TY - CHAP M1 - Book, Section TI - Acute Management of the Brain Injury Patient A1 - Boucher, Bradley A. A1 - Wood, G. Christopher A2 - DiPiro, Joseph T. A2 - Yee, Gary C. A2 - Posey, L. Michael A2 - Haines, Stuart T. A2 - Nolin, Thomas D. A2 - Ellingrod, Vicki PY - 2020 T2 - Pharmacotherapy: A Pathophysiologic Approach, 11e AB - 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, 4th edition, 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 100 to 110 mm Hg depending on age) with an SBP goal of 120 to 140 mm Hg and reversal of hypoxemia are primary goals during the initial resuscitative and intensive care of patients with severe TBI. Nonpharmacologic management of intracranial hypertension includes raising the head of the bed 30°, and ventricular drainage if an extraventricular drain (EVD) is present. The principal monitoring parameter for patients with severe TBI within the intensive care environment is increased intracranial pressure (ICP). Cerebral perfusion pressure (CPP) is also a critical monitoring parameter and should be maintained between 60 and 70 mm Hg (8.0 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 management of intracranial hypertension should include analgesics, sedatives, and antipyretics; paralytics may be advantageous under selected circumstances. Specific pharmacologic 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. Numerous investigational strategies targeted at limiting injury and/or stimulating axonal repair following severe TBI have been employed; however, no proven therapeutic benefits have been identified. Use of phenytoin (alternatively levetiracetam) for the prophylaxis of posttraumatic seizures generally should be discontinued after 7 days if no seizures are observed. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/29 UR - accesspharmacy.mhmedical.com/content.aspx?aid=1182446446 ER -