Differences between brain and rectal temperatures during routine critical care of patients with severe traumatic brain injury (original) (raw)
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Clinical review: Brain-body temperature differences in adults with severe traumatic brain injury
Critical Care, 2013
Surrogate or 'proxy' measures of brain temperature are used in the routine management of patients with brain damage. The prevailing view is that the brain is 'hotter' than the body. The polarity and magnitude of temperature diff erences between brain and body, however, remains unclear after severe traumatic brain injury (TBI). The focus of this systematic review is on the adult patient admitted to intensive/neurocritical care with a diagnosis of severe TBI (Glasgow Coma Scale score of less than 8). The review considered studies that measured brain temperature and core body temperature. Articles published in English from the years 1980 to 2012 were searched in databases, CINAHL, PubMed, Scopus, Web of Science, Science Direct, Ovid SP, Mednar and ProQuest Dissertations & Theses Database. For the review, publications of randomised controlled trials, non-randomised controlled trials, before and after studies, cohort studies, case-control studies and descriptive studies were considered for inclusion. Of 2,391 records identifi ed via the search strategies, 37 were retrieved for detailed examination (including two via hand searching). Fifteen were reviewed and assessed for methodological quality. Eleven studies were included in the systematic review providing 15 brain-core body temperature comparisons. The direction of mean brain-body temperature diff erences was positive (brain higher than body temperature) and negative (brain lower than body temperature). Hypothermia is associated with large brain-body temperature diff erences. Brain temperature cannot be predicted reliably from core body temperature. Concurrent monitoring of brain and body temperature is recommended in patients where risk of temperature-related neuronal damage is a cause for clinical concern and when deliberate induction of below-normal body temperature is instituted.
Brain Temperature and Outcome After Severe Traumatic Brain Injury
Neurocritical Care, 2006
Introduction: In humans, raised body temperature is linked to poor outcome after brain injury. Because deviations between brain and body temperature have been reported after severe traumatic brain injury (TBI), the aim of this study was to explore the relationship between initial and mean brain temperature and survival at 3 months. Methods: Intraparenchymal temperature was measured 3-4 cm within white matter. Logistic regression was used to explore linear and quadratic relationships between initial and average brain temperature and survival at 3 months. Results: In 36 patients, initial brain temperatures ranged from 33.5 to 39.2°C (median 37.4°C). There was no evidence of an association between initial brain temperature and risk of death, either linear (odds ratio [OR] 95% confidence interval [CI] = 1.3 [0.68 to 2.5], p = 0.42) or quadratic (p = 0.26). Assuming a linear relationship, patients with higher mean brain temperatures were less likely to die: OR (95% CI) for death per 1°C was 0.31 (0.09 to 1.1), p = 0.06. However, by fitting the quadratic relationship, there was a suggestion that both high and low temperatures were associated with increased risk of death: p = 0.06. Conclusion: Initial brain temperature measured shortly after admission did not predict outcome. There is a suggestion that patients with " middle range " tem peratures were less likely to die.
International Journal of Statistics in Medical Research, 2013
There is uncertainty about the reliability of using body temperature readings as a 'surrogate' measure of brain temperature. Aim: To determine the temporal interrelationship between body and brain temperature after severe traumatic brain injury (TBI). Setting and Patients: Large University teaching hospital in the North West of England. Patients admitted for emergency neurocritical care. All patients received dual-modality monitoring of brain tissue pressure and temperature via invasive intracerebral micro-sensors. Body temperature was measured using an indwelling thermistor inserted in to the rectum. Methods: Temperature was monitored continuously with values stored to a bedside data acquisition system at intervals of 10 minutes. Data were transferred to a spreadsheet at end of each individual's monitoring period for further analysis under Matlab routines. The method of functional principal components was used to determine the time-dynamics of brain and body temperature relationships. Results: In the period after severe TBI, median body and brain temperature for all readings and in all patients was 37.6 o C and 37.7 o C respectively; a statistical (p <0.001) but not clinically significant difference. A strong regression relationship between brain and body temperature was demonstrated (functional coefficient of determination, R 2 = 0.7623, p< 0.0020). Conclusions: Body temperature is a good early predictor of brain temperature but only during the first two days after severe TBI. The results will be of value for future predictive modeling of brain temperature changes, particularly where brain tissue monitoring is not clinically justified or available. In particular, results demonstrate the uncertainty in using body temperature as a surrogate for brain temperature beyond the first two days after severe traumatic brain injury.
Brain temperature, body core temperature, and intracranial pressure in acute cerebral damage
Journal of Neurology, Neurosurgery & Psychiatry, 2001
Objectives-To assess the frequency of hyperthermia in a population of acute neurosurgical patients; to assess the relation between brain temperature (ICT) and core temperature (Tc); to investigate the eVect of changes in brain temperature on intracranial pressure (ICP). Methods-The study involved 20 patients (10 severe head injury, eight subarachnoid haemorrhage, two neoplasms) with median Glasgow coma score (GCS) 6. ICP and ICT were monitored by an intraventricular catheter coupled with a thermistor. Internal Tc was measured in the pulmonary artery by a Swan-Ganz catheter. Results-Mean ICT was 38.4 (SD 0.8) and mean Tc 38.1 (SD 0.8)°C; 73% of ICT and 57.5% of Tc measurements were >38°C. The mean diVerence between ICT and Tc was 0.3 (SD 0.3)°C (range −0.7 to 2.3°C) (p=0. 0001). Only in 12% of patients was Tc higher than ICT. The main reason for the diVerences between ICT and Tc was body core temperature: the diVerence between ICT and Tc increased significantly with body core temperature and fell significantly when this was lowered. The mean gradient between ICT and Tc was 0.16 (SD 0.31)°C before febrile episodes (ICT being higher than Tc), and 0.41 (SD 0.38)°C at the febrile peak (p<0.05). When changes in temperature were considered, ICT had a profound influence on ICP. Increases in ICT were associated with a significant rise in ICP, from 14.9 (SD 7.9) to 22 (SD 10.4) mm Hg (p<0.05). As the fever ebbed there was a significant decrease in ICP, from 17.5 (SD 8.62) to 16 (SD 7.76) mm Hg (p=0.02). Conclusions-Fever is extremely frequent during acute cerebral damage and ICT is significantly higher than Tc. Moreover, Tc may underestimate ICT during the phases when temperature has the most impact on the intracranial system because of the close association between increases in ICT and ICP. (J Neurol Neurosurg Psychiatry 2001;71:448-454)
Intracerebral temperature monitoring in severely head injured patients
Acta Neurochirurgica, 1995
In a series of 6 severely head injured patients, intraventricular as well as rectal, bladder and jugular vein temperature is recorded. The relationship between these temperatures in different conditions is evaluated. Intracerebral temperature is 0.5 +0.2~ (mean + SD) higher than bladder temperature except in conditions such as brain death. It is concluded that rectal temperature is not representative and therefore not a good alternative to the measurement of brain temperature. More data on human intracerebral temperature are mandatory as well as prospective studies correlating intracerebral temperature with final outcome in head injury.
Rectal-scalp temperature difference predicts brain death in children
Pediatric Neurology, 1999
When brain death in children occurs, commonly the scalp feels cold despite a normal core temperature. This phenomenon might reflect absent cerebral blood flow and metabolic activity. The authors, therefore, measured rectal-scalp temperature differences in critically ill comatose children to test the hypothesis that a particular temperature difference may correlate with clinical brain death. In a prospective cohort study set in a pediatric intensive care unit, rectal-scalp, rectalabdomen, and rectal-mastoid temperatures in critically ill comatose children older than 18 months of age were measured before and during brain death evaluations. Twelve children were enrolled. Clinical criteria for brain death were met by seven patients, and five patients survived. All of the seven children who died had rectal-scalp temperature differences greater than 4°C (mean ؍ 6.7, range ؍ 6.0-7.4) at the time of clinical brain death. No survivor had a rectal-scalp temperature difference of 4°C at any time (mean ؍ 3.4, range ؍ 2.9-3.9). Rectal-scalp temperature differences of those who died and those who survived were significantly different at the P < 0.005 level. Rectal-abdomen and rectal-mastoid temperature differences did not correlate with clinical brain death or rectal-scalp temperature difference. In this preliminary study a rectal-scalp temperature difference of greater than 4°C correlates with clinical criteria for brain death in children.
Critical Care, 2009
Introduction Temperature measurement is important during routine neurocritical care especially as differences between brain and systemic temperatures have been observed. The purpose of the study was to determine if infra-red temporal artery thermometry provides a better estimate of brain temperature than tympanic membrane temperature for patients with severe traumatic brain injury. Methods Brain parenchyma, tympanic membrane and temporal artery temperatures were recorded every 15-30 min for five hours during the first seven days after admission. Results Twenty patients aged 17-76 years were recruited. Brain and tympanic membrane temperature differences ranged from-0.8 °C to 2.5 °C (mean 0.9 °C). Brain and temporal artery temperature differences ranged from-0.7 °C to 1.5 °C (mean 0.3 °C). Tympanic membrane temperature differed from brain temperature by an average of 0.58 °C more than temporal artery temperature measurements (95% CI 0.31 °C to 0.85 °C, P < 0.0001). Conclusions At temperatures within the normal to febrile range, temporal artery temperature is closer to brain temperature than is tympanic membrane temperature.
Body Temperature after EMS Transport: Association with Traumatic Brain Injury Outcomes
Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors, 2017
Low body temperatures following prehospital transport are associated with poor outcomes in patients with traumatic brain injury (TBI). However, a minimal amount is known about potential associations across a range of temperatures obtained immediately after prehospital transport. Furthermore, a minimal amount is known about the influence of body temperature on non-mortality outcomes. The purpose of this study was to assess the correlation between temperatures obtained immediately following prehospital transport and TBI outcomes across the entire range of temperatures. This retrospective observational study included all moderate/severe TBI cases (CDC Barell Matrix Type 1) in the pre-implementation cohort of the Excellence in Prehospital Injury Care (EPIC) TBI Study (NIH/NINDS: 1R01NS071049). Cases were compared across four cohorts of initial trauma center temperature (ITCT): <35.0°C [Very Low Temperature (VLT)]; 35.0-35.9°C [Low Temperature (LT)]; 36.0-37.9°C [Normal Temperature (N...
Brain temperature and its fundamental properties: a review for clinical neuroscientists
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.
Hypothermia and Rapid Rewarming Is Associated With Worse Outcome Following Traumatic Brain Injury
Journal of Trauma Nursing, 2010
Purpose-The purpose of the present study was to determine (1) the prevalence and degree of hypothermia in patients on emergency department admission and (2) the effect of hypothermia and rate of rewarming on patient outcomes. Methods-Secondary data analysis was conducted on patients admitted to a level I trauma center following severe traumatic brain injury (n = 147). Patients were grouped according to temperature on admission according to hypothermia status and rate of rewarming (rapid or slow). Regression analyses were performed. Findings-Hypothermic patients were more likely to have lower postresuscitation Glasgow Coma Scale scores and a higher initial injury severity score. Hypothermia on admission was correlated with longer intensive care unit stays, a lower Glasgow Coma Scale score at discharge, higher mortality rate, and lower Glasgow outcome score-extended scores up to 6 months postinjury (P < .05). When controlling for other factors, rewarming rates more than 0.25°C/h were associated with lower Glasgow Coma Scale scores at discharge, longer intensive care unit length of stay, and higher mortality rate than patients rewarmed more slowly although these did not reach statistical significance. Conclusion-Hypothermia on admission is correlated with worse outcomes in brain-injured patients. Patients with traumatic brain injury who are rapidly rewarmed may be more likely to have worse outcomes. Trauma protocols may need to be reexamined to include controlled rewarming at rates 0.25°C/h or less.