عناية اصابات الرأس

• عناية

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• Rocuronium


  0.9-1.2 mg/kg administration achieves same intubating conditions as succinylcholine at 60-90 seconds, with no transient increase in ICP but muscle paralysis lasting 30-40 minutes
• CPP target range


  60-70 mm Hg in adults
• CPP target range for children

  40-50 mm Hg
• Maintenance of CPP at 60-70 mm Hg in the first 2-3 days after TBI is probably reasonable
• Hyperventilation


  Effectiveness in reducing ICP is well confirmed, but it is potentially deleterious and should not be overused as it can result in ischemia
• Prolonged prophylactic hyperventilation with PaCO2 of 25 mm Hg or less is not recommended
• Recommendations on hyperventilation


  • Hyperventilation is recommended as a temporizing measure for the reduction of elevated ICP
  • Hyperventilation should be avoided during the first 24 hours after injury when CBF is often critically reduced
  • If hyperventilation is used, Sjv02 or brain tissue PO2 measurements are recommended to monitor oxygen delivery
• Severe intracranial HTN


  Can result in secondary injury to the brain, due to ischemia produced by reducing CPP and it can also distort and compress the brainstem
• Sjv02 monitoring


  Has been used to guide the management of patients with TBI, as a marginal or inadequate CBF results in an increasing oxygen extraction, a widening arteriovenous content difference, and reduction of Sjv02
• Normal Sjv02 values


  Between 60% and 75%, with Sjv02 less than 50% for 5 minutes commonly accepted as constituting jugular desaturation
• Interventions to improve low Sjv02 values

  • Reducing hyperventilation
  • Increasing MAP
  • Inducing hypervolemia
• Pbt02


  Has been used to guide the management of both TBI and SAH, with a PbtO2 equal to or greater than 20-25 mm Hg viewed as normal, and values equal to or less than 10-15 mm Hg assumed to convey a substantial risk of hypoxic injury
• Fever


  Increases brain metabolism and has been demonstrated to increase brain injury, so aggressive treatment of fever, including acetaminophen and mechanical cooling, is recommended in patients with increased ICP
• TBI may produce coagulopathy through the systemic release of by-products from neuronal death such as tissue factor and phospholipids leading to disseminated intravascular coagulation, so coagulation parameters should be measured immediately in acute TBI patients and any abnormal values should be identified and treated
• Hyperglycemia


  Might produce an increase in neuronal metabolism and increase neuronal death after TBI due to increased tissue acidosis through anaerobic metabolism, the creation of free radicals, and increased blood brain barrier permeability, so the ideal blood glucose level should range from 80-180 mg/dl
• Fluid therapy


  Accurate fluid management may be complicated by continuing or concealed hemorrhage but every effort must be made to restore normovolemia & prevent hypertension, using clinical & laboratory assessment of volume status and invasive hemodynamic monitoring
• Maintenance fluid


  30-40ml/kg per day, with a mix of colloids and crystalloids probably appropriate in large-volume resuscitation (greater than half of the circulating volume) to prevent reduction of serum osmolarity and profound reduction of COP
• A chronic negative fluid balance, as can occur with the combination of modest fluid restriction and liberal use of osmotic diuretics, has been shown to be deleterious and should be avoided
• Hemoglobin level


  The minimal acceptable hemoglobin level should probably be more than 7 g/dL, with 9 g/dL suggested as a hazard threshold in patients with TBI based on observations of brain tissue PO2 (Pbt02)
• Cerebral perfusion pressure (CPP)

  The amount of pressure needed to maintain blood flow to the brain, regulated by the driving force of mean arterial pressure (MAP) and the opposing force of intracranial pressure (ICP)
• Calculating CPP


  CPP = MAP - ICP