Rectal probe temperature lag during rapid saline induction of hypothermia after resuscitation from cardiac arrest
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低体温症を初発症状とした脳腫瘍の1例を経験した. 症例は84歳女性で, 直腸温にて持続的に35℃以下を示し, CT及びMRI検査にて第3脳室近傍に存在する30×30×35mm大の嚢胞性腫瘍で, 右視床下部の圧排を認め, 頭蓋咽頭腫と疑診した. 感染症罹患時には体温上昇を認め, 直腸温概日リズムは低体温時並びに発熱時において良好に保持された. 本症例の低体温発症の機序として, 視床下部圧排により体温調節機能の異常をきたし, 体温調節目標温度が正常に比してより低温に設定された可能性が示唆された.
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Hypothermia was induced in non-fasted, female rats by placing animals in individual, cylindrical screen cages under crushed ice until a rectal temperature of 15 °C was attained. No anaesthetic or artificial ventilation was provided. Hypothermic animals were sacrificed after 0, 30, and 60 minutes' maintenance at this rectal temperature and metabolites were measured in blood and liver. It was observed that, as previously reported, hypothermia caused increases in blood packed cell volume, glucose and lactic acid levels, and plasma levels of inorganic phosphorus and total ketones. Maintenance of hypothermia for 30 or 60 minutes either caused no further change or accentuated the changes observed initially in these metabolites. Liver glycogen level decreased significantly after 30 minutes but returned to an almost normal level at 60 minutes. From these observations it is concluded that attainment of a "steady state" condition of hypothermia in non-fasted rats does not alter the pattern of metabolic changes observed in acute hypothermia of short duration.
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Accidental hypothermia is not a frequent cause of death in Australia. Moreover it is rare to have an admission to hospital with a core temperature below 32°C. Among the cases described in the literature, it is clear that temperature and prognosis are related. Our patient presented with severe accidental hypothermia and even though the admission core temperature was below 26 degrees she was successfully discharged from hospital after active re-warming with three different devices. She had laboratory and ECG findings associated with severe hypothermia.
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We have previously reported high ROSC rates and excellent survival in OHCA in our region [1,2]. Prehospital emergency physicians (anesthesiologists) take active part in most resuscitation. If ROSC is not achieved, resuscitation is terminated on the scene in most cases. We want to investigate factors linked to survival in the few patients transported with ongoing resuscitation to the hospital.
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There are approximately 300,000 out-of-hospital cardiac arrests per year with less than 10% of those surviving. More than half of survivors suffer permanent neurologic deficits. Therapeutic hypothermia has proven effective at thwarting neurologic damage occurring in the 16-hour window following return of spontaneous circulation (ROSC).
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Abstract Rectal core temperature monitoring can mitigate heat injury but can be invasive and impractical. EQ02 + LifeMonitor is a less invasive estimation of core temperature. Therefore, the primary purpose of this study was to determine the validity of the EQ02 + LifeMonitor validity compared to rectal thermometer core temperatures. Thirteen participants completed simulated firefighting tasks with and without turn out gear, involving four rounds of a 5-minute walk on a treadmill at 2.8 mph/2.5% grade and 20 deadlifts over five minutes in heat [40.6°C; 50% humidity]. During each trial participants wore both an EQ02 + LifeMonitor and DataTherm II rectal thermometer. Devices were statistically equivalent [Δ upper p < 0.001, Δ lower p < 0.001] yet there was a statistically significant difference in the value (~ 0.1°C; p < 0.001).There was a significant effect of devices [ p < 0.001] and time [ p < 0.001], but no interaction effect [ p = 0.70] on core temperature drift. Estimated core temperature was marginally different from the DataTherm II and on average overestimated core temperature. These results suggest the EQ02 + LifeMonitor may be a viable, less invasive alternative of assessing core temperature compared to rectal temperature monitoring, especially during rigorous, intermittent activities.
Core temperature
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Clinical death
Targeted temperature management
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Hypothermia was induced in non-fasted, female rats by placing animals in individual, cylindrical screen cages under crushed ice until a rectal temperature of 15 °C was attained. No anaesthetic or artificial ventilation was provided. Hypothermic animals were sacrificed after 0, 30, and 60 minutes' maintenance at this rectal temperature and metabolites were measured in blood and liver. It was observed that, as previously reported, hypothermia caused increases in blood packed cell volume, glucose and lactic acid levels, and plasma levels of inorganic phosphorus and total ketones. Maintenance of hypothermia for 30 or 60 minutes either caused no further change or accentuated the changes observed initially in these metabolites. Liver glycogen level decreased significantly after 30 minutes but returned to an almost normal level at 60 minutes. From these observations it is concluded that attainment of a "steady state" condition of hypothermia in non-fasted rats does not alter the pattern of metabolic changes observed in acute hypothermia of short duration.
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