Transcript Document

Head Trauma
Presented by
Aric Storck, PGY3
Precepted by
Dr. Ian Rigby
August 12, 2004
Outline
Primary / Secondary Brain Injury
 Minor Head Injuries

Selective radiography
 Pediatrics
 Concussion


Severe Head Injuries




Intracranial hypertension
Neuroprotective measures
Seizure prophylaxis
Basilar skull fractures
Epidemiology

>1.1 million ED visits / year in NA
 Minor
head injuries (GCS 14-15) - 80%
 Moderate head injuries (GCS 9-13) - 10%
 Severe head injuries (GCS <9) - 10%
50,000 die before reaching hospital
 20% hospitalized
 200,000 permanent disability
 leading cause of traumatic death in males
<25

Primary Injury

Occurs at time of accident

Due to direct impact of mechanical forces

Irreversible damage from mechanical cellular and
microvascular disruption

Preventable with protective gear, etc.

No intervention possible in ED
Primary Injury
Skull Fractures

Linear – no specific treatment

Depressed
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

Compound depressed (open)


May tear dura or damage brain
Operative elevation may be required
Wound debridement +/- surgical elevation
Skull base

May be complicated by meningitis/abscess
Primary Brain Injury

Directly under the injury site (coup)

Remote from injury site (contre-coup)

Concussion
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Contusions

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Often frontal-temporal due to rough contour of skull
base
Intracranial hematomas
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
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Epidural hematomas
Subdural hematomas
Subarachnoid hematomas

Diffuse axonal injury
 Shearing
of brain tissue with disruption of
neuronal projections in white matter
 Microscopic injury
 Not usually visible on CT
 May be visible on MRI
Secondary injury

Injury occurring after primary insult

Generally due to poor cerebral perfusion
 All
of our therapies are directed at
reducing this!
Cerebral Blood Flow

Autoregulation possible over range of
CPP’s

Vulnerable to

Systemic hypotension
SBP<90
 Reduces cerebral perfusion … ischemia
 Doubles mortality, worsens outcome of
survivors


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Increased ICP
Hypoxia
PO2<60
 Doubles mortality


Anemia
Hematocrit <30%
 Increases mortality

Increased ICP

CSF + Blood + Brain + Mass = constant

~100-150cc extra tolerated before ICP

Multiple therapies targeting ICP
 Mannitol
 HTS
 Hyerventilation
 Ventriculostomy
 Paralysis
& sedation
2o systemic insults
Hypoxia
 Hypotension
 Anemia
 Electrolyte disturbances
 Hypo/Hyperglycemia
 Hyperthermia
 Seizures

Case 1

21 year old male. Tripped and hit head on
ground playing soccer. No LOC. Does not
remember details of the incident. Previously
healthy

What else do you want to know?

O/E





96 14 120/80 36.7 98%
PERL 4mm
Eyes open, a little confused, follows commands
Remainder of exam normal
GCS?
Glasgow Coma Scale

Eye Opening (E)
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4. Spontaneous
3 . To voice
2. To pain
1. None
Motor response (M)
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Verbal Responses (V)
―
―
―
―
―
5. Oriented
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
1. None

6. Obeys commands
5. Localizes pain
4. Withdraws from pain
3. Abnormal flexion
2. Abnormal extension
1. None
NB


Developed for evaluation
of head trauma 6 hours
post injury
Deceased have GCS 3

What is the severity of his injury?


Does he need neuroimaging?


CT, MRI, Skull Radiographs?
If you don’t image them, what are you going to do?


Minor, Moderate, Severe?
Observe, admit, discharge?
What is his risk for a “clinically important” brain injury
Minor Head Trauma

~80% of all head injuries

Originally classified as GCS 13-15

Now defined as GCS 14-15
 GCS
13 found to have outcomes more similar
to moderate (GCS 9-12) HI group. More
abnormal CT scans than GCS 14-15
Minor Head Trauma

Presentation
 HA,
disorientation, confusion, amnesia
 No focal neurological deficits
 Prognostic significance of LOC uncertain

3% will deteriorate

1% have surgical lesions

<0.5% will die
Rosen 2002:
High Risk Minor Head Injury
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
Vomiting
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 Minor Head Injury
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
CT Scans in Minor Head Injury

1,000,000 Minor HI scanned annually in
US

$750,000,000 in charges

Significant intracranial injury in <6%
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So … ~95% incur expense and radiation
exposure with negative examination
CT scan in minor head injury

An ongoing and evolving issue


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
scan everyone
scan no one
selective scanning
wide variation in inter-physician and teaching hospital
scanning rates
Conflicting goals


Minimize the number of unnecessary scans performed
Not miss any significant HI’s
“The New Orleans Rules”
Indications for CT in patients with minor HI
Haydel et al. NEJM 2000;343:100-5.

Minor HI


Any LOC or amnesia
Normal neuro exam

CT patients with 1 or
more of




Derived with 520
patients
Validated on 909
patients



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
H/A
Vomiting
Age>60
Drug or ETOH
intoxication
Amnesia
Seizure
Trauma above the
clavicles

Sens for CT abnormality 100% (95%100%)

Would reduce CT ordering rate by 22% at
study site

Would increase CT usage in Canada
Canadian CT Head Rule
Stiell, I et al. Lancet 2001;357:1391-96.


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3121 patients
Multicentred, prospective cohort
study
Inclusion criteria
 blunt trauma
 GCS 13-15 in ED
 witnessed LOC, amnesia or
disorientation
 injured within the past 24hrs

Exclusion criteria
<16 years
 no LOC, amnesia, or
disorientation
 obvious depressed skull #
 penetrating skull injury
 focal neurological deficit
 post-injury seizure
 pregnant
 congenital or acquired
bleeding disorder.

Canadian CT Head Rule

Primary outcome

need for neurological
intervention within 7 days
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
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Death from head injury
Intubation
Craniotomy
elevation of skull#
ICP monitoring
Secondary outcomes

Clinically Important Brain Injury
(CIBI)

“an injury which would normally
require admission and neuro
follow-up”

consensus of EPs,
neurosurgeons and
neuroradiologists
CIBI defined

All lesions unless
neurologically intact with

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Solitary contusion <5mm
Localized SAH <1mm
SDH<4mm
Isolated pneumocephaly
Closed and depressed
skull#, not through inner
table
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 14 days for those who
did not have a CT to determine the presence
of CIBI.
Canadian CT Head Rule

Results
1% (44) required neurosurgical intervention
 0.13% (4) died
 8% (254) clinically important brain injury
 4% (94) clinically unimportant brain injury



small SAH, contusions <5mm
67% had CT, 33% phone follow-up, 1358 eligible patients
not enrolled, 363 lost to follow-up
Canadian CT Head Rule

7 variables with good interobserver
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
 medium risk for the secondary outcome
 Low risk for either outcome
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



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hemotympanum, "raccoon" eyes, CSF otorrhea or
rhinorrhea, Battle's sign)
Vomiting 2 or more times
Age 65 or older
CT “mandatory” for these patients (4.6% chance
of requiring neurological intervention)



Sens 100% (92%-100%)
Spec 69% (67%-70%)
CT ordering proportion 32%
Canadian CT Head Rule

Medium risk (for CIBI on CT)

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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



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At risk for CIBI on CT
Not at risk for neurological intervention
Can manage with CT or observation depending on local resources
Sens. 98.4% (96%-99%)
Spec. 49.6% (48%-51%)
Canadian CT Head Rule

Questions
 Is
the sensitivity (95% confidence intervals)
high enough?
 Will
it reduce the frequency of scanning Mild
HI patients?
The Future …

NEXUS II
 National
 Taking
Emergency X-Ray Utilization Study
place in 21 US and Canadian EDs
 28,320
patients (~10x as many as next
largest study)
 Will
be published ????
Case 2
 40
y.o. homeless man
 Brought
in by EMS
 Found on bike path
 ++ intoxicated
 some vomiting with ++ coffee grounds
 Opens
eyes to pain, Inappropriate angry
words, localizes pain. VSS
 What would you do?

Same guy but you’ve been busy. Now he’s
been here 4 hours.
 Neurologically
unchanged
 Still reeks like EtOH
 Now what?

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

Actual case
Was seen by GI for
workup of hematemesis
Head injury initially
missed
On re-examination a
large, boggy scalp
lesion and palpable skull
fracture was found
Px is +++ important!
Patient died a week
later of neurogenic
pulmonary edema
Case 3

60 year old man
 Fell
4 feet off ladder
 Hit head on grass
 Initially very confused, now GCS 15
 Otherwise healthy
 Normal Exam
Case 4
16 yo boy fell and hit head while
skateboarding
 No LOC
 Was confused initially - now feels fine
 GCS 15, normal exam
 CT or not?
 What kind of head injury is this?
 Management?

Case 5
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16 year hockey player
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Checked hard and hit head on ice

Brief (~15 seconds) LOC
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He was disoriented for ~ 10 minutes but now
seems fine

You are the only doctor in the arena, the coach
asks if his star player has to go to the hospital

Can he keep playing?
Concussion

“temporary and brief interruption of
neurologic function after minor head
trauma, which may involve LOC” (Rosen
2002)

Usually have normal neuroimaging

Cerebrovascular regulation difficulties for
several days after accident
 Very
vulnerable to repeat injuries (second
impact syndrome)
AAN. Practice Parameter: The management of
concussion in sports. Neurology 1997:48-581-585.
Practice “Options”

Grade 1
Remove from contest
 Examine q5 minutes
 May return to contest if concussive
symptoms clear within 15 minutes
 A second grade 1 concussion eliminates the
player from the game. Return in one week
only if asymptomatic.


Grade 2






Remove from contest with no return that
day
Repeated neuro exams until symptoms
resolve and again the next day
MD to perform neuro exam prior to returning
to play after 1 asymptomatic week
Following 2nd grade 2 concussion no return
to play until 2 weeks asymptomatic
CT/MRI if HA or other symptoms worsen or
persist >1 week
End of season if any CT/MRI abnormality

Grade 3







Transport to ED
+/- neuroimaging
+/- admission
No return to play until asymptomatic one week
Following 2nd grade 3 concussion no return to play
until asymptomatic one month
CT/MRI if HA or other symptoms worsen or persist >1
week
End of season (or career) for any CT/MRI abnormality
Case 6
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2 year old girl
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

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Tripped and fell down stairs
Hit head on floor
Brief (~10 second) LOC
No seizures/vomiting

O/E: eyes open, normal spontaneous
movements, persistent cry

What is her GCS

CT or not?
Head Injury in Children
AAP, AAFP. The Management of Minor Closed Head Injury in Children.
Pediatrics 1999:104(6)1407-1415.
Based on evidence and expert consensus


Applies to



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2-20 year olds
Isolated minor HI
Normal neurological exam
No sign of skull fracture
Can include those with
LOC<1 minute
 Seizure immediately post
injury
 Vomited
 HA, lethargy

Does not apply to







Polytrauma
Unobserved LOC
? C-spine injury
Compounding medical
conditions (eg:bleeding
diathesis, AVM, etc.)
Non-accidental trauma
Language barrier
Summary of recommendations

Minor HI and no LOC

Observation


CT / SR not indicated


ED or at home
Side-effects (sedation, radiation, unnecessary
interventions for incidental findings, etc.) outweigh
benefits of early detection
Risk of clinically important ICI estimated at
<1/5000 (based on large adult study and 2 small
peds studies)

Minor HI and brief LOC
 Observation
or CT
 Studies suggest 0-7% may have ICI
 2-5%
 No
may need neurosurgical intervention
evidence to suggest CT better than
observation in asymptomatic patients
 $(observation) < $(CT) < $(hospitalization)
Disposition

CT Normal

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Extremely low risk for subsequent problems
3 studies

Incidence of deterioration was 0



(95% CI 0-1.4%)
Reliable observation still prudent
CT Abnormal

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D/C with observation vs admission for observation
Careful consideration of abnormalities
Case 7

9 month old boy
 Fell
2 feet from car seat and hit head on
linoleum
 Cried immediately, no vomiting, no seizures

O/E: Neurologically normal, small boggy
scalp hematoma

CT – yes or no?
Pediatric (<2 years) HI
Schutzman S et al. Evaluation and Management of Children Younger
Than Two Years Old With Apparently Minor Head Trauma: Proposed
Guidelines. Pediatrics 2001:107(5)983-993.

Little research and no clear guidelines for
management of minor HI in young
children

Evidence and expert consensus used to
derive guidelines

404 articles reviewed

Children <2 years differ from older kids
 Clinical
assessment difficult
 Asymptomatic ICI more common
 Higher risk of nonaccidental trauma
 Higher risk for skull fractures
 Leptomeningeal cysts may develop

Minor Head Injury
Defined

History, or physical signs,
of blunt trauma to the
scalp, skull, or brain in an
infant or child who is alert
or awakens to voice or
light touch

Does not attempt to
address
Birth trauma
 Penetrating trauma
 Neuro disorder
 Bleeding diatheses
 Prior neurosurgery
 Polytrauma
 Non-accidental trauma


Intracranial Injury
 Intracranial
hematoma
 Cerebral contusion
 Cerebral edema
Guidelines

Flexible and follow the general principles
 The
younger the child, the lower the
threshold for imaging
 The
greater the severity and number or
symptoms, the lower the threshold for
imaging
 Must
consider non-accidental trauma
Results
High Risk Group

CT is Indicated for any of the following

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Depressed mental status
Focal neurological findings
Signs of depressed / basilar skull fracture
Acute skull fracture by Px or skull x-rays
Irritability
Bulging fontanelle
No data to support inclusion of seizure,
vomiting, or LOC in decision making

But suggest that they be taken into consideration
Intermediate Risk Group

CT or observation (4-6 hours) are acceptable

Includes children with any of







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>2 episodes of vomiting
LOC <1 minute
History of lethargy/irritability (resolved)
Behaviour not normal as reported by caregivers
Nonacute skull fracture (>24hours old)
Concerning or unknown mechanism
Scalp hematomas (esp. temporoparietal)
CT if deterioration during observation
Low Risk Group

CT not indicated

Observation by responsible adult

Includes patients who
 Low
energy mechanisms (fall<3 feet)
 No SSx >2 hours after injury
CATCH CT Study
Clinical Indicators of Intracranial Injury in Headinjured Infants
Greenes D, et al. Pediatrics 1999:104(4) 861-867.
Prospective study of infants <2 years
 N=608
 Goal



Identify low-risk criteria to determine which
patients do not need neuroimaging
Hypotheses


Some ICI’s in asymptomatic patients will be
diagnosed by scalp hematoma on Px
Asymptomatic patients with no scalp abnormalities
can safely be discharged without neuroimaging

Subjects asymptomatic if lacked all of
 Hx
of LOC or lethargy
 Irritability
 Seizures
 >1 emesis
 Depressed mental status
 Bulging fontanelle
 Abnormal vital signs consistent with increased
ICP
 Focal neurological signs

Scalp hematomas rated as
 Small
(“barely perceptible”)
 Moderate
 Large (“obvious swelling and/or boggy
consistency”)

Scalp hematomas considered significant
if
 <1
y.o. with any hematoma
 >1 y.o. with moderate – large hematoma
Results

30 (5%) had ICI

Relationship of age and ICI
 12/92
(13%) of <2 m.o. had ICI
 13/224 (6%) of 3-11 m.o. had ICI
 5/292 (2%) of 12-24 m.o. had ICI

14 asymptomatic patients had ICI
13/14 (93%) had significant scalp hematoma
 Among patients with significant scalp hematoma who
had a CT - OR for ICI 2.78 (95% CI 1.15-6.70)



NB: the only patient missed was a 2yo with an epidural
requiring no intervention
265 patients (43%) asymptomatic with no
significant scalp hematoma


No clinically significant injury
95% CI 0-1.2%
 Clinically
significant (95%) predictors of ICI
 Hx
of lethargy
 Irritability
 Depressed mentalstatus
 Bulging fontanelle
 Abnormal vital signs
 Not
found to be significant
 LOC
 seizures
 vomiting
Blunt pediatric head trauma requiring
neurosurgical intervention:
How subtle can it be?
Brown L, et al. AJEM 2003

Retrospectively reviewed all children
<10y.o. with blunt head trauma who went
for neurosurgical intervention between
1985-2001.

110 patients met inclusion criteria
Variables assessed








LOC
Altered mental status
Seizures
Vomiting
Focal neurologic
findings
Scalp hematoma
Scalp laceration
Facial laceration
Pupillary changes
 Vital signs abnormal
consistent with high
ICP
 HA (kids >2)
 Bulging fontanelle,
irritability, apnea,
retinal hemorrhages
(kids<2)

Results

All children had at least 2 SSx of head injury

ALOC most common finding (>80%)

“Emergency physicians should feel
confident that standard history and
physical examination skills are adequate
to identify head-injured children who
require neurosurgical procedures.”
A Decision Rule for Identifying Children at Low Risk for
Brain Injuries After Blunt Head Trauma
Palchak M, et al. Annals of EM 2003:42(4)

Prospective
observational study


2043 enrolled
1271 underwent CT

Evaluated clinical
predictors for outcomes
of
1.
2.
Brain injury on CT
Need acute intervention




Neurosurgical procedure
Antiepileptic medications
> 1 week
Persistent neurological
deficits
Hospitalization at least 2
nights
Results

Significant predictors






GCS<15
Clinical skull fracture
Vomiting
Scalp hematoma if <2yo
Headache
Can safely omit CT in absence of all significant
predictors

Identified 97/98 (99% CI 94-100) patient
with head injury on CT
 The
only patient not identified was discharged
home from ED without complications
Identified 105/105 (100% CI 97-100%) of
patients requiring acute interventions
 NPV 100% (CI 99.7-100)

Conclusions

Application of rule would have eliminated ¼ CT
scans ordered

Included all severity of injuries

May be underpowered to make judgements about
minor head trauma

Are the confidence intervals acceptable?

Will this reduce use of scanning here?
SEVERE HEAD INJURY
Head Injury:
History

Key Historic Info


MVC
fall







height, landing position, assault weapon
LOC
amnesia
Sz (Hx of Sz)
vitals and GCS on scene and transport
AMPLE
current complaints
Head Injury:
Physical Exam

Key Clinical Info
ABCs --high incidence of
polytrauma
 GCS
 Head and neck

Approx 60% TBI will have a
second system injury

Up to 16% have associated cspine injury



pupils


size, reactivity, asymmetry
motor exam


?basal skull#
symmetry, abnormal
posturing, strength.
Cranial nerves

gag, corneal ref.
DTRs and pathologic
reflexes
 vitals
 ?herniation syndromes

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.
Case 8

40 y.o. woman





Rollerblading without helmet
Hit occiput on cement
GCS 12 at scene (E3 V3 M6)
Brought by EMS in full spines
In ED
90, 120/70, 16, 99% on 5L by np, 36.5
 PERL
 Confused, combative, 4 limb spontaneous movement.
 Large hematoma on occiput


Management?
Her CT

No surgical intervention indicated

She is admitted under neurosurgery for
observation

The next morning she is found to be more
drowsy than the night before


GCS 9 (E2 V3 M4)
Now what would you like to do?
Her new CT
•Uneven inner surface
•Important in contrecoup injury

ICU called
 GCS
9
 9>8
 No
need to intubate or take to ICU right now
 “Just watch her on the ward. Call us if there’s
any problems …”

Patient perks up slightly during day (GCS
10-11)

Deteriorates at bedtime (GCS 7)

What now?

You decide to intubate

As you are bagging the patient you notice
that their right pupil has become quite
dilated. It doesn’t seem to react very well
to light.

What do you do?

Mannitol / lasix attempted as temporizing
measure

Patient taken to ICU and intubated

Taken to OR for craniotomy / frontal lobectomy

Patient died 2 days later
Mannitol

Osmotic agent
 Reduces
cerebral swelling (decreases ICP)
 Intravascular volume expander (increases
MAP)
 Reduces blood viscosity
 Net effect = Increased CBF

Pitfalls
ARF in large doses
 Hyperkalemia
 Paradoxically may cause increased bleeding into
traumatic lesion by decompression of tamponade
 Causes BBB failure in large doses. Can accumulate in
brain tissue and cause reverse osmotic shift (rebound
ICP)
 Hypovolemic hypotension secondary to diuresis

Evidence???

Only one placebo controlled trial

Sayre M, et al. Out-of-hospital administration of mannitol to
head-injured patients does not change systolic BP. Acad Emerg
Med 1996;3:840-48.
 Prehospital
mannitol vs placebo
 Mannitol associated with increased risk of
death (RR 1.59 CI 0.44-5.79)

Indications
 Signs
of herniation syndrome
 Progressive neurological deterioration

Usage
 Only
in monitored setting
 Small boluses better than infusion
 0.25-1 g/kg
 Onset within minutes, lasts 6-8 hours
 Osmolarity should be kept <320
 Colloids / blood prn hypotension
Guidelines for the management of severe
traumatic brain injury
Brain Trauma Foundation (2000)

Mannitol

Standards


Guidelines


Insufficient data to support treatment standards
Mannitol is effective for control of raised ICP after severe
head injury. Effective doses range from 0.25-1g/kg
Options




Indications for mannitol prior to ICP monitoring are signs of
transtentorial herniation or progressive neurological
deterioration not attributable to extracranial explanations.
Hypovolemia should be avoided by fluid replacement
Serum osmolality should be kept below 320mOsm to prevent
renal failure
Euvolemia should be maintained by fluid replacement
Intermittent boluses may be more effective than continuous
infusion.
Hyperventilation

Hypocapnia (PCO2 30-35)

cerebral vasoconstriction


temporarily reduces ICP (~25%)
Also decreases CPP

Rapid onset ~30 sec, peak ~ 8 min

PCO2 <25 or prolonged hyperventilation can
cause ischemic injury, alkalosis, hypokalemia

Indications & usage
 Only
for brief periods during resuscitation
 Only for patients with acute neurological
deterioration
 Full monitoring (including ICP if possible)
 Method of last resort
 Do not use if CPP >70
Guidelines for the management of severe
traumatic brain injury
Brain Trauma Foundation (2000)

Hyperventilation

Standards


Guidelines


In absence of raised ICP, chronic prolonged hyperventilation
therapy (pCO2<25) should be avoided after severe TBI
Use of prophylactic hyperventilation (pCO2<35) during first
24 hours after severe TBI should be avoided b/c it can
compromise cerebral perfusion while CBF reduced
Options

Hyperventilation may be necessary for brief periods of
neurologic deterioration, or longer periods of raised ICP
refractory to sedation, paralysis, CSF drainage, and osmotic
diuretics
Guidelines for the management of severe
traumatic brain injury
Brain Trauma Foundation (2000)

ICP Monitoring
 Standards
 Insufficient
data to support standards
 Guidelines
 Appropriate
in patients with a severe head injury
(GCS 3-8) and abnormal CT scan (hematomas,
contusions, edema, compressed basal cisterns)
 Appropriate in patients with severe head injury and
normal CT scan if age >40, motor posturing, sBP
<90
 Not routinely indicated in mild or moderate head
injury
Increasing ICP: What’s new …

Hypertonic saline (HTS)
 mechanisms
 Draws
of action
water from brain tissue via osmotic
gradient
 Restores BP & cardiac output with less volume
and lower capillary hydrostatic pressure
 positive inotropic effect
 Does not impair renal function (vs mannitol)
Shackford S, et al. Hypertonic Saline Resuscitation of
Patients with Head Injury: A Prospective, RCT. Trauma
1998;44(1):50-58.
RCT
 N=34
 Compared

 Hypertonic
(1.6% HTS for resus, NS maintenance)
 Hypotonic (RL for resus, ½ NS maintenance)
HTS group had significantly lower GCS & higher
ICP to begin with
 No significant differences in ICP between
groups
 Underpowered (calculated N=320 for
significance) and inconclusive

Qureshi A, et al. Use of hypertonic (3%) saline/acetate infusion in
the treatment of cerebral edema: Effect on intracranial pressure and
lateral displacement of the brain. Crit Care Med 1998; 26(3):44046.
retrospective chart review
 N=27
 studied effect of infusion of 3% NaCl/Naacetate infusion (target Na 145-155) on
ICP
 Observed reduction of ICP correlated to
Na level in head trauma patients (R2=.91,
p=0.03)

Qureshi A, et al. Use of hypertonic saline/acetate infusion in
treatment of cerebral edema in patients with head trauma:
experience at a single center. Trauma 1999;47(4) 659

retrospective review of 36 patients treated with
2-3% HTS infusions vs 46 patients treated with
NS

HTS associated with higher likelihood or
requiring barbituate coma to control ICP
(p=0.04)

HTS associated with higher in-hospital mortality
(OR 3.1; CI 1.1-10.2)

suggested further research into HTS boluses and
short infusions
Hypertonic Saline & Pediatrics
Simma et al. A prospective, randomized, and controlled study of fluid
management in children with severe head injury: Lactated Ringers vs
hypertonic saline.Crit Care Med 1998:26(7) 1265-70.
 RCT
of 32 kids with GCS <8
 1.7% HTS vs RL for maintenance fluid
 statistically significant inverse relationship
between ICP and Na in both groups
 RL group had more ARDS (p=0.1),
complications (p=0.09), longer ICU times
(p=0.1), longer ventilation time (p=0.1)
 No difference in survival or duration of
hospital stay
Peterson B, et al. Prolonged hypernatremia controls elevated
intracranial pressure in head-injured pediatric patients. Crit Care
Med 2000;28(4):1136-43.
retrospective chart review
 N=68
 studied ability of 3% HTS infusion to
reduce ICP to <20 mmHg
 HTS controlled ICP in most cases


so same group decided to study this
prospectively ….
Khanna S, et al. Use of hypertonic saline in the treatment of
severe refractory posttraumatic intracranial hypertension in
pediatric traumatic brain injury. Crit Care Med 2000;28(4):114451.
Prospectively evaluated effect of prolonged 3% HTS
infusion on refractory elevations in ICP
 N=10
 significant reductions in ICP, and increased CPP
 avg highest Na 171, osm 365
 two patients developed ARF





one septic
one MOSF
both recovered completely
concluded HTS is well tolerated and effective in
controlling refractory ICP in pediatrics
Mannitol vs HTS
Vialet R, et al. Isovolume hypertonic solutes in the treatment of refractory posttraumatic intracranial
hypertension: 2ml/kg 7.5% saline is more effective than 2ml/kg 20% mannitol. Crit Care Med 2003. 31(6).
Prospective RCT
 N=20
 7.5% HTS (2400 mOsm) vs 20% mannitol
(1160 mOsm)
 Received 2cc/kg of solution for raised ICP
refractory to sedation, hemodynamic
optimization, CSF drainage


Results
 HTS
 Significant
reduction in raised ICP events and time
 Significant reduction in failure rate (persistant
elevated ICP despite 2 infusions)

Conclusion
 HTS
is safe and more effective than mannitol
in control of refractory ICP
HTS - Take home points
 Acceptable
as first or second line therapy to
treat elevated ICP in pediatric TBI
 In adults use is only supported for treatment
of refractory intracranial hypertension
 More research needed on concentrations and
dosing
 no evidence of significant harm, may be
helpful
 You’re
not going to use this in emerg … yet
Controversies
Hypothermia

Mild hypothermia (32-340)


neuroprotective in animal models
in mechanistic models




decreases excitatory amino acids in peritrauma region
decreases consumption of endogenous antioxidants
anti-inflammatory effects
some evidence of protective effects in cardiac arrest
Marion D, et al. Treatment of Traumatic Brain
Injury With Moderate Hypothermia. NEJM
1997;336(8):540-6.
RCT of mild hypothermia (x24h) vs
normothermia in severe TBI (GCS 3-7)
 N=87
 improvement in Glascow Outcome Scores
among GCS 5-7, but not 3-4

 12
month RR of bad outcome 0.3 (CI 0.1-1.0)
Clifton G, et al. Lack of Effect of Induction of
Hypothermia After Acute Brain Injury. NEJM
2001;344(8):556-63.
Randomized patients with GCS 3-7 to mild
hypothermia (x48 h) vs normothermia
 N=392; 11 centres
 same rates of mortality & poor
neurological outcome
 more complications (sepsis, pneumonia,
bleeding) in hypothermia group


Criticized because
 hypothermia
not achieved until 8.4 +/- 3
hours post-injury (missed treatment window)
 differences in fluid balance between groups
 differences in outcomes between centres
 Used different protocol than 1997 study

Multiple RCT’s on hypothermia and TBI still
ongoing

Back to our patient…
 Your
medical student asks if you are going to
start her on seizure prophylaxis
AAN. Practice parameter: Antiepileptic drug prophylaxis in
severe traumatic brain injury. Neurology 2003;60:10-16.

Background
 Post-traumatic
seizures are common
 2%
of all comers
 12% of severe TBI
 Seizures
are physically and psychologically
debilitating, can potentiate secondary brain
injury, and are costly
 Prophylactic use of antiepileptics poses risk
of adverse effects

Reviewed evidence for seizure prophylaxis in
preventing early (<7 days) and late seizures

Severe TBI defined as





Prolonged LOC or amnesia
Intracranial hematoma
Depressed skull fracture
Brain contusion
125 prospective studies reviewed
Does AED prophylaxis decrease risk of
developing early seizures (within 7 days) in
patients with severe TBI?

4 eligible studies
2
class I studies of IV phenytoin
 One
statistically significant
 One not statistically significant

But very low incidence of seizures in placebo group
1
class II study of carbamazepine
1
class III study of phenytoin

Combined results
 Pooled
class I evidence
 RR of seizures 0.37 (CI 0.18-0.74)

Adverse effects
 One
rash in phenytoin group
 Similar drop out rates for drug/placebo
Does AED prophylaxis decrease the risk of
developing late (after 7 days) seizures in patients
with severe TBI?

8 eligible studies
2
class I studies of phenytoin
 3 class II studies
1
phenytoin study (large loss to follow-up)
 1 valproate study (large loss to follow-up)
 1 unspecified study (quasi-randomization)
3
class III studies

Results
 Class
I studies
 Neither
 Class
 0/3
 Class
2
demonstrated statistical significance
II studies
demonstrated statistical significance
III studies
studies positive
 1 study no significant difference

Combined results



Pooled results from class I and class II studies in
attempt to narrow CI’s
RR 1.05 (CI 0.82-1.35)
Adverse effects




Higher incidence of rash in treatment group (6 vs
1.2%)
17.6% of phenytoin patients switched to
phenobarbital within 1 year in one class II study
Single episode of neutropenia in valproate group
Similar rates of discontinuation
Practice recommendations

For adults with severe TBI
 “Prophylactic
treatment with phenytoin,
beginning with IV loading dose, should be
initiated as soon as possible after injury to
decrease the risk of post-traumatic seizures
occurring within the first 7 days” (Level A)
 Prophylaxis
should not routinely be used
beyond 7 days to decrease the risk of
seizures (Level B)
limitations

Does not address
 No
proven difference in outcomes due to
prevention of early seizures
 Pediatrics
 Milder forms of head injury
 The utility of EEG in predicting seizure risk
Case 9
 24
year old male
 found
unconscious outside bar
 +++EtOH
 Unclear if assaulted or fell and hit head or neither
 O/E
 GCS
11 (E3 V3 M5)
 smells like EtOH
 blood coming from right ear
His CT
Basilar skull fracture
Clinical Features
 Cranial nerve deficits
Blood in ear canal
 facial paralysis
 hemotympanum
 decreased auditory
 rhinorrhea
acuity
 otorrhea
 dizziness
 Battle’s sign
 tinnitus, nystagmus
(retroauricular
hematoma)
 Raccoon sign
(periorbital ecchymosis)

Management

Admit for observation vs discharge?


higher risk for development of late hematomas
No good evidence

Manage concurrent TBI

How about antibiotics???


Now?
What if they come back in two days with fever?
Antibiotics in basilar skull
fracture?

For

CSF exposed to pathogens
in upper respiratory tract
 reported risk of meningitis
with BSF 9-50%
 antibiotics are theoretically
beneficial in preventing
meningitis
 think rhinorrhea higher risk
than otorrhea
(communication of
cribriform plate with CSF)

Against


antibiotics contribute
to development of
resistant organisms
and more serious
infection
no evidence for use of
antibiotic prophylaxis
Villalobos T et al. Antibiotic prophylaxis after basilar skull
fractures: A meta-analysis. Clinical Infectious Diseases
1998;27:364-9.

14 studies
 12
with extractable data
 9 retrospective
 2 prospective RCT’s
 1 combined retrospective/prospective

1241 patients
 719
antibiotics
 522 no antibiotics

Antibiotics used
 ceftriaxone
 ampicillin/sulfadiazine
 penicillin
 first
and third generation cephalosporins
 chloramphenicol
 gentamicin
 sulfonamides
Odds ratio of meningitis
(no Abx vs Abx)

All 12 studies individually
 none
differed significantly from OR = 1
 OR 0 to infinity

all 12 studies pooled
 OR=1.15;

9 retrospective studies pooled
 OR

CI 0.68-1.94l p=0.678
= 1.17; CI 0.68-2.01; p=0.706
2 prospective studies pooled
 OR
0.68; CI 0.01-13.77; p=0.187
Antibiotics with CSF leakage

Data extractable from 9 studies
 547
patients
 297

29 developed meningitis
 250

received antibiotics
received no antibiotics
34 developed meningitis

Odds ratio of meningitis (no Abx vs Abx)

Each study individually


No OR’s significantly different than 1
All studies pooled

OR 1.34; CI 0.75-2.41; p=0.358
CSF Rhinorrhea vs Otorrhea

Data from 6 studies

70 patients with rhinorrhea


109 with otorrhea



3 patients developed meningitis
No significant differences in any study
Pooled data from 6 studies


4 patients developed meningitis
OR 1.74; CI 0.26-13.36; p=0.772
NB: did not break down into Abx vs none
What about kids?
3
studies exclusively on pediatrics
 131 patients
 57
received antibiotics

2 developed meningitis
 74

 OR
received no antibiotics
2 developed meningitis
not reported
 NB: all patients developing meningitis had CSF
leak
Choi D, et al. Traumatic CSF leakage: risk factors and the
use of prophylactic antibiotics. Br J Neurosurgery
1996;10(6):571-575.

Retrospective study

293 patients with basilar skull fracture
 115
clinical CSF leak
 170 no clinical CSF leak
 8 no documentation
Incidence of meningitis in all patients with fracture of the
base of skull, regardless of the presence or absence of
clinical CSF leakage
Meningitis
No meningitis
Prophylactic
antibiotics
No antibiotics
12
0
185
73
Significant p<0.05
Incidence of meningitis in those patients with
fractures of the base of skull and clinical
evidence of CSF leakage
Prophylactic
antibiotics
No antibiotics
Meningitis
10
0
No meningitis
72
15
No significant difference p=0.170
The bottom line
All studies are small and underpowered to
detect a small difference
 there is no evidence to support the use of
prophylactic antibiotics to prevent
meningitis is asymptomatic patient with
basilar skull fracture
 Use common sense if SSx of infection
(both groups at risk for meningitis)

the end