• P J D Andrews, B Harris, and G D Murray.
• Department of Anaesthesia, Intensive Care and Pain Management, University of Edinburgh, UK. p.andrews@ed.ac.uk
• Br J Anaesth. 2005 Mar 1;94(3):330-5.

BackgroundPyrexia is common after brain injury; it is generally believed to affect outcome adversely and the usual clinical methods of reducing temperature are not effective. The normal physiological mechanisms of brain cooling are heat loss from the upper airways and through the skull, and these can produce selective brain cooling.MethodsAir at room temperature and humidity was continuously administered to 15 brain-injured, intubated and mechanically ventilated patients via a sponge-tipped oxygen catheter in each nostril at a combined rate of 115 ml kg(-1) min(-1). Brain temperature was measured using a pressure-temperature Camino catheter which is designed to site the thermistor 1 cm into the parenchyma in the frontal lobe. Oesophageal temperature was measured using an oesophageal stethoscope with a thermistor. After establishing baseline for 30 min, patients were randomized to receive airflow or no airflow for 6 h and then crossed over for a further 6 h.ResultsAirflow replicating normal resting minute volume did not produce clinically relevant or statistically significant reductions in brain temperature [0.13 (SD 0.55) degrees C; 95% CI, 0.43-0.17 degrees C]. However, we serendipitously found some evidence of selective brain cooling via the skull, but this needs further substantiation.ConclusionsA flow of humidified air at room temperature through the upper respiratory tracts of intubated brain-injured patients did not produce clinically relevant or statistically significant reductions in brain temperature measured in the frontal lobe.

31 keywords...

hide…