David BlissChris DaelTim DeakersMichael LevyKarl Maher Todd Maugans Gordon McComb Karen McVeighAlan Nager Christopher NewthCarol NicholsonNiurka Rivero Randall Wetzel

Children’s Hospital of Los Angeles

11.18.97

Management Management Guidelines for Guidelines for Head TraumaHead Trauma

Comments: R. Chestnut IComments: 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 IIComments: 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 IIIComments: 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: GCSAirway management: GCS

Patients with Glasgow coma scores of 8 or below require oral endotracheal

intubation.

Airway management: Airway management: rapid sequence intubation + Sellick rapid sequence intubation + Sellick maneuvermaneuver

– 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: Airway management: succinylcholinesuccinylcholine

• 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:Airway management: adjuncts Iadjuncts 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:Airway management: adjuncts IIadjuncts 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: Airway management: non-depolarizing agentsnon-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 IVentilation 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 IIVentilation II

There is nono indication for prophylactic hyperventilation.

Normocapnoea is good for you !Normocapnoea is good for you !

Ventilation IIIVentilation 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

odontoidatlas

Intravascular volume IIntravascular volume I

The targeted ideal for volume resuscitation in head trauma is euvolemiaeuvolemia. This should be maintained with either normal saline or Lactated Ringer's.

•Intravascular volume should be maintained with solutions containing >133meq\L Na+ (isotonic).

•Hypertonic (3%) saline may be indicated (euvolaemic hypernatraemia).

Intravascular volume IIIntravascular volume II

• Hyperglycaemia and Hypoglycaemia must be avoided.

• Glucose (D5) not indicated for children over 6 months of age.

• monitor serum glucose.

Intravascular volume IIIIntravascular volume III

Sedation and pain management ISedation and pain management I

Children who are agitated or possibly in pain, requirerequire sedation and/or analgesia.

Sedation and pain management IISedation 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 IPositioning 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 IIPositioning II

ICP monitoring IICP monitoring I

Indicated for children with head trauma with a Glasgow coma score of 7 or less or who are rapidly deteriorating.

ICP monitoring IIICP 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 ICerebral 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 IICerebral perfusion pressure II

http://neurosun.medsch.ucla.edu/BMML/nenov.44.VRM96/96MedVirReal.html

ICP waveformsICP 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 complianceIntracranial compliance

ICP: b-waves IICP: 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 IIICP: b-waves II

ICP: a-waves IICP: 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 IIICP: a-waves II

ICP: a-waves mechanism IICP: 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 IIICP: a-waves mechanism II

ICP: terminal wavesICP: terminal waves

Pentobarbital coma IPentobarbital coma I

Pentobarbital-induced coma should be considered if intracranial pressure is not controlled by:

osmotherapy

temperature regulation

sedation

Pentobarbital coma IIPentobarbital 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 IInhalational 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

• 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 IIInhalational anaesthesia II

• 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

Inhalational anaesthesia IIIInhalational anaesthesia III

Temperature regulation ITemperature 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 IITemperature 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 - TrendsSummary - Trends

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

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text:text:randall wetzel md, children's hospital of los angelesrandall wetzel md, children's hospital of los angelesjoseph dicarlo md, stanford universityjoseph dicarlo md, stanford university

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