Coagulopathie: Une affaire personnelle

Individual clotting factor contributions to mortality following trauma.

Kunitake RC et Al. J Trauma Acute Care Surg. 2017 Feb;82(2):302-308. doi: 10.1097/TA.0000000000001313.

 

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Un travail intéressant qui portant sur 1463 traumatisés d'ISS médian de 16 et qui met en avant l'existence de deux profils de coagulopathie traumatique (16% des patients pris en charge). Dans 49,30 des cas, un premier est en rapport avec des anomalies des facteurs II,VII,IX,X et protéine C . Le second profil (17% des patients) exprime des anomalies sur les facteurs V et VIII. Seuls seraient liés à une motralité à 28j. LA déplétion en facteur V serait associée à une mortalité à long terme. Ce travail milite pour une approche personnalisée de la ocaguklopathie traumatique.

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BACKGROUND:

Acute traumatic coagulopathy affects 20% to 30% of trauma patients, but the extensive collinearity of the coagulation cascade complicates attempts to clarify global clotting factor dysfunction. This study aimed to characterize phenotypes of clotting factor dysfunction and their contributions to mortality after major trauma.

METHODS:

This prospective cohort study examines all adult trauma patients of the highest activation level presenting to San Francisco General Hospital between February 2005 and February 2015. Factors II, V, VII, VIII, IX, and X and protein C activity on admission and mortality status at 28 days were assessed. Predictors of 28-day mortality in univariate analysis were included in multiple logistic regression controlling for traumatic brain injury (TBI), acidosis, age, and mechanism of injury. Principal component analysis was utilized to identify phenotypic coagulation.

RESULTS:

Complete coagulation factor data were available for 876 (61%) of 1,429 patients. In multiple logistic regression, factors V (odds ratio [OR], 0.86; 95% confidence interval [CI], 0.76-0.97), VIII (OR, 0.97; 95% CI, 0.95-0.99), and X (OR, 0.79; 95% CI, 0.68-0.92) and protein C (OR, 1.17; 95% CI, 1.05-1.30) significantly predicted 28-day mortality after controlling for age, base deficit, mechanism of injury, and TBI. Principal component analysis identified two significant principal components (Phenotypes 1 and 2) that accounted for 66.3% of the total variance. Phenotype 1 (factors II, VII, IX, and X and protein C abnormalities) explained 49.3% and was associated with increased injury, coagulopathy, TBI, and mortality. Phenotype 2 (factors V and VIII abnormalities) explained 17.0% and was associated with increased coagulopathy, blunt injury, and mortality. Only Phenotype 2 remained significantly associated with 28-day mortality in multiple logistic regression.

CONCLUSIONS:

Principal component analysis identified two distinct phenotypes within the entirety of global clotting factor abnormalities, and these findings substantiate the crucial association of factors V and VIII on mortality following trauma. This may be the first step toward identifying unique phenotypes after injury and personalizing hemostatic resuscitation.