Management Guidelines for Head Trauma

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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
Childrens Hospital of Los Angeles 11.18.97
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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 251275,1997.

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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 251275,1997.

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Comments R. Chestnut III

• However, there appears to be significant
  controversy regarding most of the component
  treatment concepts when approached individually.
• Randall Chestnut. CCM 251275,1997.

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Airway management GCS
Patients with Glasgow coma scores of 8 or below
require oral endotracheal intubation.
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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)

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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

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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)
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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)
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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

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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 75731-739, 1991.
• Crit Care Med 251402-1409, 1997.

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Ventilation II
There is no indication for prophylactic
hyperventilation.
Normocapnoea is good for you !
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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
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3 y/o boy after MVA. Spontaneouly breathing but
nasal flaring present. Atlantoaxial distraction
with severed spinal cord
atlas
odontoid
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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.
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Intravascular volume II

• Intravascular volume should be maintained with
  solutions containing gt133meq\L Na (isotonic).
• Hypertonic (3) saline may be indicated
  (euvolaemic hypernatraemia).

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Intravascular volume III

• Hyperglycaemia and Hypoglycaemia must be avoided.
  
• Glucose (D5) not indicated for children over 6
  months of age.
• monitor serum glucose.

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Sedation and pain management I
Children who are agitated or possibly in pain,
require sedation and/or analgesia.
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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.

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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)

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Positioning II
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ICP monitoring I
Indicated for children with head trauma with a
Glasgow coma score of 7 or less or who are
rapidly deteriorating.
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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.

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Cerebral perfusion pressure I

• maintain Cerebral Perfusion Pressure
  (CPPMAP-ICP)
• gt60 torr if ICP lt22 torr
• gt70torr if ICP gt 22 torr
• hypertonic resuscitation
• pressors

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Cerebral perfusion pressure II
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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

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Intracranial compliance
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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

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ICP b-waves II
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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

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ICP a-waves II
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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

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ICP a-waves mechanism II
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ICP terminal waves
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Pentobarbital coma I

• Pentobarbital-induced coma should be considered
  if intracranial pressure is not controlled by
• osmotherapy
• temperature regulation
• sedation

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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

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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

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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

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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

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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

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Temperature regulation II

• mild hypothermia for patients with measured
  elevated intracranial pressure (gt20 torr, 25 cm
  H2O) will be instituted.
• the goal is to maintain body temperatures
  between 33-35o C (less is not better).
• NEJM 336540,1997

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Summary - Trends

• No prophylactic hyperventilation
• Use of controlled hypothermia
• Euvolemic resuscitation
• Hypertonic fluids (3 saline)
• No steroids
• Propofol and Sevoflurane

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A joint production
(All net animation)
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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