Thrombocytopenia is a decrease in platelet count. This decrease may happen in up to 30% of people who have started heparin therapy. Only about 5% experience a significant decrease in platelets, which results in clotting or hemorrhage.

Type I heparin-induced thrombocytopenia, the acute form, occurs early in heparin treatment with improvement in platelet count as heparin therapy continues. Type II, the delayed from, occurs 5 to 10 days after the start of heparin in a patient’s first exposure to heparin and 3 to 9 days in a patient with previous heparin therapy. Type II reportedly has a 23–60% complication rate, and 12–18% of people die.

Treatment consists in eliminating all sources of heparin, including heparin flushes to maintain  intravascular catheter patency (keep them open)  and heparin-coated catheters.  Even very low doses of heparin can evoke a reaction.

Patients on heparin therapy should have daily platelet counts (via blood tests). A platelet count below 100,000/mm or a significant drop of more than 100,000 indicates that heparin should be stopped and platelet aggregation tests should be performed. Protamine is then administered. If continued anticoagulation is needed, medications other than heparin are used. These medications include hirudin, argatroban, danaparoid, and low molecular weight heparin. Danaparoid and low molecular weight heparin are used only after testing whether the patient reacts to them the same way he or she reacts to regular heparin. Once the patient’s blood has been sufficiently anticoagulated with one of the above agents, the patient starts coumadin if long-term anticoagulation is needed.