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Physiology
Concussion Mild TBI
Epidural Hematoma
Subdural Hematoma
Traumatic SAH
Contusion
Skull Fractures
Pathophysiology
mm Hg
Hypotension
Monro-Kellie Doctrine
Cranial vault is a fixed volume
any change in the contents either
o displaces the normal contents or
o raises the pressure inside the skull
Direct Injury
head is struck by an object or its motion is
arrested by another object
skull initially bends inward at the point of
contact (coup)
some energy is transmitted to the brain by
shock waves that travel distant to the site
of impact or compression
Indirect Injury
cranial contents are set into motion by forces other than
the direct contact of the skull with another object
acceleration-deceleration injury
as brain moves within the skull, bridging subdural
vessels are strained (subdural hematomas)
shear and strain injuries (diffuse axonal injury or
concussion)
intracranial content movement abruptly arrested
(contrecoup)
penetrating injury - pressure waves can damage
structures distal to the path of the missile.
Primary Injury
mechanical irreversible damage that occurs at the
time of head trauma:
o brain lacerations, hemorrhages, contusions, and tissue
avulsions
o mechanical cellular disruption and microvascular injury
Case
17 playing soccer
was headed by another player
o No LOC
o Pulled from game kept getting beaten
o Progressive confusion
o Amnestic of the event
Now GCS 15
No Focal Neurologic findings
o ?Imaging
o ?Follow-up
Design: prospective cohort study ( June 2000-December 2002). 9 EDs. 2707 adults
blunt head trauma witnessed LOC, disorientation, or definite amnesia and a GCS
13-15. The CCHR and NOC were compared in a subgroup of 1822 adults with minor
head injury and GCS 15.
Outcomes Neurosurgical intervention and clinically important brain injury evaluated by
CT and a structured follow-up telephone interview.
Results Among 1822 patients with GCS 15, 8 (0.4%) required neurosurgical intervention
and 97 (5.3%) had clinically important brain injury.
NOC and the CCHR both had 100% sensitivity
CCHR was more specific (76.3% vs 12.1%, P.001) (neurosurgical intervention)
CT rates (52.1% vs 88.0%, P.001)
Conclusion For patients with minor head injury and GCS score of 15, the CCHR and the
NOC have equivalent high sensitivities for need for neurosurgical intervention and
clinically important brain injury, but the CCHR has higher specificity for important
clinical outcomes than does the NOC, and its use may result in reduced imaging
rates.
Concussion
grossly normal structural neuroimaging
Signs: GCS 13-15 at 30 min post injury
Symptoms: confusion and amnesia +/- LOC
focus
orientation
slurred speech / poor coordination
emotional
Course: resolution of symptoms follows a sequential course
GCS <15
Abnormal CT scan: intracranial bleeding, cerebral edema
Seizures
Abnormal INR PTT
Return to play
McCrory P, Johnston K, Meeuwisse W, Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the 2nd
International Conference on Concussion in Sport, Prague 2004. Br J Sports Med 2005;39(4):196-204.
Case
20 year-old university student
presents after a morning game of baseball in which he
collided with another player
Brief LOC meanwhile she bled profusely from the chin
When he recovered, she offered him a ride to the
emergency room, which he declined, saying "it's just a
bump on the head"
He returned to his room and told his roommates the story,
and remained lucid through the morning.
After lunch restless with a severe HA seizure.
OE: LOC
R pupil dilated
Epidural Hematoma
Epidural Hematoma
Usually due to arterial injury
o trauma to the skull base tearing of middle meningeal artery
o results in hemorrhage
Occasionally
anterior cranial fossa rupture of the anterior meningeal artery
vertex dural arteriovenous fistula
Epidural-Pathophysiology
Blow to the head fractures the temporal bone and
ruptures branches of the middle meningeal artery, lies
outside the dura.
The ruptured artery then leaks blood between the inner
skull and the dura.
The increasing volume of blood strips the dura from the
inside of the skull, forming, in effect, a large blood blister
which pushes against the brain as it expands.
The hematoma may strip the dura from the bone as far
as the sutures of the skull.
This stripping of the dura from the calvarium may be part
of the reason for the severe headache.
Epidural Hematoma - Hx
Mean age 20-30 years
Caused by MVC, Falls, Assaults
o Skull # present 75-95% of the time
Epidural - Management
Neurologic emergency
o hematoma expansion
o elevated intracranial pressure
o brain herniation
Operative
o Craniotomy and hematoma evacuation
o Burr Hole
Non-Operative
o Close observation
o serial brain imaging
hematoma enlargement
neurologic deterioration
Epidural - ?Surgical
An EDH > 30 cm3 should be surgically evacuated
regardless of the patient's GCS
GCS < 9 with anisocoria evacuation ASAP
An EDH
o
o
o
o
o
< 30 cm3
< 15-mm thickness
< 5-mm midline shift (MLS) in patients
with a GCS > 8
w/o focal deficit
Case
83 presents with confusion
Gradually increasing over the past week
No history of trauma
GCS: 14
CN: ii-xii normal no focal findings
Urine + nitrates/leuks epithelials
CT Head
Subdural Hematoma
Subdural Hematoma
SDHs form b/w the dura and the brain
Usually they are caused by the movement of the brain
relative to the skull
o acceleration-deceleration injuries
Acute SDH
24 hours post trauma
LOC;
lucid interval: 50% - 70% mentation
Subacute SDH
symptomatic 24h - 2 wks post injury
CT: hypodense or isodense lesion
absence of sulci
shift
contrast detection of isodense lesions
Chronic SDH
>2 weeks post trauma
Hemiparesis or Weakness: ~45%
LOC: ~50%
Case
51 MVC single vehicle at highway
speeds off road and into a tree
?LOC
GCS 8 (scene) 8 (now)
Subarachnoid Hemorrhage
Traumatic SAH
TSAH is defined as blood within the CSF and
meningeal intima
o results from tears of small subarachnoid vessels
Traumatic SAH
contrast CT: density in basilar cisterns
density interhemispheric fissures/sulci
prognosis reasonable
cerebral vasospasm cerebral ischemia
Chicken vs Egg
Did this patient lose consciousness while driving
because of spontaneous SAH and subsequently
crash his car, or did the patient sustain head
injury from the motor vehicle accident causing
traumatic SAH?
cerebral angiogram to exclude an underlying
aneurysm or vascular malformation
SKULL FRACTURES
Fractures
Sutures
Craniectomy
o underlying brain is damaged and swollen
?CSF Leak
Dab fluid on a tissue paper,
a clear ring of wet tissue beyond the blood
stain, called a "halo" or "ring" sign
Focused Hx
Mechanism
LOC
Ambulatory at scene
GCS at scene
Focused Physical
ABCs
ATLS protocol
GCS
Signs of external injury
Pupils
Check Ears/Nose
Extremities - movement
4. Spontaneous
3. To voice
2. To pain
1. None
6. Obeys commands
5. Localizes pain
4. Withdraws from pain
3. Abnormal flexion
2. Abnormal extension
1. None
Emergent Management of
Closed Head Injury
Case
22 bicycle vs truck
LOC
Agitated at the scene
GCS
o Opens eyes to pain 2
o Withdraws 4
o Sounds no inteligible words 2
Outline
Airway
Avoid Hypoxia
Avoid Hypotension
Brain Specific Therapies
o
o
o
o
o
Position
Hyperventilation
Mannitol
Hypertonic Saline
Cooling
Airway
Capture it!
How you do it probably does not have a great
effect on neurological outcome unless you
cause hypoxemia or hypotension
There is little evidence-based medicine to
guide the choice of agents
Intubation Indications*
*Eastern Association For The Surgery of Trauma, 2003; NICE guidelines, 2003
Case
Paramedics state his GCS was 7 or 8
at the scene
Should they have intubated?
Methods: BeforeAfter system wide controlled clinical trial conducted in 17 cities. Adult patients who
had experienced major trauma in a BLS phase and a subsequent ALS phase (during which
paramedics were able to perform intubation and administer fluids and drugs intravenously). The
primary outcome was survival to hospital discharge.
Results:
Survival did not differ overall (81.1% ALS v. 81.8% among those in the BLS; p=0.65)
Among patients with GCS < 9, survival was with ALS (50.9% v. 60.0%; p=0.02)
The adjusted odds of death for the advanced life-support v. basic life-support phases were nonsignificant (1.2, 95% confidence interval 0.91.7; p=0.16)
Interpretation: The OPALS Major Trauma Study showed that systemwide implementation of full
advanced life-support programs did not decrease mortality or morbidity for major trauma patients.
We also found that during the ALS phase, mortality was greater among patients with GCS < 9.
Airway
Preparation and Preoxygenation
Prevent ICP rise
o Lidocaine 1.5-2 mg/kg IV
o Rocuronium 0.06 - 0.1 mg/kg (defasciculating dose)
o Fentanyl 3 ug/kg IVP
Sedation
o
o
o
o
Airway - Intubation
Lidocaine (1.5 to 2 mg/kg IV push)
may cough reflex, HTN response, ICP
Case
22 with presumed CHI
Now intubated.
What are your priorities?
AVOID HYPOXEMIA
Main Results: Mean arterial saturation was 81% (SD 24.24); mean arterial systolic
pressure was 112 mm Hg (SD 37.25). Airway obstruction was detected in 22
cases. Twenty-seven patients showed an arterial saturation lower than 90% on
the scene, and 12 had a systolic arterial pressure of less than 100 mm Hg. The
outcome was significantly worse in cases of hypotension, desaturation, or both.
Results:
Worse outcomes were strongly correlated (p < 0.05) with GCS score, age,
pupillary response and size, hypoxia, hyperthermia, and high intracranial
pressure (ICP).
Even a single O2 sat reading < 90% was associated with a significantly worse
outcome
AVOID HYPOTENSION
100
90
80
70
60
50
40
30
20
10
0
Favourable outcome
Unfavourable outcome
none
early
late
both
Timing of hypotension (SBP < 90 mmHg)
Hypotension
Single occurrence of BP (SBP<90mmHg)
o doubles mortality*
o disability in survivors of head injury*
duration and frequency = prognosis**
*Chesnut et al., 1993; Management and Prognosis of Severe Traumatic Brain Injury, 2000
**Schierhout and Roberts, 2000
Hypotension
Case
Asymetric Pupils L fixed and dilated
What is happening?
What would you like to do?
Herniation
Position
Maximize venous outflow from the head
o excessive flexion or rotation of the neck
o avoid restrictive neck taping
o minimize stimuli that could induce Valsalva
(i.e. suctioning)
Hyperventilation
Once a mainstay for treatment of ICP
Concerns about cerebral ischemia
o difficult to demonstrate
ml/100g/min
ml/100g/min
60
60
PaCO2: 38 mmHg
PaCO2: 25 mmHg
Mannitol
Mannitol
Benefits:
o Plasma expanding effect
o Reduces hematocrit and viscosity
o cerebral blood flow
o Osmotic effect creates a fluid gradient out
of cells. This osmotic effect initially
decreases intracellular edema, thus
decreases ICP
Mannitol
Drawbacks:
o Osmotic diuresis
o HYPOTENSION
o May accumulate in the brain and result is a
reverse osmotic shift potentially increasing
ICP
o Acute renal failure
Mannitol
Indications: (prior to ICP monitoring)
1. Signs of transtentorial herniation
2. Progressive neurological deterioration
Hypertonic Saline
Hyperosmotic agents
Mannitol effective through non- osmotic effects
Problems with big fluid shifts from diuresis
Increasing interest in use of hypertonic saline (3-24%)
? more effective with fewer side effects.
Outcome with Na+; survival with Na+ 180 mmol/l!
Methods: Consecutive patients with clinical TTH treated with 23.4% saline (30 to
60mL) were included in a retrospective cohort. Factors associated with successful
reversal of TTH were determined.
Results: 76 TTH events. In addition to 23.4% saline, TTH management included
hyperventilation (70% of events), mannitol (57%), propofol (62%), pentobarbital (15%),
ventriculostomy drainage (27%), and decompressive hemicraniectomy (18%).
Reversal of TTH occurred in 57/76 events (75%).
Reversal of TTH was predicted by a 5 mmol/L rise in serum sodium concentration (p
0.001) or an absolute serum sodium of 145 mmol/L (p 0.007) 1 hour after 23.4%
saline.
Adverse effects included transient hypotension in 13 events (17%); no evidence of
central pontine myelinolysis was detected on post-herniation MRI (n 18). Twenty-two
patients (32%) survived to discharge, with severe disability in 17 and mild to moderate
disability in 5.
Conclusion: Treatment with 23.4% saline was associated with rapid reversal of
transtentorial herniation (TTH) and reduced intracranial pressure, and had few adverse
effects. Outcomes of TTH were poor, but medical reversal may extend the window for
adjunctive treatments.
Case
The R2 ER resident on NSx asks what
you think his chances are of putting in a
EVD?
What are the indications for ICP
monitoring?
Antiepileptic therapy
Antiepileptic therapy
Seizure incidence
12% blunt trauma
50% penetrating head injury
Anti-epileptic
Acute Treatment
Lorazepam (0.05-0.15 mg/kg IV, over 2-5 min - max 4 mg)
Diazepam (0.1 mg/kg, up to 5 mg IV, Q10 min - max20 mg)
Prophylaxis
phenytoin (13 to 18 mg/kg IV)
fosphenytoin (13 to 18 phenytoin equivalents/kg)
Selection criteria
o
Two reviewers
Relative risks and 95% confidence intervals (95%CI) were calculated
Main results
o
o
o
o
All randomised trials of anti-epileptic agents, in which study participants had a clinically defined
acute traumatic head injury of any severity. Trials in which the intervention was started more than
eight weeks after injury were excluded.
Authors' conclusions
o
o
o
o
Prior Hx of seizures
*Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed.
Blood Glucose
Blood Glucose
Lam et al found 43% of patients with severe
brain injury to have admission blood glucose
levels above 11.1 mM
Rovlias and Kotsou showed postoperative
glucose levels, independent of their relationship
with GCS, significantly contributed to the
prediction of the patients prognosis
Brain pH
Brain pH
7.5
6.5
6
0
10
Glucose
15
20
Steroids
Steroids
Beneficial in tumors
Decreases cerebral edema
Many reasonable sized RCTs that have
failed to show benefit.
Some have shown mild benefits in
subgroup analysis
Not recomended
Cooling
Therapeutic Hypothermia:
Experimental Evidence
NABIS:H I
AIM
To determine whether surface-induced moderate
hypothermia (33.0o C), begun rapidly after severe
traumatic brain injury (GCS 3-8) and maintained for 48
hours will improve outcome with low toxicity
NABIS:H I
Outcomes
NABIS:H I
Data
Target Temp
8.4 + 3 hrs
Temperature
Future Directions
Questions?
Acknowledgements
Dr. Jason Lord
Dr. David Zygun
Trauma CT
Communicating vs non-communicating
Infarction/Inflammation/Tumor
Is there Hydrocephalus?
o
Small ventricles
Small basilar cisterns
General effacement of cortical sulci
Diffuse loss of grey-white differentiation
Effacement of sulci
Head CT
Blood Can Be Very Bad
Blood
Cisterns
Brain
Ventricles
Bone
Blood
Cisterns
Brain
Ventricles
Bone
Blood
Cisterns
Brain
Ventricles
Bone
Blood
Cisterns
Brain
Ventricles
Bone
Blood
Cisterns
Brain
Ventricles
Bone
CT Scan Basics
A CT image is a computer-generated
picture based on multiple x-ray
exposures taken around the periphery
of the subject
X-rays are passed through the subject,
and a scanning device measures the
transmitted radiation
The denser the object, the more the
beam is attenuated, and hence fewer xrays make it to the sensor
CT Scan Basics
Posterior Fossa
Brainstem
Cerebellum
Skull Base
Clinoids
Petrosal bone
Sphenoid bone
Sella turcica
Sinuses
Sagittal View
Cisterns
CT Scan
Cisterns at Cerebral
Peduncles Level
CT Scan
CT Scan
CT Scan
Ventricles
CSF Production
Produced in choroid plexus in the lateral
Ventricles Foramen of Monroe IIIrd
Ventricle Acqueduct of Sylvius IVth
Ventricle Lushka/Magendie
0.5-1 cc/min
Adult CSF volume is approx. 150 ccs
Adult CSF production is ~ 500-700 cc/day
B is for Blood
Is blood present?
o If so, where is it?
o If so, what effect is it having?
Blood becomes
isodense at approx 1
week
Blood becomes
isodense at approx 1
week
Epidural Hematoma
Lens shaped
Does not cross sutures
Classically described with
injury to middle meningeal
artery
mortality if treated prior to
unconsciousness (< 20%)
CT Scan
CT Scans
Subdural Hematoma
CT Scan
CT Scan
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
Blood in the cisterns/cortical gyral surface
o Aneurysms responsible for 75-80% of SAH
o AVMs responsible for 4-5%
o Vasculitis accounts for small proportion (<1%)
o No cause is found in 10-15%
o 20% will have associated acute hydrocephalus
163
164
C is for CISTERNS
4 key cisterns
o Circummesencephalic
o Suprasellar
o Quadrigeminal
o Sylvian
Cisterns
2 Key questions to answer regarding
cisterns:
o Is there blood?
o Are the cisterns open?
B is for BRAIN
(Blood Can Be Very Bad)
171
Tumor
Atrophy
Abscess
Hemorrhagic Contusion
Mass Effect
Stroke
Intracranial Air
Intracranial Air
Intracranial Air
V is for VENTRICLES
(Blood Can Be Very Bad)
BONE
No Worries
If
No blood is seen
All cisterns are present/open
The brain is symmetric
with Normal gray-white diff
The ventricles are symmetric
without dilation
There is no fractured bone
Practice CT