Summary

  1. There is Level 1b evidence that head elevations of 15°, 30°, and 45° effectively reduce elevated intracranial pressure post ABI when compared to a flat position.
     
  2. There is conflicting (Level 1b and Level 4) evidence as to whether head elevation improves cerebral perfusion pressure post ABI. 
     
  3. There is Level 1a evidence that therapeutic hypothermia effectively reduces elevated intracranial pressure post ABI.
     
  4. There is Level 1a evidence that therapeutic hypothermia is associated with an increased incidenceof pneumonia and other complications post ABI.
     
  5. There is conflicting (Level 1a and Level 2 evidence) as to whether therapeutic hypothermia reduces mortality and improves long-term outcomes post ABI.
     
  6. There is Level 1b evidence that ventricular cerebrospinal fluid drainage effectively lowers elevated intracranial pressure post ABI.
     
  7. There is conflicting (Level 2 and Level 3) evidence as to whether an external ventricular drain yields lower intracranial pressure, better long-term outcomes, reduced therapeutic intensity, and fewer complications than an intraparenchymal fiberoptic monitor post ABI.
     
  8. There is Level 3 evidence that continuous ventricular cerebrospinal fluid drainage is more effective than intermittent drainage at lowering elevated intracranial pressure post ABI.
     
  9. There is Level 4 evidence that lumbar cerebrospinal fluid drainage effectively lowers elevated intracranial pressure post ABI.
     
  10. There is Level 1a evidence that decompressive craniectomy effectively reduces elevated intracranial pressure post ABI.
     
  11. There is conflicting evidence (Level 1a) as to whether decompressive craniectomy is associated with higher Glasgow Outcome Scale scores and lower mortality when compared to standard care.
     
  12. There is Level 2 evidence that standard craniectomy with a larger bone flap is more effective than limited craniectomy with a smaller bone flap in lowering elevated intracranial pressure and yielding higher Glasgow Outcome Scale scores.
     
  13. There is conflicting evidence (Level 3) as to whether decompressive craniectomy improves long-term outcomes when compared to craniotomy.
     
  14. There is Level 4 evidence that hyperventilation lowers elevated intracranial pressure post TBI.
     
  15. There is Level 4 evidence that hyperoxia counteracts the detrimental effects of brief hyperventilation post TBI.
     
  16. There is Level 1b evidence that tromethamine counteracts the detrimental effects of prolonged hyperventilation and yields better outcomes than hyperventilation alone in severe TBI.
     
  17. There is Level 4 evidence that continuous rotational therapy does not improve intracranial pressure following severe TBI.
     
  18. There is Level 4 evidence that the prone position may increase intracranial pressure but improve cerebral oxygenation post ABI.
     
  19. There is Level 4 evience that the use of hypertonic saline is effective in increasing cerebral perfusion pressure.  
     
  20. There is Level 1b evidence that the use of hypertonic saline results in similar clinical outcomes when compared to Ringer's lactate solution.
     
  21. There is Level 2 evidence that the use of hypertonic saline is similar to Ringer's lactate solution and sodium bicarbonate in lowering elevated intracranial pressure.
     
  22. There is Level 1b evidence that the use of hypertonic saline results in lower rates of mortality when compared to albumin.
     
  23. There is conflicting evidence (Level 1b) as to whether hypertonic saline lowers elevated intracranial pressure more effectively than mannitol.
     
  24. There is Level 2 evidence that the use of hypertonic saline is more effective than mannitol in increasing CPP, Cerebral Blood Flow, and Brain Tissue Oxygen Tension.
     
  25. There is Level 4 evidence that mannitol is effectie in controlling elevated intracranial pressure.    
     
  26. There is Level 2 evidence that early administration of mannitol does not effectively lower elevated intracranial pressure, but does not adversely affect blood pressure. 
     
  27. There is Level 2 evidence that high-dose mannitol is more effective than conventional mannitol in reducing mortality rates and improving clinical outcomes.
     
  28. There is Level 1b evidence that mannitol is no more effective than hypertonic saline in controlling elevated intracranial pressure.
     
  29. There is Level 1b evidence that mannitol is less effective than sodium lactate in controlling elevated intracranial pressure.
     
  30. There is Level 1b evidence that propofol reduces intracranial pressure and the need for other intracranial pressure interventions when used in conjunction with morphine compared to morphine alone.
     
  31. There is Level 1b evidence that a high does of propofol improves intracranial pressure and cerebral perfusion pressure compared to a low dose of propofol.
     
  32. There is Level 2 evidence that propofol is not significantly different from dexmedetomidine in its effect on intracranial pressure. 
     
  33. There is Level 2 evidence that propofol is not significantly different from morphine and midazolam in its effect on intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and long-term outcomes.
     
  34. There is Level 4 evidence that propofol improves intracranial pressure and cerebral perfusion pressure.
     
  35. There is Level 4 evidence that midazolam reduces mean arterial pressure, cerebral perfusion pressure, and systolic blood pressure, but has no effect on intracranial pressure.  
     
  36. There is Level 2 evidence that midazolam is not different from propofol in its effect on intracranial pressure or cerebral perfusion pressure.
     
  37. There is Level 1b evidence that midazolam is not different than propofol in its effect on long-term outcomes.
     
  38. There is Level 1a evidence that morphine, sufentanil, and alfentanil result in increased intracranial pressure post ABI.
     
  39. There is conflicting evidence (Level 1b) regarding the effects of fentanyl on intracranial pressure post ABI.
     
  40. There is conflicting evidence (Level 2) that remifentanil does not affect intracranial pressure post ABI.
     
  41. There is conflicting (Level 1b, Level 2, Level 3) evidence regarding the efficacy of pentobarbital in improving intracranial pressure over conventional management measures.
     
  42. There is Level 2 evidence that thiopental is more effective than pentobarbital for controlling elevated intracranial pressure.
     
  43. There is Level 2 evidence that pentobarbital is not more effective than mannitol for controlling elevated intracranial pressure.
     
  44. There is Level 3 evidence that high-dose barbiturate results in increased length of stay and does not improve outcomes when compared to low-dose barbiturate.
     
  45. There is Level 4 evidence that barbiturate therapy may cause reversible leukopenia, granulocytopenia, and systemic hypotension, as well as supressed bone marrow production.
     
  46. There is Level 4 evidence that a combination barbiturate therapy and therapeutic hypothermia may result in improved clinical outcomes up to 1 year post injury. 
     
  47. There is Level 1a evidence that methylprednisolone increases mortality rates in patients post ABI and should not be used.
     
  48. There is Level 1b evidence that dexamethasone does not lower elevated intracranial pressure levels and may worsen outcomes.
     
  49. There is Level 2 evidence that triamcinolone may improve outcomes in patients with a GCS<8 and a focal lesion.
     
  50. There is Level 3 evidence that glucocorticoid administration may increase the risk of developing first late seizures.
     
  51. There is Level 1a evidence that progesterone does not lower intracranial pressure levels post TBI when compared to placebo.
     
  52. There is Level 1a evidence that progesterone is not associated with adverse events when compard to placebo.    
     
  53. There is conflicting evidence (Level 1a) as to whether progesterone improves long-term outcomes and reduces mortality post TBI when compared to placebo. 
     
  54. There is Level 1a evidence that Bradycor is effective at preventing acute elevations in intracranial pressure and reducing therapeutic intensity levels post ABI when compared to placebo
     
  55. There is Level 1b evidence that Anatibant is no more effective than placebo in improving long-term outcomes and may result in serious adverse events post ABI.
     
  56. There is Level 4 evidence that dimethyl sulfoxide temporarily reduces intracranial pressure elevations that may not be sustained over the long-term.
     
  57. There is Level 1b evidence that conivaptan lowers elevated intracranial pressure post ABI when compared to standard acute are alone (e.g. osmolar therapy, sedation, analgesia).
     
  58. There is Level 1b evidence that vasopressin and catecholamine are similarly effective in lowering elevated intracranial pressure post ABI.
     
  59. There is Level 4 evidence that paracetamol effectively lowers elevated intracranial pressure post ABI.  
     
  60. There is Level 1a evidence that multisensory stimulation and familiar auditory stimulation are more effective at improving consciousness and cognitive function post ABI than standard care. 
     
  61. There is Level 1b evidence that multisensory stimulation delivered five times per day is more effective at improving consciousness and cognitive function post ABI than standard care.
     
  62. There is Level 1b evidence that multisensory stimulation delivered by a family member is more effective at improving consciousness and cognitive function post ABI when compared to stimulation delivered by a nurse
     
  63. There is Level 2 evidence that specific, directed, and regulated sensory stimulation is more effective at improving consciousness and cognitive function post ABI than indiscriminate stimulation
     
  64. There is Level 2 evidence that sensory stimulation may improve clinical outcomes, physiological parameters, and behaviours indicative of consciousness post ABI.
     
  65. There is Level 4 evidence that music therapy as an adjunct to other modes of sensory stimulation may be used to promote emergence from coma post ABI.
     
  66. There is Level 1b evidence that median nerve electrical stimulation does not improve emergence from coma post ABI when compared to sham stimulation. 
     
  67. There is Level 1a evidence that amantadine effectively improves consciousness, cognitive function, and disability when compared to placebo.
     
  68. There is Level 1b evidence that citicoline is not effective at restoring consciousness post ABI.
     
  69. There is Level 2 evidence that antiepileptics are not effective at restoring consciousness post ABI.