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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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head trauma


August, 22, 2002

Adam Oster PGY2

Dr. Mark Yarema

head trauma1


  • Epidemiology
  • Biomechanics of HI
  • Minor HI
    • Canadian CT Head Rule
    • future developments
  • Severe HI
    • physiology
    • management issues and controversies
    • future developments
  • Pediatric HI
head trauma2
  • Epidemiology
    • approx 1 000 000 HI evaluated in ED in N.A/yr
    • majority (80%) are minor or minimal
      • majority of these can be discharged home safely
      • small percentage will deteriorate and require neurosurgery
      • early diagnosis of these NSx lesions is important and effects long short and long term outcome
    • 50 000 die before reaching the ED
    • leading cause of traumatic death in males <25 y.o
head truma biomechanics

Direct Injury

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

Indirect Injury

occurs when the cranial contents are set in motion within the skull

SDH, DAI, coup-contra-coup pattern, concussion.

head truma biomechanics1
Secondary Injury


includes seizures


Decreased CPP



Systemic and Metabolic insults


areas of brain suffering irreversible primary injury are surrounded by a penumbra of tissue that is injured but potentially salvageable.

head injury classification
  • MINOR (80%)
    • GCS 13-15
  • MODERATE (10%)
    • GCS 9-13
  • SEVERE (10%)
    • GCS 3-8
30 yo woman fell from a ladder 45 minutes ago while painting her house, witnessed by her husband. No LOC. Previously healthy.
  • What else do you want to know?
  • O/E
    • eyes are open
    • converses but not sure why she’s in the hospital
    • obeys commands
    • no focal deficits
        • GCS --
    • remainder of exam normal
minor hi
Minor HI
  • CT scan?
  • What is her risk of a NSx lesion
  • A “clinically important” brain injury
  • death from this HI
minor hi1
GCS 13-15

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

Minor HI
ct scan in minor hi
CT scan in Minor HI
  • An ongoing and evolving issue
    • scan everyone
    • scan no one
    • selective scanning
    • wide variation in inter-physician and teaching hospital scanning rates
history of the debate
History of the debate
  • Haydel, 2000
    • H/A
    • Vomiting
    • Age>60
    • Drug or ETOH intoxication
    • Amnesia
    • Seizure
    • Trauma above the clavicles
  • Sens 100% (95%-100%) for CT abnormality
  • Sens. for NSx intervention 54%-100% (N=6)
rosen 2002 high risk
Rosen 2002: High Risk

Focal neurologic findings

Asymmetric pupils

Skull fracture

Multiple trauma

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


Posttraumatic seizure

History of bleeding disorder/anticoagulation

Recent ingestion of intoxicants

Unreliable/unknown history of injury

Suspected child abuse

Age >60 yr, <2 yr

rosen 2002 low risk
Rosen 2002: Low Risk

Currently asymptomatic

No other injuries

No focality on examination

Normal pupils

No change in consciousness

Intact orientation/memory

Initial Glasgow Coma Scale score of 14 or 15

Accurate history

Trivial mechanism

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

<5mins 5.9%

>5mins 8.5%

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

Signs and Symptoms:Correlation with IC Lesion Emergency Medicine Clinics Of North America vol 17, no.1. Feb., 1999.
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

>3mm, 43%

Basal Skull #

53%-90% IC lesion

Signs and Symptoms:Correlation with IC Lesion Emergency Medicine Clinics Of North America vol 17, no.1. Feb., 1999.
canadian ct head rule
Canadian CT Head Rule
  • 3121 patients multicentred, prospective cohort study
  • inclusion criteria
    • GCS 13-15
    • witnessed LOC, amnesia or disorientation
    • injured within the past 24hrs
  • Excluded; <16, no LOC/amnesia/disorientation, obvious depressed skull #, penetrating skull inj., focal neuro deficit, Sz post-injury, pregnant, congenital or acquired bleeding disorder.
canadian ct head rule1
Primary outcome

need for neurosurgical intervention

intubation or death within 7d, craniotomy, elevation of skull#, ICP monitoring.

Secondary outcomes

Clinically Important Brain Injury

“an injury which would normally require admission and neuro follow-up”

consensus of EPs, neurosurgeons and neuroradiologists


Solitary contusion <5mm

Localized SAH


Isolated pneumocephaly

Closed and depressed skull#, not through inner table

Canadian CT Head Rule
canadian ct head rule2
Canadian CT Head Rule
  • Study Design
    • Patients assessed for 22 standardized findings on Hx, PE and neurological exam.
    • CT scan at discretion of physician
    • Follow-up by phone at 14days for those who did not have a CT to determine the presence of CIBI.
canadian ct head rule3
Canadian CT Head Rule
  • Results
    • 1% (44) required neurosurgical intervention
    • 0.13% (4) died
    • 8% (254) CIBI
    • 4% (94) CUIBI
        • small SAH, contusions <5mm
      • 67% had CT, 33% phone follow-up, 363 (%) lost to follow-up
canadian ct head rule4
Canadian CT Head Rule
  • 7 variables with good IO agreement and strong association with the outcome
    • Goal was highest sensitivity while still achieving greatest specificity
    • Stratifies patients into three groups
      • high risk for the primary outcomes measure or
      • medium risk for the secondary outcome
      • Low risk for either outcome
canadian ct head rule5
Canadian CT Head Rule
  • High risk (for neurological intervention)
    • GCS score <15 at 2 hours after injury
    • Suspected open or depressed skull fracture
    • Any sign of basal skull fracture
      • hemotympanum, "raccoon" eyes, CSF otorrhea or rhinorrhea, Battle's sign)
    • Vomiting > 2 episodes
    • Age > 65 years
  • Sens 100% (92%-100%)
  • Spec. (67%-70%)
canadian ct head rule6
Canadian CT Head Rule
  • Medium risk (for brain injury on CT)
    • Amnesia before impact >30 minutes
    • Dangerous mechanism
      • pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from height >3 feet or 5 stairs
  • Sens. 98.4% (96%-99%)
  • Spec. 49.6% (48%-51%)
canadian ct head rule7
Canadian CT Head Rule
  • Questions
    • Is the sensitivity high enough?
    • Will it reduce the frequency of scanning Mild HI patients
35 y.o intoxicated male brought in by EMS. Witnessed fall from own height at an LRT station approx. 45 minutes ago.
    • Open eyes to shouting, sleeping but easily roused with pain, swearing, moves all 4 limbs vigorously. VSS.
    • Obvious scalp lacerations. Remainder of exam normal.
    • Image now or observe?
Same guy but you’ve been busy. Now injury was approx. 6hrs ago.
    • Opens eyes to shouting, swears, moves all four limbs spontaneously.
    • Now what?
50 y.o woman with chronic a.fib.. Husband saw her fall from the first rung of a step ladder. She cannot remember what happened. Otherwise healthy.
    • GCS 15.
    • Disposition?
16 yo boy fell while skateboarding. LOC approx 10 secs. Now feels fine.
    • GCS 15, normal exam.
    • Disposition?
  • “A brief alteration in mental function after minor head trauma.” (Rosen, 2002).
  • Absent cerebral autoregulation for days following
  • Advice on discharge?
    • Depends on extent of concussion
  • Grade 1 = confusion without amnesia, no LOC
  • Grade 2 = confusion with amnesia, no LOC
  • Grade 3 = LOC
concussion grade 1
Concussion: Grade 1
  • Remove from sporting event immediately. Examine immediately and serially for development of amnesia and post-concussive symptoms at rest and with exertion.
  • Consider return to sport if amnesia does not appear and no symptoms appear for at least 20
concussion grade 2
Concussion: Grade 2
  • Remove from event. Re-examine next day.
  • May return to practice only after 1 full week without symptoms.
concussion grade 3
Concussion: Grade 3
  • Transport to hospital for evaluation. Admit and observe if concerns of clinically significant brain injury. If no concern, discharge with instructions to family for overnight observation.
  • May return to practice only after 2 full weeks without symptoms
30 yo helmeted male mountain biking in Edworthy. Came off bike while travelling downhill. Struck side of head on tree. Brief LOC. Immediate neck pain. Friends helped him up and they walked him out to their car. Drove him to the ED.
GCS 15, PERL 3mm
  • No focal neurologic deficits.
  • Central c-spine tenderness.
  • Rest of exam wnl.
hi and pediatrics
HI and Pediatrics
  • Important to separate the traumatic or accidental from the non-accidental.
  • Adult resuscitation principles apply, e.g avoiding hypoxia, hypotension, hyperthermia.
  • Challenge is predicting who is low risk enough to be observed and discharged home.
pediatric hi general principles
Pediatric HI:General Principles
  • The younger the child the lower your threshold should be for imaging
  • The greater the forces the lower your threshold should be
  • The more physical symptoms the lower your threshold should be
  • Consider intentional injury/neglect.
  • Can get hypovolemic hypotension
pediatric hi predictors for intracerebral injury trauma reports 2000
Pediatric HI: Predictors for Intracerebral Injury Trauma Reports, 2000.
  • Skull #
    • better predictor than clinical symptoms
    • Sens. 60% to 100%
    • Scalp hematoma (sens 80% to 100%) and young age are predictors for SF
  • Altered mental status
  • Focal neurological findings
  • Scalp swelling,
  • HI without a clear history of trauma
  • In the <6mo. May be asymptomatic
  • LOC and vomiting are not predictive.
pediatric hi risk stratification 2 y o pediatrics vol 17 no 5 may 2001
High Risk

Decreased LOC

Focal findings

Basal or any skull #


bulging fontanelle

*LOC>1min, post-injury SZ, worsening vomiting

*Consensus guideline

Low Risk

Trivial (low energy) mechanism

Fall <3feet

No signs/symptoms at >2yrs post-injury

Age >3mo

Require a period of observation for deterioration.

Pediatric HI:Risk Stratification < 2 y.o Pediatrics. Vol 17, no. 5. May, 2001
pediatric hi normal ct and discharge
Pediatric HI: Normal CT and Discharge
  • 3 studies
    • HI and Normal CT
    • Incidence of deterioration was 0
      • (95% CI 0-1.4%)
rosen 2002 pediatric minor hi and management
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…)

Rosen, 2002: Pediatric minor HI and Management
26 yo male, brought in by STARS from Canmore for CHI.
    • EMS on scene -- GCS 11, full spines
    • STARS called for transport to FMC
    • In ED
      • 90, 120/70, 16, 99% on 5L by np, 36.5
      • opens eyes to shouting his name, moaning, 4 limb spontaneous movement.
head injury history
Key Historic Info



height, landing position, assault weapon



Sz (Hx of Sz)

vitals and GCS on scene and transport


current complaints

26 yo previously healthy male. Unrestrained passenger in high-speed single vehicle rollover. No airbags.


No alcohol/drugs involved

Head Injury:History
head injury physical exam
Key Clinical Info

ABCs --high incidence of polytrauma


Head and neck

?basal skull#


size, reactivity, asymmetry

motor exam

symmetry, abnormal posturing, strength.

Cranial nerves

gag, corneal ref.

DTRs and pathologic reflexes


?herniation syndromes

Approx 60% TBI will have a second system injury

16% associated c-spine injury

Head Injury: Physical Exam
head injury glasgow coma scale
Head Injury:Glasgow Coma Scale
  • *GCS
      • developed for assessment at 6hrs post-injury
      • isolated HI and hemodynamically stable
      • use at <6hrs is limited
        • hemodynamics, intubation, ETOH, sedation/paralysis
      • does not assess brainstem function
severe hi
  • Prevention of secondary injury
    • 1 episode of hypotension (SBP<90) increased mortality by 150%.
    • Hypoxia (paO2<60) also significantly increased mortality (but less than hypotension).
    • Combined hypotension and hypoxia more detrimental than either alone.

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)

Hemodynamically stable

no focal complaints


Airway and Breathing



CT head nil acute

c-spine films normal


Normal brain

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

intra-axial mass

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

hemodynamics normal

bagged by EMS to FMC


airway and breathing


neuro exam


does not open eyes

Moaning and very agitated

moves all four limbs vigorously

withdraws from painful stimuli



Rt 4 Lt 2, reactive

motor exam

no posturing

brainstem function normal



toes downgoing

rectal tone normal

What’s your management plan?
    • Airway capture?
      • Indications for intubation
    • Imaging
    • Disposition
indications for intubation
Indications for Intubation
  • Failure to protect
  • inability to oxygenate
  • inability to ventilate
  • anticipated clinical course
    • loose airway in near future
    • transport
    • DI
challenges during the intubation
Challenges during the Intubation
    • challenges during intubation
      • MAP
      • ICP
    • decreasing MAP
    • increasing ICP
        • RSRL
        • reflex inc. ICP due to laryngoscopy
rsi the chosen one
RSI: the chosen one
  • Preparation
  • pre-oxygenate
  • pre-treatment
      • L -- lidocaine
      • O -- opiates
      • A -- atropine
      • D -- defasciculator or low dose sux
  • paralysis with induction
      • etomidate is agent of choice; thiopentol
  • protection/positioning
  • placement/proof
  • Pitfalls
    • paralysis in a patient with potential neurologic deficits requiring serial exams
    • monitoring for Sz
CT head read as normal
  • now what?
    • Serial exams
    • ?extubation and to NSx
    • remain intubated to ICU
29 yo male, witnessed fall from a 2nd storey building with LOC. Brought in by EMS in full spinal precautions on O2.
    • On scene, hemodynamically stable.
    • GCS 9 (E2, V2, M5), PERL 3mm
    • stable throughout transport (20mins) to FMC
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



what else?

Raise bed 30 deg.


pCO2 to 30-35



Seizure prophylaxis

acute deterioration increasing icp




no response?

Role for prophylactic hyperventilation?

Hypocapnia pitfalls

reduced CBF can cause ischemia

temporary measure

Acute Deterioration: Increasing ICP
acute deterioration increasing icp1


decreased blood viscosity

increases BP

reduces ICP through osmotic cerebral dehydration

lasts 90mins to 6hrs

use smaller doses and boluses

Mannitol pitfalls

causes BBB failure and will build up in cerebral tissue causing a reverse osmotic shift.

Acute Deterioration: Increasing ICP
acute deterioration increasing icp3
Acute Deterioration: Increasing ICP
  • Needs a craniotomy stat
  • If delayed and no effect from hypocapnia and mannitol
    • next line
      • phenobarbitol
        • must be hemodynamically stable
        • dose
          • load 10mg/kg over 3hrs
          • then 1mg/kg/hr maintenance
seizure prophylaxis
Seizure Prophylaxis
  • Depressed skull #
  • intubated and paralysed patient
  • Seizure at time of injury
  • History of seizures
  • penetrating HI
  • severe HI
increasing icp controversies
Increasing ICP: Controversies
  • Hypertonic saline (HTS)
    • science
      • improves CBF, MAP and CPP
      • studies to date (HTS of 1.6% to 23.4%). Some add dextran.
        • RCTs
          • Shackford et al. 1.6% HTS vs LR;underpowered and inconclusive
          • Simma et al. 1.6% HTS vs LR. HTS group had shorter ICU stays and fewer interventions
increasing icp controversies1
Increasing ICP: Controversies
  • HTS
      • Case controlled
        • Khanna et al. 3% HTS vs conventional therapy in refractory ICP (peds)
          • effectively decreases ICP and safely tolerated.
          • ?outcomes measured
      • Retrospective
        • Quereshi, Annals of EM 2000. 2% or #5 HTS vs 0.9%. Did not lessen requirements for other interventions or decrease in-hosp. Mortality.
  • Take-home; no harm, maybe effective, few RCTs (none against mannitol) and wide range of concentrations used.
increasing icp controversies2
Increasing ICP: Controversies
  • Hypothermia
    • Niemann Annals of EM 2001
      • random assignment of 392 pts with CHI to hypothermia (33 deg.) vs normothermia within 6hrs post-injury for 48hrs.
      • No improvement in outcomes and trend to longer length of hospitalisation and higher rate of complications.
  • bradycardia
  • irregular respirations
  • the Cushing reflex
Dilated and sluggish Lt pupil
  • Rt sided Babinski
  • early Lt. uncal herniation
Dilated, non-reactive Rt pupil
  • Rt sided hemiparesis
  • Rt Babinski
  • late Rt uncal herniation (Kernohan’s notch phenomenon)
Bilaterally pinpoint pupils
  • bilateral decerebrate posturing
  • hyperventilation
  • central transtentorial herniation
Pinpoint pupils
  • flaccid quadriplegia
  • cerebellar tonsillar herniation
35 yo woman. Restrained driver in a high-speed single vehicle collision. Passenger dead at scene. Patients airbag deployed and she remained the vehicle. Significant incursion of the light standard into the drivers side.
  • GCS 11 on scene and initial BP 90/60 but up to 105/80 after 1L NS en route.
  • In ED; GCS 8, no lateralizing signs
    • 110, 90/60.
    • Abdomen rigid, LUQ pain.
17 yo male passenger in the back of a pickup. Thrown from vehicle. LOC on scene for 3 mins.
    • On scene; eyes closed, moaning, moves left side more than right. Intubated. GCS?
    • In ED; eyes closed, grunting, spontaneously moves left more than right . Lt pupil 5mm, sluggish, Rt pupil 2mm, reactive.
      • 110, 100/80, 100%. Abdomen hard.
    • You give mannitoland hyperventilate.
    • What next?
You’re the STARS doc flying to Golden to pick-up an 18 yo CHI who is intubated and being hyperventilated for increasing ICP evidenced by a new Lt. sided blown pupil. His pupils became symmetric soon after. Mannitol was given.
  • When you get there the treating physician tells you his Lt. Pupil has blown again.
  • Emergency burr hole?