ABSTRACT
I had no choice but to develop an interest in heparin-induced thrombocytopenia (HIT). As a medical resident in 1976, I had just read papers in the New England Journal of Medicine and Annals of Internal Medicine (Babcock et al., 1976; Bell et al., 1976) championing different mechanisms of this phenomenon, when a 50-yr-old man came under my care at the Veterans Administration hospital with deep-vein thrombosis (DVT) following back surgery. After intravenous (iv) heparin was infused for 1 wk, he experienced worsening leg signs, new pulmonary emboli (PE), and a fall in platelet count from 441 to 83 · 109/L. Proud of my astuteness, I immediately stopped the heparin, gave a ”loading dose” of warfarin (10 mg), protected his lungs with an inferior vena cava (IVC) filter, and confirmed the diagnosis by observing that heparin produced in vitro aggregation of normal platelets in the presence of the patient’s platelet-poor plasma. Within days, a necrotic thigh lesion emerged, sepsis and death ensued, leaving me to marvel at the incredibly bad luck that could deal a person both HIT and warfarin-induced skin necrosis. Today we understand that these two drug reactions are not coincidental and that the warfarin therapy likely contributed to the catastrophic outcome. We published this case 27 yr later, including it within a case series illustrating the dangers of warfarin use during acute HIT (Srinivasan et al., 2004).
