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Mild therapeutic hypothermia to improve neurologic outcome after cardiac arrest

Objective

An estimated 7 million people in the European Union suffer from brain damage due to cardiac arrest, stroke, head trauma or disease. Recovery without residual neurologic damage after cardiac arrest with global cerebral ischemia is still a rare event. Severe impairment of bodily or cognitive functions is often the result. The individual, emotional and social aspects of brain damage and rehabilitation are seldom taken into account. Efforts to improve the prevention of brain damage immediately after successful resuscitation of patients are missing. Patient recruitment for a prospective randomized study in one center will not be enough. In Europe only few centers oriented in clinical resuscitation research are existing. Therefore progress in this area clearly depends on the cooperative interaction of these emergency medical service systems.
The efficacy of hypothermia in preserving neurologic function when instituted before and during certain no - flow cardiovascular states has been well documented both clinically and experimentally since the 1950's. Most studies have used moderate to deep hypothermia in order to demonstrate these protective effects. Considering the use of hypothermia for preservation and resuscitation, the lack of controlled outcome trials, the long period of time required to reach therapeutic hypothermia, and the incidence of rewarming complications such as infection, arrhythmia and coagulopathy have made it difficult to apply these methods to emergency situations such as cardiac arrest. Recent experimental evidence in dogs has shown that hypothermia induced after cardiac arrest does indeed mitigate the effects of the post resuscitation syndrome and improve neurologic function. More importantly, such benefits can be demonstrated with mild hypothermia, thus minimizing complications and requiring less time for induction of hypothermia.

In a three year randomized, prospective, multicenter clinical trial we expect that mild therapeutic cerebral hypothermia (32 -34 °C tympanic temperature) will improve neurologic outcome after prolonged cardiac arrest (cerebral performance category after 6 months) without causing deleterious side effects. We are planing to lower brain temperature by 3 - 5 °C immediately after admission of the patient to the emergency department and to continue cooling for at least 24 hours post-arrest in conjunction with advanced cardiac life support. The cooling technique chosen will be external head cooling with a cooling device in conjunction with a blanket and total body cooling with a mattress.
External auditory canal temperature e.g. tympanic membrane temperature changes could provide an approximation to brain temperatures. Therefore, before a central pulmonary artery thermistor probe will be inserted, we are planning to monitor infrared tympanic thermometry. Temperature monitoring is needed to avoid temperatures below 30 °C.
Mild hypothermia may prove to be an important and secure component for cerebral preservation and resuscitation during and after global ischemia. Mild hypothermia may prove to be a useful method of cerebral resuscitation after global ischemic states and therefore promote the prevention of neuro - mental diseases.

Funding Scheme

CSC - Cost-sharing contracts

Coordinator

Universität Wien

Participants (2)

Algemeen Ziekenhuis St.Jan
Belgium
Address
10,Ruddershove
8000 Brugge
University of Helsinki
Finland
Address
4,Haartmaninkatu
00290 Helsinki