Thromboelastographic (TEG) Characterization of Patients with Hematologic Malignancy and Chemotherapy Induced Thrombocytopenia (CIT).

The decision to provide prophylactic platelet transfusions to patients with hematologic malignancy and chemotherapy induced thrombocytopenia (CIT) is often based solely on the platelet count being below a somewhat arbitrary threshold. The ability to rapidly assess the overall (net) coagulation status (thrombotic and hemorrhagic tendencies) of these patients may help limit transfusion to those with a measurable bleeding tendency and reduce overall platelet product consumption. We performed pre- and post-platelet transfusion whole blood thromboelastography (TEG) in 20 pts with leukemia (16) or lymphoma (4) and CIT. Citrated venous blood was obtained prior to and 1 hour after single transfusions of 5 units of random donor platelets. Normal ranges were derived from TEG evaluation of 18 normal controls. Correlation between absolute and % changes in maximum TEG amplitude (MA, mm) and time to initial clot formation (R, min) and absolute and % changes in platelet count was assessed. Pts were defined as normal if MA = 45.7 to 64.9 and R = 8.3 to 19.9; hypocoagulable if MA<45.7 and/or R>19.9; hypercoagulable if MA>64.9 and/or R<8.3; and “mixed” for all other result patterns. Pre-transfusion TEG revealed 17/20 (85%) patients to be hypocoagulable, 1/20 (5%) to be hypercoagulable, and 2/20 (10%) to have a mixed pattern. All hypocoagulable patients had a baseline MA<45.7 and 12/17 had an R>19.9. Pre-transfusion platelet count correlated with baseline MA (r =.47, p=.038). No statistically significant correlation between absolute and % change in platelet count and absolute change in MA, % change in MA, absolute change in R, and % change in R existed. Post transfusion, 17/20(85%) patients had normal MA. Post transfusion, 7/17(41%) hypocoagulable patients had normal TEG, 7/17(41%) remained hypocoagulable, and 3/17(18%) became hypercoagulable. Both “mixed” patients became hypercoagulable; the hypercoagulable patient became normal. 3/5 patients with poor transfusion response (platelet count increase < 10,000/mL) went from hypocoagulable to normal while the remaining 2/5 had MA but not R normalization. Based on our TEG data, 15% of hematologic malignancy patients with CIT did not have a baseline hypocoagulable pattern and may not have needed platelet transfusion. In the 85% who were hypocoagulable at baseline, 41% remained hypocoagulable despite platelet transfusion and may have benefited from additional hemostatic therapy. The patients that normalized did so with variable and at times minimal increases in platelet count. The 18% of baseline hypocoagulable patients that became hypercoagulable post-transfusion may have become transiently prone to thrombosis. Our data supports further evaluation of surrogate markers of overall hemostatic potential, like TEG, as a means of guiding and optimizing platelet transfusion practices.