SEARCH RESULTS FOR: Heparin-Induced-Thrombocytopenia

Heparin-Induced Thrombocytopenia

Non-Immune Mediated: Type 1 (within two days of heparin administration) Platelets aggregate within the bloodstream ↓ Free unbound platelets in bloodstream Mild Thrombocytopenia: platelet count between 100 x 109/L - 150 x 109/L Fewer platelets available for thrombosis (formation of a pathological blood clot) Self limiting with no thrombotic risk Legend: Heparin-Induced Thrombocytopenia (HIT): Pathogenesis and clinical findings Obesity Hypertension Macrovascular disease Hyperlipidemia Heparin (often unfractionated) complexes with platelet factor 4 (PF4) on the platelet surface, due to heparin’s negative charge & PF4’s affinity for long-chain polysaccharides Immune-Mediated: Type 2 (within 5-15 days of heparin administration) Anti-heparin/PF4 Immunoglobulin G antibodies binds to the heparin-PF4 complex in the blood Splenic macrophages remove platelet- immunoglobulin G complexes in the spleen Thrombocytopenia: Platelet count < 100 x 109/L (though < 20 x 109/L should prompt consideration of other diagnoses) ↑ Vascular inflammation & endothelial dysfunction activate platelets Authors: Kelle Edgar, Hadi Hassan Sergio F. Sharif Reviewers: Haotian Wang, Jessica Asgarpour Yan Yu*, Lynn Savoie* Kareem Jamani* * MD at time of publication Activated platelets release PF4 Anti-heparin/PF4 antibodies activate adjacent platelets Activated platelets release inflammatory mediators Circulating anti- heparin/PF4 antibodies bind adjacent cellular targets Anti-heparin/PF4 antibodies bind endogenous heparan sulfate on endothelium Activated endothelium releases procoagulants thrombin & tissue factor Activated platelets release procoagulants (factors promoting blood clotting) Free platelets are consumed from formation of thrombi Hypercoagulable state (↑ risk of thrombosis) ↓ Platelets available to clot at different area of the body Thrombosis in coronary, peripheral or cerebral arteries Bleeding (rare) Myocardial infarction Acute ischemia Stroke Inflammatory mediators disrupt hypothalamic body thermoregulation Fever/ chills Inflammatory mediators promote vasodilation of arterioles under the skin ↑ Blood to surface of skin Flushing of skin Venous thrombosis in lower leg or lung Deep vein thrombosis Pulmonary embolism Microthrombi occlude vessels surrounding injection site, limiting nutrient supply Necrosis (tissue death) at heparin injection site Published Aug 29, 2014; updated Jun 16, 2025 on www.thecalgaryguide.com Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications