What is the management of heparin-induced thrombocytopenia (HIT)?

Management of Heparin-Induced Thrombocytopenia (HIT)

When heparin-induced thrombocytopenia is suspected, all heparin products must be immediately discontinued and replaced with a non-heparin anticoagulant at therapeutic doses. 1, 2

Diagnosis and Initial Assessment

• For patients with suspected HIT, use the 4T score to determine pre-test probability (low ≤3, intermediate 4-5, high ≥6) 1
• If pre-test probability is intermediate or high, perform anti-PF4 antibody testing while simultaneously initiating alternative anticoagulation 1
• If clinical probability is high (4T ≥6), do not wait for laboratory confirmation before stopping heparin and starting alternative anticoagulation 1
• If clinical probability is low (4T ≤3), HIT can be excluded and heparin can be continued with close platelet count monitoring 1

Immediate Management

• Immediately discontinue all forms of heparin, including heparin flushes and heparin-coated catheters 1, 2
• Start therapeutic-dose non-heparin anticoagulation, even if thrombosis is not present 1, 2
• Avoid platelet transfusions as they may worsen thrombosis in HIT patients 2

Alternative Anticoagulant Options

For Most Patients:

• Argatroban: Initial dose 2 mcg/kg/min as continuous IV infusion (reduce to 0.5-1 mcg/kg/min in critically ill, cardiac surgery, or moderate hepatic impairment) 1, 3

  • Monitor aPTT to maintain 1.5-3 times baseline value 1, 3
  • First-line choice for patients with renal impairment (creatinine clearance <30 mL/min) 1, 2
  • Contraindicated in severe hepatic failure (Child-Pugh C) 1, 2

• Bivalirudin: Alternative to argatroban with shorter half-life (20-30 minutes) 1

  • Useful for procedures requiring short-acting anticoagulation 1
  • Avoid in severe renal impairment 1, 2

• Danaparoid: Alternative parenteral option 1

  • Not recommended in severe renal failure 1
  • Requires monitoring of anti-Xa activity with specific calibration 1
  • Use curative doses, not prophylactic doses 1

• Fondaparinux: Can be considered when other options are unavailable 1, 4

  • Effective and safe alternative with similar outcomes to argatroban and danaparoid 4

• Direct Oral Anticoagulants (DOACs): Can be used in stable patients without severe organ dysfunction 1, 5

  • More cost-effective and easier to administer than parenteral options 5

Special Situations:

• Severe renal impairment: Use argatroban (preferred) 1, 2
• Severe hepatic impairment: Use bivalirudin, danaparoid, or fondaparinux 1
• Severe HIT (massive PE, extensive thrombosis, venous gangrene): Use argatroban or bivalirudin with strict monitoring 1

Transitioning to Oral Anticoagulation

• Wait for platelet count recovery (>150,000/μL or return to baseline) before transitioning to vitamin K antagonists (VKAs) 1, 5
• When transitioning to VKAs, continue parenteral anticoagulant until therapeutic INR is achieved 1, 5
• DOACs can be used directly after parenteral therapy without overlap 5

Perioperative Management

• For patients with acute HIT (<1 month), postpone elective surgery beyond the first month if possible 1
• If surgery cannot be delayed, use argatroban or bivalirudin due to their short half-lives 1
• Before cardiac surgery in patients with history of HIT, perform ELISA for anti-PF4 antibodies 1
• If antibodies are negative, short-term unfractionated heparin can be used during the procedure 1

Duration of Anticoagulation

• For HIT without thrombosis: 4-6 weeks of anticoagulation 1, 5
• For HIT with thrombosis: 3-6 months of anticoagulation 2, 5

Long-term Management

• Provide patients with documentation of HIT diagnosis and laboratory results 1
• For future anticoagulation needs, use oral anticoagulants (VKA or DOAC) or fondaparinux 1
• Schedule follow-up with hematology within 3 months of HIT diagnosis 1
• Re-exposure to heparin should be avoided, especially within 3 months of HIT diagnosis 1

Common Pitfalls to Avoid

• Delaying alternative anticoagulation while waiting for laboratory confirmation in high-probability cases 1
• Using prophylactic rather than therapeutic doses of alternative anticoagulants 1
• Transitioning to VKAs before adequate platelet recovery, which can increase thrombotic risk 1, 5
• Failing to document HIT diagnosis for future reference 1
• Administering platelet transfusions, which can precipitate thrombosis 2