Traumatic Brain Injury (Neuroanesthesia)



When resuscitating neurosurgical patients with other trauma, even in the presence of severe head injury, adequate volume resuscitation is far more important than the fear of excessive fluid overload [Andrews]

Cardiopulmonary concerns

Blood pressure management is controversial – often hypertension is secondary to pain, which should be treated. Other potential causes include cerebral ischemia and elevated ICP – if analgesia does not work, use short-acting beta blockers in most cases to keep SBP < 180 mm Hg [Andrews] – when cerebral ischemia or ICP is an issue, keep SBP < 220 mm Hg but do not treat until then

Anesthetic Considerations

Podcast on with Dr. Michael Todd on airway management in cervical spine injury, the DECRA trial, hypothermia and neuroprotection:  

Always suspect cervical spine injury and full stomach. Comatose patients require intubation to prevent hypercarbia and subsequent ICP changes. Awake intubation can often not be performed because they require significant cooperation. Hypotension and hypoxemia have been proven to correlate with poor outcomes. Postoperatively these patients often remain intubated, as ICP must be controlled and they often have reduced airway protection. Beware DIC in these patients, as it is a common complication of traumatic brain injury


A-line is mandatory. TLC is recommended. A CVP < 5 mm Hg suggests dehydration in this patient population and should likely be corrected (no data). In elderly patients with ventricular disease, spinal cord injury patients, and patients with ARDS, Andrews recommends a PA catheter and maintenence of wedge 12-14 mm Hg. All severe TBI patients should be intubated. Continuous hyperventilation loses its effect as soon as 4-6 hours [Andrews] but always by 20-24 hours as by this time serum and CSF pH will normalize [Br J Anesth 46: 348, 1974; Scand J Clin Lab Invest 22: 247, 1968] – return of PaCO2 to more normal values then leads to overdilation of arterioles and subsequent elevations in ICP, thus continuous hyperventilation should be avoided. In an experiment involving seven hyperventilated rabbits, vessel diameter was reduced by 13% at 4 hours, 3% at 24 hours, and at 52 hours the vessel diameters were 105% of baseline at a pCO2 of 25 mm Hg and 122% at a pCO2 of 38 mm Hg [J Neurosurg 69: 923, 1988]

Intracranial Pressure

To manage ICP, remove all potential underlying causes (hematoma). For medical management – raise the head of bed, drain CSF, give temporary doses of IV mannitol and/or hyperosmolar therapy, and sedate with propfol (shown by Class I evidence to be superior to morphine in managing elevated ICP [Bullock R: Guidelines]). Limit free water intake, and consider diuretics, ex. furosemide. The goal is not dehydration but euvolemia – Na 135-145 and mOsm 300-330 are optimal, as is a CVP of 2-5 mm Hg

Barbiturate coma may be indicated for failure of all other methods, however, based on three available randomized controlled trials, the 2004 Cochrane Database review stated “There is no evidence that barbiturate therapy in patients with acute severe head injury improves outcome. Barbiturate therapy results in a fall in blood pressure in one of four treated patients. The hypotensive effect of barbiturate therapy will offset any ICP lowering effect on cerebral perfusion pressure”

Hypothermia has been shown to lower ICP [NEJM 336: 540, 1997;J Neurosurg 79: 363, 1993; J Neurosurg 89: 206, 1998] and may improve outcomes in patients with severe head injury [J Neurotrauma 10: 263, 1993; J Neurosurg 79: 354, 1993]. There may be, however significant toxicities associated with hypothermia, thus beware. The Brain Trauma Foundation Guidelines state that there is Class III evidence suggesting that “Prophylactic hypothermia is associated with significantly higher Glasgow Outcome Scale (GOS) scores when compared to scores for normothermic controls.” However, Class III data also suggest that “prophylactic hypothermia is not significantly associated with decreased mortality when compared with normothermic controls.”

Who to admit to the NICU

Any patient with severe TBI, open calvarial, or penetrating injury to the skull. All post-craniotomy patients. Many moderately injured patients, and even some mildly injured patients if they have significant other injuries. Note that 20% of patients with a linear or depressed skull fracture will require operative intervention [J Neurosurg 65: 203, 1986]


Load Phenytoin 15-18 mg/kg with 5 mg/kg after. Temkin’s study of 404 TBI patients given dilantin within 24 hours of injury and showed that a year of therapy was no more effective than seven days (short term incidence reduced from 13.3 to 3.4% [NEJM 323: 497, 1990]) – no other therapy has proven superior. Valproate shows no benefit and may increase mortality [J Neurosurg 91: 593, 1999], magnesium may be detrimental [Lancet Neurol 6: 29, 2007], and steroids do not work [Epilepsia 45: 690, 2004]

Traumatic Brain Injury Miscellanei Traumatic Brain Injury Miscellanei – Only use 0.9% NaCl without glucose and tight glucose control – Keep Na < 150 mEq/L and Osm < 330 mOsm/L – TPN does not affect mortality – Phenytoin is superior to valproate, magnesium, and steroids for early seizure prophylaxis.