To understand the gradient between rectal and brain temperature in children after severe traumatic brain injury. We hypothesized that the rectal temperature and brain temperature gradient will be influenced by the child's body surface area and that this relationship will persist over physiologic temperature ranges.
Retrospective review of a prospectively collected pediatric neurotrauma registry.
Academic, university-based pediatric neurotrauma program.
Consecutive children (n = 40) with severe traumatic brain injury (Glasgow coma scale of <8) who underwent brain temperature monitoring (July 2003 to December 2008) were studied after informed consent was obtained. A subset of children (n = 24) were concurrently enrolled in a randomized, controlled clinical trial of early-moderate hypothermia for neuroprotection.
Data extraction of multiple clinical variables, including demographic data, body surface area, and rectal and brain temperature at recorded at hourly intervals.
Paired brain and rectal temperature measurements (in degrees Celsius, n = 4369) were collected hourly and compared by using Pearson correlations. Patients were stratified according to body surface area (<1.0 m, 1.0-1.99 m, 2.0-2.99 m, and >3.0 m) and based on brain temperature (≤34.0, 34.1-36.0; 36.1-38, ≥38.1). Body surface area and brain temperature were compared between groups by using Pearson correlations with correction for repeated measures. Mean brain temperature-rectal temperature difference was calculated for stratified brain temperature ranges. Overall, brain and rectal temperatures were highly correlated (r = .86, p < .001). During brain hyperthermia, brain temperature-rectal temperature was similar to that reported in previous studies with brain temperature higher than rectal temperature (1.75 ± 0.4; r = .54). Surprisingly, this relationship was reversed during brain hypothermia (brain temperature-rectal temperature = -1.87 ± 0.8; r = .37), indicating a reversal of the brain-systemic temperature gradient. When stratified for body surface area, the correlation between rectal temperature and brain temperature remained strong (r = .78, 0.91, 0.79 and 0.95, respectively, p < .001). However, the correlation between brain temperature and rectal temperature was substantially decreased when stratified for brain temperature (r = .37, 0.58, 0.48, 0.54, p < .001). In particular, during moderate brain hypothermia (brain temperature ≤34), the correlation between brain temperature and rectal temperature was weakest, indicating the greatest variability during this condition which is often targeted for therapeutic trials.
Brain temperature and rectal temperature are generally well-correlated in children with traumatic brain injury. This relationship is different at the extremes of the physiologic temperature range, with the temperature gradient reversed during brain hypothermia and hyperthermia. Given that studies showing neuroprotection from hypothermia in animal models of brain injury generally target brain temperature, our data suggest the possibility that, if brain temperature were the therapeutic target in clinical trials, this would result in somewhat higher systemic temperature and potentially fewer side effects. This relationship may be exploited in future clinical trials to maintain brain hypothermia (for neurologic protection) at slightly higher systemic temperatures (and potentially fewer systemic side effects).
"On average, deep brain temperature is less than 1 • C higher than body temperature in humans, unless cerebral injury is severe enough to significantly disrupt the brain-body temperature regulation (Soukup et al., 2002). Theoretically, the maximal brain temperature elevation over blood temperature, under physiological conditions, would be approximately 0.9 • C for a typical hematocrit level of 40% (Yablonskiy et al., 2000), and both the magnitude and direction of the difference can be temperature dependent (Nybo et al., 2002b; Smith et al., 2011). The temperature gap may become more accentuated at higher body temperatures and diminish or even reverse in its relationship at lower body temperatures. "
[Show abstract][Hide abstract] ABSTRACT: Brain temperature, as an independent therapeutic target variable, has received increasingly intense clinical attention. To date, brain hypothermia represents the most potent neuroprotectant in laboratory studies. Although the impact of brain temperature is prevalent in a number of common human diseases including: head trauma, stroke, multiple sclerosis, epilepsy, mood disorders, headaches, and neurodegenerative disorders, it is evident and well recognized that the therapeutic application of induced hypothermia is limited to a few highly selected clinical conditions such as cardiac arrest and hypoxic ischemic neonatal encephalopathy. Efforts to understand the fundamental aspects of brain temperature regulation are therefore critical for the development of safe, effective, and pragmatic clinical treatments for patients with brain injuries. Although centrally-mediated mechanisms to maintain a stable body temperature are relatively well established, very little is clinically known about brain temperature's spatial and temporal distribution, its physiological and pathological fluctuations, and the mechanism underlying brain thermal homeostasis. The human brain, a metabolically "expensive" organ with intense heat production, is sensitive to fluctuations in temperature with regards to its functional activity and energy efficiency. In this review, we discuss several critical aspects concerning the fundamental properties of brain temperature from a clinical perspective.
Frontiers in Neuroscience 10/2014; 8(307). DOI:10.3389/fnins.2014.00307 · 3.66 Impact Factor
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