What every physician needs to know about thrombocytopenia:
The evaluation of a patient with thrombocytopenia requires two initial steps.
The first step is to exclude life-threatening conditions associated with thrombocytopenia:
– Besides a low platelet count, white blood cells, and hemoglobin levels are usually abnormal and constitutional symptoms, such as fever and weight loss are frequently present. Blasts are frequently present on the blood smear.
Disseminated intravascular coagulation (DIC)
– DIC usually occurs in association with sepsis, trauma, or critical illness and may be associated with serious bleeding or clotting complications.
Thrombotic thrombocytopenic purpura (TTP)
– TTP is characterized by fragmented red blood cells (schistocytes) on the blood smear. If TTP is suspected, plasma exchange should be promptly instituted.
Antiphospholipid antibody syndrome
– The antiphospholipid antibody syndrome is characterized by recurrent thromboses or pregnancy loss in the presence of antiphospholipid antibodies.
Severe drug-induced thrombocytopenia (DITP)
– When severe immune-mediated thrombocytopenia occurs as a side effect of drugs (most commonly in hospitalized patients), bleeding complications may be severe or life-threatening. Heparin-induced thrombocytopenia (HIT) is a special type of thrombocytopenic reaction characterized by predisposition to thrombosis.
Post-transfusion purpura (PTP)
– PTP is a rare, life threatening complication of red blood cell transfusion that occurs mostly in sensitized females. Severe thrombocytopenia occurring 5-10 days after the transfusion can result in severe bleeding complications.
The second step is to assess the risk of bleeding, according to the severity of the thrombocytopenia. This is critical to determine if urgent correction of the thrombocytopenia is required.
A platelet count less than 150,000/uL
– A platelet count less than 150,000/uL is the definition of thrombocytopenia but platelet counts between 100,000-150,000/uL are unimportant for bleeding risk, even with surgery or trauma.
Platelet counts between 50,000-100,000/uL
– Platelet counts between 50,000 and 100,000/uL may indicate a risk for bleeding with certain types of surgery or trauma, but will not be associated with spontaneous bleeding and are probably safe in patients taking drugs that impair platelet function, such as aspirin and clopidogrel.
Platelet counts between 30,000-50,000/uL
– Platelet counts between 30,000-50,000/uL do suggest a possible risk for bleeding with surgery or trauma, but are rarely associated with petechiae, purpura, and spontaneous bleeding.
Platelet counts between 10,000-30,000/uL
– Platelet counts between 10,000 and 30,000/uL may be associated with petechiae, purpura, and spontaneous bleeding, as well as excessive bleeding with surgery or trauma.
Platelet counts less than 10,000/uL
– Platelet counts less than 10,000/uL may be associated with spontaneous bleeding; but even in these patients, spontaneous, severe, and life-threatening bleeding is uncommon unless other disorders are present, such as DIC.
What features of the presentation will guide me toward possible causes and next treatment steps:
Key points in the initial physical examination are:
Petechiae must be distinguished from vasculitic purpura
– Thrombocytopenic petechiae are asymptomatic and not palpable.
– Vasculitic purpura, such as caused by an adverse drug reaction, is preceded by symptoms of burning or stinging, and the petechiae are palpable.
Presence or absence of splenomegaly
– This is important because the normal spleen transiently retains approximately 1/3 of circulating platelets within its vascular sinusoids. A large congested spleen, typically the result of liver cirrhosis and portal hypertension, can transiently retain 90% of platelets, causing mild or moderate thrombocytopenia – although the total number of circulating platelets (systemic circulation + spleen vasculature) remains normal. This is described as “platelet pooling” in the spleen and is the result of abnormal distribution of platelets between the spleen and the systemic circulation.
Presence of fever, chills, and hypotension – suggesting sepsis
Presence of transient, focal neurologic abnormalities
– This may suggest microvascular thrombosis, as in thrombotic thrombocytopenic purpura (TTP).
– Abnormalities such as lymphadenopathy or lung consolidation, may suggest infectious disease or malignancy.
Heart murmur may suggest bacterial endocarditis or platelet destruction across an abnormal valve
Skin rash, arthritis, alopecia
– Skin rash, arthritis, alopecia may suggest autoimmune disorders such as systemic lupus erythematosus (SLE).
What laboratory studies should you order to help make the diagnosis and how should you interpret the results?
Complete blood count and peripheral blood smear
Key points in the laboratory evaluation begin with the complete blood count (CBC) and examination of the peripheral blood smear.
Confirm the presence of thrombocytopenia by directly observing decreased numbers of platelets on the blood smear. Exclude the presence of platelet clumps from improper collection and processing techniques or “pseudothrombocytopenia” caused by platelet clumping that results from a naturally occurring platelet agglutinin present in approximately 1 in 1,000 normal people that can cause platelet clumping in the presence of EDTA (ethylenediaminetetraacetic acid), the anticoagulant used in routine CBC collection tubes.
If thrombocytopenia is confirmed
Is the platelet morphology normal?
Some inherited thrombocytopenic disorders, such as May-Hegglin, are associated with giant platelets (equal to the size of red cells) or, rarely, abnormally small platelets, such as in Wiskott-Aldrich syndrome.
Is the hemoglobin concentration normal?
If anemia is present and there is no evidence of bleeding as the cause, does the anemia appear to be hemolytic or related to decreased production?
Hemolytic anemia may be caused by immune or non-immune mechanisms
– Autoimmune hemolysis is typically associated with the presence of microspherocytes on the blood smear and confirmed by a positive direct antiglobulin test (DAT). This may suggest that the etiology of the thrombocytopenia is also autoimmune, as in ITP.
– Non-immune hemolysis is typically due to red cell fragmentation, which can be caused by diffuse microvascular thrombosis, and therefore described as thrombotic microangiopathy. It is typically associated with fragmented red cells, described as schistocytes. This suggests TTP. Other causes of turbulent circulation, such as a defective prosthetic heart valve, can cause hemolytic anemia.
– Unless there is a process preventing bone marrow response, all etiologies of hemolysis are associated with the presence of increased numbers of reticulocytes, noted on the blood smear as large, irregular polychromatophilic (blue-gray) red cells.
Anemia caused by decreased red cell production, which is associated with thrombocytopenia, can have multiple etiologies
– Megaloblastic anemia, resulting from a deficiency of vitamin B12 or folic acid, is characterized by leukopenia, in addition to anemia and thrombocytopenia. Red cells are large and oval shape, and neutrophils are hypersegmented (contain five or more nuclear lobes). Thrombocytopenia is common, but rarely severe in megaloblastic anemias.
– Anemia resulting from replacement of marrow by exogenous tumor or granulomatous disease (such as tuberculosis) causes a leukoerythroblastic (myelophthisic) reaction, with nucleated red cells, schistocytes, and also immature granulocytes.
– Anemia resulting from marrow hypoplasia may have normal red cell morphology.
Is the white blood cell count (WBC) and morphology normal?
A low WBC most often is associated with marrow failure, and therefore associated also with thrombocytopenia and anemia
– Marrow failure related to replacement by exogenous tumor or granulomatous disease can cause release of immature granulocytes (myelocytes, promyelocytes, myeloblasts) and nucleated red cells, described as a leukoerythroblastic or myelophthisic reaction.
– Marrow failure can be related to leukemia, acute or chronic. Acute leukemia can be associated with high or low white blood cell counts.
A low WBC commonly occurs in patients with SLE
Other laboratory evaluations may include:
– Chemistry values may demonstrate increased levels of lactate dehydrogenase (LDH) or indirect bilirubin, consistent with hemolysis. Increased LDH may also be consistent with systemic malignancy.
– Autoimmune hemolysis is documented by a positive direct Coombs’ test (direct antiglobulin test, or DAT) that detects immunoglobulin G (IgG) antibodies and/or complement on the red cell surface. The indirect Coombs’ test, which detects red cell antibodies in serum, is irrelevant and unimportant for this diagnostic evaluation; it is only relevant in blood bank testing for red cell transfusions.
What conditions can underlie thrombocytopenia:
Many conditions are associated with thrombocytopenia. The most common underlying causes are immune thrombocytopenia (either primary ITP or secondary ITP associated with drugs, systemic lupus erythematous [SLE], HIV, hepatitis C, lymphoma or chronic lymphocytic leukemia), pseudothrombocytopenia, splenomegaly or hypersplenism, sepsis, gestational thrombocytopenia (incidental thrombocytopenia of pregnancy), HELLP (hemolysis, elevated liver function tests, low platelets syndrome), antiphospholipid syndrome, DIC, and TTP.
Examples of clinical presentations
Previously healthy person, moderate thrombocytopenia (for example, platelet count 60,000/uL) incidentally discovered on a routine CBC. No bleeding or other symptoms, normal physical exam, remainder of laboratory evaluation normal.
Pseudothrombocytopenia is possible. Diagnosis will be made by examination of the blood smear.
Primary immune thrombocytopenia (ITP) is the most likely diagnosis if the blood smear confirms that true thrombocytopenia is present.
It is important to review historical platelet counts. A normal platelet count in the past excludes a hereditary thrombocytopenia.
– This is a common presentation for adults with ITP. In young children, usually less than age 5, ITP typically presents with sudden, severe, and symptomatic thrombocytopenia.
Previously healthy young woman at 35 weeks of an uncomplicated pregnancy with mild thrombocytopenia (for example, platelet count 80,000/uL). No bleeding or other symptoms, normal physical exam, remainder of routine laboratory evaluation normal.
– Occurs in 5% of normal pregnancies during late gestation; platelet count rarely less than 70,000/uL; recovers following delivery. Cannot be distinguished from mild ITP (except that patients do not respond to ITP treatment) but spontaneous recovery following delivery supports the diagnosis of gestational thrombocytopenia.
Previously healthy person, mild thrombocytopenia (for example, platelet count 70,000/uL) incidentally discovered on a routine CBC. No bleeding or other symptoms, physical examination reveals spider angiomata on the chest and shoulders and splenomegaly, laboratory evaluation reveals mild anemia with target cells and low serum albumin.
Thrombocytopenia associated with occult liver disease, portal hypertension, and splenomegaly with platelet pooling
Previously healthy person, sudden onset of severe thrombocytopenia (for example, platelet count 8,000) with purpura, no other symptoms or abnormalities on physical examination, remainder of CBC and other laboratory evaluation normal.
DITP is possible
– Additional history must identify drugs taken within hours of the onset of purpura, and focus on new prescription drugs begun in the previous 1-3 weeks, or any drugs taken intermittently over years. Quinine and sulfa drugs such as trimethoprim-sulfamethoxazole are the most common. Consult the registry of drugs that can cause thrombocytopenia at www.ouhsc.edu/platelets. Ask specifically about quinine taken occasionally, perhaps from a family member or friend, because patients often interpret doctors’ questions about drugs only to mean regular prescription medications. Ask about beverages that contain quinine (e.g., tonic water, Schweppes bitter lemon) and nutritional supplements or herbal remedies that are taken occasionally.
DITP typically has a prompt recovery to a normal platelet count
– Beginning within 2-3 days of stopping the suspected drug and achieving a normal platelet count in 1-2 weeks.
DITP can be confirmed by documentation of drug dependent, platelet reactive antibodies
– This test is not routinely available in clinical laboratories. One source for this test is the Blood Center of Wisconsin (www.bcw.edu).
Primary immune thrombocytopenia (ITP) is also possible
– Especially in young children in whom the sudden onset of thrombocytopenia is typical and petechiae/purpura are common.
Previously healthy person, gradual onset of occasional bleeding symptoms including purpura, associated with menorrhagia over several months, moderate thrombocytopenia (for example, platelet count 18,000), remainder of CBC and other laboratory evaluation normal, no other symptoms, remainder of physical exam normal.
This is the typical presentation of ITP in an adult
– Confirmation of the diagnosis of ITP requires exclusion of other causes of thrombocytopenia, such as HIV or hepatitis C. If the remainder of the history, physical examination, and blood counts are normal, no further testing is required.
Previously healthy person, weakness and abdominal discomfort for the past week, purpura noted 2 days ago, no other symptoms, physical exam normal except for minor purpura. Laboratory evaluation demonstrates a platelet count of 12,000/uL, normal WBC, hemoglobin 6 gm/dL, bilirubin 3.5 mg/dL (3.1 mg/dL indirect reacting), LDH 1250 U/L (normal less than 200), creatinine 0.9 mg/dL.
This is the typical presentation of TTP
– Although neurologic abnormalities, often transient focal deficits, are described as classic, one third of patients have no neurologic abnormalities at presentation. Half of patients have normal renal function. Fever is rare; high fever with chills probably never occurs and should suggest systemic infection. Examination of the blood smear will demonstrate fragmented red cells (schistocytes) and polychromatophilic red cells.
Previously healthy young woman at 35 weeks of a previously uncomplicated pregnancy develops hypertension (BP 155/95), edema of her feet and ankles, right upper quadrant abdominal pain and tenderness, and transient visual scotomata. Laboratory evaluation demonstrates moderate thrombocytopenia (platelet count 25,000/uL) and anemia (hemoglobin 9 gm/dL), abnormal liver function with elevated transaminase levels, LDH 550 U/L (normal less than 200), and normal creatinine. Examination of the blood smear demonstrates fragmented red cells.
This is the typical presentation of preeclampsia with the associated HELLP syndrome
– This is a pregnancy related complication which should spontaneously resolve with urgent delivery. The thrombocytopenia and hemolytic anemia with fragmented red cells can suggest TTP, but consideration of TTP can be deferred to observe recovery with delivery.
Hospitalized patient with chronic renal failure requiring maintenance hemodialysis who has had bacteremia related to his vascular access graft. His admission blood pressure was 211/139, potassium 6.7 meq/L, and platelet count 211,000/uL. His platelet count was normal for the first week in the hospital, and then rapidly decreased to 8,000/uL on day 11. His vital signs are normal, his clinical status is stable, his hemoglobin level is unchanged at 8.4 gm/dL, and his white blood cell count is normal. There are several possible, as well as several unlikely, etiologies for the acute thrombocytopenia.
Recurrent bacteremic sepsis is a possible etiology, but unlikely because of the patient’s stable clinical status
– Sepsis may be associated with thrombocytopenia without disseminated intravascular coagulation (DIC), possibly caused by microvascular thrombi that may occur with some organisms (for example, Aspergillus, Cytomegalovirus).
Recurrent bacteremic sepsis with DIC is a possible etiology
– Coagulation studies demonstrated a normal INR (international normalized ratio), activated partial thromboplastin time (aPTT), and fibrinogen concentration, excluding DIC.
Heparin-induced thrombocytopenia (HIT) is a possible etiology
– The patient did not have a new venous or arterial thrombosis, but half of patients with HIT present without evidence of thrombosis. A platelet activation assay for heparin-dependent antibodies was negative, which is evidence against HIT. Most compelling against HIT is the severity of thrombocytopenia. Platelet counts less than 20,000/uL are rare in HIT.
TTP can first occur in a hospitalized patient, apparently triggered by an acute inflammatory disorder such as systemic infection or pancreatitis
– However, TTP was unlikely in this patient because of his stable hemoglobin, examination of the blood smear that demonstrated no schistocytes, and a normal LDH level of 112 U/L.
DITP related to the patient’s antibiotics is the most likely etiology
– The best evidence would be to assess the time course of antibiotic administration and onset of thrombocytopenia. Vancomycin and piperacillin are both common causes of DITP. This patient had been treated with piperacillin for vascular graft-related sepsis several months previously, was treated with piperacillin on this admission for 2 days, then piperacillin was resumed on day 9, followed by the development of thrombocytopenia. The piperacillin etiology was confirmed by documentation of piperacillin-dependent, platelet-reactive antibodies.
Hospitalized patient who had coronary angiography that included treatment with heparin and abciximab as well as aspirin and clopidogrel. He had never been previously exposed to any of these medicines, except aspirin. His platelet count was 255,000/uL before his procedure, but at the time of a routine CBC 2 hours after the procedure, his platelet count is 10,000/uL. He has extensive purpura and blood blisters in his mouth.
The etiology is almost certainly abciximab
– This class of antithrombotic agents that blocks platelet fibrinogen binding by GP (glycoprotein) IIb-IIIa can cause sudden severe thrombocytopenia with the initial exposure. This occurs in approximately 1% of patients receiving abciximab, eptifibatide, and tirofiban. In contrast to other drugs that cause thrombocytopenia, the GP IIb-IIIa inhibitors can cause immediate thrombocytopenia at the time of the first exposure. All other drugs (with rare exceptions) require a period of time, usually 1-3 weeks, to develop sensitization. Although the patients had been previously exposed to aspirin, DITP caused by aspirin is extremely rare. Heparin rarely causes sudden, severe thrombocytopenia. Appropriate management is administration of platelet transfusions and cessation of the offending agent. Thrombocytopenia will resolve within 1 week.
When do you need to get more aggressive tests?
Additional diagnostic testing is rarely required for evaluation and management of patients with thrombocytopenia, beyond the tests previously described in the patient vignettes.
Bone marrow aspiration and biopsy are appropriate in several clinical situations:
When marrow failure is suspected by the additional presence of anemia and leukopenia
When the peripheral blood smear has the features of a leukoerythroblastic (myelophthisic) reaction which suggests marrow replacement by exogenous tumor or granulomatous disease
When the thrombocytopenia does not respond to appropriate management for the initial clinical diagnosis
– Such as presumed ITP with no response to steroids, intravenous immunoglobulin (IVIG), and additional treatments, or presumed TTP with no response to plasma exchange and immunosuppressive treatment.
Bone marrow aspiration and biopsy are not necessary in patients with the typical presentation and clinical course of ITP, TTP, DITP, or liver disease with splenomegaly.
Testing for drug-dependent, platelet-reactive antibodies can be critically important when DITP is suspected and the diagnosis supported by prompt recovery of the platelet count after drugs were stopped, but often multiple drugs are stopped and which caused the thrombocytopenia is uncertain. This test is not routinely available in clinical laboratories. One source for this test is the Blood Center of Wisconsin (www.bcw.edu).
What imaging studies (if any) will be helpful?
Imaging studies have no routine role in the evaluation and management of patients for a primary problem of thrombocytopenia. Abdominal ultrasound may be indicated when splenomegaly is suspected.
What therapies should you initiate immediately and under what circumstances – even if root cause is unidentified?
Platelet transfusion is always appropriate for patients with severe thrombocytopenia (for example, less than 20,000/uL) and clinically important bleeding. Although platelet transfusions have been described as dangerous for patients with TTP because of the potential risk of exacerbating the microvascular thrombosis, this has never been supported by more than rare anecdotes.
Recent clinical evidence suggests that platelet transfusions are actually commonly given to patients with TTP before the diagnosis is considered, with no adverse effect. In patients with ITP or DITP, platelet transfusions generally only produce a very brief platelet count increment (lasting hours), but hemostasis will be helped by the platelet transfusion, regardless of the level or even absence of an increment.
Platelet transfusion is generally not appropriate for patients who are not bleeding, or who have only cutaneous purpura.
In patients with known ITP who present with severe thrombocytopenia and bleeding, intravenous immune globulin (1-2 g/kg) should be administered with corticosteroids.
What other therapies are helpful for reducing complications?
Not applicable for patients evaluated and managed for thrombocytopenia.
What should you tell the patient and the family about prognosis?
“What if” scenarios.
Thrombocytopenia may be due to many causes. The etiology can be anticipated by the history.
Key points in the history are onset, context, severity, timing, and bleeding:
Onset of thrombocytopenia
– Previously normal subjects with unexpected thrombocytopenia suggest an acquired disorder like immune thrombocytopenia (ITP).
– Long standing history and/or family history of thrombocytopenia may suggest an inherited form of thrombocytopenia like May-Hegglin anomaly.
– Surgical patients: Dilutional thrombocytopenia is mild and expected in the first 1-4 days following major surgical procedures.
– Intensive care unit (ICU) patients: Thrombocytopenia in critically ill patients is often multifactorial and may be associated with DIC, sepsis, or drugs.
– Cancer: A history of malignancy may suggest DIC or marrow metastases.
– Age: Neonatal thrombocytopenia that is severe and present at birth or within a few days of birth may be caused by neonatal alloimmune thrombocytopenia, which is the result of maternal platelet alloantibodies. HIT is less common in children than adults.
The severity of thrombocytopenia may provide a clue to the underlying diagnosis
– Severe (below 20,000/uL) is typical of immune causes.
– Moderate (20,000-100,000/uL) is typical of HIT.
– Mild to moderate (50,000-100,000/uL) is typical of splenomegaly/hypersplenism.
Timing of thrombocytopenia with respect to exposures
– Within hours of drug exposures: Acute-onset HIT or other immune-mediated reactions (drug-induced thrombocytopenia [DITP]) following previous intermittent exposure (for example, quinine), recent new drugs, or rarely following the first exposure to certain drugs including tirofiban, eptifibatide, or abciximab.
– 1-4 days after major surgery: Typical of post-operative dilution.
– 5-10 days after drug exposure to a newly prescribed drug taken daily: Immune mediated drug reactions (including classic HIT).
– 5-10 days after red blood cell transfusion: Typical of PTP.
Characterization of bleeding symptoms
– Thrombocytopenia causes immediate bleeding after minor cutaneous cuts. This is distinguished from bleeding related to a coagulation disorder, such as hemophilia, which does not result in bleeding from small cuts (such as razor nicks), and only occurs hours after a larger cut, because the normal platelets provide temporary hemostasis.
– Thrombocytopenia typically causes cutaneous bleeding (purpura and petechiae). Petechiae are typically more frequent on feet (except for the soles, where firm tissue support of cutaneous vessels prevents petechiae), ankles, and legs, where vascular pressure is greater.
– Bleeding is often absent in HIT, despite severe thrombocytopenia.
– Rate of onset of bleeding symptoms. Sudden, unexpected bleeding is typical of acute childhood ITP. Gradual, over weeks to months is common in adults with ITP.
– Severe thrombocytopenia can result in blood blisters in mucous membranes of the mouth and conjunctiva, nosebleeds, or menorrhagia that may be described as “wet purpura”.
– Rarely bleeding from the gastrointestinal (GI) tract will be sufficiently severe to require red cell transfusion support.
– Critical or fatal bleeding, such as intracranial, is very rare and usually associated with head trauma.
What other clinical manifestations may help me to diagnose thrombocytopenia?
What other additional laboratory studies may be ordered?
What’s the Evidence?
Neunert, C, Lim, W, Crowther, M, Cohen, A. “The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia”. Blood. vol. 117. Apr 21. pp. 4190-207. [This is an update of the 1996 ASH ITP Practice Guideline. The format is based on case scenarios that provide easily understood principles for evaluation and management of children and adults with ITP.]
George, JN.. “How I treat patients with thrombotic thrombocytopenic purpura – 2010”. Blood. vol. 116. 2010. pp. 4060-4069. [A practical review of the differential diagnosis of TTP, the appropriate diagnostic considerations, management with plasma exchange and immunosuppressive agents, and the long-term prognosis for patients who have recovered from an acute episode.]
Aster, RH, Curtis, BR, McFarland, JG, Bougie, DW.. “Drug-induced thrombocytopenia: pathogenesis, diagnosis, and management”. J Thromb Haemost.. vol. 7. 2009. pp. 911-918. [This is an excellent resource for understanding the mechanisms of DITP and the clinical course and management.]
Roussan, TA, Aldoss, IT, Cowley, BD. “Recurrent acute thrombocytopenia in the hospitalized patient: sepsis, DIC, HIT, or antibiotic-induced thrombocytopenia”. Amer J Hematol.. vol. 85. 2010. pp. 71-74. [A case problem-solving format that concludes with the diagnosis of piperacillin-induced thrombocytopenia and emphasized the principles of evaluation and management of acute, unexpected thrombocytopenia in a hospitalized patient with multiple concomitant disorders.]
Warkentin, TE.. “Think of HIT”. Hematology (Education Program Book of the Amer Soc Hematology). vol. 1. 2006. pp. 408-414. [This article is a very practical lesson in the evaluation of the hospitalized patient suspected of having heparin-induced thrombocytopenia and/or thrombosis.]
Burrows, RF, Kelton, JG.. “Fetal thrombocytopenia and its relation to maternal thrombocytopenia”. New Eng J Med.. vol. 329. 1993. pp. 1463-1466. [This is a landmark article that describes maternal and infant platelet counts at birth in 15,471 consecutive women. This study defined the previously unrecognized entity of gestational thrombocytopenia.]
Connell, NT, Sweeney, JD.. “Does my patient have a life-or- limb-threatening thrombocytopenia?”. Hematol Oncol Clin North Am.. vol. 26. 2012 Apr. pp. 369-82. [This review article focuses on causes and management of severe thrombocytopenia typically characterized by platelet counts <10,000/uL.]
Wei, Y, Ji, XB, Wang, YW. “High-dose dexamethasone vs prednisone for treatment of adult immune thrombocytopenia: a prospective multicenter randomized trial”. Blood. vol. 127. 2016 Jan 21. pp. 296-302. [A recent clinical trial comparing two commonly used corticosteroids in the treatment of adults with acute ITP demonstrating that pulse dexamethasone is as effective as daily prednisone but with fewer side effects.]
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- What every physician needs to know about thrombocytopenia:
- What features of the presentation will guide me toward possible causes and next treatment steps:
- What laboratory studies should you order to help make the diagnosis and how should you interpret the results?
- What conditions can underlie thrombocytopenia:
- When do you need to get more aggressive tests?
- What imaging studies (if any) will be helpful?
- What therapies should you initiate immediately and under what circumstances – even if root cause is unidentified?
- What other therapies are helpful for reducing complications?
- What should you tell the patient and the family about prognosis?
- “What if” scenarios.
- What other clinical manifestations may help me to diagnose thrombocytopenia?
- What other additional laboratory studies may be ordered?