effect of mild hypothermia on jugular venous bulb oxygen saturation and CSF glutamate in severe head trauma

Hypothermia has been used as a method of brain protection in patients with traumatic brain injury for many years. The protective effects of hypothermia are related to the inhibition of the excitatory amino acids [EAA] release including glutamate. The hypothermic decline of the cerebral metabolic rate of oxygen [CMRO[2]] is also another mechanism of brain protection because it maintains the aerobic metabolism of the brain. To study the effect of mild hypothermia on brain oxygenation and the release of the EAA glutamate in severe head trauma. Forty two patients [16 - 60 years old] with severe head trauma [Glasgow coma scale < 8] were classified according to the diagnosis by computed tomography into group 1 [global brain damage] [n=20] and group 2 [focal brain damage] [n=22] two cases in group 2 were died before completion of the study so they were excluded. The cerebrospinal [CSF] glutamate, the jugular venous bulb oxygen saturation, the jugular venous lactate, the Glasgow coma scale [GCS], the acute physiological and chronic health evaluation score [APACHE II] and the length of lCU stay and other hemodynamic variables were measured and recorded. Hypothermia decreased the cerebrospinal [CSF] glutamate, improved the jugular venous bulb oxygen saturation, decreased the jugular venous lactate, improved the Glasgow coma scale [GCS] and decreased the acute physiological and chronic health evaluation score [APACHE II], There were significant statistical differences [p < 0.001] in each group but there were no statistical significant differences between both groups. The length of ICU stay was shorter in the group 1 than in group 2. Mild Hypothermia is one of the mechanisms of brain protections through decreasing the level of the neurotoxic cerebrospinal excitatory amino acid glutamate and by improving the cerebral oxygenation and preventing the anaerobic metabolism by decreasing the level of serum lactate

Fever in brain death

Forty-one brain dead patients were included in this study. Information about age, sex, type of brain lesion and positive bacterial cultures was collected. Their temperature was recorded hourly from day 0 [day of brain stem testing] till they died [expired]. Two patients died [expired] on the same day of testing and the temperature of the remaining 39 patients was evaluated. Seven out of the 39 patients did not show any fever at all, while two patients were persistently febrile. The remaining 30 patients had some febrile bouts interchanging with the a febrile [normal and/or subnormal temperature] ones. So, the total number of patients who showed fever was 32 out of 39, whereas those who showed normal and/or subnormal temperature were 37 patients. Fever was not related to sex, type of brain lesion, positive bacterial cultures or the initial Glasgow coma scale [GCS] score. However, its pattern was related to age; young patients expressed more febrile bouts and their fever was maximally expressed more lately. Accordingly, fever in brain dead patients may not be as uncommon as previously suggested