title: Fever control using external cooling in septic shock: a randomized controlled trial.
abstract: BACKGROUND
  Fever control may improve vascular tone and decrease oxygen consumption, but fever may contribute to combat infection.
  
  
  OBJECTIVE
  To determine whether fever control by external cooling diminishes vasopressor requirements in septic shock.
  
  
  METHODS
  In a multicenter randomized controlled trial, febrile patients with septic shock requiring vasopressors, mechanical ventilation, and sedation were allocated to external cooling (n = 101) to achieve normothermia (36.5-37°C) for 48 hours or no external cooling (n = 99). Vasopressors were tapered to maintain the same blood pressure target in the two groups. The primary endpoint was the number of patients with a 50% decrease in baseline vasopressor dose after 48 hours.
  
  
  RESULTS
  Body temperature was significantly lower in the cooling group after 2 hours of treatment (36.8 ± 0.7 vs. 38.4 ± 1.1°C; P < 0.01). A 50% vasopressor dose decrease was significantly more common with external cooling from 12 hours of treatment (54 vs. 20%; absolute difference, 34%; 95% confidence interval [95% CI], -46 to -21; P < 0.001) but not at 48 hours (72 vs. 61%; absolute difference, 11%; 95% CI, -23 to 2). Shock reversal during the intensive care unit stay was significantly more common with cooling (86 vs. 73%; absolute difference, 13%; 95% CI, 2 to 25; P = 0.021). Day-14 mortality was significantly lower in the cooling group (19 vs. 34%; absolute difference, -16%; 95% CI, -28 to -4; P = 0.013).
  
  
  CONCLUSIONS
  In this study, fever control using external cooling was safe and decreased vasopressor requirements and early mortality in septic shock.
authors.affiliation: Service de Réanimation Médicale, CHU Henri Mondor, 94000 Créteil, France. frederique.schortgen@hmn.aphp.fr
authors.forename: Frédérique
authors.initials: F
authors.lastname: Schortgen
authors.forename: Karine
authors.initials: K
authors.lastname: Clabault
authors.forename: Sandrine
authors.initials: S
authors.lastname: Katsahian
authors.forename: Jerome
authors.initials: J
authors.lastname: Devaquet
authors.forename: Alain
authors.initials: A
authors.lastname: Mercat
authors.forename: Nicolas
authors.initials: N
authors.lastname: Deye
authors.forename: Jean
authors.initials: J
authors.lastname: Dellamonica
authors.forename: Lila
authors.initials: L
authors.lastname: Bouadma
authors.forename: Fabrice
authors.initials: F
authors.lastname: Cook
authors.forename: Olfa
authors.initials: O
authors.lastname: Beji
authors.forename: Christian
authors.initials: C
authors.lastname: Brun-Buisson
authors.forename: François
authors.initials: F
authors.lastname: Lemaire
authors.forename: Laurent
authors.initials: L
authors.lastname: Brochard
mesh_terms: D000368:Aged; D001831:Body Temperature; D003422:Critical Care; D017679:Cryotherapy; D004837:Epinephrine / Q000627:therapeutic use; D005260:Female; D005334:Fever / Q000209:etiology / Q000628:therapy*; D006801:Humans; D057194:Intention to Treat Analysis; D053208:Kaplan-Meier Estimate; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000627:therapeutic use; D016012:Poisson Distribution; D012772:Shock, Septic / Q000150:complications* / Q000188:drug therapy / Q000401:mortality; D016896:Treatment Outcome; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
chemical_list: D014662:Vasoconstrictor Agents; D009638:Norepinephrine; D004837:Epinephrine