Fanny Vardon Bounes1, Géraldine Faure2, Antoine Rouget3, Jean-Marie Conil4, Bernard Georges5, Thomas Geeraerts6, Olivier Fourcade7, Vincent Minville8, Clément Delmas9. 1. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France; Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université Paul Sabatier, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Bounes.f@chu-toulouse.fr. 2. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Faure.g@chu-toulouse.fr. 3. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Rouget.a@chu-toulouse.fr. 4. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Conil.jm@chu-toulouse.fr. 5. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Georges.b@chu-toulouse.fr. 6. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Geeraerts.t@chu-toulouse.fr. 7. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Fourcade.o@chu-toulouse.fr. 8. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France; Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université Paul Sabatier, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Minville.v@chu-toulouse.fr. 9. Critical Care Unit, Toulouse University Hospital, Avenue du Pr Jean Poulhès, 31059 Toulouse, France; Institut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université Paul Sabatier, Avenue du Pr Jean Poulhès, 31059 Toulouse, France. Electronic address: Delmas.clement@chu-toulouse.fr.
Abstract
BACKGROUND: Metabolic response to severe trauma requires early nutritional resuscitation. Carnitine is essential for lipolysis, the energy source during this hypercatabolic phase. However l-carnitine is not present in nutritional replacement solutions. Furthermore, free carnitine depletion, defined as carnitine plasma level under 36μmol/L, was not adequately reported in adult patients with severe trauma. The aim of this study was to assess plasma free carnitine levels and factors of variation in severe trauma. METHOD: Our observational study concerned 38 trauma patients including 18 with traumatic brain injury (TBI). On the third day after trauma, plasma free carnitine concentration was determined (by enzymatic method) while patients received artificial nutrition. RESULTS: Low plasmatic free carnitine concentration was evidenced in 95% of the patients with a median value of 18μmol/L (11-47). Univariate analysis showed that mean arterial pressure, serum urea, CKD-EPI and patients with TBI were significantly associated with plasma free carnitine concentration less than 18μmol/L. Lower plasma free carnitine concentration was observed in the group of patients with TBI with 17.72μmol/L (11-36) versus 21.5μmol/L (11-47) for others patients (p=0.031). Logistic regression analysis showed that severe trauma with TBI and CKD-EPI above 94mL/min/1.73m2 appeared to be independent predictor of lower free carnitine plasmatic concentration (Goodness of fit=0.87 and AUC=0.89). CONCLUSION: Our observations support hypotheses that plasma free carnitine concentration is lowered in severe injured patients especially for TBI patients and patients with estimated GFR above 94mL/min/1.73m2.
BACKGROUND: Metabolic response to severe trauma requires early nutritional resuscitation. Carnitine is essential for lipolysis, the energy source during this hypercatabolic phase. However l-carnitine is not present in nutritional replacement solutions. Furthermore, free carnitine depletion, defined as carnitine plasma level under 36μmol/L, was not adequately reported in adult patients with severe trauma. The aim of this study was to assess plasma free carnitine levels and factors of variation in severe trauma. METHOD: Our observational study concerned 38 traumapatients including 18 with traumatic brain injury (TBI). On the third day after trauma, plasma free carnitine concentration was determined (by enzymatic method) while patients received artificial nutrition. RESULTS: Low plasmatic free carnitine concentration was evidenced in 95% of the patients with a median value of 18μmol/L (11-47). Univariate analysis showed that mean arterial pressure, serum urea, CKD-EPI and patients with TBI were significantly associated with plasma free carnitine concentration less than 18μmol/L. Lower plasma free carnitine concentration was observed in the group of patients with TBI with 17.72μmol/L (11-36) versus 21.5μmol/L (11-47) for others patients (p=0.031). Logistic regression analysis showed that severe trauma with TBI and CKD-EPI above 94mL/min/1.73m2 appeared to be independent predictor of lower free carnitine plasmatic concentration (Goodness of fit=0.87 and AUC=0.89). CONCLUSION: Our observations support hypotheses that plasma free carnitine concentration is lowered in severe injured patients especially for TBIpatients and patients with estimated GFR above 94mL/min/1.73m2.