Heparin-induced thrombocytopenia (HIT)

Types

1. Type I HIT (non-immune):
   • Mild, early platelet fall within 1-4 days.
   • Due to direct platelet effect of heparin.
   • Usually transient and clinically insignificant. Heparin can generally be continued.
2. Type II HIT (immune-mediated, clinically important):
   • Usually occurs 5-10 days after starting heparin, or sooner with recent prior exposure.
   • Caused by IgG antibodies against heparin-platelet factor 4 (PF4) complexes.
   • Antibody complexes activate platelets and generate thrombin, causing thrombocytopenia with paradoxical thrombosis.

Clinical features

• Platelet count falls by more than 50% from baseline, often to 20,000-150,000/µL.
• Venous thrombosis is common: DVT, pulmonary embolism.
• Arterial thrombosis may cause limb ischemia, myocardial infarction, or stroke.
• Skin necrosis at heparin injection sites or acute systemic reaction after IV heparin may occur.
• Bleeding is uncommon despite thrombocytopenia.

Diagnosis

• Assess pretest probability using the 4Ts score:
  • Thrombocytopenia
  • Timing of platelet fall
  • Thrombosis or other sequelae
  • Other causes of Thrombocytopenia
• Confirm with PF4-heparin antibody immunoassay and, where needed, a functional platelet activation assay.

Management

1. Stop all heparin immediately, including heparin flushes and LMWH.
2. Start a non-heparin anticoagulant because thrombosis risk remains high: argatroban, bivalirudin, fondaparinux, danaparoid, or selected DOACs.
3. Do not give platelet transfusions unless there is major bleeding.
4. Avoid starting warfarin until platelet recovery. If already given, stop it and administer vitamin K.
5. Document HIT clearly and avoid future heparin exposure unless specialist-directed.