Background-Ear thermometers are becoming popular as a method for measuring deep body (core) temperature. Aim-To determine the variability of a single user's tympanic membrane (ear) temperature measurements. Subjects-Forty two, afebrile, healthy children, and 20 febrile children with acute burns. Results-In afebrile children measurements made in both ears (and within just a few minutes of each other) diVered by as much as 0.6°C. Operator measurement error, s w of three consecutive measurements, in the same ear, was 0.13°C. In the group of febrile, burned children, core temperature was measured hourly at a number of sites (ear, rectum, axilla, bladder). A peak in core temperature occurred approximately 10-12 hours after the burn. Measurement error was calculated in 14 febrile, burned children with a peak temperature in excess of 38°C. For the left ear, measurement error was 0.19°C and for the right ear, 0.11°C. In the febrile children agreement between the ears was poor. The limits of agreement were 0.4°C to −0.8°C. It was not possible to predict the occasions when the temperature diVerences between the ears would be large or small. Conclusions-The measurement error of one recording from the next is probably acceptable at about 0.1 to 0.2°C. To limit the variations in temperature of one ear to the other, measurements should be restricted to one of the ears whenever possible and the same ear used throughout the temperature monitoring period. Nurses and parents should take more than one temperature reading from the same ear whenever possible. (Arch Dis Child 1999;80:262-266)
Type 2 diabetes is associated with biochemical evidence of low-grade inflammation, and experimental studies have suggested that both insulin and glucose affect inflammatory responses. To determine the effect of in vivo changes in glucose availability and plasma insulin concentrations in humans, we administered 20 U/kg Escherichia coli lipopolysaccharide (LPS) or saline (control) to 14 subjects during a euglycemic hyperinsulinemic clamp (n = 6) or an infusion of sterile saline (n = 8). Parallel in vitro studies on human whole blood were undertaken to determine whether there was a direct effect of glucose, insulin, and leptin on proinflammatory cytokine production. Infusion of glucose and insulin significantly amplified and/or prolonged the cardiovascular, plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and counterregulatory hormone responses to LPS, whereas the effects on fever, plasma norepinephrine concentrations, and oxygen consumption were unaffected. In vitro studies showed no modulation of LPS-stimulated IL-6 or TNF-alpha production by glucose, insulin, or leptin at physiologically relevant concentrations. Hyperinsulinemia indirectly enhances key components of the systemic inflammatory and stress responses in this human model of infection.
SummaryTheoretical models suggest that small differences only exist between brain and body temperature in health. Once the brain is injured, brain temperature is generally regarded to rise above body temperature. However, since reports of the magnitude of the temperature gradient between brain and body vary, it is still not clear whether conventional body temperature monitoring accurately predicts brain temperature at all times. In this prospective, descriptive study, 20 adults with severe primary brain trauma were studied during their stay in the neurointensive care unit. Brain temperature ranged from 33.4 to 39.9°C. Comparisons between paired brain and rectal temperature measurements revealed no evidence of a systematic difference [mean difference )0.04°C (range )0.13 to 0.05°C, 95% CI), p = 0.39]. Contrary to popular belief, brain temperature did not exceed systemic temperature in this relatively homogeneous patient series. The mean values masked inconsistent and unpredictable individual brain-rectal temperature differences (range 1.8 to )2.9°C) and reversal of the brain-body temperature gradient occurred in some patients. Brain temperature could not be predicted from body temperature at all times. Brain temperature is seldom measured during routine neurointensive care but there is a long-held assumption that since the temperatures of healthy internal organs differ only slightly [1], temperature measurements of the rectum, bladder, pulmonary artery and tympanum can be used as surrogates for brain temperature. Using these conventional body sites, temperatures greater than 38.5°C are commonly encountered during neurocritical care [2,3] and cause concern. In animal models of cerebral ischaemia [4][5][6][7] and trauma [8,9] a rise in body core temperature in excess of 38°C is associated with increased neuronal damage. In stroke patients a rise in body temperature independently predicts poor outcome [10] and increased mortality [11][12][13][14] but when the human brain is injured by trauma, the evidence for a relationship between raised body temperature and worse neurological outcome is not as clear [15,16]. However, it is assumed that the deleterious metabolic, inflammatory and biochemical mechanisms associated with raised body temperature in animal models of stroke and trauma may operate similarly in the brain injured human [17]. This assumption underpins current opinion that even a small increase in body temperature (1-2°C) above normal (37°C) accelerates ischaemic damage and increases the size of the primary brain lesion [9,18] and should therefore be prevented [13].Little is known about human brain temperature, but theoretical models suggest that during normothermia the temperature of the brain is close to that of internal carotid arterial blood before the blood enters the circle of Willis [19]. In man, direct measurement of brain temperature Anaesthesia, 2005, 60, pages 759-765
Temperature has a major effect on survival in all animal species. Despite wide variations in climate, organ temperature is regulated 'tightly' by homeostatic mechanisms controlling heat production and conservation, as well as heat loss. Although less is known about the temperature of the healthy or injured human brain, mammalian brain homeothermy involves interplay between neural metabolic heat production, cerebral blood flow and the temperature of incoming arterial blood. Recent advances in invasive and non-invasive thermometry have allowed measurement of brain temperature to be made in man. In health, small differences only exist between local brain and body core temperature. Large (negative) brain-body temperature dissociation, observed in some patients after severe brain damage, does not appear to be a feature of cerebral homeothermy in healthy people. The extent to which changes in brain temperature reflect, or 'drive', secondary cerebral pathology remains uncertain in patients with traumatic brain injury (TBI). Raised temperature may be due to a regulated readjustment in the hypothalamic 'set-point' in response to inflammation and infection, or it may occur as a consequence of damage to the hypothalamus and/or its pathways. Diagnosis of the mechanism of raised temperature; fever v. neurogenic hyperthermia (regulated v. unregulated temperature rise) is difficult to make clinically. Whatever the cause, a 1-2 degrees C rise in brain or body temperature, especially when it develops early after injury, is widely regarded as harmful. There is no clear evidence that fever per se leads directly to worsened neurological damage or poor outcome, nor evidence that antipyretic treatments (pharmacological or cold-induced therapies) preserve damaged brain tissue or result in a better outcome. Part 2 follows part one with a detailed analysis of the evidence for the significance of raised temperature on outcome after TBI.
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 differences 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 identified 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 differences was positive (brain higher than body temperature) and negative (brain lower than body temperature). Hypothermia is associated with large brain-body temperature differences. 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.
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