OBJECTIVE: To ascertain the incidence and timing of fever in patients at risk for temperature modulation of brain injury resulting from ischemia or trauma. DESIGN: We retrospectively reviewed the medical records of patients admitted between January 1991 and December 1994. MATERIAL AND METHODS: We investigated three groups of hospitalized patients considered at risk for ongoing brain injury resulting from a prior cerebral insult: successful resuscitation from out-of-hospital cardiac arrest (CA), subarachnoid hemorrhage (SAH), or traumatic closed-head injury (CHI). Forty patients per condition were randomly selected from those who survived for more than 24 hours after hospital admission. RESULTS: During the initial 72 hours of hospitalization, temperature increases to 38 degrees C or more (that is, temperatures previously reported to worsen neurologic outcome after brain injury) were noted in 83% of patients with CA, 70% of those with SAH, and 68% of those with CHI. Within the cohort of febrile patients, 18 to 44% of all temperature measurements were 38 degrees C or higher, and the febrile episodes occurred randomly throughout the study interval. Fewer than one-eighth of the febrile patients received drugs possessing antipyretic properties (such as aspirin or acetaminophen) in a dose appropriate to treat fever. No other method of temperature control (for example, physical means) was used in any patient. The fractions of patients who were dismissed from the hospital with permanent neurologic injury were as follows: CA, 20%; SAH, 45%; and CHI, 43%. CONCLUSION: In these hospitalized patients at risk for ongoing brain injury, the incidence of temperature increases within the range reported to worsen neurologic outcome (elevations of 1.0 degree C or more) was very high. The characterization of these potentially injurious, randomly occurring, and traditionally undertreated temperature increases may have implications for the design of future protocols aimed at providing cerebral protection.
OBJECTIVE: To ascertain the incidence and timing of fever in patients at risk for temperature modulation of brain injury resulting from ischemia or trauma. DESIGN: We retrospectively reviewed the medical records of patients admitted between January 1991 and December 1994. MATERIAL AND METHODS: We investigated three groups of hospitalized patients considered at risk for ongoing brain injury resulting from a prior cerebral insult: successful resuscitation from out-of-hospital cardiac arrest (CA), subarachnoid hemorrhage (SAH), or traumatic closed-head injury (CHI). Forty patients per condition were randomly selected from those who survived for more than 24 hours after hospital admission. RESULTS: During the initial 72 hours of hospitalization, temperature increases to 38 degrees C or more (that is, temperatures previously reported to worsen neurologic outcome after brain injury) were noted in 83% of patients with CA, 70% of those with SAH, and 68% of those with CHI. Within the cohort of febrile patients, 18 to 44% of all temperature measurements were 38 degrees C or higher, and the febrile episodes occurred randomly throughout the study interval. Fewer than one-eighth of the febrile patients received drugs possessing antipyretic properties (such as aspirin or acetaminophen) in a dose appropriate to treat fever. No other method of temperature control (for example, physical means) was used in any patient. The fractions of patients who were dismissed from the hospital with permanent neurologic injury were as follows: CA, 20%; SAH, 45%; and CHI, 43%. CONCLUSION: In these hospitalized patients at risk for ongoing brain injury, the incidence of temperature increases within the range reported to worsen neurologic outcome (elevations of 1.0 degree C or more) was very high. The characterization of these potentially injurious, randomly occurring, and traditionally undertreated temperature increases may have implications for the design of future protocols aimed at providing cerebral protection.
Authors: Neeraj Badjatia; Joan O'Donnell; John R Baker; David Huang; Cenk Ayata; David M Greer; Bob S Carter; Christopher S Ogilvy; Colin T McDonald Journal: Neurocrit Care Date: 2004 Impact factor: 3.210
Authors: J Steven Hata; Constance R Shelsky; Bradley J Hindman; Thomas C Smith; Jonathan S Simmons; Michael M Todd Journal: Neurocrit Care Date: 2008 Impact factor: 3.210