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Management Guidelines for Head Trauma. David Bliss Chris Dael Tim Deakers Michael Levy Karl Maher Todd Maugans Gordon McComb Karen McVeigh Alan Nager Christopher Newth Carol Nicholson Niurka Rivero Randall Wetzel . Children’s Hospital of Los Angeles 11.18.97.
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Management Guidelines for Head Trauma David Bliss Chris Dael Tim Deakers Michael Levy Karl Maher Todd Maugans Gordon McComb Karen McVeigh Alan Nager Christopher Newth Carol Nicholson Niurka Rivero Randall Wetzel Children’s Hospital of Los Angeles 11.18.97
Comments: R. Chestnut I “As a result of tumultuous growth and somewhat erratic emergence of neurotraumatology, there is little consensus at this time regarding pathophysiologic mechanisms and methods of management.” Randall Chestnut. CCM 25:1275,1997.
Comments: R. Chestnut II “It is generally accepted that an organised concatenation of individually unproven but collectively apparently successful therapies is associated with improved outcome from traumatic brain injury.” Randall Chestnut. CCM 25:1275,1997.
Comments: R. Chestnut III “However, there appears to be significant controversy regarding most of the component treatment concepts when approached individually.” Randall Chestnut. CCM 25:1275,1997.
Airway management: GCS Patients with Glasgow coma scores of 8 or below require oral endotracheal intubation.
Airway management: rapid sequence intubation + Sellick maneuver • succinylcholine : its rapid onset and rapid reversibility make it desirable in the trauma patient • succinylcholine : can lead to increased ICP, cerebral blood flow and CO2 production • these potential adverse effects can be minimized, making our first choice for neuromuscular blockade in the acute trauma setting succinylcholine (1-2 mg/kg IV)
Airway management: succinylcholine • can elevate I.C.P. independent of laryngoscopy and intubation • related to increased muscle spindle activity • partially blocked by precurarisation • succinylcholine can be given to severely head injuried patients in the ICU without detrimental effects
Airway management:adjuncts I 2-5 minutes before the succinylcholine: atropine (0.01mg/kg) lidocaine (1.5-2.0 mg/kg) defasciculation: pancuronium (0.03 mg/kg) vecuronium (0.03 mg/kg)
Airway management:adjuncts II sedation: midazolam (0.05 - 2.0 mg/kg) sodium thiopentone (1 -4 mg/kg IV bolus) [only if hemodynamics are stable] analgesia: fentanyl (1-5 mcg/kg)
Airway management: non-depolarizing agents In controlled circumstances, where large doses of non-polarizing neuromuscular blocking agents can be safely administered and sufficient personnel are available, an alternative (non-depolarizing) neuromuscular blocking agent might be used: • rocuronium 1-1.5 mg/kg IV • vecuronium 0.2-0.4 mg/kg IV
Ventilation I • regional blood flow is decreased by hyperventilation in head injured children • hyperaemia is less common than once thought • CMRO2 is decreased more than perfusion • outcomes are worse in the mild to moderate injury group. J Neurosurg 75:731-739, 1991. Crit Care Med 25:1402-1409, 1997.
Ventilation II There is noindication for prophylactic hyperventilation. Normocapnoea is good for you !
Ventilation III The recommended standard of care at CHLA is to monitor end tidal pCO2 following oral endotracheal intubation, during transport, during neuroradiologic procedures and in the intensive care unit. Normocapnoea is the goal
3 y/o boy after MVA. Spontaneouly breathing but nasal flaring present. Atlantoaxial distraction with severed spinal cord atlas odontoid
Intravascular volume I The targeted ideal for volume resuscitation in head trauma is euvolemia. This should be maintained with either normal saline or Lactated Ringer's.
Intravascular volume II • Intravascular volume should be maintained with solutions containing >133meq\L Na+ (isotonic). • Hypertonic (3%) saline may be indicated (euvolaemic hypernatraemia).
Intravascular volume III • Hyperglycaemia and Hypoglycaemia must be avoided. • Glucose (D5) not indicated for children over 6 months of age. • monitor serum glucose.
Sedation and pain management I Children who are agitated or possibly in pain, require sedation and/or analgesia.
Sedation and pain management II Midazolam and fentanyl are adequate, short acting drugs to be used in this setting. No other drugs are necessary routinely for sedation and analgesia in the first 12 hours. • fentanyl: 1-3 mcg/kg/min q 1 hr prn • midazolam: 0.05 to 0.1 mg/kg over 2 minutes Propofol has been considered; however, it has a propensity for hypotension in the acute setting.
Positioning I • In-line traction for intubation • (all head injury is neck injury) • Do Not occlude venous drainage • watch the neck collars • avoid Trendelenberg (central lines)
ICP monitoring I Indicated for children with head trauma with a Glasgow coma score of 7or less or who are rapidly deteriorating.
ICP monitoring II • In children who require neuromuscular blockade or deep sedation or anesthesia, intracranial pressure monitoring may be indicated at a higher GCS. • Anaesthesia makes clinical monitoring of elevated intracranial pressure extremely difficult and thus, in selected cases ICP should be directly measured if surgery is necessary.
Cerebral perfusion pressure I • maintain Cerebral Perfusion Pressure (CPP=MAP-ICP) • >60 torr if ICP <22 torr • >70torr if ICP > 22 torr • hypertonic resuscitation • pressors
Cerebral perfusion pressure II http://neurosun.medsch.ucla.edu/BMML/nenov.44.VRM96/96MedVirReal.html
ICP waveforms • The normal ICP waveform contains three phases: • P1 (percussion wave) from arterial pulsations • P2 (rebound wave) reflects intracranial compliance • P3 (dichrotic wave) represents venous pulsations
ICP: b-waves I • B - waves are frequent elevations (up to 50 mm Hg) lasting several seconds, occuring in two minute cycles. • b - waves are suggestive of poor intracranial compliance
ICP: a-waves I • A-waves (plateau waves) last 5-20 minutes, and often accompany symptoms of brainstem dysfunction. • cerebral perfusion pressure may be decreased • a-waves often herald decompensation
ICP: a-waves mechanism I • A-waves (plateau waves) result when mean systemic blood pressure decreases below threshold. • cerebral perfusion pressure (CPP) falls below ischemic threshold • cerebrovasodilation occurs in response • in a non-compliant cranium, this vasodilation results in greatly increased intracranial pressure
Pentobarbital coma I Pentobarbital-induced coma should be considered if intracranial pressure is not controlled by: • osmotherapy • temperature regulation • sedation
Pentobarbital coma II ICP should be monitored when pentobarbital coma is induced. Neurometric monitoring can be facilitated by: • continuous cerebral function monitoring (Neurotrack) • continuous EEG
Inhalational anaesthesia I Ideally, with inhalational anaesthesia, one would like to see: • decreased CMRO2 • CMRO2 and CBF remain linked • no alteration in CSF dynamics • no alteration in ICP
Inhalational anaesthesia II • Nitrous oxide: increases CBF, CBV; ICP not CO2 responsive worse than halothane or isofluorane • Halothane: increases CBF and ICP; decreases CSF production • Desflurane: decreased CMRO2, increased CBF, increased ICP, decreased cerebral compliance
Inhalational anaesthesia III • Isoflurane: decreases (or has no effect on) CBF (coupled). Minimal effect on CSF volume or ICP • Sevoflurane: decreases CMRO2, coupled, decreased CBF, low B-G solubility coefficient
Temperature regulation I Temperatures should, at all times, be maintained below 37.5.0 C (higher temperatures are associated with elevated ICP, increased CMRO2) • acetominophen, 15-20 mg/kg q 4-6 hours prn • body exposure • direct cooling
Temperature regulation II • mild hypothermia for patients with measured elevated intracranial pressure (>20 torr, 25 cm H2O) will be instituted. • the goal is to maintain body temperatures between 33-35o C (less is not better). • NEJM 336:540,1997
Summary - Trends • No prophylactic hyperventilation • Use of controlled hypothermia • Euvolemic resuscitation • Hypertonic fluids (3% saline) • No steroids • Propofol and Sevoflurane
A joint production (All net animation)
A joint production text: randall wetzel md, children's hospital of los angeles joseph dicarlo md, stanford university graphics: dogbyte productions dana braner md, oregon health sciences university all net joseph dicarlo md, stanford university webpath, university of utah ucla dept of neurosurgery