Hypothermia Hypothermia and barbiturate anesthesia fairly consistently reduce ICP but relatively few patients respond to such measures for long and their clinical outcome is not improved. The main problem, aside from the difficulty maintaining lower body temperatures, is that rewarming induces substantial brain swelling and a return of ICP to prior levels or higher. An early randomized controlled trial of cooling adult patients with severe closed head injury (Glasgow Coma Scale scores of 3 to 7) to 33°C (91.4°F) for 24 h appeared to hasten neurologic recovery and may have modestly improved outcome (Marion et al), but a larger and better-conducted study led by Clifton showed that attaining hypothermia of 33°C (91.4°F) within 8 h of injury failed to improve outcome and this approach cannot be endorsed except in special circumstances. A trial reported by Andrews and colleagues came to the same conclusion when hypothermia of 32 to 35°C was added to standard treatment for raised ICP. The same lack of effect has been shown in studies with children (Hutchinson et al, 2008).
Although barbiturates lower ICP, they lower the blood pressure as well; hence, they may diminish cerebral perfusion. However, an uncontrolled series by Marshall and coworkers (1979) claimed improved survival by using barbiturates even in cases where the ICP exceeded 40 mm Hg. The more definitive randomized study by Eisenberg and associates showed no benefit from barbiturate-induced anesthesia in head-injured patients, and this class of drugs has been largely abandoned except for brief, acute control of ICP while other measures are being instituted.
Glucocorticoids Several controlled studies have established that the administration of high-dose steroids does not improve the clinical outcome of severe head injury. Eclipsing smaller prior studies was the well-designed Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage (CRASH) trial, conducted in more than 10,000 adults and controlled for varying degrees of injury as judged by the Glasgow Coma Scale and imaging features. The effect of the infusion of methylprednisolone 2 g, followed by 0.4 g/h for 48 h, favored survival in the untreated patients by a small but clear margin, leading to the current recommendation that steroids not be used routinely following head injury.
Blood pressure management The management of posttraumatic systemic hypertension represents a difficult problem. Within hours after head injury, the sympathoadrenal response and elevation of blood pressure recedes spontaneously in a matter of a few hours or days. Unless the blood pressure elevation is extreme (greater than 180/95 mm Hg), it can be disregarded in the early stages. In animal experiments, it has been found that severe hypertension leads to increased perfusion of the brain and an augmentation of the edema surrounding contusions and hemorrhages. As mentioned earlier, edema is the main element in the genesis of brain swelling and of raised ICP in most head-injured patients (Marmarou et al). This reflects a failure of autoregulatory vascular mechanisms, with resulting transudative edema in damaged areas of the brain. The control of high blood pressure must be balanced against the risk of reducing cerebral perfusion pressure and the observation that even a brief period of mild hypotension may provoke a cycle of cerebral vasodilatation, increased cerebral blood volume, and elevated ICP in the form of plateau waves (Rosner and Becker). Observations such as these emphasize the need for immediate correction of hypotension in severely head-injured patients.