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 - Talbert, Robert L. A2 - Yee, Gary C. A2 - Matzke, Gary R. A2 - Wells, Barbara G. A2 - Posey, L. Michael Y1 - 2017 N1 - T2 - Pharmacotherapy: A Pathophysiologic Approach, 10e 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, 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. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/29 UR - accesspharmacy.mhmedical.com/content.aspx?aid=1145190801 ER -