Therapeutic hypothermia in traumatic brain injury

Jonathan Kj Rhodes

doi:10.1186/cc11269

Abstract

Hypothermia has profound effects on the brain function but importantly is potentially protective against both focal and global injuries. Aspects of the biochemical response to acute ischaemia and trauma, which are associated with poor outcome, can be inhibited by cooling. Unlike many pharmacological treatments that tend to antagonise a single neurochemical process, hypothermia offers a simple method of inhibiting multiple pathological processes simultaneously. It therefore has the potential, if applied correctly, to improve outcomes after acute brain injuries, where drug trials have so far failed. The systemic cooling of patients after acute brain injury is an established treatment modality in many neuro-ICUs. It is a strategy for protecting the injured brain that makes intuitive sense and can reduce both intracranial pressure and the potential for ischaemic secondary insults. Basic science evidence also suggests that cooling can attenuate many secondary biochemical cascades that are activated after acute injury. However, despite these multiple lines of supportive evidence there is as yet no confirmation from a high-quality randomised controlled trial that prophylactic hypothermia improves outcome or reduces mortality. This talk will look at the potentially beneficial effects of hypothermia on the biochemistry of acute brain injury, consider the reasons for the failure to demonstrate clinical efficacy and review the supportive data from meta-analysis, suggesting how hypothermia might be best delivered. Finally I will discuss EuroTherm3235, a European Society of Intensive Care Medicine funded multicentre randomised controlled trial investigating prophylactic hypothermia in traumatic brain injury, which draws on the lessons from the available literature.

Highlights

A1 Update on therapeutic temperature management Gregor Broessner1*, Marlene Fischer1, Gerrit Schubert2, Bernhard Metzler3, Erich Schmutzhard1 1Department of Neurology, Medical University, Innsbruck, Austria; 2Department of Neurosurgery, Medical University, Innsbruck, Austria; 3Department of Cardiology, Medical University, Innsbruck, Austria Critical Care 2012, 16(Suppl 2):A1It is a pleasure to announce the 2nd Innsbruck Hypothermia Symposium
Mild therapeutic hypothermia after cardiac arrest has become standard in post-resuscitation care in many hospitals as it is recommended by current guidelines
Some authors report that both b1-adrenoceptors and aadrenoceptors increase their sensitivity to catecholamines during hypothermia [18,20,21,22] as b1-adrenoceptor activity was potentiated by low temperature, and they claim the existence of hypothermia-induced supersensitivity and increased agonist activity for b1-adrenoceptors

Summary

Introduction

A1 Update on therapeutic temperature management Gregor Broessner1*, Marlene Fischer, Gerrit Schubert, Bernhard Metzler, Erich Schmutzhard1 1Department of Neurology, Medical University, Innsbruck, Austria; 2Department of Neurosurgery, Medical University, Innsbruck, Austria; 3Department of Cardiology, Medical University, Innsbruck, Austria Critical Care 2012, 16(Suppl 2):A1It is a pleasure to announce the 2nd Innsbruck Hypothermia Symposium. It could be shown that hypothermia may lead to increased rate of infections, hypotension, shivering, disturbances in blood clotting, rewarming injuries and significant changes in pharmacokinetics and pharmacodynamics possibly limiting outcome effects of the treated patients [4,5,6,7,8]. Aggressive treatment of fever in the ICU without risk elevation through the side effects of therapeutic hypothermia led to the concept of controlled prophylactic normothermia This concept is based upon strict control of body core temperature with a target of 36.5°C beginning as early as possible with the goal of complete fever prevention. All planned measures to reduce reperfusion damage before revascularization should preferably be applied in a very short time

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