Traumatic Brain Injury
• 1.6 million head injuries in US
annually
• 250,000 hospital admissions
• 60,000 deaths
• 70,000 - 90,000 permanent
neurologic disabilities
• Causes
– Motor vehicle accidents
– Falls
Primary Survey
1.
2.
3.
4.

Stabilize the spine
Establish adequate airway
Ensure adequate ventilation
IV access to initiate volume resuscitation
Avoid secondary insults to brain
Hypoxia
Hypotension
 Determine level of
consciousness
examine pupils
Secondary Survey
• Once relatively stable
• Includes a complete neurologic examination
• Severity of the head injury is classified clinically by
GCS
– 13 to 15 mild
– 9 to 12 moderate
– 8 or less severe
• Assess strength, sensation
Overall goal with neurologic injury
• Presume injury until proven otherwise
• Identify early
• Allow injured tissue the best chance to repair itself
– Adequate delivery of oxygen and glucose
– Avoid infection
• Preserve residual nervous tissue
Primary Brain Injury
• Trauma: concussion, contusion,
diffuse axonal injury
• Ischemia: global, regional
• Inflammation
• Direct Injury: hemorrhage,
penetrating injury
• Compression: tumor, edema,
Hematoma
• Metabolic insults
• Excitatory toxicity: seizures, illicit
drugs, severe hyperthermia
Secondary Brain Injury
• Hypoperfusion: hypotension, high intracranial pressure,
vasospasm
– Single episode SBP <90 mm Hg increases morbidity & doubles
mortality*
• Hypoxemia* **
– pO2 ≤ 60 mm Hg increases poor outcome from 28% to 71% *
– Increases mortality
 50% from 14.3% **
• Harmful mediators: reperfusion, inflammation
• Electrolyte changes
*Chestnut RM, et al. J Trauma 1993;34:216-222
**Jones PA, J Neurosurg Anesth 1994;6:4-14
Basic Premises:
1. Monro-Kellie hypothesis
 3 compartments: brain, blood, & CSF
 Increase in one must be compensated by
decrease in others or the ICP will increase
2. Compliance

volume to pressure relationship
Basic Premises:
1. Monro-Kellie hypothesis
2. Compliance
3. Cerebral autoregulation
Intact autoregulation
Lang et al JNNP 2003;74:1053-1059
Intact autoregulation
Intact autoregulation
Lang et al JNNP 2003;74:1053-1059
Defective autoregulation
Basic Premises:
Monro-Kellie hypothesis
2. Compliance
3. Cerebral autoregulation
4. CPP = MAP – ICP
Optimal cerebral perfusion pressure (CPP) in patients
with acute traumatic brain injury by current guidelines
is:
A. Maintaining a mean arterial pressure
of greater than 90 mm Hg.
B. 50-70 mm Hg.
C. greater than 70 mm Hg.
D. determined without an ICP monitor.
E. not important, ICP is the parameter to
follow
Cerebral perfusion pressure
CPP = MAP - ICP
Normal is 70-100 mm Hg
Adequate 50-60 mm Hg
Ischemia 30-40 mm Hg
High MAP
• WARNING ! ↑ in BP may be a sign of ↑ICP
DO NOT TREAT/OVERTREAT BP alone
CPP = MAP - ICP
70 = 75 - 5
70 mm Hg = ↑ ← ↑
70 = 110 - 40
35 = 75 - 40
Cerebral perfusion pressure
CPP=MAP-ICP
Current AANS guidelines specify ICP <20
& CPP of 50-70 mmHg
• Lower CPP : poorer outcome (ischemic)
• Higher CPP: more ARDS
J Neurotrauma. 2007; 24:S59-64
Initial Management – Pre-hospital
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ABCD
Intubate early if GCS <8
Systolic BP of < 110 requires fluid resuscitation
Rapid transport to trauma center
Avoid sedation if possible to preserve neuro exam
Early Hospital Management
• Intubate if GCS <8
• Rapid sequence preferred
– Avoid increased ICP with placement of ETT
• Preferred drugs
– Etomidate – rapid acting, short duration, min BP effect
– Rocuronium- short duration, no BP effect, no increased ICP
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100% O2 until transferred to ICU
Initial target PCO2 should be 35 to 40 mm Hg
MAP goal 90
Use only LR or NS – NO HYPOTONIC FLUID
Maintain Oxygenation!
Hypoxemia ≤ 60 mm
Hg increases poor
outcome from 28%
to 71% (trauma)
• CT head – non contrast
– All patients at risk
• GCS <15
• Depressed skull or evidence of basilar skull fracture
• Focal neuro deficits
– GCS 15, +LOC
• Neurosurgical consultation
– Surgical evacuation
• all acute traumatic extra-axial hematoma >1 cm
• subdural or epidural hematoma > 5 mm
with an equivalent midline shift and GCS<8
• depressed, open, and compound skull fractures
• recommended if hematoma > 20 ml with mass effect
ICU Management
• Serial neurologic exams
• ICP monitor recommended in patients with a GCS
score < 8
– intracranial HTN > 60%
• No RCT’s to support improved outcomes with ICP
monitor
• Studies demonstrate outcome is inversely proportional
to max ICP reading and time spent >20
ICP Monitoring
 Different sites
1) IntraventricularGold standard
2) Intraparenchymal
3) Subarachnoid
4) Subdural
5) Epidural
 Different modalities
1) Fiberoptic
2) Fluid-coupled
Jugular Venous Oximetry
 Continuous SjVO2
 Blood Draws for
CvO2
Value
SjVO2
Normal Ischemia
> 60% <50% (10 min.)
Tissue PO2 Monitoring:
Pbto2 Licox- Integra
• Direct measurement of tissue oxygen
tension (?)
• Local measurement
• Part of ICP-bolt system
• Experimental use in Europe since
1992
• Approved for use in Europe, Canada,
and US
Management of Intracranial HTN
• 3 targets
– Intracranial blood volume reduction
– CSF drainage
– Brain parenchyma reduction
Cerebral blood volume
• Decrease
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Elevate head to 30 degrees
Midline position of head
Sedation
Muscle relaxation
Decrease airway pressure
• Increase
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Ischemia
Acidosis
Hypercapnia
Increased venous
pressure
– Hyperthermia
Hyperventilation
Begins almost immediately
Peak effect in 30 minutes
Lowers ICP by 25-30% in most patients
May decrease cerebral blood flow:
 No lower than pCO2 of 30mm Hg
Normalize within hours
Ventilation: Hyperventilation
 PaCO2 of 25-30 mm Hg can cause
significant vasoconstriction and
reduction in cerebral blood flow
Coles JP, Crit Care Med 2002;30:1950-1959
Diringer MN. J Neurosurg 2002;96:103-108
Imberti R. J Neurosurg 2002;96:97-102
Muizelaar J Neurosurg 1991;75:731-739
Cold. Acta Neurochir 1989;96:100-106
Raichle, et al. Stroke 1972;3:566-575
Hyperventilation
 Hyperventilation lowers CBF, and therefore ICP, by
raising the extracellular pH in the CNS
• CO2 is not the direct mediator of this response
 Hyperventilation does not ‘stop working;’ however,
The choroid plexus exports bicarbonate to lower the pH
 6 hour time course
• The cause of the ICP elevation is usually progressive
• Further attempts at hyperventilation will raise
intrathoracic pressure, decreasing jugular venous return
and thereby raising ICP
Hemodynamic
• CBF is independent of MAP between 50-150
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Autoregulation
With injury 50% pts lose autoregulation ability
GOAL – Normal MAP or MAP >90
Treat hypotension with thoughts of cause
Treat HTN with B-blockers, nicardipine
Use vasodilators with caution
Cerebral autoregulation in normal subjects and patients with chronic
hypertension
Marik, P. E. et al. Chest 2002;122:699-711
Osmotic Agents: Mannitol
 Acts within 20-30 minutes
 Dosage: 0.25-1 g/kg bolus
 Filtered needles!
 Actions:
1) osmotic gradient
2) may increase cardiac preload, output
and elevate MAP
3) improves rheology of red blood cells
4) decreases CSF production
5) free radical scavenger
Osmotic Agents: Mannitol
• Serum osmolality <320 mOsm/L vs
osmolar gap <10
• Measured osmoles –
(2Na +glu/18+BUN/2.8)
• Watch for osmotic diuresis: Dehydration
and hypotension
• MAINTAIN EUVOLEMIA
Hypertonic Saline
3% saline 250cc bolus (run in as fast as
possible)
7% saline bolus
23.4% saline 30cc bolus
Fever
 Each increase in 1degree Celsius increases cerebral
metabolic rate by 7%
 One study w/ exercise: 1.5º C increased CMRO2 by 23%
increase in CMRO2
Vasodilation
CBV
ICP
 Increases O2 requirements
 Increases CO2 production (may need to adjust ventilator
minute ventilation!!!)
Nunnely SA et al. J Appl Physiol 2002;92:846-851.
McIntyre L et al JAMA 2003
Pentobarbital coma may result in:
A. hyperthermia.
B. hypertension.
C. increased respiratory drive.
D. unreactive large pupils.
E. increased electrographic activity
Additional methods to decrease ICP
for when conventional management fails
No demonstrated benefit
• Barbiturate coma
– Reduce O2 demand
– No cellular toxicity
– Burst suppression by
continuous EEG
• Hypothermia
– Reduce O2 demand
– Do not actively rewarm
cold patients
• Decompressive
Craniectomy
– Last resort
Sedation
• Fentanyl is analgesic of choice
– Min BP effect, depresses cough
• Propofol
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easily titratable, rapidly reversible
decreases cerebral metabolic rate
Potentiates GABA inhibition
Inhibitions methyl-D-aspartate glutamate receptors
Inhibits voltage-dependent calcium channels
Potent antioxidant
Inhibits lipid peroxidation
• Can paralyze if needed, but keep to minimum
Seizure Prophylaxis
• Anti-seizure medication
– 7 days after severe injury
– Usually phenytoin
• Avoid abnormal electrolytes
• Hyponatremia
– SIADH
– Cerebral salt wasting
• Hypomagnesemia
Hemicraniectomy:
4 types of acute post-traumatic intracranial hemorrhage:
Subarachnoid
hemorrhage
Periventricular
and frontal lobe
contusions with
intraparenchymal
hematoma
Subdural
hematoma
EPIDURAL HEMATOMA
Mattiello, J. A. et al. N Engl J Med 2001;344:580
EPIDURAL HEMATOMA
Acute
subdural
hematoma
Chronic
subdural
hematoma
EPIDURAL HEMATOMA
Subarachnoid
hemorrhage
Multiple
intraparenchymal
hematomas with
surrounding edema
Diffuse Axonal Injury
• May cause immediate and prolonged unconsciousness
• High morality, high morbidity, often persistent
vegetative state
• Identified by diffusion-weighted MRI
• Caused by shearing forces affecting axons leading to
dysfunction of the reticular activating system
• Axons are not torn but sequential, focal changes that
lead to swelling and disconnection over multiple hours
• Apoptosis may play role in axonal injury
CT in Patients with Craniocerebral Trauma
Multiple
Intraparenchymal
hemorrhages
Subarachnoid
hemorrhage
Gilman, S. N Engl J Med 1998;338:889-896
Depressed skull
fracture
Poor prognosis
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Advanced age
Female <50
Anticoagulation at time of trauma
Low GCS at arrival
Hypotension
Abnormal pupillary widening
Traumatic SAH
Things to keep in mind…
• Spine injury until proven otherwise
• Many intraparenchymal hematomas may be delayed,
appearing on the CT scan 24 h after the initial insult
• Low threshold to repeat CT scan
– Clinical changes
– Continued uncontrollable intracranial HTN
Acute Spinal Injury
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10,000 new cases annually
Males 16-30 make up 80%
Most due to MVA 36%, violence 29%, falls 21%
Quadriplegia is slightly more common than paraplegia
Rare to completely transect cord
6-8% of head trauma will also have spine injury
Main goal is early identification
Insult is associated with an injury response that results
in neuronal destruction
Secondary injury
• cascade of tissue injury
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vascular compromise
inflammatory changes
cellular dysfunction
free radical generation
• hallmark is spinal cord edema
• peaks 3 to 6 days after injury
• subsides over a period of weeks
Initial Resuscitation
• Regular ABC’s
• Immobilize neck until cleared or
stabilized
– Head between two sandbags
– Placement of cervical collar
• Immobilize entire spine
– Transportation on a rigid spine board
– Log rolling
• 25-50% of cervical spine injuries also
have head injury
Neurologic exam
• Early
• Sequential
• Include
– Strength
– Sensation – pain, position
• Neurologic level: most caudal segment of the spinal cord with normal
bilateral motor (strength >3/5) and sensory (light touch and pinprick)
function
The NEXUS Low-Risk Criteria
Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518
The Canadian C-Spine Rule
Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518
Imaging
• Cervical spine films
– AP, lateral, and odontoid
– Additional laterals
• If entire c-spine or C7–T1 space not seen
• Abnormal vertebral alignment, bony structure,
intervertebral space, and soft tissue thickening
• Flexion and extension films
• SCIWORA (spinal cord injury without radiologic abnormality)
• CT scan – best for bones
– If not adequate visualization by X-ray
• MRI
– Modality of choice for characterizing acute cord injury
– Best for edema, hemorrhage, ligamentous injury
Neuroresuscitative Agents
• High dose steroids
– 30mg/kg bolus
– 5.4mg/kg/hr x 23H
– Give for 48H if not given within 3H
• Effective if given in first 8 hours
Injury classification
– Stable
– Unstable
– Soft tissue or fracture
Surgery
• Decompress neural tissue
• Prevent cord injury by ensuring stability
• Options include
– bed rest in traction (rarely done)
– external immobilization
– open reduction with internal fixation
Order of injury Repair
• Any open fractures first
• Then any closed fracture
– Tibia
– Femur – within 24h
– Pelvis
– Spine
– Upper extremity
Ligamentous injury
Odontoid Fracture
Atlas fracture
C2 Hangman’s Fracture
C6 Fracture with retropulsion
to cord
subluxation of C4-C5 with
spinal cord compression
Soft tissue swelling
Lumbar
Burst
fracture
Compression fracture
Cord Injury Syndromes
• Complete cord lesion - all sensory and motor function below
the lesion is abolished
• Central cord lesion – motor function lost upper>lower
suspended sensory loss in cervicothoracic dermatomes
• Posterior Cord syndrome – diminished proprioception and fine
touch
• Brown-Sequard syndrome - cord hemisection ipsilateral loss
of pain and proprioception, contralateral pain and temp loss,
suspended ipsilateral loss of all sensation
• Spinal shock – lack of neurologic function after trauma that can
last until 4 weeks
Systemic Effects of SCI
• Respiratory
• Cardiovascular
– Almost solely related to
interruption of sympathetic
pathway at T1-L2
– Bradycardia
• Resolves with stimulation
• Resolves after 2 months
• Rare to need pacemaker
– Hypotension
• Give volume
• Low dose pressors
– Related to level of injury
– Thoracic levels eliminates
intercostals
– Diaphragm alone to inspire –
phrenic nerve (C3-5)
– Cervical lesions decreases cough
and secretion clearance
– Decreased tidal volumes
– Minimal expiratory help
– Status improves with time
Autonomic hyperreflexia
• Loss of central inhibition
• hyper-reactive sympathetic
reflexes to cord below level of
lesion
• Bladder or bowel distention
usual causes
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HTN
Arrythmias
Headaches
Vasodilation above lesion
level
In Summary
• Appropriate pre-hospital care is essential
• Assume injury until proven otherwise
• Evaluate as early as possible to prevent
unnecessary immobilization
• Earlier steroids with spinal injury
• Follow clinical exam
References
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Czosnyka M. Pickard JD. Monitoring and interpretation of intracranial pressure.
Journal of Neurology, Neurosurgery & Psychiatry. 75(6):813-21, 2004 Jun.
Gunnarsson T. Fehlings MG. Acute neurosurgical management of traumatic brain
injury and spinal cord injury. Current Opinion in Neurology. 16(6):717-23, 2003 Dec.
Hutchinson PJ. Kirkpatrick PJ. Decompressive craniectomy in head injury. Current
Opinion in Critical Care. 10(2):101-4, 2004 Apr
Longhi L. Stocchetti N. Hyperoxia in head injury: therapeutic tool?. Current Opinion
in Critical Care. 10(2):105-9, 2004 Apr
Marik, PE. Varon, J. and Trask, T Managament of Head Trauma*Chest. 2002; 122: 699
- 711.
Marshall LF. Head injury: recent past, present, and future. Neurosurgery. 47(3):54661, 2000 Sep
Patel RV. DeLong W Jr. Vresilovic EJ. Evaluation and treatment of spinal injuries in the
patient with polytrauma.Clinical Orthopaedics & Related Research. (422):43-54, 2004
May.