INTRODUCTION
Heparin-induced thrombocytopenia (HIT) precipitates an extreme prothrombotic diathesis, with 50% of patients presenting with complicating venous or arterial thromboemboli.1 Without prompt and effective treatment, the likely outcome is limb amputation in 10% to 20%, death in 20% to 30%, and residual deficits in survivors related to strokes, myocardial infarctions, and pulmonary emboli.2-3 Those without a thrombus on presentation (isolated HIT) have a risk approaching 50% of developing one and suffering a similar outcome.1, 4 Key to preventing catastrophes is awareness, vigilance, and the application of recently refined treatment strategies. From managing many hundreds of cases over 25 years and frequently discussing this topic nationwide, I seek to expose persistent myths and misconceptions that impede life- and limb-saving care for patients with HIT.
THE MYTHS AND MISCONCEPTIONS
HIT Is a Rare Disorder (So I Don't Have to Worry or Learn About It)
Heparin-induced thrombocytopenia occurs in 3% to 5% of patients receiving intravenous unfractionated heparin.5 The incidence is on the order of 0.5% with subcutaneous low-molecular-weight heparins, catheter flushes, and even . . . [Full Text of this Article]
HIT Is Overblown in the Medical Literature (and Overdiagnosed)
We Can Use Low-Molecular-Weight Heparin (and Forget About It)
This Can't Be HIT Because the Patient Is Not Now Receiving Heparin
This Can't Be HIT Because It Is Too Early (or Too Late)
This Can't Be HIT Because the Platelet Count Is Not Low (or Too Low)
We Can Wait for the Test to Come Back
We Can Just Stop Heparin
We Can Just Start Warfarin
We Can Protect the Patient With a Vena Cava Filter
I Don't Believe That Direct Thrombin Inhibitors Improve Outcome (There Are No Randomized Studies)
We Don't Need a Hematology Consultation (We Can Handle This Ourselves)
THE BOTTOM LINE
