Heparin-Induced Thrombocytopenia (HIT)

Stop all heparin - The whole management is complete heparin avoidance: no unfractionated or low-molecular-weight heparin, no heparin flushes, no heparin-bonded catheters. Flag it everywhere in the chart.

Use a non-heparin anticoagulant - Thrombosis risk persists, so anticoagulate with a direct thrombin inhibitor (argatroban, bivalirudin) rather than simply stopping the heparin.

Don't just transfuse platelets - Despite the thrombocytopenia the state is prothrombotic; platelet transfusion is generally avoided unless there is active bleeding.

Cardiac and vascular surgery is a special problem - Cases that normally rely on heparin, such as bypass and vascular surgery, need an alternative strategy — bivalirudin, or delaying until antibodies clear — planned with hematology and perfusion.

Vigilance for thrombosis - Watch for new DVT or PE, arterial thrombosis, and limb ischemia; it's the platelet-count trend, not an absolute number, that drives suspicion.

Communicate the avoidance - Make sure the heparin avoidance carries through every handoff and to the postoperative team.

Heparin-induced thrombocytopenia is an immune reaction to heparin: antibodies form against the heparin-platelet factor 4 complex and activate platelets, causing a falling platelet count and, paradoxically, a strongly prothrombotic state.

Despite the low platelets, the danger is thrombosis — venous and arterial — not bleeding. It typically appears 5 to 10 days after heparin exposure (sooner with prior sensitization) as a platelet drop of at least 50%, with or without new thrombosis. Recognition matters enormously in the perioperative setting because heparin is everywhere: flushes, coatings, prophylaxis, and bypass, and any re-exposure can be catastrophic.