title: Therapeutic Hypothermia Reduces Intracranial Pressure and Partial Brain Oxygen Tension in Patients with Severe Traumatic Brain Injury: Preliminary Data from the Eurotherm3235 Trial.
abstract: Traumatic brain injury (TBI) is a significant cause of disability and death and a huge economic burden throughout the world. Much of the morbidity associated with TBI is attributed to secondary brain injuries resulting in hypoxia and ischemia after the initial trauma. Intracranial hypertension and decreased partial brain oxygen tension (PbtO2) are targeted as potentially avoidable causes of morbidity. Therapeutic hypothermia (TH) may be an effective intervention to reduce intracranial pressure (ICP), but could also affect cerebral blood flow (CBF). This is a retrospective analysis of prospectively collected data from 17 patients admitted to the Western General Hospital, Edinburgh. Patients with an ICP >20 mmHg refractory to initial therapy were randomized to standard care or standard care and TH (intervention group) titrated between 32°C and 35°C to reduce ICP. ICP and PbtO2 were measured using the Licox system and core temperature was recorded through rectal thermometer. Data were analyzed at the hour before cooling, the first hour at target temperature, 2 consecutive hours at target temperature, and after 6 hours of hypothermia. There was a mean decrease in ICP of 4.3±1.6 mmHg (p<0.04) from 15.7 to 11.4 mmHg, from precooling to the first epoch of hypothermia in the intervention group (n=9) that was not seen in the control group (n=8). A decrease in ICP was maintained throughout all time periods. There was a mean decrease in PbtO2 of 7.8±3.1 mmHg (p<0.05) from 30.2 to 22.4 mmHg, from precooling to stable hypothermia, which was not seen in the control group. This research supports others in demonstrating a decrease in ICP with temperature, which could facilitate a reduction in the use of hyperosmolar agents or other stage II interventions. The decrease in PbtO2 is not below the suggested treatment threshold of 20 mmHg, but might indicate a decrease in CBF.
authors.affiliation: 1 Center for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kindgom.
authors.forename: Liam M C
authors.initials: LM
authors.lastname: Flynn
authors.affiliation: 2 Department of Anesthesia and Critical Care, University of Edinburgh and NHS Lothian , Western General Hospital, Edinburgh, United Kingdom .
authors.forename: Jonathan
authors.initials: J
authors.lastname: Rhodes
authors.affiliation: 1 Center for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kindgom.
authors.forename: Peter J D
authors.initials: PJ
authors.lastname: Andrews
mesh_terms: D000328:Adult; D001930:Brain Injuries / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D005260:Female; D006801:Humans; D007036:Hypothermia, Induced / Q000009:adverse effects / Q000379:methods; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D019586:Intracranial Hypertension / Q000209:etiology; D007427:Intracranial Pressure; D008297:Male; D010101:Oxygen Consumption; D015599:Trauma Severity Indices; D016896:Treatment Outcome