Abstract
A critical evaluation was done about the guidelines and effects of the hyperventilation maneuver on prevention and treatment of increased intracranial pressure (ICP) that follows severe traumatic brain injury (TBI). The prophylactic use of hyperventilation should be avoided after severe TBI acute phase, unless high venous O2 values are recorded at jugular bulb blood (SjO2), or to allow time when there are evidences of neurologic deterioration with posturing. The lack of cerebrovascular response to hyperventilation to low the ICP means that the blood brain barrier (BBB) function is extensively impaired. Then, hyperventilation may be used as a screening therapeutic test in acute severe TBI, since BBB impairment is the pointer that other available clinical procedures for high ICP control (sedation, paralysis and osmotic diuretics) are not workable. A new pathogenetic hypothesis about traumatic brain edema and its therapeutic approach is presented.
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