Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. Mild hypothermia (34-36°C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 ± 0.4°C in the normothermic group to 38.2 ± 0.5°C in the hyperthermic group, 35.3 ± 0.5°C in the mild therapeutic hypothermia group, and 34.3 ± 1.5°C in the hypothermia group without active cooling. The mean ?Tbr-rect was positive for patients with a Tbr above 36.0°C (0.0 ± 0.5°C) and negative for patients during mild therapeutic hypothermia (-0.2 ± 0.6°C) and also in those with a brain temperature below 36°C without active cooling (0.8 ± -1.4°C)-the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0°C and 37.5°C was 37.8 ± 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0°C and a negative brain-rectal temperature difference (17.1 ± 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.
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N2 – Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. Mild hypothermia (34-36°C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 ± 0.4°C in the normothermic group to 38.2 ± 0.5°C in the hyperthermic group, 35.3 ± 0.5°C in the mild therapeutic hypothermia group, and 34.3 ± 1.5°C in the hypothermia group without active cooling. The mean ?Tbr-rect was positive for patients with a Tbr above 36.0°C (0.0 ± 0.5°C) and negative for patients during mild therapeutic hypothermia (-0.2 ± 0.6°C) and also in those with a brain temperature below 36°C without active cooling (0.8 ± -1.4°C)-the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0°C and 37.5°C was 37.8 ± 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0°C and a negative brain-rectal temperature difference (17.1 ± 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.
AB – Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood caffmos online flow, and outcome after 3 months. Mild hypothermia (34-36°C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 ± 0.4°C in the normothermic group to 38.2 ± 0.5°C in the hyperthermic group, 35.3 ± 0.5°C in the mild therapeutic hypothermia group, and 34.3 ± 1.5°C in the hypothermia group without active cooling. The mean ?Tbr-rect was positive for patients with a Tbr above 36.0°C (0.0 ± 0.5°C) and negative for patients during mild therapeutic hypothermia (-0.2 ± 0.6°C) and also in those with a brain temperature below 36°C without active cooling (0.8 ± -1.4°C)-the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0°C and 37.5°C was 37.8 ± 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0°C and a negative brain-rectal temperature difference (17.1 ± 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.