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Background: Fluid bolus (FB) contribute to positive fluid balance and may not have a beneficial effect. Following cardiac surgery FB are common but often based on simple physiology (heart rate, blood pressure, urine output) as measures of fluid responsiveness are more complex and may not be valid in this cohort. Method(s): Post-operative cardiac surgical patients who received a FB in ICU in the first 24 hours were included. Using a questionnaire based tool, the reasons for a FB and the perceived efficacy by the prescriber were recorded. Physiological data were recorded before and one hour after each FB. A FB was said to be "mean arterial pressure (MAP) responsive" if the FB caused a sustained increase in MAP of at least 5 mmHg. Result(s): Over 5 months, 74 patients (95% on-pump surgery) were recruited. A total of 135 FBs were administered. Each patient received a median of 1(1-2) FB, with a median volume of 0.25 (0.25-0.5) liters. Postoperatively 47% of patients received one FB, 31% received two FBs and 22% received three or more FBs. The most common fluid used was 4% albumin (85%). The main reasons for giving a FB were low MAP (72%), low urine output (21%) and low filling pressure (11%). Overall, 1 hour after a FB, there was an increase in MAP and central venous pressure, and a decrease in urine output, hemoglobin and serum calcium level. However, there was no change in heart rate, vasopressor rate, central venous oxygen saturation or serum lactate levels (Table). Overall, FBs contributed to 45% of fluid balance and only 48% of FB were MAP responsive. Conclusion(s): Lower MAP was the most common reason for FB and sustained physiological efficacy of FB were small.

Background: Fluid bolus (FB) contribute to positive fluid balance and may not have a beneficial effect. Following cardiac surgery FB are common but often based on simple physiology (heart rate, blood pressure, urine output) as measures of fluid responsiveness are more complex and may not be valid in this cohort. Method(s): Post-operative cardiac surgical patients who received a FB in ICU in the first 24 hours were included. Using a questionnaire based tool, the reasons for a FB and the perceived efficacy by the prescriber were recorded. Physiological data were recorded before and one hour after each FB. A FB was said to be "mean arterial pressure (MAP) responsive" if the FB caused a sustained increase in MAP of at least 5 mmHg. Result(s): Over 5 months, 74 patients (95% on-pump surgery) were recruited. A total of 135 FBs were administered. Each patient received a median of 1(1-2) FB, with a median volume of 0.25 (0.25-0.5) liters. Postoperatively 47% of patients received one FB, 31% received two FBs and 22% received three or more FBs. The most common fluid used was 4% albumin (85%). The main reasons for giving a FB were low MAP (72%), low urine output (21%) and low filling pressure (11%). Overall, 1 hour after a FB, there was an increase in MAP and central venous pressure, and a decrease in urine output, hemoglobin and serum calcium level. However, there was no change in heart rate, vasopressor rate, central venous oxygen saturation or serum lactate levels (Table). Overall, FBs contributed to 45% of fluid balance and only 48% of FB were MAP responsive. Conclusion(s): Lower MAP was the most common reason for FB and sustained physiological efficacy of FB were small.

Background: In a recent multicenter randomized trial comparing unfractionated heparin (UFH) with low-molecular-weight heparin (dalteparin) for thromboprophylaxis in 3,746 critically ill patients, 17 patients (0.5%) developed heparin-induced thrombocytopenia (HIT) based on serotoninrelease assay-positive (SRA 1) status. A trend to a lower frequency of HIT with dalteparin vs UFH was observed in the intention-to-treat analysis (fi ve vs 12 patients, P = .14), which was statistically signifi cant (three vs 12 patients, P = .046) in a prespecifi ed per-protocol analysis that excluded patients with DVT at study entry. We sought to characterize HIT outcomes and to determine how dalteparin thromboprophylaxis may reduce HIT frequency in patients in the ICU. Method(s): In 17 patients with HIT, we analyzed platelet counts and thrombotic events in relation to the study drug and other open-label heparin, to determine whether the study drug plausibly explained seroconversion to SRA 1 status and/or breakthrough of thrombocytopenia/thrombosis. We also compared antibody frequencies (dalteparin vs UFH) in 409 patients serologically investigated for HIT. Result(s): HIT-associated thrombosis occurred in 10 of 17 patients (58.8%) (8:1:1 venous:arterial:both). Dalteparin was associated with fewer study drug-attributable HIT-related events (P = .020), including less seroconversion (P = .058) and less breakthrough of thrombocytopenia/thrombosis (P = .032). Antiplatelet factor 4/heparin IgG antibodies by enzyme-linked immunosorbent assay were less frequent among patients receiving dalteparin vs UFH (13.5% vs 27.3%, P < .001). One patient with HIT-associated DVT died after UFH bolus (anaphylactoid reaction), whereas platelet counts recovered in two others with HIT-associated VTE despite continuation of therapeuticdose UFH. Conclusion(s): The lower risk of HIT in patients in the ICU receiving dalteparin appears related to both decreased antibody formation and decreased clinical breakthrough o

Background: In a recent multicenter randomized trial comparing unfractionated heparin (UFH) with low-molecular-weight heparin (dalteparin) for thromboprophylaxis in 3,746 critically ill patients, 17 patients (0.5%) developed heparin-induced thrombocytopenia (HIT) based on serotoninrelease assay-positive (SRA 1) status. A trend to a lower frequency of HIT with dalteparin vs UFH was observed in the intention-to-treat analysis (fi ve vs 12 patients, P = .14), which was statistically signifi cant (three vs 12 patients, P = .046) in a prespecifi ed per-protocol analysis that excluded patients with DVT at study entry. We sought to characterize HIT outcomes and to determine how dalteparin thromboprophylaxis may reduce HIT frequency in patients in the ICU. Method(s): In 17 patients with HIT, we analyzed platelet counts and thrombotic events in relation to the study drug and other open-label heparin, to determine whether the study drug plausibly explained seroconversion to SRA 1 status and/or breakthrough of thrombocytopenia/thrombosis. We also compared antibody frequencies (dalteparin vs UFH) in 409 patients serologically investigated for HIT. Result(s): HIT-associated thrombosis occurred in 10 of 17 patients (58.8%) (8:1:1 venous:arterial:both). Dalteparin was associated with fewer study drug-attributable HIT-related events (P = .020), including less seroconversion (P = .058) and less breakthrough of thrombocytopenia/thrombosis (P = .032). Antiplatelet factor 4/heparin IgG antibodies by enzyme-linked immunosorbent assay were less frequent among patients receiving dalteparin vs UFH (13.5% vs 27.3%, P < .001). One patient with HIT-associated DVT died after UFH bolus (anaphylactoid reaction), whereas platelet counts recovered in two others with HIT-associated VTE despite continuation of therapeuticdose UFH. Conclusion(s): The lower risk of HIT in patients in the ICU receiving dalteparin appears related to both decreased antibody formation and decreased clinical breakthrough o