[The use of hypothermia in intensive therapy].

The authors discuss the usefulness of therapeutic hypothermia for neuroprotection in patients with hypoxic cerebral damage. Although first reports on this method were published more than 50 years ago, it gained wider popularity at the end of 20th century. This popularity was related to the fact that deep hypothermia (below 30 degrees C) was displaced by mild hypothermia using higher temperatures (32-35 degrees C). The therapeutic benefit of mild hypothermia is based on the decrease of cerebral metabolism (5-7% per one degree Celsius). The ATP consumption by neurons is decreased despite the lack of glucose and oxygen associated with cardiac arrest, and membrane function is longer preserved. Hypothermia also prevents cerebral oedema, both of vascular and cytotoxic origin, and other reactions associated with reperfusion injury. Recently, the American Heart Association and European Resuscitation Council recommended the use of mild hypothermia (32-34 degrees C) in adult patients after ventricular fibrillation. Some clinical data also indicates that induced hypothermia reduces cerebral hypoxic ischemic injury. Randomized clinical trials in newborns with hypoxic ischemic encephalopathy confirm improved neurological outcomes and survival at 18 months of age with therapeutic hypothermia. The use of hypothermia after craniocerebral and spinal trauma, or ischemic brain damage is controversial, and not widely recommended. The authors describe various methods of inducing hypothermia in clinical settings; perhaps the most effective is intravenous infusion of cold fluids together with superficial cooling. Side effects and complications are discussed. They conclude that mild hypothermia can be regarded as a useful therapy in adult patients after VF cardiac arrest, and in neonates with hypoxic cerebral brain damage.