by Drewry, Anne M.; Mohr, Nicholas M.; Ablordeppey, Enyo A.;
Dalton, Catherine M.; Doctor, Rebecca J.; Fuller, Brian M.; Kollef, Marin H.;
Hotchkiss, Richard S.
Critical Care Medicine: June 2022 -
Volume 50 - Issue 6 - p 924-934
OBJECTIVES:
To test the hypothesis that forced-air warming of critically
ill afebrile sepsis patients improves immune function compared to
standard temperature management.
DESIGN:
Single-center, prospective, open-label, randomized
controlled trial.
SETTING:
One thousand two hundred-bed academic medical center.
PATIENTS:
Eligible patients were mechanically ventilated septic adults
with: 1) a diagnosis of sepsis within 48 hours of enrollment; 2)
anticipated need for mechanical ventilation of greater than 48 hours; and 3) a
maximum temperature less than 38.3°C within the 24 hours prior to enrollment.
Primary exclusion criteria included: immunologic diseases, immune-suppressing
medications, and any existing condition sensitive to therapeutic hyperthermia
(e.g., brain injury). The primary outcome was monocyte human leukocyte antigen
(HLA)-DR expression, with secondary outcomes of CD3/CD28-induced interferon
gamma (IFN-γ) production, mortality, and 28-day hospital-free days.
INTERVENTIONS:
External warming using a forced-air warming blanket for 48
hours, with a goal temperature 1.5°C above the lowest temperature documented in
the previous 24 hours.
MEASUREMENTS AND MAIN RESULTS:
We enrolled 56 participants in the study. No differences
were observed between the groups in HLA-DR expression (692 vs 2,002; p =
0.396) or IFN-γ production (31 vs 69; p = 0.678). Participants
allocated to external warming had lower 28-day mortality (18% vs 43%; absolute
risk reduction, 25%; 95% CI, 2–48%) and more 28-day hospital-free days
(difference, 2.6 d; 95% CI, 0–11.6).
CONCLUSIONS:
Participants randomized to external forced-air warming did
not have a difference in HLA-DR expression or IFN-γ production. In this pilot
study, however, 28-day mortality was lower in the intervention group. Future
research should seek to better elucidate the impact of temperature modulation
on immune and nonimmune organ failure pathways in sepsis.
