Until the early 1980s, management of severe traumatic brain injury involved fluid restriction. This practice, accompanied by use of hyperosmolar therapy to treat cerebral oedema, often produced dehydration, which could be severe. Subsequent work identified special concerns with dehydration in patients with traumatic brain injury (ie, a reduction in cerebral perfusion pressure by hypotension produces cerebral vasodilation, exacerbating intracranial hypertension).2 Dehydration also increases the riskof acute renal failure, a complication that adds serious challenges to the management of patients with traumatic brain injury. These concerns with hypovolaemia and dehydration ushered in an era in which the production of a euvolaemic hyperosmolar state became the target in severe traumatic brain injury.
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