- 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 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 to 35 mm Hg [4.0 to 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 (i.e., 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 (e.g., calcium antagonists, glutamate antagonists, antioxidants, free-radical scavengers, and progesterone) targeted at interrupting the pathophysiologic cascade of events occurring following severe TBI have been employed, but no proven therapeutic benefits have been identified.
On completion of the chapter, the reader will be able to:
Describe the most common causes of severe traumatic brain injury (TBI) and the typical age distribution for patients sustaining such injuries.
Differentiate between primary and secondary brain injury.
Explain the central role of ischemia in triggering secondary neuronal injury following severe TBI.
Compare and contrast the processes of cellular necrosis and apotosis along the spectrum of secondary neuronal injury.
Discuss the cascade of biochemical events proposed to occur following a severe TBI.
Evaluate the neurological state of a severe brain injury patient using the Glasgow Coma Scale (GCS) and factors that may affect the GCS in addition to TBI.
Summarize the impact of the Brain Trauma Foundation Guidelines for the Management of Severe Brain Injury on the consistency of care for severe TBI patients.
Outline several ...