Head Trauma - HomePage Personali
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Management
Guidelines for
Head Trauma
Children’s Hospital of
Los Angeles
11.18.97
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
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
no indication
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
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)
Positioning II
ICP monitoring I
Indicated for children with head trauma with
a Glasgow coma score of 7 or 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=MAPICP)
– >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
Intracranial compliance
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: b-waves II
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 II
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
ICP: a-waves mechanism II
ICP: terminal waves
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 3335o 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