Thrombocytopenia

Platelets come from megakariocytes and are produced in bone marrow and lung. Their development is stimulated by thrombopoeitin produced in liver and kidney. They are 2-3 um across. Platelet function follows the pattern: Adhesion -> Activation -> Aggregation. Platelet aggregation forms a platelet plug (primary hemostasis), which is stabilized by coagulation factors culminating in a fibrin mesh/net which stabilizes the platelet plug.

Spurious

• Clumping

Sequestration

• Hypersplenism

Destruction/Consumption

• HIGH IPF%, Prolonged PT / aPTT
• What happens to platelets after they help form a clot?

• DIC
  • Most Common Etiologies
    • Bacterial sepsis (83%), Trauma (31%), Cancer (e.g. APML, 6.8%), placental abruption, preeclampsia, amniotic fluid embolism, burn, hyperthermia, rhabdomyolysis, infection, transfusion reaction (ABO incompatibility), snake venom, aortic aneurysm
  • Pathogenesis
    • Expression of the transmembrane glycoprotein TF (which activates factor VII and the extrinsic pathway)
    • Consumption of clotting factors
    • Widespread micro and macrovascular thrombosis, depletion of fibrinogen and fibrin clot formation
    • Platelets are trapped in the clots
    • Plasminogen --> Plasmin also upregulated, leading to large increase in clot breakdown and release of FDPs.
  • Diagnostic Algorithm: Score of 5+ points strongly associated with DIC
    • Presence of a disease known to be associated with DIC (2 pts)
    • Platelets < 100k (1 pt), < 50k (2 pt)
    • Fibrin degradation products (FDPs) (e.g. d-dimer): moderate increase (2 pt), strong increase (3 pt)
    • PT > 3s (1 pt), > 6s (2 pt)
    • Fibrinogen < 1 g/L (1 pt)
  • Treatments and Evidence Behind Them:
    • Basically don't get it.
    • Treat underlying condition
    • Treatment is lousy. Evidence behind treatment is likewise lousy.
    • Platelets, cryo, FFP
  • Morbidity/Mortality is 20-50%

• ITP
• TTP
• HUS
• HIT

Decreased Production

• LOW IPF%
• Parvo
• Aplastic Anemia
• Cancer
• Chemotherapy
• Liver disease?