Chapter 58: Acute Management of the Brain Injury Patient

KEY CONCEPTS

• Cerebral ischemia is the key pathophysiologic event triggering secondary neuronal injury following severe traumatic brain injury (TBI). Intracellular accumulation of calcium is postulated to be a central pathophysiologic process in amplifying and perpetuating secondary neuronal injury via inhibition of cellular respiration and enzyme activation.

• Guidelines for the Management of Severe Brain Injury, published by the Brain Trauma Foundation (BTF)/American Association of Neurological Surgeons (AANS), serve as the foundation on which clinical decisions in managing adult neurotrauma patients are based; comparable guidelines for infants, children, and adolescents have also been published.

• Correcting and preventing early hypotension (systolic blood pressure [SBP] less than 90 mm Hg) and hypoxemia (PaO₂ less than 60 mm Hg [8.0 kPa]) are primary goals during the initial resuscitative and intensive care of severe TBI patients.

• Nonpharmacologic treatment in the management of intracranial hypertension includes raising the head of the bed 30°, short-term mild hyperventilation (PaCO₂ 30-35 mm Hg [4.0-4.7 kPa]), ventricular drainage if a ventriculostomy is present, and decompressive surgery.

• The principal monitoring parameter for severe TBI patients within the intensive care environment is intracranial pressure (ICP). Cerebral perfusion pressure (CPP) is also a critical monitoring parameter and should be maintained between 50 and 70 mm Hg (6.7 and 9.3 kPa) (greater than 40 mm Hg [5.3 kPa] in pediatric patients) through the use of fluids, vasopressors, and/or ICP normalization therapy.

• Nonspecific pharmacologic treatment in the management of intracranial hypertension should include analgesics, sedatives, antipyretics, and paralytics under selected circumstances.

• Specific pharmacologic treatment in the management of intracranial hypertension includes mannitol, hypertonic saline, furosemide, and high-dose pentobarbital. Neither routine use of corticosteroids nor aggressive hyperventilation (ie, PaCO₂ less than 25 mm Hg [3.3 kPa]) should be used in the management of intracranial hypertension.

• Use of phenytoin for the prophylaxis of posttraumatic seizures usually should be discontinued after 7 days if no seizures are observed.

• Numerous investigational strategies targeted at limiting injury and/or stimulating axonal repair following severe TBI have been employed, but no proven therapeutic benefits have been identified.