Mechanisms of Injury

Traumatic Brain Injury

Blunt(Closed)
Explosion
Blast

Fall

Penetrating
GSW
Stab
Fragment

Motor vehicle crashes (MVC)

CURS

TRAUMATISMELE CRANIO-CEREBRALE

Relative Proportion of Levels of Care for TBI

Source: CDC: Traumatic Brain Injury in the United States, October
2004

50,000
Deaths

235,000
Hospitalizations

1,111,000
Emergency Department Visits

???
Other Medical Care or No Care

Military Context

Blast Wave Physics

Courtesy of Keith Prusaczyk, Ph.D.

Types of Injuries
Primary Injuries

Scalp lacerations
Skull fractures (Linear, depressed, basiliar)
Facial fractures (Le Forte 1 3)
Concussion (mild traumatic brain injury): amnesia
Cerebral contusion
Axial / Extra-axial haematomas
Diffuse axonal injury

Concussion

The diagnostic sign is amnesia

Takes few months to resolve
No morphological abnormality
No abnormalities on radiology
Beware of Second Impact Syndrome

Cerebral Contusions
Frontal & Temporal
regions commonly
Can be multiple and
bilateral
An area of haemorrhage
& oedema
Diagnose by CT / MRI
It is primary injury but
produces secondary
injury due to increased
ICP

Diffuse Axonal Injury

Rotational Forces
Acceleration Deceleration injuries
Neuronal tearing in white matter
Seen on MRI
Suspect if many cerebral contusions
on CT scan and patient has prolonged
coma (>6hrs) with no evidence of a
SOL.

Secondary Injury
Cellular changes
Hypoxia
Hypercarbia
Hypotension
Cerebral oedema
Vasogenic
Cytotoxic

Increased Intra Cranial Pressure

Why Worry?
Increasing ICP
Decreased cerebral perfusion pressure
causing ischaemia
Midline shift causing ventricular obstruction
Herniation

Uncal
Central
Cingulate (subfalcine)
Cerebellar
Transcalvarial

Herniation
Uncal Herniation
Medial temporal lobe (Uncus)
compresses midbrain with
increasing ICP
Pressure in the region of
kernohans notch causes
ipsilateral pupillary dilatation,
ipsi / contralateral
hemiparesis and possible
posterior cerebral artery
compression
Decreased level of
consciousness
Respiratory pattern change
Goal is to prevent this from
occuring

Recognition and
Management of Specific
Head Injuries

Skull Fracture

Cause of Injury
Most common cause is blunt trauma

Signs of Injury
Severe headache and nausea
Palpation may reveal defect in skull
May be blood in the middle ear, ear canal, nose,
ecchymosis around the eyes (raccoon eyes) or behind the
ear (Battles sign)
Cerebrospinal fluid may also appear in ear and nose

Care
Immediate hospitalization and referral to neurosurgeon

Recognition and
Management of Specific
Eye Injuries

Mechanisms of Injury

Collisions

Car hits object

Head hits
windshield
Brain hits inside
of skull

Mechanisms of Injury

Mechanisms of Injury
Brain movement inside the skull
Base of skull is very rough
Most brain movement is at the top
Brain suspended by vessels and
brain tissue that can be torn by
movement, especially at the base

Mechanism of Injuries,
cont.
Rotational injuries
injury occurs accelerationdeceleration of the brain does
not follow straight linear path.
Brain twists and moves at
angles causing stretching and
shearing of brain tissue and
potential vascular injury.

Penetrating
include missile injuries, GSW
or impalement.

Penetrating Mechanism

Response to Injury
Due to increased

blood volume

(not edema)
Natural response
to injury anywhere
on your body
Body rushes
nutrients to heal
injured area

Response to Injury
Increase in
cerebral edema
(water) develops
after 24-48 hours
and peaks in 3-5
days
Not an acute
concern, per say

Intracranial Pressure
The pressure of the brain contents
within the skull is intracranial pressure
(ICP)
The pressure of the blood flowing
through the brain is referred to as the
cerebral perfusion pressure (CPP)
The pressure of the blood in the body is
the mean arterial pressure (MAP)

Intracranial Pressure
MAP (Mean Arterial Pressure) can
be determined by a simple
formula:

MAP = systolic + 2x diastolic

3

Intracranial Pressure
Example of MAP
B/P is 120/80
MAP = 120 + 160 = 280 = 93
mm/hg
3
3

Intracranial Pressure
Intracranial pressure (ICP)is
measured by a device that is
implanted through the skull by a
surgeon
The normal value for ICP is
0 - 10 mm/hg

Intracranial Pressure
Cerebral Perfusion Pressure (CPP)
can be determined by the following
formula:

CPP = MAP - ICP

Normal CPP range is 60 - 150 for
autoregulation to work well!

Intracranial Pressure
Example of CPP
Blood Pressure is 140/80
ICP is 30

CPP = 100 - 30 = 70 mm/hg

Is this enough for autoregulation?
What would happen if the ICP was
80?

Assessment Findings
Cushings Triad
hypertension
bradycardia
altered respirations

LATE SIGN!
Why do we get into
Cushings Triad?

Assessment Findings
BP of 250/130
MAP would be 170!
Why is the MAP so high?
The ICP is 100!
Is this a good thing?
Should we lower the blood
pressure?

 Concussions (Mild Head Injuries)

Characterized by immediate and transient post-traumatic
impairment of neural function

Cause of Injury
Result of direct blow, acceleration/deceleration forces
producing shaking of the brain
Coup mechanism
Contra-coup mechanism

Signs of Injury
Brief periods of diminished consciousness or unconsciousness
that lasts seconds or minutes
Headache, tinnitus, nausea, irritability, confusion,
disorientation, dizziness, posttraumatic amnesia, retrograde
amnesia, concentration difficulty, blurred vision, photophobia,
sleep disturbances

 Care
The decision to return an athlete to competition
following a brain injury is a difficult one that
takes a great deal of consideration
If any loss of consciousness occurs the ATC
must remove the athlete from competition
With any loss of consciousness (LOC) a cervical
spine injury should be assumed
Objective measures (BESS and SAC) should be
used to determine readiness to play
A number of guidelines have been established
in an effort to aid clinicians in their decisions

 Scalp Injuries

Cause of Injury

Blunt trauma or penetrating trauma tends to be

the cause
Can occur in conjunction with serious head trauma

Signs of Injury

Athlete complains of blow to the head

Bleeding is often extensive (difficult to pinpoint exact site)

Care

Clean w/ antiseptic soap and water (remove debris)

Cut away hair if necessary to expose area
Apply firm pressure or astringent to reduce bleeding
Wounds larger than 1/2 inch in length should be referred
Smaller wounds can be covered w/ protective covering
and gauze (use extra adherent)

 Facial Lacerations
Cause of Injury
Result of a direct impact,
and indirect compressive
force or contact w/ a sharp
object

Signs of Injury
Pain
Substantial bleeding

Care
Apply pressure to control
bleeding
Referral to a physician will
be necessary for stitches

 Care
Control bleeding and refer to a physician for Xray,examination and reduction
Uncomplicated and simple fractures will pose
little problem for the athletes quick return
Splinting may be necessary

Recognition and
Management of Specific Ear
Injuries

 Rupture of the Tympanic Membrane

Cause of Injury
Fall or slap to the unprotected ear or sudden underwater variation
can result in a rupture

Signs of Injury
Complaint of loud pop, followed by pain in ear, nausea, vomiting,
and dizziness
Hearing loss, visible rupture (seen through otoscope)

Care
Small to moderate perforations usually heal spontaneously in 1-2
weeks
Infection can occur and must be continually monitored
Should not fly until condition is resolved

Rupture Tympanic
Membrane

Recognition and
Management of Specific
Eye
Injuries
Orbital Hematoma (Black Eye)
Cause of Injury
Blow to the area surrounding the eye

Signs of Injury
Signs of a more serious condition may be
displayed as a subconjunctival hemorrhage
Swelling and discoloration

Care
Cold application for at least 30 minutes,
24 hours of rest if athlete has distorted vision
Do not blow nose after acute eye injury may
increase hemorrhaging

 Orbital Fracture
Cause of Injury
Direct trauma to the eyeball

Signs of Injury

Blurred vision
Diplopia
Restricted eye movement
Downward displacement of the eye
Soft-tissue swelling and hemorrhaging
Numbness
Infraorbital nerve entrapment

Care
X-ray will be necessary to confirm fracture
Antibiotics
Decrease risk of infection (due to proximity of maxillary sinus
and bacteria)

Treat surgically or allow to resolve spontaneously

Orbital Fracture

Management in
Traumatic Brain
Injury
Dr.(Mrs.) Bibhukalyani Das
Prof. & HOD Neuroanaesthesiology,
Neuro ICU & Pain Clinic
Bangur Institute of Neuroscience &
Psychiatry

 TBI is a global public health problem.

Urbanization : Vehicles
Incidence in Developing Countries.
70% victims of RTA sustain TBI
70% of RTA deaths are due to TBI
Majority death occur in 72 hrs.
Victims :Young males in productive age group
Children constitute 25-30% of all TBI victims
Loss of life, Rehab of
disabledSig.Econo.burdn

Pathophysiology:TBI
A. Primary Injury (Br. damage @ impact)
Minor Concussion DAI BS dysf.
Followed by series of secondary events :
(i) Focal hematoma / contusion
(ii)Changes in CBF & CMRO2
(iii) ICP
(iv) Biochemical changes @ Cellular level

B. Secondary Brain Injury (hours to days)

TBI : Clinical Grading

Duration of Unconsciousness & GCS
Mild :
< 30 minutes
13-15
Moderate:
> 30 min. < 6 hours
9-12
Severe :
> 6 hours
8

Mortality in severe TBI is 20-25% even in

neurological centers of excellence.
Intensive care needed to secondary insult

TBI : Management Protocol

Mild -

Discharge with advice

OR watch for 24hrs.

Moderate Imaging

Admission Investigation &

Conservative

OR

Operative management as per

need.

ICU management: Severe

TBI
Aim is to :
1. Optimize O2 & substrate delivery
2. Detect harmful events.
ICU management include :
Intensive monitoring
Intensive therapy

&

ICU management: Severe

TBI
Aim is to :
1. Optimize O2 & substrate delivery
2. Detect harmful events.
ICU management include :
Intensive monitoring
Intensive therapy

&

TBI : ICU Monitoring

1. Clinical Neurological Assessment & serial CT
2. CVS monitoring (HR, ECG, NIBP/IBP, CVP, PCWP)
3. Respiratory : SpO2 , EtCO2, ABG, Serial chest X-ray
4. ICP monitoring
5. Jugular venous O2 saturation & ABG
6. Transcranial Doppler monitoring
7. Evoked potential monitoring
8. Core Temp. monitoring
9. Metabolic monitoring with PET, Br. Microdialysis.
10. Fluid intake /output, Sr. electrolytes, Glucose, BUN
etc.

TBI : ICP monitoring

Importance:
To predict & optimize CPP (MAP-ICP)
Cl. Signs of ICH are late , nonconsistent
Episodic ICP may occur in pts. normal CT /MRI.
Intraventricular Catheter Method is gold standard,
but carries 1 2 % risk of Hmrge ; 8 10% risk of
infection
Epidural & Subdural devices less accurate
Intraparenchymal F.O. probes easy to use,
infection

ICP monitoring(contd.)
3 types of WAVES described by Lundberg A wave : ICP>40mmHg, lasts for 5-20 mins
indicates severe in IC compliance
&
needs aggressive management.
B wave : ICP 20-25 mmHg
Frequency 1-2 /min . Indicate compliance
Needs treatment.
C wave : No clinical significance.

TBI : TCD monitoring

Useful non-invasive CBF monitor

To diagnose Post-traumatic vasospasm
Indirect estimation of ICP or CPP.
MCA commonly used (75-80% IC flow)
Shows Systo., Diasto., Mean CBF velocity
Normal FV = 35 90 cm /sec; > 100 cm/sec in
TBI ;
> 200 cm/sec shows angiographic vasospasm
Contd. ICP Initial & then loss DCBF isolated
systo.spike oscillating flow pattern (onset of IC
circulatory arrest)

TBI : Jugular venous

oxymetry
The device offers 3 indices to assess CBF:
1. Jugular venous oxygen saturation( SjVO2)
60-80% - Normal , > 90% -Hyperaemia
< 50% -Hypoperfusion
2. Cerebral arterio-venous O2 diff.(A-VDO2)
A-VDO2 = CMRO2/ CBF: 5-7.5 vol% Normal
<5 vol % Hyperaemia , >7.5 vol% Hypoperfusion
3. Cerebral O2 extraction (CEO2) 20-40% Normal
> 40% hypoperfusion.

Newer modalities
Direct tissue oximetry : detects regional
ischemia. Normal PbtO2 = 20 40 mmHg ; 8 10
mmHg critical
PbtO2 8.5 mmHg correlates 50% SjvO2
Near infra red spectroscopy (NIRS) : not
quantitative ; Contusion, extracereberal collection
interferes.
Cerebral microdialysis

These are very expensive, not available in many

centers & provide regional information.

Multimodal Evoked
Potential
Functional assessment of neuronal activity
Good predictor of Outcome in TBI
(A) Somato sensory evoked potential (SSEP)
(B) Auditory brainstem evoked potential ( ABEP
)
70-80% good outcome when EP Normal
Poor prognosis when absent
Complex electrical environment of ICU
makes this monitoring difficult.

TBI : Intensive Therapy

Aim is to achieve optimum cerebral perfusion
and prevent secondary ischaemic insults
CPP = MAP ICP : Ideally 60-70 mmHg
ing MAP : volume expansion , ionotrops &
vasopressor
ing ICP : head-up position, hyperventilation ,
diuretics , CNS depressants, drainage of CSF.

Intracranial Pressure (ICP)

The Monro-Kellie Doctrine
Monro, 1783 Constant intracranial volume
Incompresible brain substance
Kellie, 1824
because

Constant intracranial compartments

the skull is a rigid box

Compensatory mechanisms
Drainage of CSF to spinal
compartment
Vasoconstriction

Intracranial Pressure (ICP)

Monitoring
1951

Guillaume and Janny - continuous

monitoring of ventricular pressure in humans

1952

Strain gauge pressure transducers and

polygraph correlation of ICP to physiologicial
manipulations

1953
1960

Ryder - CSF pressure / volume curve

1965
1975

Langfitt - volume / pressure relationship

Lundberg - continuous recording of ICP in

patients, ICP waves
Miller - volume / pressure response
(brain compliance)

CSF pressure / volume curve

Intracranial Pressure (ICP)

ICP Waves
ICP levels

Severely increased 40 mm Hg
Moderately increased
20 -40 mm Hg
Slightly increased
10-20 mm Hg

ICP waves

A waves

50-100 mm Hg, for 5-20

min
headache, nausea, vomiting
B waves
20-40 mm Hg, 1-2 / min
periodic breathing, somnolence
C waves
10-20 mm Hg, 4-8 / min
BP waves

Pathphysiology of Increased ICP

Hydrocephalus
Communicating
Non-communicating
Space occupying lesion (SOL)
Tumor, hematoma/blood clot, contusion
Brain swelling - accumulation of brain
water
Brain edema
Vasogenic
Cellular (cytotoxic)
Vascular congestion - increase CBV

Treatment of Intracranial
Hypertension
Oxygenation and hydration
300 head elevation
Sedation and paralysis
Ventricular CSF drainage
Osmotic therapy - urea, mannitol
Nonosmotic diuretics - furosemide
Corticosteriods
Hyperventilation
Barbiturates, Propofol

The Role of Anti-Seizure Prophylaxis

Following TBI
High risk patients for developing posttraumatic seizure
GCS <10
cortical contusions
depressed skull fracture
subdural hematoma
epidural hematoma
intracerebral hematoma
penetrating head injury
seizure within 24 hrs. of injury
Recommendation

routine seizure prophylaxis later than

1 week after TBI is not recommended.

Cerebral Perfusion Pressure (CPP)

CBF
The critical parameter for brain function
Difficult to quantify and continuously
measured
CPP - estimation of CBF

CPP = MAP - ICP

Mean systolic BP minus intracranial pressure

Cerebral Blood Flow (CBF)

The brain - high metabolically
active organ
2% of total body weight
20% of cardiac output
20% of total body oxygen consumption
Glucose
Glycogen
Oxygen

the main energy source

limited energy reserves
no reserves

Constant supply of nutrients is required

Decreases CBF causes brain ischemia

Cerebral Blood Flow (CBF)

Threshold of CBF and Ischemia
50 ml/100 g/min Normal
25 ml/100 g/min Alteration in consciousness
Abnormal EEG
18 ml/100 g/min Paralysis, aphasia
Loss of evoked potentials Partial Na/K
pump failure
16 ml/100 g/min Complete pump failure
Cytotoxic edema
Calcium channels open
12 ml/100 g/min Cell death

Intracranial Hypertension
Signs and Symptoms
Headache, vomiting, confusion, lethargy, drowsiness,
coma
Changes in vital signs, medullary compression
Cushings triad - experimental, rare in human and trauma,
trminal stages
Herniation signs - pupillary signs: ipsilateral and bilateral
mydriasis
Hemiparesis
Papilledema - in chronic elevation of ICP

Cerebral Autoregulation
Intrinsic mechanisms control cerebral arterioles
diameter - maintain adequate cerebral perfusion in
response to physiological changes
1) Metabolic theory - metabolic requirements
2) Myogenic / pressure theory - systemic BP controls
cerebral perfusion
3) Carbon dioxide (CO2) reactivity - vasodilation and
vasoconstriction in response to PaCO 2
4) Blood viscosity - rheological properties of blood
are
altered by blood viscosity can change CBF

Cerebral Autoregulation
Metabolic Theory
Metabolic requirements control vasomotor
changes
Coupling between metabolism and CBF in
normal conditions
High activity (seizure, fever)
increased metabolism > increases CBF
Low activity (coma, anesthesia, hypothermia)
low metabolism > decreases CBF

Barbiturates in the Control of Intracranial

Hypertension
Cerebral Metabolism

Cerebral Metabolic Demand

(glucose, oxygen)

CBF

CBV
ICP

Side
Effect

BP

CPP

Treatment
Intracranial
pressure
monitoring
Intraparenchymal
Intraventricular
Direct CSF
drainage

Epidural

 CPP managment
Target euvolaemia
Vasopressors
If ICP is less than 20 then continue to monitor and
treat patient
If ICP>20 drain CSF

Assess patient

If ICP is greater than 20 then hyperventilate.

If still then mannitol
If still consider transfer
Consider decompressive craniectomy (DECRA trial)
If still and GCS <4 then think potential organ
donation

Randomised Evaluation of
Surgery with Craniectomy for
Uncontrollable Elevation of
Intra-Cranial Pressure

Stage 1 - initial treatment measures:

Patients will be sedated, analgesed and ventilated. Patients
may or may not be paralysed but this must be noted. They will
be nursed head up with no venous obstruction. Invasive
monitoring (central venous pressure and arterial lines as a
minimum will be applied). Targets for physiological parameters
will be:
Cerebral perfusion pressure > 60 mmHg (central venous
pressure 6-10),
Oxygen saturation >97%,
Arterial CO2 = 4.0-4.5 kPa,
Temperature <37C,
Blood sugar 4-7 mmol/l.

The ICP will be assessed at this stage. If the ICP<20mmHg, the

above medical treatment will continue. If the ICP>20mmHg, a
repeat scan will be considered to investigate the presence of an
evolving mass lesion and stage 2 will be applied.

An external ventricular drain - depending on the size of the

lateral ventricles
Mannitol
Inotropes to increase the mean arterial pressure to maintain a
cerebral perfusion pressure of >60 mmHg.
Arterial carbon dioxide 3.5 to 4.5kPa (can be monitored with
jugular venous oxygen saturation sensors maintaining SjvO2
>55%)
Hypertonic saline
Moderate cooling (35-36C) but not severe hypothermia <34C
Loop diuretics
Steroids (
as physiological replacement or treatment of severe sepsis).

Barbiturates are not implemented as part of stage 2, but are

reserved as part of continued medical treatment following
randomisation. This clause enables a direct comparison
between the efficacy of decompressive craniectomy and
extended medical treatment including the introduction of
barbiturate coma.

Nurse head up
Ventilation
Sedation
Analgesia
+/- Paralysis
Monitoring:
CVP
Arterial line
ICP
ICP > 25
mm Hg
Stage 3
RANDOMISE
MEDICAL
SURGICAL
Continued Medical Treatment*
(stage 2 options) + barbiturates permitted
Decompressive craniectomy**

Stage 2
OPTIONS:
Ventriculostomy
Inotropes
Mannitol
Hypertonic saline
Loop diuretics
Hypothermia 36-34
BARBITURATES NOT
PERMITTED
ICP > 25 mm Hg
1-12 hours post
start stage 2

[Summary of RESCUEicp protocol]

References:
Hutchinson PJ et al; Surgery for Brain Edema, Neurosurgery Focus,May 2007,15;22.
Sahuquillo.J, Arikan.F; Decompressive Craniectomy for the treatment of refractory high intra-cranial
pressure in
traumatic brain injury, The Cochrane Collabaration, Volume(1) 2006.