Charmaine Childs

Tympanic membrane temperature as a measure of core temperature.

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) differed by as much as 0.6°C. Operator measurement error, sw 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 differences 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.

Determination of regional brain temperature using proton magnetic resonance spectroscopy to assess brain–body temperature differences in healthy human subjects

Proton magnetic resonance spectroscopy (1H MRS) was used to determine brain temperature in healthy volunteers. Partially water‐suppressed 1H MRS data sets were acquired at 3T from four different gray matter (GM)/white matter (WM) volumes. Brain temperatures were determined from the chemical‐shift difference between the CH3 of N‐acetyl aspartate (NAA) at 2.01 ppm and water. Brain temperatures in 1H MRS voxels of 2 × 2 × 2 cm3 showed no substantial heterogeneity. The volume‐averaged temperature from single‐voxel spectroscopy was compared with body temperatures obtained from the oral cavity, tympanum, and temporal artery regions. The mean brain parenchyma temperature was 0.5°C cooler than readings obtained from three extra‐brain sites (P < 0.01). 1H MRS imaging (MRSI) data were acquired from a slice encompassing the single‐voxel volumes to assess the ability of spectroscopic imaging to determine regional brain temperature within the imaging slice. Brain temperature away from the center of the brain determined by MRSI differed from that obtained by single‐voxel MRS in the same brain region, possibly due to a poor line width (LW) in MRSI. The data are discussed in the light of proposed brain–body temperature gradients and the use of 1H MRSI to monitor brain temperature in pathologies, such as brain trauma. Magn Reson Med 57:59–66, 2007.

Differences between brain and rectal temperatures during routine critical care of patients with severe traumatic brain injury

Theoretical 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.

A survey into toxic shock syndrome (TSS) in UK burns units

Toxic shock syndrome (TSS) is a rare complication of a Staphylococcus aureus infection and is primarily seen in children with small burns. The true incidence of TSS in burns patients is not known and the number of presumptive cases rarely reported. This survey was undertaken to determine if the incidence of TSS in children with burns could be related to the type of dressing used to cover the wound. A questionnaire was compiled and sent to the Senior Nurse in charge of each of the UK burns units. General information on the number of admissions, age of the patient, cause of injury and burn wound management was sought. An 81% response was obtained after two mailshots and follow up telephone calls. Seventy percent (23/33) of units which answered the survey nursed children. Of these, eight units had either not encountered TSS previously or not had a case within the past two years. These units were small, admitting a maximum of 50 patients each year. Of the units where TSS was encountered, approximately 2.5% of children admitted showed symptoms of TSS. Of the units who nursed both adults and children, seven units had seen TSS in burned adult patients which has not been reported in the literature. Of the eight units where TSS had not been recently encountered, four routinely administered prophylactic antibiotics to prevent infection whereas routine administration of antibiotics occurred in only two of the 15 units where TSS was seen. Although wound management procedures differed slightly there were many similarities. These included wound cleaning with normal saline, covering with either silver sulphadiazine (1%) or povidone iodine (10%), depending upon the infection status, and dressing with a paraffin tulle, gauze and crepe bandages. No association between the management of the burn wound and subsequent development of TSS could be established.

Human brain temperature: regulation, measurement and relationship with cerebral trauma: Part 1

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°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.

Patterns of Staphylococcus aureus colonization, toxin production, immunity and illness in burned children.

Toxic shock syndrome toxin-one (TSST-1) produced from some but not all strains of Staphylococcus aureus is considered to be responsible for the development of the serious illness, toxic shock syndrome (TSS). The aim of this study was to establish the importance of S. aureus in the aetiology of suspected cases of TSS in acutely burned children. The pattern of colonization of S. aureus, and in particular toxic shock syndrome toxin-one (TSST-1) producing isolates, was studied in 53 burned children admitted as consecutive cases. S. aureus was not normally present on admission. Although it was the most common wound pathogen, it was acquired during the first few days after admission. Antibody status to TSST-1 on admission and at discharge was determined. Only half (49 per cent) of the children had antibodies to TSST-1. When it was possible to obtain paired admission and discharge samples in patients who had been given blood products, an assessment of seroconversion could be made. Two of the four patients given blood products during the resuscitation and postoperative period were antibody negative on admission (the other two were TSST-1 antibody positive). By discharge they had antibodies to TSST-1. Whilst the majority of donated blood products had antibodies to TSST-1 (76 per cent), some (24 per cent) did not. Seven of 53 children (13 per cent) developed a toxic shock-like illness which caused clinical concern.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain temperature and outcome after severe traumatic brain injury

IntroductionIn 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.MethodsIntraparenchymal 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.ResultsIn 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.ConclusionInitial brain temperature measured shortly after adminission did not predict outcome. There is a suggestion that patients with “middle range” temperatures were less likely to die.

Using Abbreviated Injury Scale (AIS) codes to classify Computed Tomography (CT) features in the Marshall System

BackgroundThe purpose of Abbreviated Injury Scale (AIS) is to code various types of Traumatic Brain Injuries (TBI) based on their anatomical location and severity. The Marshall CT Classification is used to identify those subgroups of brain injured patients at higher risk of deterioration or mortality. The purpose of this study is to determine whether and how AIS coding can be translated to the Marshall ClassificationMethodsInitially, a Marshall Class was allocated to each AIS code through cross-tabulation. This was agreed upon through several discussion meetings with experts from both fields (clinicians and AIS coders). Furthermore, in order to make this translation possible, some necessary assumptions with regards to coding and classification of mass lesions and brain swelling were essential which were all approved and made explicit.ResultsThe proposed method involves two stages: firstly to determine all possible Marshall Classes which a given patient can attract based on allocated AIS codes; via cross-tabulation and secondly to assign one Marshall Class to each patient through an algorithm.ConclusionThis method can be easily programmed in computer softwares and it would enable future important TBI research programs using trauma registry data.

Infra-red thermometry: the reliability of tympanic and temporal artery readings for predicting brain temperature after severe traumatic brain injury

IntroductionTemperature 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.MethodsBrain parenchyma, tympanic membrane and temporal artery temperatures were recorded every 15–30 min for five hours during the first seven days after admission.ResultsTwenty 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).ConclusionsAt temperatures within the normal to febrile range, temporal artery temperature is closer to brain temperature than is tympanic membrane temperature.

Transfer times for patients with extradural and subdural haematomas to neurosurgery in Greater Manchester

Delay in transfer of patients with acute extradural (EDH) or subdural (SDH) haematoma to definitive neurosurgical evacuation has a detrimental effect on outcome. From July 2003 to December 2005 we undertook a prospective analysis of patients admitted to our unit for neurosurgical evacuation of their haematoma, who were transferred from non-neurosurgical hospitals. Data was collected for: 1) overall transfer time, 2) time taken from injury or deterioration to CT scan, 3) time from CT scan to arrival at our unit, and 4) time from arrival at our unit to surgery.  Overall 81 patients were eligible, of which 39 had an EDH and 42 a SDH. The median transfer times for EDH and SDH were 5.25 hours and 6.0 hours respectively. This paper discusses the factors that may prolong delays in the transfer of patients between hospitals and the way in which our unit is trying to improve the local service for the population of Greater Manchester.