Anesthesia for Traumatic brain injury TBI

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Anesthesia for Traumatic brain injury (TBI)

• By ???
• 2008.10.01

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Intubation

• Glasgow Coma Scale (GCS) of 7 to 8 or less
• Controlled ventilation for ICP or airway control

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Intubation Technique

• The anesthesiologist may encounter a number of
  conflicting constraints,
• (1) elevated ICP
• (2) a full stomach
• (3) an uncertain cervical spine
• (4) an uncertain airway (presence of blood,
• possible laryngeal-tracheal injury,
• possible skull base fracture)
• (5) an uncertain volume status
• (6) an uncooperative/combative patient
• (7) hypoxemia.

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• no "correct" or the "best" approach
• determined by the relative weight of these
  various factors along with the degree of urgency
• Keep sight of the ABCs of resuscitation
• stabilizing the circulation are higher initial
  priorities than control of ICP
• Do not risk losing the airway or causing severe
  hypotension for the sake of preventing coughing
  on the tube or brief hypertension with
  intubation.

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Cervical Spine

• Approximately 2 of patients with a closed-head
  injury who survive to reach a hospital will have
  a fracture of the cervical spine
• mostly injured in the atlanto-occipital region,
  difficult to identify radiologically
• Any uncertainty regarding the airway or the
  cervical spine, direct laryngoscopy (with
  vigorous atlanto-occipital extension) should
  probably be avoided unless the exigencies of
  airway control demand it.

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• Occasional failed intubation
• Cricothyrotomy
• LMA
• SCC ? increase ICP
• Increments are small and probably do not
• SCC should not be viewed as contraindicated in a
  TBI victim

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Choice of Anesthetics

• Craniotomies will most commonly be performed for
  the evacuation of subdural, epidural, or
  intracerebral hematomas.
• Anesthetics known to be cerebral vasoconstrictors
  will be preferable to those having the potential
  to dilate the cerebral circulation
• All of the intravenous anesthetics, except
  perhaps ketamine, cause some cerebral
  vasoconstriction, are reasonable choices, are
  consistent with hemodynamic stability.
• All of the inhaled anesthetics (N2O and all of
  the vapors) have some cerebral vasodilatory
  effect

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• patients remained tracheally intubated
  postoperatively ? anesthetic based primarily on a
  narcotic (e.g., fentanyl) and a muscle relaxant

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Monitoring

• Anesthesiologist should appreciate that the
  priority is to open the cranium as rapidly as
  possible
• After achieving intravenous access, the
  craniotomy should never be delayed significantly
  by line placement.
• arterial line? often placed after induction in
  urgent situations, is appropriate for essentially
  all acute trauma craniotomies.
• The decision to achieve central venous access can
  be based on the patient's hemodynamic status.

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Blood Pressure Management

• The concept that the injured brain is extremely
  vulnerable to what would otherwise be a minor
  insult, for example, modest hypotension or
  moderate hypoxia, has been well confirmed in the
  laboratory.
• several clinical surveys are strongly supportive
  of the adverse effect of minor degrees of
  hypotension in the post-TBI period ? patients in
  the postinjury period have regions of brain with
  low CBF, autoregulation is defective.

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• Normal CBF 50 mL/100g/min
• CBF lt 18 20 mL/100g/min ? ischemia with failure
  of electrical activity
• CBF lt 8 10 mL/100g/min ? energy metabolism
  fail, cell death
• CBF gt 55 60mL/100g/min
• (beyond brains metabolic demand) ?
• hyperemia ? brains metabolic demand
• decreased ? cerebral infarction

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• Low postinsult CBF values correlates with a poor
  eventual outcome, patients die after TBI have
  pathologic changes consistent with ischemia.
• appropriate blood pressure ?
• evidence that indices of the adequacy of cerebral
  perfusion derived from Sjvo2 and transcranial
  Doppler data begin to deteriorate below a mean
  CPP of
• 70 mmHg. (CPP MAP - ICP)
• CPP of 60 mmHg

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• The characteristic behavior of CBF after head
  injury is an initially low CBF followed by a
  gradual increase over a period of 48 to 72 hours
  to normal or sometimes even slightly hyperemic
  levels
• 
  

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• in the absence of measures of CBF or brain tissue
  well-being (both of which are uncommonly
  available), careful maintenance of a CPP of 60 to
  70 mm Hg in the first 72 hours after TBI will be
  appropriate and is common practice in a
  head-injured adult
• A CPP target of 45 mm Hg has been recommended for
  children
• In the ideal situation, management of CPP is
  "targeted" to the pathophysiology that prevails
  in the individual patient

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• Recent study suggested that hypotension was the
  most significant secondary brain injury factor
  that had an adverse effect on outcome, hypocapnia
  was also significantly related.
• Jeremitsky E, Omert L, Dunham, CM, et al
  Harbingers of Poor Outcome. The Day After Severe
  Brain Injury Hypothermia, Hypoxia and
  Hypoperfusion. J Trauma 200354312-318

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• The prevention of secondary brain damage is thus
  the major concern for the treatment of traumatic
  brain injury.

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• Early resuscitation should be based on the VIP
  (ventilate, infuse, pump) rule.
• Hypoxemia clearly worsens outcomes, and oxygen
  administration should be generous to maintain an
  SpO2 of ?95 at all times.
• Vincent JL, Berre J. Primer on medical
  management of severe brain injury. Critical Care
  Medicine 2005331392-1399

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• If cerebral trauma is severe, the systolic
  arterial pressure should be kept gt 120 mmHg (MAP
  gt 90 mmHg)
• Combined inotropes/ vasopressors
• Positioning head routinely elevated at 30 degree
  to improve jugular venous return and decrease
  ICP.
• Analgesia-sedation
• Primer on medical management of
  severe brain injury.
• 
  Critical Care Medicine 2005331392-1399

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Guidelines for the management of severe traumatic
brain injury. Blood pressure and oxygenation

• A significant proportion of traumatic brain
  injury (TBI) patients have hypoxemia or
  hypotension in the prehospital setting as well as
  inhospital. Hypotension or hypoxia increase
  morbidity and mortality from severe TBI. At
  present, the defining level of hypotension is
  unclear. Hypotension, defined as a single
  observation of a systolic blood pressure of less
  than 90 mm Hg, must be avoided if possible, or
  rapidly corrected in severe TBI patients. A
  similar situation applies to the definition of
  hypoxia as apnea cyanosis in the field, or a PaO2
  lt60 mm Hg. Clinical intuition suggests that
  correcting hypotension and hypoxia improves
  outcomes however, clinical studies have failed
  to provide the supporting data.
• 
  National Guideline Clearinghouse
• 
  www.guideline.gov

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IICP Protocol

• First Tier
• Head Position
• Prevent hypotension and hypoxia
• Sedation and analgesics
• Mannitol or Hypertonic Saline
• Brain CT Scan if IICP gt 20 mmHg

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IICP Protocol

• Craniectomy and / or lobectomy
• Barbiturate Coma (Citosol)
• Moderate Hypothermia (32-35 ?)
• Hyperventilation 25-30 mmHg

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Hyperventilation

• Hyperventilation has long been a standard
  component of the management of TBI patients
  perceived to be at risk for increased ICP
• However, evidence is increasing that
  hyperventilation is potentially deleterious
• evidence suggests that hyperventilation and the
  concomitant vasoconstriction can result in
  ischemia, especially when baseline CBF is low, as
  is likely to be the case in the first 48 to 72
  hours after head injury

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• hyperventilation should be used selectively
  rather than routinely in the management of TBI
  patients

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• Controversy
• Conflicting data from the enthusiastic overuse of
  hyperventilation to the avoidance of
  hyperventilation
• Conclusion Careful use of hypocapnia for the
  short-term control of raised ICP remains a useful
  therapeutic tool
• 
  Hyperventilation in Head Injury
• 
  A Review
• 
  Chest 20051271812-1827

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Fluid Management

• Principles fluids should invariably be chosen to
  prevent a reduction in serum osmolarity and
  should probably be chosen to prevent a profound
  reduction in colloid oncotic pressure
• specifically, in the circumstances of
  large-volume resuscitation (arbitrarily, greater
  than half a circulating volume), a mix of
  colloids and crystalloids is probably appropriate
  
• Maintenance of intravascular normovolemia, as an
  adjunct to MAP and CPP support.

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• 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

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• Fluid either Ringers lactate or normal saline
  are appropriate first-line fluids, but hypertonic
  saline may have a role.
• Vincent JL, Berre J. Primer on medical
  management of severe brain injury.
• Critical Care Medicine 2005331392-1399
• Hypertonic saline decreases ICP without adversely
  affecting hemodynamic status1,2, and may have
  beneficial effects on excitatory
  neurotransmitters and on the immune system3
• Munar F, Ferre AM, de Nadal M, et al Cerebral
  hemodynamic effects of 7.2 hypertonic saline in
  patients with head injury and raised intracranial
  pressure. J Neurotrauma 2000 1741-51
• Hart R, Ghajar J, Hochleuthner H, et al
  Hypertonic/hyperoncotic saline reliably reduces
  ICP in severely head-injured patients with
  intracranial hypertension. Acta Neurochir Suppl
  (Wien) 1997 70 126-129
• Dutton RP, McCunn M Traumatic brain injury. Curr
  Opin Crit Care 2003 9503-509

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• To correct vasodilatory shock after traumatic
  brain injury, a resuscitation strategy that
  combined either phenylephrine or argining
  vasopressin plus crystalloid was superior to
  either fluid alone or pressor alone.
• Resuscitation with
  Pressors after Traumatic
• Brain
  Injury.
• J Am
  Coll Surg 2005201536-545

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Jugular Venous Oxygen Saturation

• use of Sjvo2 monitoring as a guide to the
  clinical management of head-injured patients
• The underlying concept is that marginal or
  inadequate CBF will result in increasing oxygen
  extraction, a widening arteriovenous content
  difference, and decreasing jugular venous Sjvo2

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• Sjvo2 measurement makes an assessment of global
  oxygen extraction
• it might be expected to have limited sensitivity
  in highly focal events
• technical limitations
• Catheter placement must be very precise to avoid
  contamination by noncerebral venous blood or
  attenuation of light return (with optical
  catheters) because of vessel wall abutment

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• false-positive rate can be significant
• an average side-to-side difference
• Normal value 50 75
• Abnormal value lt 50 for 5 minutes

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• Jugular venous oxygen saturation (SjO2) lt 60
  indicates an inadequate cerebral blood flow in
  relation to the oxygen requirements of the brain.
  
• Vincent JL, Berre J. Primer on medical
  management of severe
• brain injury. Critical Care Medicine
  2005331392-1399

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Brain Tissue Po2 Monitoring

• Small-diameter intraparenchymal electrodes are
  available that allow measurement of brain tissue
  Ptio2
• Normal Ptio2 20mmHg
• Abnormal Ptio2 lt 10 mmHg
• They are very focal monitors that assess the
  oxygenation status of only small regions of brain
  surrounding the tip

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Hypothermia

• Mild induced hypothermia has already crept into
  the management of neurosurgical procedures in
  which there is a perceived risk of ischemic
  injury
• because these single-center trials appeared to
  indicate good patient tolerance of sustained mild
  hypothermia (32C to 34C), as well as
  improvement in ICP, cerebral oxygen
  supply/demand, and outcome, a multicenter trial
  was performed. That trial revealed no overall
  benefit of hypothermia

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• RESULTS
• Intracranial pressure decreased significantly at
  brain temperatures below 37C
• and decreased more sharply at temperatures 35 to
  36C, but no differences
• were observed at temperatures below 35C.
  Cerebral perfusion pressure
• peaked at 35.0 to 35.9C and decreased with
  further decreases in temperature.
• Jugular venous oxygen saturation and mixed venous
  oxygen saturation
• remained in the normal range during hypothermia.
  Oxygen delivery
• and oxygen consumption decreased to abnormally
  low levels at rectal
• temperatures below 35C, and the correlation
  between them became less
• significant at less than 35C than that when
  temperatures were 35C or higher.
• Brain temperature was consistently higher than
  rectal temperature by 0.5 0.3C.
• CONCLUSION These results suggest that, after
  traumatic brain injury,
• decreasing body temperature to 35 to 35.5C can
  reduce intracranial
• hypertension while maintaining sufficient
  cerebral perfusion pressure without
• cardiac dysfunction or oxygen debt. Thus, 35 to
  35.5C seems to be the optimal
• temperature at which to treat patients with
  severe traumatic brain injury.
• OPTIMAL TEMPERATURE FOR THE MANAGEMENT OF

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The End !