HEAD TRAUMA. August, 22, 2002 Adam Oster PGY2 Dr. Mark Yarema. HEAD TRAUMA. Outline Epidemiology Biomechanics of HI Minor HI Canadian CT Head Rule future developments Severe HI physiology management issues and controversies future developments Pediatric HI. HEAD TRAUMA.
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August, 22, 2002
Adam Oster PGY2
Dr. Mark Yarema
occurs at the moment of the injury
damage can occur directly beneath the area involved;
#, EDH, ICH, contusion
or occur remotely from propagation of energy
occurs when the cranial contents are set in motion within the skull
SDH, DAI, coup-contra-coup pattern, concussion.
Systemic and Metabolic insults
areas of brain suffering irreversible primary injury are surrounded by a penumbra of tissue that is injured but potentially salvageable.
amnesia, disorientation and confusion are common
no focal neurologic deficits
Controversy about including GCS 13 in minor HI since the rates of NSx lesions and sequelae are closer to moderate HI (GCS9-12) than minor (GCS 14-15(
3% will deteriorate
1% have surgical lesions
<0.5% will die
Focal neurologic findings
Serious, painful, distracting injuries
External signs of trauma
Initial Glasgow Coma Scale score of 13
Loss of consciousness (>2 min)
Posttraumatic confusion/amnesia (>20 min)
Progressively worsening headache
History of bleeding disorder/anticoagulation
Recent ingestion of intoxicants
Unreliable/unknown history of injury
Suspected child abuse
Age >60 yr, <2 yr
No other injuries
No focality on examination
No change in consciousness
Initial Glasgow Coma Scale score of 14 or 15
Injury >24 hr ago
Reliable home observers
incidence of IC lesions range 1.3% to 17.2%
GCS 15 and LOC
6.1% to 9.4%
IC lesion incidence rises with increasing with LOC duration
H/A, nausea and vomiting
about 2x as likely to occur in HI without IC lesion as in HI with IC lesion.
no correlation with IC lesion incidence
GCS 15 Shackford et. al
IC lesion rate 14.8%
3.2% required crani.
GCS 15 Miller et. al.
IC lesion in 6.1%
0.2% required NSx.
incidence of IC increased with extent.
>1mm, 30% IC lesion
Basal Skull #
53%-90% IC lesion
need for neurosurgical intervention
intubation or death within 7d, craniotomy, elevation of skull#, ICP monitoring.
Clinically Important Brain Injury
“an injury which would normally require admission and neuro follow-up”
consensus of EPs, neurosurgeons and neuroradiologists
Solitary contusion <5mm
Closed and depressed skull#, not through inner table
Basal or any skull #
*LOC>1min, post-injury SZ, worsening vomiting
Trivial (low energy) mechanism
No signs/symptoms at >2yrs post-injury
Require a period of observation for deterioration.
No LOC and Normal Exam
observe for up to 24hrs by a competent adult
LOC and normal exam
may consider observation by competent adult
CT if high risk mechanism or currently symptomatic (e.g vomiting, seizure…)
Key Historic Info
height, landing position, assault weapon
Sz (Hx of Sz)
vitals and GCS on scene and transport
26 yo previously healthy male. Unrestrained passenger in high-speed single vehicle rollover. No airbags.
No alcohol/drugs involved
Key Clinical Info
ABCs --high incidence of polytrauma
Head and neck
size, reactivity, asymmetry
symmetry, abnormal posturing, strength.
gag, corneal ref.
DTRs and pathologic reflexes
Approx 60% TBI will have a second system injury
16% associated c-spine injury
Chestnut, RA. Analysis of the role of Secondary Brain Injury in determining the outcome from severe head injury. J. Neurosurg 1990;72:360.
26 yo male, brought in by STARS from Canmore for CHI.
EMS on scene -- GCS 11, full spines
STARS called for transport to FMC
90, 120/70, 16, 99% on 5L by np, 36.5
opens eyes to shouting his name, moaning, 4 limb spontaneous movement.
12 (E3, V3, M6)
no focal complaints
Airway and Breathing
CT head nil acute
c-spine films normal
CBF is constant over a wide range of pressures (MAP 60-150)
will vary linearly outside this range
cerebral vessel diameter also varies linearly with paCO2 and inversely with pa O2
Cannot measure CBF so use surrogate
what increases ICP
edema, CSF obstruction.
Intracranial compensatory mechanisms can accommodate approx. 50cc to 100cc of increased volume.
Beyond this ICP (and CPP) will increase dramatically.
MAP transmitted directly to ICP.
18 yo girl. Motorcross with family. Witnessed fall off bike while jumping.
+LOC, no Sz.
GCS 8 on scene
bagged by EMS to FMC
airway and breathing
does not open eyes
Moaning and very agitated
moves all four limbs vigorously
withdraws from painful stimuli
Rt 4 Lt 2, reactive
brainstem function normal
rectal tone normal
Triaged to resusc room
O2 and monitors applied
80, 120/80, 20, 99%
Rt pupil 5mm, sluggish to light
Lt pupil 3mm, reactive
no eye opening
withdraws to pain
Raise bed 30 deg.
pCO2 to 30-35
Role for prophylactic hyperventilation?
reduced CBF can cause ischemia
decreased blood viscosity
reduces ICP through osmotic cerebral dehydration
lasts 90mins to 6hrs
use smaller doses and boluses
causes BBB failure and will build up in cerebral tissue causing a reverse osmotic shift.