Major mechanisms of thrombocytopenia and typical clinical scenarios in the ICU
| 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 |
| 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 |
CLL, chronic lymphatic leukemia; CMV, cytomegaly virus; EBV, Epstein-Barr virus; HCV, hepatitis C virus; HELLP, hypertension, elevated liver enzymes, proteinuria; HPA, human platelet antigen; HUS, hemolytic uremic syndrome; ITP, immune thrombocytopenia; IVIG, intravenous immunoglobulin G; SLE, systemic lupus erythematosus; TTP, thrombotic thrombocytopenic purpura.