Traumatic Brain Injury

Shantaveer
Gangu
MentorDr.Baldauf MD

Demographics
Account for 75% all pediatric trauma
hospitalizations
80% of trauma related deaths in children
Domestic falls, MVAs, recreational injuries
and child abuse account for majority of
them.
Gang and drug related assaults are on a rise.
Firearm injuries to brain account for 12%
pediatric deaths.

Pathophysiology of Brain
Injury

Primary Brain Injury

Cerebral
Contusion
Most common Focal
brain Injury
Sites Impact site/
under skull #
Anteroinferior frontal
Anterior Temporal
Occipital Regions
Petechial
hemorrahges
coalesce
Intracerebral
Hematomas later on.

DAI
Hallmark of severe
traumatic Brain Injury
Differential Movement
of Adjacent regions of
Brain during
acceleration and
Deceleration.
DAI is major cause of
prolonged COMA after
TBI, probably due to
disruption of
Ascending Reticular
connections to Cortex.
Angular forces >
Oblique/ Sagital Forces

The shorn Axons

retract and are
evident
histologically as
RETRACTION BALLS.
Located
predominantly in
1.CORPUS
CALLOSUM
2.PERIVENTRICULAR
WHITE MATTER
3.BASAL GANGLIA
4.BRAIN STEM

Secondary Brain Injury

Biochemical
Cascade
AA/Neurotransmitter
release

Blood Flow
changes(Global/reg
ional)
Uncoupling of
Substrate delivery
and extraction
CBF
CMRoxy

Intracellular Ca++ OEF/GEF CMRgluco

se
accumulation and
cytoskeletal/
enzymatic breakdown
Extracellular
Cytokines and GF
Generation of free
radicals

External
Compression
Intraparenchymal
Extraxial
(subdural/epidural)

Pneumocephalus
Depressed skull
fracture

Initial Stabilization
Initial assessment and resuscitative
efforts proceed concurrently.
Few things to watch for,
1.Airway
2.Cervical spine injury
3.Hypotension
4.Hypothermia
5.Neurogenic Hypertension

Cervical Spine X-ray: Lateral view.1,Vertebral body

(TH1).2,Spinous process of C7.3,Lamina.4,Inferior articular
process.5,Superior articular process.6,Spinous process of
C2.7,Odontoid process.8,Anterior arch of C1 (Atlas).9,Trachea.

Neurological Assessment
Rapid Trauma Neurological Examination
1.
2.
3.
4.
5.
6.
7.
8.
9.

Level Of Consciousness
Pupils
Eom
Fundi
Extremity Movement
Response To Pain
Deep Tendon Reflexes
Plantar Responses
Brainstem Reflexes

Level Of Consciousness
Glasgow Coma Scale
Eye Opening
Spontaneous
To Voice
3
To Pain
None
1

Best Verbal
4 Oriented

Best Motor
Obeys
Command

Localizes

Withdraws

Incomprehensible 2

Flexion

None

Extension

None

Confused
2 Inappropriate

Children's Coma Scale

Ocular response

Verbal response

Motor response

Opens eyes spontaneously

4

Smiles, orientated
to sounds, follows
objects, interacts.
5

Infant moves spontaneousl

or purposefully 6

EOMI, reactive pupils

( opens eyes to speech)
3

Cries but
consolable,
inappropriate
interaction 4

Infant withdraws from touch

5

EOM impaired, fixed pupils

(opens eyes to painful
stimuli)
2

Inconsistently
inconsolable,
moaning
3

Infant withdraws from pain

4

EOM paralyzed, fixed pupils

( doesnt open eyes)
1

Inconsolable,
agitated
2

Abnormal flexion to pain fo

an infant (decorticate
response) 3

No verbal response
1

Extension to pain
(decerebrate response) 2
No motor response

Pupillary
Exam
Pupillary size is
balance b/n
Sympath and
parasympatheti
c influences.
Size, shape and
reactivity to
light are tested
parameters.

Mydriasis

Miosis

3 Cr.N.
damageMydriasis

Carotid A.
injury in neck
or skull base

Unilateral
mydriasis
Transtentorial (
Uncal)
Herniation

Horners
syndromeMiosis with
Ipsilateral
ptosis and
anhydrosis.

Traumatic
iridoplegia

Hypothalamic,
cervicothoracic
or direct orbital
injury.

Seizure/
postictal state
Atropine /
Sympathomim
etics

Eye Movements
SO4,LR6, All3
Injury location

Abnormality

Cavernous sinus/Sup Orbital

fissure

All 3 Cr.Ns ( 3,4,6) are affected +

V1 division

Transtentorial ( Uncal ) herniation

3 Cr.N

Raised ICP ( false localizing sign)

Isolated Abducens(6) palsy

Frontal eyes field ( brodmans

area 8)

Ipsilateral tonic conjugate

deviation

Seizure involving frontal eyes field Conjugate deviation to

contralateral side
Occipital lobe injury ( unilateral)

Hemianopsia + ipsilateral
conjugate gaze preference

Brainstem Reflexes
Facial palsy unilateral

7 N injury- Basilar skull #

Corneal reflex ( V1+V2)

Rostral Pontine function

Dolls eye maneuver

Vestibuloocular function

Ice water caloric test ( never in

awake child)

COWS normal response

Coma same side deviation
Stuporous/obtunded nystagmus
to contralateral rapid component

Gag and cough reflex

9,10th N + brainstem swallowing

centers

Periodic( Cheyne-stokes)

b/l hemispheric/diencephalic
injury to as caudal as upper pons

Apneustic ( prolonged ispiratory

plateau)

Mid- caudal pons injury

Ataxic breathing( irregular

stuttering resp)

Medullary respiratory generator

center.

Deep tendon and superficial

reflexes
DTRs exaggerated after TBI due to cortical
disinhibition
Decreased / absent after Spinal cord injury
Asymmetric DTRs unilateral brain/spine
injury
Superficial lost/decreased in corticospinal
dysfunction and helpful in localizing lesions
Plantar response
Normal reflex

Intact descending corticospinal

inhibition

Positive Babinski

Interrupted inhibition pathways

Neurodiagnostic Evaluation
Skull Radiograph

Controversial usage, costs>

benefits

CT
Contiguous slices from vertex to
foramen Magnum.
Extend to C3 if upper spine #
suspected
Brain, Blood and Bone windows
May miss # that run parallel to CT
slice and located at vertex.

Indications controversial, a must in

1.Penetrating head trauma
2.basilar/ depressed skull #
3.Posttraumatic seizure
4.Severe head injury
In addition anyone with,
1.Altered level of consiousness
2.Focal deficits
3.Persistent headaches/ repeated
emesis

MRI

Better than CT in subacute and chronic

phases of injury to detect
contusions/shearing in white
matter/c.callosum
Invaluable in spinal cord injury

Cerebral angiography

Carotid/vertebrobasilar
dissections/occlusions

Clinical Features In Head

Trauma

Scalp Injuries
Skull Fractures
Depressed Skull Fractures
Basilar Skull Fractures
Vascular Injuries
Penetrating Head Injury
Intracranial Hemorrhage

Epidural Hematoma
Subdural Hematoma
Subarachnoid Hemorrhage
Intracerebral Hemorrhage

Scalp Injuries
Most are laceration
Simple Linear/ Stellate ED Rx
Extensive, Degloving/Avulsion Repair
GA
Overlying Depressed Skull#, Infections
Repair+ Elevation Of #

Hematomas
Subgaleal
Cephalohematomas
Galeal Apo & Periost

Periost & Skull

Cross Suture Lines

Limited By S.Lines

Hypotension & Anemia(bp,hct)

Calcify And Disfiguring Sx

Skull Fractures
Thin skull #s common place.
Risk of # associated intracranial injuries?
CT to R/o
1. Open
2. Closed
3. Linear (3/4)
4. Comminuted ( multiple branches)
5. Diastatic ( edges split
apart)<3yrleptomeningeal cyst,
cephalomalacia,
6. Depressed
7. Basilar

Depressed Skull #
From focal blow
Closed 10% FND/15% seizures Rx,
for cosmetic reasons
< skull thickness- no elevation
Open/ frontal sinus intracranial wall
elevate and Sx + frontal sinus irrigation
Free floating remove/replace wrt size
and after soaking in abx

Basilar Skull #

Epidural Hematomas (EDH)

Peak incidence in 2nd decade
Source meningeal vessel, Dural
venous sinus, diploic vein from skull #
H/o minor head injury Viz fall
C/f wrt size, location, rate of
accumulation
Lucid interval (33%), non specific
Confusion, lethargy, agitation, focal
neurological deficits.

Diagnosis
CT is diagnostic
Initial Ct Hyperdense Lentiform
collection beneath skull
Actively bleeding- Mixed densities
Severe anemia- isodense/hypodense
Untreated EDH imaging over days
Hyperdense Isodense Hypodense
w.r.t. brain

Treatment
Non surgical
Minimal / no symptoms
Should be located outside of
Temporal or Post fossae
Should be < 40 ml in volume
Should not be associated with
intradural lesions
Should be discovered 6 or more
hours after the injury

Surgical

Subdural Hematoma
Common in infants.
Cause high velocity impact/
assault/ child abuse/ fall from
significant height.
Associated with cerebral contusions
+ DAI
Adults
Source cortical bridging
Child/infantsveins/
Cerebral
convexities
over frontal/
Occipital + Parietal cortex
Dural
venous
sinuses.
temporal regions

Parafalcine ( post falx cerebri),

supratentorial
{ abuse}

50% are unconscious

immediately.
Focal deficits common
Hemiparesis 50%
Pupillary abnormality28-78%
Seizures 6-22%
Rx- larger- urgent
removal
with mass
SmallSmall
effect/ significant
change in conscious/
focal deficits
Small with significant
brain injuries + mass
effect out of proportion
to size of clot

Removed

Non operative approach

SDHs are High density

collections on CT
conforming to convex
surface of brain
Cant cross falx cerebri/
tentorium cerebelli
{ compartmentalized}
Can cross beneath
suture lines
Distorstion of cortical
surface/ effacement of
ipsilateral ventricle/
shift of midline often
noted.

SAH

Trauma is leading cause.

Acute from disruption of
perforating vessels
around circle of Willis in
basal cistern
Delayed from ruptured
pseudo aneurysm.
Rx maintain intravascular
vol to prevent ischemia
from vasospasm.
Mortality 39%
{ national traumatic
coma databank}

Intracere
bral
Rare in Peds.
60%
from small
Bleed
contusions coalesce to
form larger hematoma.
Rarely , violent angular
acceleration bleed in
deep white matter, basal
ganglia, thalamus
Transtentorial Herniation
midbrain bleed ( Duret
hemorrhages)
Common sites
Ant Temporal and Inf
Frontal lobes { impact
against lateral sphenoid
bone/ floor of ant fossa}

CT- hyperdense/mixed
MRI- small petechial
bleed+ DAI
Rx- small- non
operative. Resolve in 23 weeks
Large- Sx drainage.
Repeat CT in small
bleeds after 12-24 hr is
warranted to r/o
coalescence to form
large hematoma.

Penetratin
Infantsg
andHead
children fall on sharp objects
with thin skull and open foraminae could
predispose
for these injuries.
Injury

R/o child abuse

Rx Surgical.
Entry wound debrided and FB removed with in
driven bone fragments.
Peri and post op ABX
Prophylactic anticonvulsants
Adolescents and children Gun Shot Wounds.
( 12%) and increasing annually.
Higher mortality when
1.Low GCS on presentation (3-4)
2.B/L hemispheric /brainstem injury/
intraventricular tracking
3.Hemodynamic instability/ apnea/both
4.Uncontrolled ICP.

CT- localizes bullet

and bone fragments
MRI- non advised till
magnetic properties
of bullet known.
Rx. Surgical
Debridement of entry
and exit wounds
Remove accessible
bullet and bone
Control hemorrhage
Repair Dural
lacerations + closure
of wounds.
NO ATTEMPT TO
REMOVE BULLET OR
BONE BEYOND ENTRY
AND EXIT WOUNDS.

Intracranial Hypertension
Pathophysiology
ICP monitoring and control are the
cornerstones of TBI management
Normal ICP
Adults <10mmhg
Children 3-7mmhg
Infants 1.5- 6mmhg

When to treat?
Adults > 20
Children >15
Infants >10 { Arbitrary numbers most
commonly used, pending outcome studies}

CBF Autoregulation
CPP = MAP- ICP { mmhg}
Normal Brain
CBF maintained within CPP
range of 50-150mmhg as
vessels can expand / constrict
accommodate p changes.
<50 CPP maximal Dilation
occurs CBF falls as CPP drops
>150CPP maximal
Constriction occurs CBF
raises with CPP
TBI
CBF falls b/n 50-80 mmhg of
CPP Range of Hypo perfusion
Auto regulation may be ,
1.Completely lost linear
relation B/n CBF & CPP
2.Incompletely lost Plateau
after CPP of 80 mmhg

Monro-Kellie doctrine
Vol of intracranial
compartment must
remain constant
because of
inelastance of skull
Normal State- ICV is a balance
b/n Blood, brain & CSF.
With ICSOL ICP remains
normal till compensation can
occur
At the Point of decompensation
The ICP starts to increase.
The brains compensatory
reserve is called Compliance
Measure of compliance
1.Volume pressure response
2.Pressure Volume Index
( PVI)
=
V/ LOG P1P2

Transient elevation
in ICP
Lundberg Waves
1. A wave
Duration = 2-15 min
Amplitude = 50-80mmhg
Results from
Transient occlusion of venous
outflow as bridging veins
occlude against
compressed dura. Or
transient vasodialtion and
hence increase CBF as a
response to ischemia
Sustained A waves may
indicate sustained
elevation in ICP and hence
low brain compliance
2. B waves changes in ICP
w.r.t. Ventilation
3. C waves short lived waves
w.r.t. arterial TraubeHerring waves

Shape of ICP wave

form as an
indicator of
Compliance

Normal ICP has 3 wave

forms.
1.Percussion wave- first
and highest amplitude
wave
2.Dicrotic wave
second wave
3.Tidal wave- third and
lowest amplitude
In reduced brain
compliance the Dicrotic
and Tidal waves
augment exceeding the
percussion waves.

ICP measurement
Intraventricular Cath coupled
to ICP transducer is Gold
standard.
Which patients need ICP
monitoring??
1.TBI + abnormal CT scan who
are not following commands
( 50-63%)
2.Comatose + Normal CT had
lower risk ( 13%) unless
associated with
1. Older age
2. Systemic Hypotension ,
<90mmhg
3. Motor posturing, with
these risk is upto 60%
3.Most clinicians use abnormal
CT scan result + low GCS scores
( < 8) as candidates for ICP
monitoring

Device / method

Risk / benefit

1. Intraventricular catheter

Adv- drainage of CSF to reduce

ICP
DisAdv- infection/ ventricular
compression leads to inaccuracy

2. subdural/ subarachnoid bolts

( Philadelphia, Leeds, Richmond
bolts)

Occlusion of port in device leads

to inaccuracy

3. Fiberoptic cath ( Camino labs)

Improved fidelity & longevity

Can be placed Intraparenchymal/
intraventricular/ subdural
Used to drain CSF
Accuracy maintained even with
fully collapsed ventricles
Single cath can be used as long
as needed

Non invasive ICP

measurement
Ultrasonographic tech

Pediatr Crit Care Med 2010

Vol. 11, No. 5

Audiological tech- displacement

of TM and perilymphatic pressure
as a correlate of ICP
Infrared light- thickness of CSF
from reflected light as a correlate
of ICP
Arterial BP wave contours and
blood flow velocity
mathematical model
Changes In optical nerve head
with optical coherent tomography
IOP as correlate of ICP

With ICP cutoff of 20mmhg it has

Specificity of 0.7 and sensitivity
of 0.97

Mangement of ICP
Goal to maintain CPP by
Reducing ICP, and/or
Increasing MAP { hyper/normo volumia preffered as
opposed old school Hypovol}
Brief periods of hypotension can double the mortality rates
CPP should be match with cerebral metabolic demand to
avoid hypoperfusion / hypeeperfusion.
Cerebral OEF is helpful as,
Decrease in CBF increase OEF increase AvDo2 fraction
AvDo2= diff b/n O2 content of Arterial jugular mixed
venous blood.
Considering Ao2 as constant, venous O2 alone can solely
be assessed.
Normal svJo2 is 65%, a drop to 50-55% global cerebral
ischemia

Hyperdynamic therapy
To maintain CPP of about >70, by increasing
MAP
{ CPP= MAP-ICP}
IVF- crystalloid/colloid
PRBC if low HCT(<30%)
Pressors as needed ( Dopa, Dobu,Phenylephri)
if autoregulation is intact? incres CPP
vasoconstriction constant CBFless
volume reduction in ICP.
Systemic Hypo ? Vice versa

Increasing CPP by reducing

ICP
Sedation and pain control

Fentanyl/ midazolam drip

Etomidate in initial phase

Quiet envir + min extern stimuli

Pharmacological paralysis if
needed

Increase in Pneumonia+ sepsis

IV/ ET lidocaine ( ET > IV)

During intubation, before ET

suctioning,ET manipulation

Elevation of head end by 2030deg

Red venous press ICP

Can cause orthostatic
changesfall CPP rebound ICP
rise

Excessive PEEP, tight cervical

collar, neck flexion/ rotation

Can rise ICP

Bladder distention rise

Contin drainage

Occult seizures unexplained rise Prophylactic Anticonvulsants

Fever rise

Rx + hypothermia.

Specific measures to reduce

ICP
Hyperventilation

Rapid & effective response.

Red Paco2/incr pH
vasoconstricton Red CBF

Disadvantages
1.paco2 < 30 torr red CBF to
ischemic level
2.Regional variation in autoreg
hyperventilation induced reverse
vascular steal

Current recommendations
1. routine hypervent ( 35 ) not be
used in first 24 hrs
2.Chronic hypervent be avoided
in absence of documented ICP
rise
3.Reserved for deterioration not
responding to other measures.
4.When needed with caution,
PaCo2 never <30 torr.
5.svJo2 can be used as indicator
of extreme ischemia( CBF fall)
6.If used, withdrawn slowly to
avoid rebound rise

 CSF drainage- effective and safe.

Provides gradient for bulk flow of
edema fluid from parenchyma of
brain to ventricles.
Continous 5-10 torr gradient
Intermittent for 1-5 min when
needed.

Diuretics
Mannitol works as osmotic
diuretic extract extra and
intra cellular edema fluid from
brain

Disadv- may preferentially

affect normal areas ( intact
BBB) vs affected zones
( disrupted BBB)

Additional mech reduces blood

viscocity ( by hemodilution) and
improves Rheology Increas
CBF vasocons decreas
volume red ICP.
Risks
1. Repeated dose reduced
osmotic gradient
2. Hyperosmolar state ( serum
osm>320 mOsm) renal
failure, rhabdomyolysis,
hemolysis

3 dosing methods
intermittant boluses when ICP
15-20
Intermittant Q6 hrly
Continous infusion

 Steroids No role currently in TBI

Barbiturates- usually last resort
med.
Pros

Cons

Reduce ICP , CBF,

CMRO2
Inhibit free lipid
peroxidation reduce
cellular damage

Close ICU monitoring

Hypotension
Hyponatremia
Myocardial depression

ALGORITH for
treatment of
elevated ICP with
severe head injury.
( Brain trauma
Foundation,
American
Association of
neurological
Surgeons, Joint
section of
Neurotrauma and
critical care)

Bispectral Index

Bispectral index(BIS) is
one of several recently
developed technologies
which purport to monitor
depth of anesthesia.
Uses ,
1. Monitor depth of anesthesia
2. Reduce incidence of
intraoperative awareness
3. Monitor recovery from brain
injury
4. With ICP to monitor during
therapeutic burst
suppression.
5. 0-100 scale.
6. 40-60 good depth of
Anesthesia.

POST TRAUMATIC SEIZURES

Complicate 10% pediatric head

injuries
1. Impact seizures follow minor
injury , occur on impact
2. Early posttraumatic seizures
within min to hours of injury.
1. No radiological intracranial
injury noted in many cases
2. Do not portend later epilepsy
3. Most do not need Rx
4. Outcome good.

Late seizure >24 hrs after injury

Visible intracranial injury.
Penetrating injuries/
depressed #/ SDH/ Lower GCS
score
Long term risk of epilespy
high- need Rx for 6-12 mo.

Seizure prophylaxis
Only during first week Or
till intracranial
hypertension phase is
passed.
Prolonged usage has
cognitive deficits on
long term follow ups.
Phenytoin commonly used

Thank You