the ligand for platelet aggregation, and in patients
with major bleeding, it is required to a
larger extent than any other hemostatic protein.8
In such patients, this requirement reflects increased
consumption, loss, dilution, and fibrino
genolysis. On the basis of these multiple roles,
even in the absence of evidence from randomized,
controlled trials, guidelines for the management
of traumatic bleeding now indicate that
the trigger level for supplementing fibrinogen
should be 1.5 to 2.0 g per liter rather than 1.0 g
per liter.9 It is unknown whether early fibrinogen
supplementation and the use of prothrombin
complex concentrate, as compared with the
use of fresh-frozen plasma, improves clinical
outcomes in patients with major bleeding. Future
randomized, controlled trials should assess the
overall benefit and safety, including the rate of
hospital-acquired venous thromboembolism.10,11
Similarly, the use of recombinant factor VIIa,
which has been shown to reduce the use of red
cells in bleeding but not to reduce mortality,
needs further evaluation. Data from placebocontrolled
trials have shown that the off-label
use of recombinant factor VIIa significantly increased
the risk of arterial thrombosis.12,13
the ligand for platelet aggregation, and in patientswith major bleeding, it is required to alarger extent than any other hemostatic protein.8In such patients, this requirement reflects increasedconsumption, loss, dilution, and fibrinogenolysis. On the basis of these multiple roles,even in the absence of evidence from randomized,controlled trials, guidelines for the managementof traumatic bleeding now indicate thatthe trigger level for supplementing fibrinogenshould be 1.5 to 2.0 g per liter rather than 1.0 gper liter.9 It is unknown whether early fibrinogensupplementation and the use of prothrombincomplex concentrate, as compared with theuse of fresh-frozen plasma, improves clinicaloutcomes in patients with major bleeding. Futurerandomized, controlled trials should assess theoverall benefit and safety, including the rate ofhospital-acquired venous thromboembolism.10,11Similarly, the use of recombinant factor VIIa,which has been shown to reduce the use of redcells in bleeding but not to reduce mortality,needs further evaluation. Data from placebocontrolledtrials have shown that the off-labeluse of recombinant factor VIIa significantly increasedthe risk of arterial thrombosis.12,13
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