ABSTRACT
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