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개인파산 CtiveISS 34.0a 2008 -196 (68.0 )NoneDa Luz et al. Critical Care 2014, …

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작성자 TOaci Embry 댓글 0건 조회 10회 작성일 23-11-17 06:43

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CtiveISS 34.0a 2008 -196 (68.0 )NoneDa Luz et al. Critical Care 2014, 18:518 http://ccforum.com/content/18/5/Page 9 ofTable 1 Characteristics of the studies included in the systematic review (Continued)Kornblith 2014 [47] Prospective ISS 9.0a Years not reported 251/1 4-Bromo-5-nitro-1H-indazole 35.0a 202 (80.7 ) TEG?- 37 Citrated blood, recalcified Kaolin and TF activated and functional fibrinogen test Branco 2014 [48] Prospective 4CzIPN ISS 1 - 51 2011 118/1 36.9b 97 (77.1 ) TEG?- T not PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8086425 reported Citrated blood, recalcified Kaolin addedMedian, AA ?arachidonic acid, ADP PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/22901180 ?adenosine diphosphate, AIS ?abbreviated injury score, bMean, CaCl 2 ?calcium chloride, CRYO ?cryoprecipitate, DVT ?deep vein thrombosis, FC ?fibrinogen concentrate, FFP ?fresh frozen plasma, GCS ?Glasgow Coma Scale, HCR ?hemostatic control resuscitation, HF ?hyperfibrinolysis, ISS ?injury severity score, LMWH ?low molecular weight heparin, MinT ?minimal transfusion, ModT ?moderate transfusion, MT ?massive transfusion, MTP ?massive transfusion protocol, Na ?sodium, PCC ?prothrombin complex concentrate, PE ?pulmonary embolism, PLT ?platelets, PM ?platelet mapping, RBC ?red blood cells, ROTEM?- rotational thromboelastometry, RSCT ?routine screening coagulation tests, r-TEG?- rapid thromboelastography, TBI ?traumatic brain injury, TEG?- thromboelastography, TF ?tissue factor, TXA ?tranexamic acid.aNoneNonethat that did not evaluate diagnostic performance against a reference standard are represented in Table 4.OutcomesThe included studies collectively reported on hypocoagulability, hypercoagulability, platelet dysfunction, and hyperfibrinolysis. We summarize the parameters of TEG? ROTEM?used for diagnosis, turnaround times (TATs), and results concerning prediction, reduction, or guidance of transfusion and prediction or reduction of mortality. Details of all studies without a control group (for clinical outcomes) or a reference standard (for diagnostic performance) are given in Table 5.complications (OR, 1.25; 95 CI, 1.12 to 1.39), after controlling for thromboprophylaxis and using the reference standards discussed earlier. When TEG?[27] was performed 24 hours after injury, trauma patients were more hypercoagulable compared with healthy volunteers across a broad range of temperatures (32 to 38 ). Finally, a cohort study [34] suggested an association between admission MA and pulmonary embolism (OR, 3.5 for MA >65; 95 CI, 1.69 to 7.23; and OR, 5.8 for MA >72; 95 CI, 2.85 to 11.77), after controlling for gender, race, age, and ISS. Hyperfibrinolysis (HF) Only one study [14] compared HF detected with ROTEM?with a laboratory gold standard and showed that ROTEM?had satisfactory diagnostic properties for HF, defined by laboratory measurement of euglobin lysis time (ELT). However, the sample size was very small (n = 23, of which five had HF), limiting the strength of inferences. Platelet dysfunction With TEG?platelet-mapping (PM) test, a study [13] showed that patients with TBI had more platelet dysfunction on admission, measured by lower platelet response to arachidonic acid (AA) but not to adenosine diphosphate (ADP), compared with non-TBI trauma patients, alcohol abusers, and healthy volunteers (P <0.001). Another study [41], using the same technique, found lower platelet response to both AA and ADP in trauma patients versus healthy volunteers (P <0.0001). With ROTEM? one study [42], comparing healthy volunteers with trauma patients, speculated that an observed difference in clot strength arose from platelet d.

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