Head Trauma

Mark Bromley PGY2

Jason Lord FRCPC

 Physiology
Concussion Mild TBI

Epidural Hematoma
Subdural Hematoma
Traumatic SAH
Contusion
Skull Fractures

ED Approach to Head Trauma

Severe Head Injury Mgmt
How to Read a Head CT Brain Death

Pathophysiology

Cerebral Blood Flow

CBF is maintained @ MAP of 60-150

mm Hg

Hypertension, alkalosis, and hypocarbia

promote cerebral vasoconstriction
Hypotension, acidosis, and hypercarbia
cause cerebral vasodilation

Hypotension

Cerebral Blood Flow

In Trauma,
CBF with a disrupted BBB vasogenic edema
CBF CPP
CPP = MAP ICP
CBF is constant when CPP is 50-160 mm Hg
If CPP < 40 mm Hg
o autoregulation of CBF CBF tissue ischemia

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

The cranial vault is normally filled by three things

o brain
o blood
o cerebral spinal fluid.

If a person were to have a brain tumor:

o it displaces one of the normal components (i.e. spinal fluid)
o ICP

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

No specific intervention exists to repair or reverse

primary brain injury
Public health interventions aimed at reducing the
occurrence of head trauma

Secondary Brain Injury

intracellular and extracellular
derangements (metabolic, ischemic, ion
shifting)
All currently used acute therapies for
TBI are directed at reversing or
preventing secondary injury

Secondary Brain Injury

Neurologic outcome is influenced by the extent
and degree of secondary brain injury
Hypotension (sBP < 90 mm Hg) reduces
cerebral perfusion (ischemia and infarction)
Hypoxia (PO2 < 60 mm Hg)
o apnea caused by brainstem compression or injury
o partial airway obstruction
o injury to the chest wall that interferes with normal
respiratory excursion
o pulmonary injury that reduces effective oxygenation

Secondary Brain Injury

Anemia (reduced oxygen-carrying
capacity of the blood)
o Increased mortality when Hct < 30%

Other potential reversible causes of

secondary injury in head injury include
hypercarbia, hyperthermia, coagulopathy,
and seizures

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

Note: Minor Head Injury is defined as a witnessed loss of consciousness,

definite amnesia, or witness disorientation in a patient with a GCS 13-15.

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 and Mild TBI

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

Observation and disposition

Observation is recommended for 24 hours after a mild
TBI because of the risk of intracranial complications
Hospital admission is recommended for patients at risk
for immediate complications from head injury
o
o
o
o

GCS <15
Abnormal CT scan: intracranial bleeding, cerebral edema
Seizures
Abnormal INR PTT

 His Dad take you aside and says theres a

big tourney on the weekend with scouts
flying in to watch.
can he play?

Return to play

Rest until all symptoms have resolved

Graded program of exertion
> 1 day at each level is needed
If any symptoms appear, patients drop back to the previous
asymptomatic level and try again after 24 h

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.

Take Home Concussion

Players should not be allowed to return to play in
the current game or practice
Players should not be left alone, and regular
monitoring for deterioration is essential during
the initial few hours after injury
Return to play must follow a medically
supervised series of steps
Players should never return to play while
symptoms persist

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

In ~15 % of cases, injury to one of the dural sinuses, or

the confluence of sinuses in the posterior cranial fossa,
is the source of hemorrhage

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

Transient LOC with a lucid interval

Symptoms: HA, N/V, drowsiness,
confusion, aphasia, seizures, and
hemiparesis

Epidural Hematoma - Imaging

Head CT fast, simple
lens-shaped pattern
collection is limited by dural attachments
at cranial sutures

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

non-operative mgmt with serial CTs and close

neurological observation in a neurosurgical center

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

Common in patients with brain atrophy (EtOH or elderly)

Superficial bridging vessels traverse greater distances
than in patients with no atrophy (more likely to rupture
with rapid movement of the head)
Occurs in ~30% of patients with severe head trauma
slow bleeding of venous structures delays clinical signs

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

detected on the first CT scan in up to 33% of

patients with severe TBI (incidence of 44% in all
cases of severe head trauma)
incidence of skull fractures and contusions
o GCS SAH
o SAH Outcome

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

Linear skull fracture

low-energy blunt trauma over a wide surface
area of the skull.
Full thickness through bone
of little significance except
when it runs through a vascular channel,
venous sinus groove
suture

Then, it may cause

epidural hematoma
venous sinus thrombosis and occlusion
sutural diastasis

Fractures

Sutures

Greater than 3 mm in width

Widest at the center and
narrow at the ends
Runs through both the outer
and the inner lamina of bone,
hence appears darker
Usually over temporoparietal
area
Usually runs in a straight line
Angular turns

Less than 2 mm in width

Same width throughout
Lighter on x-rays compared
with fracture lines
At specific anatomic sites
Does not run in a straight line
Curvaceous

Basilar skull fracture

Petrous temporal bone: CSF otorrhea and bruising over mastoids

(Battle sign)
Anterior cranial fossa: CSF rhinorrhea and bruising below eyes
(raccoon eyes)
Longitudinal temporal bone ossicular chain disruption and
conductive deafness Facial palsy, nystagmus, and facial numbness
are 2 to VII, VI, and V CN palsy
Transverse temporal bone: VIII CN palsy and labyrinth injury
nystagmus, ataxia, and permanent neural hearing loss
Occipital condylar fracture: coma and have other associated cspine injuries
Vernet syndrome or jugular foramen syndrome is involvement of
IX, X, and XI CN difficulty in phonation, aspiration and ipsilateral
motor paralysis of the vocal cord, soft palate (curtain sign), superior
pharyngeal constrictor, sternocleidomastoid, and trapezius.

Depressed Skull Fracture

Elevation
o depressed segment is > 5mm below inner
table
o gross contamination,
o dural tear with pneumocephalus
o underlying hematoma

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

ED Approach to Head Trauma

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

Glasgow Coma Scale*

Eye Opening (E)

Motor response (M)

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

Verbal Responses (V)

5. Oriented
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
1. None

*Developed for evaluation of head trauma 6 hours post injury

Deceased and rocks have GCS 3

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

Indications for ICP Monitoring

Surgical Management

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*

Coma (i.e. GCS 8) or significantly deteriorating LOC

Loss of protective laryngeal reflexes
Copious bleeding into mouth
Respiratory arrhythmia
Ventilatory insufficiency
o clinical decision - not necessarily requiring ABG

Bilateral mandibular fracture

Any facial injury compromising airway
Seizures
Any other injury that requires ventilation/intubation

*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

Prevent Vagally stimulated bradycardia

o Atropine 0.01 mg/kg IV (Minimum dose: 0.1 mg)

Sedation
o
o
o
o

Etomidate 0.3 mg/kg IVP OR

Thiopental (Pentothal) 4 mg/kg IVP (IF BP stable) OR
Propofol 2mg/kg IVP OR
Midazolam 0.1mg/kg (max 5mg) IVP

Apply cricoid pressure

Muscle relaxants
o Succinylcholine 1.5 mg/kg IV OR
o Rocuronium 0.6 mg/kg IV

Airway - Intubation
Lidocaine (1.5 to 2 mg/kg IV push)
may cough reflex, HTN response, ICP

Succinylcholine fasciculations ICP

premedicate w a subparalytic dose of a nondepolarizing agent

Etomidate (0.3 mg/kg IV)

good effect on ICP CBF and metabolism
minimal adverse effects on BP
Minimal respiratory depressant effects

Methods: Medline literature search was undertaken for evidence of the

effect of succinylcholine (SCH) on the intracranial pressure (ICP) of
patients with acute brain injury and whether pretreatment with a
defasciculating dose of competitive neuromuscular blocker is beneficial
in this patient group.
Conclusions: Studies were weak and small
For those patients suffering acute TBI the authors could find no studies
that investigated the issue of pretreatment with defasciculating doses of
competitive neuromuscular blockers and their effect on ICP in patients
given SCH.
SCH caused ICP for patients undergoing neurosurgery for brain
tumours with elective anaesthesia and that pretreatment with
defasciculating doses of neuromuscular blockers reduced such
increases. ?impact on outcome.

Background: laryngeal instrumentation and intubation is

associated with a marked, transient rise in ICP.
Methods: A literature search was carried out to identify studies
in which intravenous lidocaine was used as a pretreatment for
RSI in major head injury. Any link to an improved neurological
outcome was also sought.
Results: No evidence was found to support the use of
intravenous lidocaine as a pretreatment for RSI in patients with
head injury and its use should only occur in clinical trials.

Case
22 with presumed CHI
Now intubated.
What are your priorities?

AVOID HYPOXEMIA

Hypoxemia and Arterial Hypotension at the Accident

Scene in Head Injury
Stocchetti, Nino MD; Furlan, Adriano MD; Volta, Franco MD

Design: Prospective, observational study.

Materials and Methods: Arterial Hbo2 was measured before tracheal intubation
at the accident scene in 49 consecutive patients with head injuries. Arterial
pressure was measured using a sphygmomanometer.

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.

Conclusions: Hypoxemia and shock are frequent findings on patients at the

accident scene. Hypoxemia is more frequently detected and promptly corrected,
while arterial hypotension is more difficult to control. Both insults may have a
significant impact on outcome
Volume 40(5) May 1996 pp 764-767

Methods: 846 cases of severe TBI (GCS 8) were analyzed retrospectively to

clarify the effects of multiple factors on the prognosis of patients.

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

Conclusions: These findings indicate that prevention of hypoxia, control of high

ICP, and prevention of hyperthermia may improve outcome in patients with TBI

desaturation occurs rapidly below

SpO2 of 9092%

AVOID HYPOTENSION

% of patients in outcome group

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)

Traumatic Coma Data Bank 1991

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

Mean Arterial Pressure

What is adequate?
o Enough to maintain CBF
Normally (MAP 60-150 mmHg and ICP ~10 mmHg)
o CPP is normally between 70 and 90 mmHg
o <70 mmHg for a sustained period ischemic injury

Outside of the limits of autoregulation

o MAP raises CPP
o ICP lowers CPP

Blood pressure control

BP should maintain CPP>60 mmHg
o pressors can be used safely without further ICP
in the setting of sedation ?iatrogenic BP
o Hypertension should generally not be treated

Avoid CPP <60 mmHg or

o normalization of BP in chronic HTN
the autoregulatory curve has shifted to the right

Case
Asymetric Pupils L fixed and dilated
What is happening?
What would you like to do?

Herniation

1) The brain squeezes under the falx cerebri in cingulate herniation

2)The brainstem herniates caudally
3) The uncus and the hippocampal gyrus herniate into the tentorial notch
4)The cerebellar tonsils herniate through the foramen magnum in tonsillar herniation.

 Uncus can squeeze the third cranial nerve

which controls ipsilateral parasympathetic
input to the eye
o pupillary dilatation
o deviation of the eye to "down and out"

Brain Specific Therapies

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)

Position the head above the heart (30o)

o head elevation may lower CPP

Hyperventilation
Once a mainstay for treatment of ICP
Concerns about cerebral ischemia
o difficult to demonstrate

Outcome worse with hyperventilation in

some studies of head injury

Adverse effects of prolonged hyperventilation in patients

with severe head injury: a randomized clinical trial
Methods: RCT
normal ventilation PaCO2 35Hg
hyperventilation PaCO2 25Hg
hyperventilation plus THAM
Outcome: GCS at 3/6/12 months
Results:
Those in the 25 mm Hg group did worse

Muizelaar et. al. 1991

Acute head injury (6 hrs post impact)

Areas in red show regions with rCBF < 20 ml/100g/min)

ml/100g/min

ml/100g/min

60

60

(Coles et al. Crit Care Med 2002)

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

not attributable to extra-crainal complications

Dose: 0.25 1g/kg IV bolus

Avoid hypovolemia
(foley recommended)

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!

Dose: 2-4 ml/Kg 5% NaCl

Max Na+ ~ 160 mmol/l
Max osmol ~ 325 mOsm/l

Munar et al. J Neurotrauma 2000. 17:41-51.

Horn et al. Neurol Res 1999;21: 758-64
Quereshi et al. J Trauma 1999;47:659-65.
Simma et al. Crit Care Med 1998;26:1265-70.
Clark & Kochanek. Crit Care Med 1998;26:1161-2.
Doyle et al. J Trauma 2001; 50: 367-383.
Petersen et al. Crit Care Med 2000;28:1136-1143

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

Seizures can contribute to

Hypoxia, Hypercarbia
Release of excitatory neurotransmitters
ICP

Anticonvulsant therapy if seizing

?Prophylaxis
o There are no clear guidelines
o ? high-risk mass lesions

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

Data collection and analysis

o
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.

10 eligible RCTs, 2036 participants

(RR) for early seizure prevention was 0.34 (95%CI 0.21, 0.54)
risk of early seizures by 66%
Seizure control in the acute phase did not show mortality (RR = 1.15; 95%CI 0.89, 1.51)
death/disability (RR = 1.28; 95%CI 0.90, 1.81)

Authors' conclusions
o
o
o
o

Prophylactic anti-epileptics reduce early seizures

No reduction in late seizures
No effect on death and neurological disability
Insufficient evidence is available to establish the net benefit of prophylactic treatment at any time
after injury.

Seizure Prophylaxis in Severe Head Trauma

Indications*

Depressed skull fracture

Paralyzed and intubated patient
Seizure at the time of injury
Seizure at ED presentation
Penetrating brain injury
Severe head injury (GCS 8)
Acute subdural hematoma
Acute epidural hematoma
Acute intracranial hemorrhage

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

Hyperglycemia-Induced Neuronal Injury

? increased tissue lactic acidosis
Brain tissue acidosis is associated with mortality following
head injury
glucose supply during incomplete ischemia may allow
continuation of anaerobic glycolysis, which would lead to
accumulation of lactate and subsequently to tissue acidosis
Injured brain cells may not be able to metabolize excess or
even normal levels of glucose through the oxidative
pathway.

Hyperglycemia-Induced Neuronal Injury

Intracellular acidosis triggers calcium entry into
the cell, lipolytic release of cytotoxic free fatty
acids and glutamate and eventually cell death
glucose available to the glycolytic pathway,
treatment of hyperglycemia could theoretically
lactate production, pH, result in less neuronal
damage, and improve patient outcome

Brain Tissue pH and Blood Glucose

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

a man will survive longer in winter than in

summer, whatever be the part of the head in
which the wound is situated.

On Injuries of the Head

400 B.C.E

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

Therapeutic Hypothermia: Cardiac Arrest

Hypothermia Treatment Window

Future Directions

ER physicians role in brain death

Hope Program
http://iweb.calgaryhealthregion.ca/hope

Questions?

Acknowledgements
Dr. Jason Lord
Dr. David Zygun

How to Read a Head CT

How to Read a Head CT

Has assumed a critical role in the daily practice
of Emergency Medicine for evaluating
intracranial emergencies
Most practitioners have limited experience with
interpretation
In many situations, the Emergency Physician
must initially interpret and act on the CT without
specialist assistance

Trauma CT

Is there evidence of hemorrhage?

o
o
o
o

Is there mass effect?

o

Communicating vs non-communicating

Have the cisterns been scrutinized for hemorrhage and size?

Is there evidence of infarction?
Is there calcification?
Have the midline structures been examined?
Have all images been analyzed?
o

Infarction/Inflammation/Tumor

Is there Hydrocephalus?
o

Small ventricles
Small basilar cisterns
General effacement of cortical sulci
Diffuse loss of grey-white differentiation

Is there local loss of grey-white differentiation?

o

Effacement of sulci

Is there cerebral edema?

o
o
o
o

Within the ventricles

Within the subdural space
Within the subarachnoid space
Within the epidural space

Scout and bone windows

Will contrast be helpful?

Is the CT interpritation consistent with clinical findings

Head CT
Blood Can Be Very Bad

Blood Can Be Very Bad

Blood
Cisterns
Brain
Ventricles
Bone

Blood Can Be Very Bad

Blood
Cisterns
Brain
Ventricles
Bone

Blood Can Be Very Bad

Blood
Cisterns
Brain
Ventricles
Bone

Blood Can Be Very Bad

Blood
Cisterns
Brain
Ventricles
Bone

Blood Can Be Very Bad

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

The denser the object, the whiter it is on CT

Bone is most dense = + 1000 Hounsfield U
Air is the least dense = - 1000 Hounsfield U

CT Scan Basics: Windowing

Focuses the spectrum of gray-scale used on a particular image

Posterior Fossa

Brainstem
Cerebellum
Skull Base
Clinoids
Petrosal bone
Sphenoid bone
Sella turcica
Sinuses

Sagittal View

Cisterns

CT Scan

Brainstem Lateral View

2nd Key Level

2nd Key Level

2 Key Level Sagittal View

nd

Cisterns at Cerebral
Peduncles Level

CT Scan

CT Scan

3rd Key Level

Cisterns at High Mid-Brain Level

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?

Acute blood is bright white on CT

(once it clots)

Blood becomes
isodense at approx 1
week

Blood becomes hypodense

at approx 2 weeks

Acute blood is bright white on CT

(once it clots)

Blood becomes
isodense at approx 1
week

Blood becomes hypodense

at approximately 2 weeks

Acute blood is bright white on CT

(once it clots)

Blood becomes isodense

at approximately 1 week

Blood becomes hypodense

at approximately 2 weeks

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

Typically falx or sickle-shaped

Crosses sutures
Does not cross midline
Acute subdural is a marker
for severe head injury
(Mortality ~ 80%)
Chronic subdural usually slow
venous bleed and well
tolerated

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

(Blood Can Be Very Bad)

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