Mechanisms of Injury

Traumatic Brain Injury

Blunt(Closed) Penetrating

Explosion Fall GSW Stab

Blast 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
kernohan’s 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 (Battle’s 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

• 3 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 acceleration-deceleration
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
• Cushing’s Triad
– hypertension
– bradycardia
– altered respirations
• LATE SIGN!

• Why do we get into

Cushing’s 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 X-ray,examination
and reduction
– Uncomplicated and simple fractures will pose little problem for
the athlete’s 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
Critical Care Management in
Traumatic Brain Injury

Dr.(Mrs.) Bibhukalyani Das

Prof. & HOD Neuroanaesthesiology, Neuro ICU &
Pain Clinic
Bangur Institute of Neuroscience & Psychiatry
Kolkata
• 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 ē in 72 hrs.
• Victims :Young males in productive age group
• Children constitute 25-30% of all TBI victims
• Loss of life, Rehab of disabledSig.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 - Admission Investigation & Imaging

Conservative OR
Operative management as per need.
Severe - ICU Management .
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. ē 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 ē 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 Constant intracranial compartments because
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 Ryder - CSF pressure / volume curve
1960 Lundberg - continuous recording of ICP in patients, ICP
waves
1965 Langfitt - volume / pressure relationship
1975 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 the main energy source
Glycogen limited energy reserves
Oxygen 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
Cushing‘s 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 PaCO2
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
BP CPP
Effect
 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 <37ºC,
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.
 Stage 2 - advanced treatment measures:
In stage 2 the following measures can be considered, all of which are optional:
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 (35-36°C) but not severe hypothermia <34°C
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.
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 36-34оС
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.