Synopsis
Estimate HIT probability from platelet timing and thrombosis, stop every heparin source, use rational PF4 testing, and begin safe non-heparin anticoagulation before limb- or life-threatening thrombosis.
- Immune HIT is caused by IgG against platelet-factor-4–heparin complexes, activating platelets, monocytes and coagulation and creating a high risk of venous and arterial thrombosis.
- The platelet count typically falls by more than 50% beginning five to ten days after heparin, and the nadir can remain above 150 × 10^9/L.
- Rapid-onset HIT can occur within 24 hours when heparin exposure in the preceding weeks has left circulating antibodies; delayed presentations can occur after heparin stops.
Key red flags
Pain, pallor, pulselessness or neurological loss with a compatible count fall needs immediate vascular and haematology intervention.
Investigation priorities
Define percentage fall and timing from heparin exposure.
Management branches
Platelets fall or thrombosis appears during or after heparin exposure.
- Calculate the exact percentage fall, exposure timing, thrombosis features and strength of competing causes using the 4Ts score.
- For a low score, seek the alternative cause and avoid indiscriminate PF4 testing unless new evidence changes probability.
Key medicines
ArgatrobanBegin a specialist intravenous infusion at the licensed weight-based rate, using a lower starting dose in critical illness or liver dysfunction and titrating to the local APTT target.
FondaparinuxFor stable selected adults, use the licensed weight-based once-daily subcutaneous therapeutic dose off label for HIT under local guidance, adjusted or avoided in renal impairment.