RT Book, Section
A1 Moore, Hunter B.
A1 Moore, Ernest E.
A2 Feliciano, David V.
A2 Mattox, Kenneth L.
A2 Moore, Ernest E.
SR Print(0)
ID 1175131893
T1 Trauma-Induced Coagulopathy
T2 Trauma, 9e
YR 2020
FD 2020
PB McGraw Hill
PP New York, NY
SN 9781260143348
LK accesssurgery.mhmedical.com/content.aspx?aid=1175131893
RD 2024/04/19
AB KEY  POINTSThe  pathogenesis  of  trauma-induced  coagulopathy  is  multifactorial  and  includes  impaired  thrombin  generation,  defective  fibrinogen,  platelet  dysfunction,  and  dysregulated  fibrinolysis.Metabolic  acidosis  has  a  more  significant  effect  on  trauma-induced  coagulopathy  than  hypothermia  at  clinically  relevant  levels.Fibrinolysis  is  the  active  degradation  of  polymerized  fibrin  through  the  co-localization  of  tissue  plasminogen  activator  or  urine-type  plasminogen  activator  with  the  lysine  avid  binding  plasminogen  and  subsequent  conversion  to  plasmin.Systemic  hyperfibrinolysis  occurs  in  10%  to  15%  of  those  requiring  a  massive  transfusion.Impaired  fibrinolysis  (shutdown)  is  present  in  the  majority  of  severely  injured  patients  and  may  result  in  microvascular  occlusion  and  organ  dysfunction.Tranexamic  acid  should  be  used  selectively  and  only  in  patients  with  active  bleeding  and  severe  shock  (systolic  blood  pressure  6)  and  optimally  with  documented  hyperfibrinolysis.Prehospital  plasma  improves  survival  in  patients  with  transport  times  that  are  anticipated  to  exceed  20  minutes.Goal-directed  hemostatic  strategies  employing  viscoelastic  assays  improve  survival.Cryoprecipitate  contains  fibrinogen,  factor  VIII,  von  Willebrand  factor,  fibronectin,  factor  XIII,  and  platelet  microparticles.Weight-based  low  molecular  weight  heparin  and  antifactor  Xa–guided  dosing  are  advantageous  in  the  prevention  of  venous  thromboembolism.