Abstract
BACKGROUND: Thrombelastography (TEG) fibrinolysis shutdown after trauma is associated with increased mortality due to hypercoagulability-associated organ failure. However, a lack of mechanistic data has precluded the development of novel interventions to treat shutdown. OBJECTIVES: To define the pathophysiology of TEG shutdown in severely injured, bleeding patients through secondary analysis of the PROPPR trial. METHODS: Fibrinolysis was characterized in PROPPR subjects using admission TEG lysis at 30 min (LY30) or plasmin-antiplasmin (PAP) levels. LY30 categories were low (<0.9%), moderate (0.9-2.9%), or high (≥ 3%). PAP was classified as low (<1,500 μg/L), moderate (1,500-20,000 μg/L), or high (>20,000 μg/L). Demographics, outcomes, admission TEG values, platelet count and function, standard coagulation tests, and coagulation proteins were compared. RESULTS: Five hundred forty-seven patients had TEG data and 549 patients had PAP data available. Low LY30 was associated with reduced platelet count and aggregation, poorer TEG clot formation, prolonged clotting times, and reduced fibrinogen and alpha2 antiplasmin. Compared to moderate PAP, low PAP subjects had similar platelet parameters, TEG values, fibrinogen, and alpha2 antiplasmin, but reduced tPA, and elevated PAI-1. D-Dimer values increased as PAP increased, however patients with low LY30 had elevated D-Dimer compared with moderate LY30 patients. Most low LY30 deaths were due to TBI (45%) and hemorrhage (42%) versus one of each cause (TBI, hemorrhage, MOF) in low PAP patients. CONCLUSIONS: Low TEG LY30 does not reflect shutdown of enzymatic fibrinolysis with hypercoagulability, but rather a coagulopathic state of moderate fibrinolysis with fibrinogen consumption and platelet dysfunction that is associated with poor outcomes.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 273-283 |
| Number of pages | 11 |
| Journal | Shock (Augusta, Ga.) |
| Volume | 51 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1 2019 |
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ASJC Scopus subject areas
- Emergency Medicine
- Critical Care and Intensive Care Medicine
Cite this
TEG Lysis Shutdown Represents Coagulopathy in Bleeding Trauma Patients : Analysis of the PROPPR Cohort. / PROPPR Study Group.
In: Shock (Augusta, Ga.), Vol. 51, No. 3, 01.03.2019, p. 273-283.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - TEG Lysis Shutdown Represents Coagulopathy in Bleeding Trauma Patients
T2 - Analysis of the PROPPR Cohort
AU - PROPPR Study Group
AU - Cardenas, Jessica C.
AU - Wade, Charles E.
AU - Cotton, Bryan A.
AU - George, Mitchell J.
AU - Holcomb, John B.
AU - Schreiber, Martin
AU - White, Nathan J.
PY - 2019/3/1
Y1 - 2019/3/1
N2 - BACKGROUND: Thrombelastography (TEG) fibrinolysis shutdown after trauma is associated with increased mortality due to hypercoagulability-associated organ failure. However, a lack of mechanistic data has precluded the development of novel interventions to treat shutdown. OBJECTIVES: To define the pathophysiology of TEG shutdown in severely injured, bleeding patients through secondary analysis of the PROPPR trial. METHODS: Fibrinolysis was characterized in PROPPR subjects using admission TEG lysis at 30 min (LY30) or plasmin-antiplasmin (PAP) levels. LY30 categories were low (<0.9%), moderate (0.9-2.9%), or high (≥ 3%). PAP was classified as low (<1,500 μg/L), moderate (1,500-20,000 μg/L), or high (>20,000 μg/L). Demographics, outcomes, admission TEG values, platelet count and function, standard coagulation tests, and coagulation proteins were compared. RESULTS: Five hundred forty-seven patients had TEG data and 549 patients had PAP data available. Low LY30 was associated with reduced platelet count and aggregation, poorer TEG clot formation, prolonged clotting times, and reduced fibrinogen and alpha2 antiplasmin. Compared to moderate PAP, low PAP subjects had similar platelet parameters, TEG values, fibrinogen, and alpha2 antiplasmin, but reduced tPA, and elevated PAI-1. D-Dimer values increased as PAP increased, however patients with low LY30 had elevated D-Dimer compared with moderate LY30 patients. Most low LY30 deaths were due to TBI (45%) and hemorrhage (42%) versus one of each cause (TBI, hemorrhage, MOF) in low PAP patients. CONCLUSIONS: Low TEG LY30 does not reflect shutdown of enzymatic fibrinolysis with hypercoagulability, but rather a coagulopathic state of moderate fibrinolysis with fibrinogen consumption and platelet dysfunction that is associated with poor outcomes.
AB - BACKGROUND: Thrombelastography (TEG) fibrinolysis shutdown after trauma is associated with increased mortality due to hypercoagulability-associated organ failure. However, a lack of mechanistic data has precluded the development of novel interventions to treat shutdown. OBJECTIVES: To define the pathophysiology of TEG shutdown in severely injured, bleeding patients through secondary analysis of the PROPPR trial. METHODS: Fibrinolysis was characterized in PROPPR subjects using admission TEG lysis at 30 min (LY30) or plasmin-antiplasmin (PAP) levels. LY30 categories were low (<0.9%), moderate (0.9-2.9%), or high (≥ 3%). PAP was classified as low (<1,500 μg/L), moderate (1,500-20,000 μg/L), or high (>20,000 μg/L). Demographics, outcomes, admission TEG values, platelet count and function, standard coagulation tests, and coagulation proteins were compared. RESULTS: Five hundred forty-seven patients had TEG data and 549 patients had PAP data available. Low LY30 was associated with reduced platelet count and aggregation, poorer TEG clot formation, prolonged clotting times, and reduced fibrinogen and alpha2 antiplasmin. Compared to moderate PAP, low PAP subjects had similar platelet parameters, TEG values, fibrinogen, and alpha2 antiplasmin, but reduced tPA, and elevated PAI-1. D-Dimer values increased as PAP increased, however patients with low LY30 had elevated D-Dimer compared with moderate LY30 patients. Most low LY30 deaths were due to TBI (45%) and hemorrhage (42%) versus one of each cause (TBI, hemorrhage, MOF) in low PAP patients. CONCLUSIONS: Low TEG LY30 does not reflect shutdown of enzymatic fibrinolysis with hypercoagulability, but rather a coagulopathic state of moderate fibrinolysis with fibrinogen consumption and platelet dysfunction that is associated with poor outcomes.
UR - http://www.scopus.com/inward/record.url?scp=85061481102&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85061481102&partnerID=8YFLogxK
U2 - 10.1097/SHK.0000000000001160
DO - 10.1097/SHK.0000000000001160
M3 - Article
C2 - 29664836
AN - SCOPUS:85061481102
VL - 51
SP - 273
EP - 283
JO - Shock
JF - Shock
SN - 1073-2322
IS - 3
ER -