Thrombocytopenia: investigation

Synopsis

Confirm a genuine low platelet count, use film and clinical context to separate production, destruction, consumption and sequestration, and identify TTP, DIC, HIT and critical bleeding without delay.

• Confirm that thrombocytopenia is real: EDTA-dependent platelet clumping, difficult sampling and platelet satellitism can produce a spuriously low automated count.
• Repeat the count in a citrate or other validated alternative tube and inspect a blood film when clumping or an unexpected isolated result is reported.
• First determine urgency from bleeding, physiology, neurological or renal features, pregnancy, sepsis, thrombosis and the direction and speed of count change.
• The blood film can reveal schistocytes, blasts, dysplasia, giant platelets, malaria, clumping and a leucoerythroblastic pattern and should be reviewed early.
• Isolated thrombocytopenia with otherwise normal film and no systemic illness suggests ITP or a drug effect after HIV, hepatitis and other secondary causes are considered.
• Anaemia with schistocytes, raised LDH and low haptoglobin indicates microangiopathic haemolysis and activates TTP, HUS, DIC, malignant hypertension or pregnancy pathways.
• Prolonged PT and APTT, low fibrinogen and high D-dimer support consumptive DIC in the right clinical setting but normal early coagulation does not exclude evolution.
• A fall beginning five to ten days after heparin with new thrombosis is assessed using the 4Ts score before PF4 laboratory testing and alternative anticoagulation.
• Liver disease and splenomegaly cause sequestration, while alcohol, medicines, B12 or folate deficiency, marrow failure and malignancy reduce platelet production.
• Do not transfuse platelets simply because the count is low; bleeding, procedure, mechanism and diagnosis determine benefit, and platelets can be harmful in TTP or HIT.