Causes of Thrombocytopenia in the ICU
Multiple mechanisms contribute to thrombocytopenia in ICU patients, including decreased production, increased destruction, sequestration, and dilution, with sepsis and trauma being the most common underlying causes. 1
Common Causes of Thrombocytopenia in ICU Patients
Decreased Platelet Production
- Bone marrow failure developing gradually over 5-7 days 2
- Antimitotic chemotherapies affecting platelet production 3
- Sepsis-induced bone marrow suppression 4
Increased Platelet Destruction
- Heparin-induced thrombocytopenia (HIT) - typically occurs 5-10 days after heparin initiation or earlier if exposed to heparin within previous 3 months 3
- Immune thrombocytopenia (ITP) - often an isolated finding without systemic illness 5
- Drug-induced immune thrombocytopenia - abrupt decrease in platelet count 1-2 weeks after starting medication 2
- Post-transfusion purpura - typically presents with major and sudden decrease in platelets with hemorrhagic context 3
- GPIIb-IIIa glycoprotein inhibitors - can cause early and profound thrombocytopenia 3
Consumption Coagulopathies
- Disseminated intravascular coagulation (DIC) - often associated with sepsis 3
- Thrombotic microangiopathies (TMA) - including thrombotic thrombocytopenic purpura (TTP) 3, 5
- Consumption thrombocytopenia after cardiac surgery 3
- Ventricular assistance devices causing platelet consumption 3
- Extracorporeal membrane oxygenation (ECMO) and other extracorporeal circuits 3
Sequestration
Dilutional Causes
- Perioperative hemodilution from massive fluid resuscitation 3
- Massive transfusion with inadequate platelet replacement 4
Other Important Causes
- Antiphospholipid syndrome - can present with both thrombocytopenia and thrombosis 3
- HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) - obstetric emergency 5
- Pseudothrombocytopenia - laboratory artifact due to platelet clumping 5
- Sepsis - most common cause of thrombocytopenia in ICU 1
- Trauma - second most common cause in ICU settings 1
Diagnostic Approach
Timing of Platelet Count Changes
- Early thrombocytopenia (within first 2 days): Consider direct effect of unfractionated heparin, hemodilution, or early HIT in previously sensitized patients 3
- Gradual decline over 5-7 days: Consider consumptive coagulopathy or bone marrow failure 2
- Abrupt decrease after initial recovery (1-2 weeks post-surgery): Strongly suggests immunologic causes like HIT or drug-induced thrombocytopenia 2
Assessment Tools
- 4T score for suspected HIT - evaluates thrombocytopenia severity, timing, thrombosis, and other potential causes 3
- Evaluate for pseudothrombocytopenia by collecting blood in tubes containing heparin or sodium citrate 5
- Distinguish acute from chronic thrombocytopenia by reviewing previous platelet counts 5
Clinical Implications
- Platelet counts >50 × 10³/μL: Generally asymptomatic 5
- Platelet counts 20-50 × 10³/μL: May have mild skin manifestations (petechiae, purpura, ecchymosis) 5
- Platelet counts <10 × 10³/μL: High risk of serious bleeding 5
- Thrombocytopenia in ICU patients is independently associated with increased mortality regardless of cause 4
Management Considerations
- Treat underlying cause when possible (sepsis, trauma) 1
- Platelet transfusion indicated for active hemorrhage or platelet counts <10 × 10³/μL 5
- For HIT, discontinue heparin and provide alternative anticoagulation at therapeutic doses 1
- Avoid unnecessary platelet transfusions in conditions with increased intravascular platelet activation as they may be harmful 1
- Ensure adequate platelet counts before invasive procedures 5
Common Pitfalls
- Failing to recognize pseudothrombocytopenia, leading to unnecessary interventions 5
- Missing HIT diagnosis, which requires prompt heparin discontinuation 3
- Not considering that some conditions (HIT, antiphospholipid syndrome, TTP) can present with both thrombocytopenia AND thrombosis 3
- Overlooking drug-induced causes, which are common in ICU patients on multiple medications 3
- Attributing thrombocytopenia to a single cause when multiple mechanisms are often present in critically ill patients 4