Mechanisms and differential diagnoses of thrombocytopenia








Mechanisms and differential diagnoses of thrombocytopenia
Clinical scenario and/or diagnostic clues
Pseudothrombocytopenia

Platelet aggregates in EDTA-anticoagulated blood; therapy with GPIIbIIIa-receptor antagonists
Thrombocytopenia is unexpected, and bleeding symptoms are absent; preceding therapy with GPIIbIIIa-receptor antagonists; repeat platelet count in citrated blood and control for aggregates in the blood smear (Note: glycoprotein IIbIIIa antagonists often induce pseudothrombocytopenia in citrated blood)
Hemodilution

Infusion of fluids and/or plasma
Massive infusion/transfusion due to bleeding
Platelet consumption

 Blood loss
Bleeding, anemia, and prolonged clotting times as signs of coagulation factor loss and/or consumption
 Massive blunt trauma
History, physical, and radiological examination
Disseminated intravascular coagulation
Shock, infection, obstetrical complications, or other typical underlying causes; prolonged clotting times; increased fibrin split products; nucleated red cells in the differential
Sepsis
Fever, further sepsis criteria, and positive blood cultures
Extracorporeal circuit
Organ failure requiring extracorporeal circuit; consider areas of high shear stress in the circuit
Platelet sequestration

Hepatosplenomegaly
History, typical comorbidity (e.g. liver cirrhosis or osteomyelofibrosis), and sonography or other diagnostic radiology

Decreased platelet production

Intoxication (alcohol and other drugs)
History of abuse or medication; toxicology screening
Viral infection (HIV, HCV, EBV, CMV)
Diagnostic workup of viral infections
Bone marrow infiltration (leukemia, tumors)
Bone marrow examination, nucleated red cells in the differential blood film, and teardrop cells
Radiation
History
Chemotherapy
History
Platelet destruction

Immune thrombocytopenia
Antiplatelet antibodies, normal or increased megakaryocytes in bone marrow, platelet count response to IVIG or steroids, comorbidities typical for secondary ITP (eg, SLE, hepatitis C, CLL)
DITP
Medication history (new drug started during the last 7-14 d), platelet counts < 20 × 109/L, increase of platelet counts after cessation of suspected/detected medication, confirmation by detection of drug-dependent antibodies
Heparin-induced thrombocytopenia
50% decrease in platelet count (typical nadir 20-80 × 109/L) between days 5 and 14 of heparin treatment, without thromboembolic events with ongoing heparin therapy, heparin-dependent, platelet activating anti-PF4/heparin antibodies
Thrombotic microangiopathies (TTP, HUS, HELLP syndrome)
Hemolysis with negative direct Coombs test, fragmented red cells in blood smear, typical platelet count nadir 10-30 × 109/L, thrombotic events with neurological (TTP) or renal (HUS) symptoms, pregnancy (HELLP-syndrome), elevated lactate dehydrogenase
Posttransfusion purpura
Transfusion history, history of pregnancy, platelet count nadir < 10 × 109/L, bleeding symptoms, high titer anti–HPA-1a antibodies
Passive alloimmune thrombocytopenia
Abrupt, transient fall in the platelet count after transfusion of plasma containing blood products (which passively transmit the platelet alloantibody), typically from a multiparous donor

Source: bloodjournal.org

Read also:  Activated clotting time (ACT) vs aPTT


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