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KEY CONCEPTS

KEY CONCEPTS

  • Image not available. 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.

  • Image not available. 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.

  • Image not available. 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.

  • Image not available. Nonpharmacologic management of intracranial hypertension includes raising the head of the bed 30°, and ventricular drainage if an extraventricular drain (EVD) is present.

  • Image not available. 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.

  • Image not available. Nonspecific pharmacologic management of intracranial hypertension should include analgesics, sedatives, and antipyretics; paralytics may be advantageous under selected circumstances.

  • Image not available. 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.

  • Image not available. 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.

  • Image not available. Use of phenytoin (alternatively levetiracetam) for the prophylaxis of posttraumatic seizures generally should be discontinued after 7 days if no seizures are observed.

PATIENT CARE PROCESS

Patient Care Process for Acute Management of the Brain Injury Patient

Image not available.

Collect

  • Glasgow Coma Scale (GCS: Table 75-1), vital signs, physical exam and head computed tomography (CT) scan findings, arterial blood gases, ICP and CPP (if available), laboratory data (see "Clinical Presentation" section)

  • Prior and current medications, including alcohol and illicit drugs

Assess

  • Consistency between with the GCS/physical exam and injuries on head CT scan (ie, could there be other reasons for the neurologic deficit such as intoxication)

  • ICP (goal <22 mmHg [2.9 kPa]) and CPP (goal 60-70 mm Hg [8.0-9.3 kPa]) (Fig. 75-2)

  • Need for general ICU supportive care including: mechanical ventilation/appropriate oxygenation, stress ulcer prophylaxis, and sedation/analgesia

  • For VTE prophylaxis, it is important to determine if pharmacologic prophylaxis is contraindicated due to intracranial bleeding

  • Need for other supportive care measures more specific to TBI including: spine immobilization, seizure prophylaxis, avoiding fever and excessive hyperglycemia, appropriate fluid therapy with a goal of euvolemia, ...

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