (picture 20), while dysplastic changes suggest a myelodysplastic disorder (picture 21 and picture 22).

●Granulomata, increased reticulin or collagen fibrosis (picture 23 and picture 24), or infiltration with malignant cells (picture 25) establishes the diagnosis of bone marrow invasion, especially when a leukoerythroblastic blood picture is also present.

GENERAL MANAGEMENT PRINCIPLES

There are some general management principles that apply to all patients with thrombocytopenia regardless of the cause, and for which questions may arise before a diagnosis has been established.

●Activity restrictions – Patients who are otherwise healthy and have no manifestations of petechiae or purpura may not require activity restrictions.

Individual considerations apply to participation in certain activities. As an example, individuals with severe thrombocytopenia (less than 50,000/microL) generally should not participate in extreme athletics such as boxing, rugby, and martial arts. However, no restrictions are necessary for usual activities or low-impact exercise.

●Anticoagulant and anti-platelet medications – For anticoagulant and anti-platelet medications, the clinical indications and risks associated with discontinuation (eg, thrombosis) are balanced against the bleeding risk associated with the degree of thrombocytopenia and of continuing the anticoagulant and/or anti-platelet medication [7]. Input from the consulting specialist who prescribed the medication and/or the hematologist may be sought. A discussion of anticoagulation in adults with thrombocytopenia is presented separately.

It is also important to note that thrombocytopenia by itself does not protect against venous or arterial thrombosis, and appropriate use of thromboprophylaxis or anticoagulants should not be withheld from a patient with mild to moderate thrombocytopenia (eg, greater than 50,000/microL) if it is indicated (eg, postoperatively). For patients with more severe thrombocytopenia, decisions are made on a case-by-case basis regarding the risks of bleeding and benefits of anticoagulation.

●Over-the-counter remedies – Patients should be educated about which non-prescription remedies interfere with platelet function (eg, aspirin, nonsteroidal anti-inflammatory drugs, ginkgo biloba). In general, these agents are avoided unless there is a specific indication for which equivalent alternatives are lacking.

●Safe platelet count for invasive procedures – Most platelet count thresholds for invasive procedures are based on weak observational evidence at best. In general, procedures with a greater risk of bleeding are performed at higher platelet counts. While there is some flexibility in individual circumstances, anesthesiologists and surgeons performing these procedures will have the last word. A listing of general guidelines used for different procedures is presented separately.

Optimal methods for raising the platelet count in preparation for an invasive procedure depend on the underlying condition (eg, corticosteroids or intravenous immune globulin (IVIG) for presumptive ITP; platelet transfusion for myelodysplastic syndromes). These approaches are discussed in detail in separate topic reviews.

Individuals with impaired platelet function may require platelet transfusions despite adequate platelet counts, depending on the procedure. Attention should also be paid to correcting coagulation abnormalities if present.

●Emergency management of bleeding – Urgent management of critical bleeding in the setting of severe thrombocytopenia requires immediate platelet transfusion, regardless of the underlying cause.

#thrombocytopenia #low platelet count #low platelets #thrombocytopenia wu

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