Relationship between brain temperature, brain chemistry and oxygen delivery after severe human head injury: The effect of mild hypothermia

Abstract

We studied brain temperature and the effect of mild hypothermia in 58 patients after severe head injury (SHI). Brain tissue oxygen tension (p_tiO₂), carbon dioxide tension (p_tiCO₂), tissuie pH (pH_ti) and temperature (T_br) were measured using a multiparameter probe. Microdialysis was performed to measure glucose, lactate, glutamate, and aspartate in the extracellular fluid. Mild hypothermia (34° – 36°C) was employed in 33 selected patients who had persistent increased intracranial pressure (ICP > 20 mmHg). Mild induced hypothermia decreased brain oxygen significantly from 33 ± 24 mmHg to 30 ± 22 mmHg (p < 0.05). The p_tiCO₂ (46 ± 8 mmHg) was also significantly lower during mild hypothermia (40.4 ± 4.0 mmHg), p < 0.0001). The pH _i increased from 7.13 ± 0.15 to 7.24 ± 0.10 (p < 0.0001) under hypothermic conditions. Induced hypothermia may protect patients from secondary ischemic events by lowering the critical p_tiO₂ threshold, reducing anaerobic metabolism, and decreasing the release of excitatory aminoacids. However, patients with spontaneous brain hypothermia on admission (T_br < 36.0°C) showed significantly higher levels of glutamate as well as lactate, compared to all other patients, and had a worse outcome. Spontaneous brain hypothermia carries a poor prognosis, and was characterized by markedly abnormal brain metabolic indices. [Neurol Res 2002; 24: 161-168]

Keywords:

• BRAIN OXYGEN
• EXCITATORY AMINOACIDS
• MILD HYPOTHERMIA
• SEVERE HEAD INJURY