[Pathophysiologic principles, emergency medical aspects and anesthesiologic measures in severe brain trauma].

In 60%-90% of cases head injury is a part of multisystem trauma and of very decisive importance for the post-traumatic prognosis. Hypoxia, hypercarbia, and hypotension increase the primary lesion and cause secondary brain damage. Therefore, emergency measures must be directed to the essentials of sustaining vital functions, i.e. intubation/ventilation/oxygenation and stabilization of the circulatory system. All trauma-specific measures should avoid additional increases in intracranial pressure or should decrease it if already elevated. Moderate hyperventilation not only causes cerebral vasoconstriction with a concomitant decrease in intracranial blood volume and intracranial pressure, but also partly restores the disturbed cerebral autoregulation, and is therefore an important part of the emergency care and anesthetic procedure in patients with severe head injuries. It is supplemented by analgesia and sedation to prevent intracranial pressure increases due to painful external stimuli. Elevation of the head and upper part of the body by 30 degrees causes a decrease in intracranial pressure by decreasing intracranial blood volume due to improved venous return from the brain; however, this measure is to be applied only in stable circulatory conditions. The head should be put in mid-position avoiding sideways rotation, flexion, and hyperextension. Osmotically active agents are only indicated in emergency situations when there are signs of clinical deterioration. High-dose barbiturate therapy is reserved as a "last resort", under intensive care conditions, for controlling an otherwise intractable intracranial pressure rise. Calcium antagonists have no indication in this context. Anesthesia in patients with severe head injury must involve only those techniques that do not further increase an already elevated intracranial pressure. As inhalational anesthetics, including nitrous oxide, elevate the intracranial pressure to varying extents due to cerebral vasodilation with a concomitant rise in intracranial blood volume, these substances have to be avoided whenever raised intracranial pressure cannot be excluded. Narcotics, benzodiazepines, small dosages of barbiturates, and long-lasting muscle relaxants can be regarded as useful.