++
KEY CONCEPTS
Cerebral ischemia is the key pathophysiologic event that triggers secondary neuronal injury following severe traumatic brain injury (TBI). Intracellular calcium accumulation 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 100-110 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 and 50 mm Hg [5.3 and 6.7 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.
++
BEYOND THE BOOK
Watch the video entitled “Overview of Traumatic Brain Injury (TBI)” (https://www.youtube.com/watch?v=T0WBMM7WKL4) presented by Dr. Christopher Wolf and moderated by Brent Ghan at the University of Missouri School of the Health Professions. This 7.5-minute video provides a general overview of human brain anatomy and physiology and a succinct introduction to the more detailed pathophysiology outlined in the chapter and a context for understanding TBI pharmacologic and nonpharmacologic management. This includes TBI pathophysiology including cerebral contusions, diffuse axonal injury, secondary brain injury, in addition to TBI recovery.
++
TBI is one of the leading causes of death and disability in the United States.1 A focus on TBI prevention, improved acute care, and rehabilitation remain national priorities. This chapter summarizes TBI epidemiology and pathophysiology, and highlights the major guidelines ...