TRAUMATIC BRAIN INJURY

DR VISHNU V K
JR EMERGENCY MEDICINE , 2ND YEAR
AIIMS ,NEW DELHI
CASE 1
• 25 year old male with h/o RTA 1 hr back , presented to ED
• A- ? Threatened
• B- RR - 15/min , SpO2 – 90%
• C- PR - 60/min , BP – 170/ 100
• D- E1 V2 M3 ; pupils : left - dilated & fixed ,
right – sluggish reaction
secondary survey – laceration over the temporal region
CASE 2
• 19 year old male brought to ED by his friends . while he was playing football he
collided with the opponent player while heading the ball..f/b brief loss of
consciousness..
• A - patent
• B- RR – 18 , SpO2 – 98% , Air entry equal b/l
• C – BP- 110/ 70 , PR – 90/ min ,regular
• D – GCS 13 , pupils – B/L NSRL
• Secondary survey - No injuries
• Disoriented to time & place ; opens eyes only on command
INTROUCTION
• Injury caused to the brain by an external force to head
• Results range in severity from concussion to coma
• Statistics : US
• 2.2 million TBI visits per year
• 280000 hospitalizations per year
• Of them 52000 die

www.brain trauma.org
CPP , ICP & AUTOREGULATION
• Cerebral perfusion pressure = MAP - ICP
• Normal ICP 7 to 15 mm Hg
• Abnormal > 20 mm Hg
• Cerebral auto regulation
• Constant cerebral blood flow over a wide range
of CPP (60 – 150)
MONRO KELLIE DOCTRINE
• VBrain + Vblood + VCSF =
constant
• Increase in volume of any
component in the expense of
other
• Brain is the least compressible
RAISED ICP
• Stage I – compensatory phase
• Stage II – when Lesion continues to
increase ICP increases
• Compromise of oxygenation
• Systemic vasoconstriction

• Stage III – small change in volume cause

drastic elevations in ICP
• Brain herniation
• Cardio respiratory arrest
PRIMARY INJURY SECONDARY
INJURY

Raised ICP Ischemia

ED EVALUATION
• Airway & C spine stabilization
• B - Respiratory rate & pattern , SpO2 ; CCT
differential air entry ?? , Subcutaneous emphesema ?
• C - BP? , Pulse – brady?? ; E -FAST
• D - GCS ?? ; pupils ?
Any FND??
• E - hypothermia ??
AMPLE HISTORY
• A - any known allergies ??
• M – Any medications ??
• Anticoagulants , Anti platelets , B blockers , Insulin

• P - Past medical/surgical history? ; pregnancy?

• T2DM , HTN , Liver disease

• L - last meal ? ; LMP ?

• E – Events related to injury??
• RTA ? Fall? Co passenger injury?
• Treatment received outside
 SECONDARY SURVEY
• Head to toe examination
• Any visible injuries over scalp
• Raccon eyes ? Sub conjunctival haemorrhage ?
• Discharge from nose ?
• Ecchymosses over mastoid?
• Hemotympanum?
• Visible injuries over chest abdomen
• Injury to extremities ? any long bone fracture ?
GCS & PUPILLARY RESPONSE
• GCS – developed by Teasdale & Jennet in 1974
• Predictive ability validated by several studies since
introduction.
• Age + pupillary reflex + GCS = 84% accurate in
predicting out come
• Classification TBI
• Mild – GCS 13 – 15
• Moderate – GCS 9 – 13
• Mild - GCS < 8

J Neurosci Nurs. 2007;39(2):68-72

PUPILLARY RESPONSE
• Abnormalities in pupillary response +
anisocoria – poor neurological outcome
• Levin HS et al
• Choi et al

• Assesing onset of transtendorial herniation +

brain stem compression with pupillary
response
• Gober et al

• Pupillary changes correlated with brainstem

oxygenation & perfusion
• Ritter AM et al.
 PATTERN OF DESCRIPTION OF LOCALIZATION

RESPIRATORY PATTERN
RESPIRATIO PATTERN
N
Cheyne- Rhythmic crescendo bilateral deep
Stokes and decrescendo of rate cerebral lesions or
breathing and depth of some cerebellar
respiration; includes lesions
brief periods of apnea
Central Very deep, very rapid midbrain and
neurogenic respirations with no upper pons
hyperventila apneic periods
tion
Apneustic Prolonged inspiratory middle to lower
breathing and/or expiratory pons
pause of 2-3 seconds
Cluster Clusters of irregular, lower pons or
breathing gasping respirations upper medulla
separated by long
periods of apnea
Ataxic Irregular, random medulla
respirations pattern of deep and
shallow respirations
with irregular apneic
periods
CUSHINGS REFLEX & HERNIATION
• Cushings reflex :
• Hypertension + bradycardia + respiratory depression
• Indicates ICP reached life threatening levels

• Cerebral herniation:
• Increasing cranial volume & ICP overwhelm natural
compensatory capacities of CNS
• Uncal herniation
• Central
• Subfalcine
• Upward Transtentorial
• Tonsillar
UNCAL HERNIATION
• Most common clinically significant herniation
• Compression of ipsilateral uncus on edge of
tendorium cerebelli
• Structures affected :
• Ipsilateral 3rd nerve
• Ipsilateral peduncle (corticospinal fibers)
• Ipsilateral NR & dialated pupil + CL hemiplegia

• Kernohans notch syndrome

• Controlateral cerebral peduncle forced against
opposite tendorial hiatus
• Ipsilateral hemiperisis + ipsilateral non reacting pupil
SEVERE TBI ( GCS < 8)
• Airway management – require intubation with C spine stabilization
• Preinduction agents to lower ICP
• Induction agents
• Short acting preferred
• Etomidate 0.3 mg/kg iv
• Propofol 1-3 mg/kg iv

• Paralytics
• SCH 1 – 1.5 mg/kg iv (avoid in burns ,crush injury)
• Rocuronium 0.6 – 1 mg/kg
POST INTUBATION..
• Place orogastric tube ( avoid naso gastric tube)
• Maintain sedation
• Ventillation strategies
• saturation > 90%
• PaO2 > 60
• Pco2 35 - 45

• No prophylactic hyperventilation
• Muizellar et al. – RCT 77 patients with severe TBI (PaCO2 25 vs PaCO2 35 )
• Worse outcomes for PaCO2 25 at 6 months
CIRCULATION
• Aggressive fluid resuscitation to Prevent hypotension
• Keep SBP > 90 & MAP >80
• Hypotension – independant predictor of outcome
• Chesnut et al . ; Fearnside et al .

• Single episode of hypotension + hypoxia increases mortality by 150%

• Marmarou A et al
RAISED ICP MANAGEMENT
• Look for signs & symptoms
Severe headache
• Patient positioning Visual changes
• MAP must be > 80 Numbness
Change in mental status
• head end elevation 30 deg FND
Seizure
• Mannitol
Bradycardia
• Osmotic diuretic ; expands plasma volume Pupillary dialatation
• Bolus of 0.25 – 1 gm/kg Hemeperisis
• CI in haemorrhage & hypotension
HYPERTONIC SALINE
• Osmotic mobilization of water across intact blood brain barrier
• Studies on polytrauma patients + TBI – survival benefit
• Wade CE et al .
• Rocha e Silva M et al .

• HS Initial fluid resuscitation ?

• Vasser et al. – RCT , 250 ml of HS vs normal saline
• Survival rate of HS higher compared to RL for GCS <8

• Continous infusion?
• Qureshi et al. – 3% saline(50-75 ml/hr) vs NS maintanence
• HS group had high inhospital mortality
OPTIC NERVE SHEATH DIAMETER
• Optic nerve sheath – anatomical extension of dura & subarachnoid
space around optic nerve is continuous with IC subarachnoid space.
• Dialatation of ONS – earlier manifestation of ICP rise
• Technique :
• Highfrequency linear probe used
• Diameter measured 3mm behind posterior scleral surface

• Wide variation in optimal cut off values ( 4.8 – 5.9)

• Amini et al. – opening CSF pressure & ONSD
• Cut off of > 5.5 mm has high sensitivity & specificity for ICP >20 cm
• Kimberly et al – cut off >5 correlates with ICP > 20 (invasive icp
monitoring)

Indian J Crit Care Med 2014 Nov 18(11) 707-708

ANTIEPILEPTICS?
• Seizures after head injury
• Worsen head injury
• Interfere with neurological examination

• Acute seizure ?
• BZDs – lorazepam

• Prophylactic phenytoin if GCS < 10

• Decrease post traumatic seizures within 1st week
• Levetiracetam has comparable efficacy to phenytoin

Torbic H et al , Am J Health Syst Pharm.2013 May 1; 70(9)

TEMPERATURE & GLYCEMIC CONTROL
• Maintain normothermia ( 36 – 38.3)
• Fever worsens the outcome
• No sufficient evidence for recommendation of hypothermia

• Hyperglycemia worsens neurologic injury

• Maintain range b/w 100 – 180
• Avoid hypoglycemia
EMERGENCY CT HEAD
• Most commonly performed in head injury

• Systematic approach in emergency CT interpretation

“BLOOD CAN BE VERY BAD”

BLOOD CISTERNS BRAIN VENTRICLES BONE

EMERGENCY CT HEAD
• Blood :
• Acute bleed will appear hyperdense on cranial CT
• Globulin molecules are relatively dense and effectively absorbs x-ray beams
• Globulin molecules breakdown – loses hyperdensity

• Isodense – 4 days - 2 weeks( depends on clot size)

• Hypodense then brain - > 2- 3 weeks
EMERGENCY CT HEAD
• Cisterns : CSF collecting spaces in brain
• 4 key cisterns
• Circummesencephalic – ring around the mid brain
• Suprasellar – location of circle of willis (star shaped)
• Quadrigeminal – W shaped at top of midbrain
• Sylvian – b/w temporal & frontal lobes

• Examined for blood , asymmetry , effacement

EMERGENCY CT HEAD
• Brain :
• Symmetry
• Grey white differentiation
• Loss – Early sign in CVA ; Diffuse axonal injury
• Midline shift
• Hyperdensity
• Blood ,
• calcification
• iv contrast
• Hypodensity
• Air
• fat
• ischemia
• tumour
EMERGENCY CT HEAD
• Ventricles :
• Dialatation
• Compresion/shift
• Blood

• Bone
• Fracture – unilateral (suture is b/l & symmetric)
• Blood in the air sinuses??
Type of Type of patient Anatomical CT findings Common cause Classic symptoms
injury location

epidural Young , rare in Potential space b/w Biconvex hematoma Skull fracture with Immediate LOC with a “
elderly & < 2 yr skull & dura tear of middle LUCID” interval (20%)
meningeal artery
Subdural Elderly & Space b/w dura & Crescent or sickle Tearing of cortical Acute – LOC; lucid
alcoholics arachnoid shaped hematoma bridging veins period possible
Chronic – AMS , gradual
worsening of
consciousness
Subarachnoid Any age group Subarachnoid space Blood in the basilar Tearing of Signs of TBI with
cisterns & subarachnoid meningeal signs
hemispheric sulci & vessels
fissures
Contusions& Any age group Anterior temporal May be normal Severe or Symptoms range from
IC hematoma or posterior frontal initially with delayed penetrating normal to loc
lobe bleed trauma
MILD TRAUMATIC BRAIN INJURY
• Concussion injury without overt haemorrhage or lesions
• GCS 14 – 15
• Physical examination usually normal
• Mild cognitive impairment
• Symptoms may be delayed from days to weeks
• Repeated concussions – long term structural damage
PATHOPHYSIOLOGY SYMPTOMS & SIGNS

Cognitive Symptoms Physical Signs and Behavioral Changes

Symptoms
Attention difficulties Headaches Irritability
Concentration problems Dizziness Depression
Amnesia and perseveration Insomnia Anxiety
Short-term and long-term Fatigue Sleep disturbances
memory problems Uneven gait Emotional lability
Orientation problems Nausea, vomiting Loss of initiative
Altered processing speed Blurred vision Loneliness and helplessness
Altered reaction time Seizures Problems related to job,
Calculation difficulties and relationship, home, or school
problems with executive function management
MILD TBI
• Which patient needs urgent imaging?
• Which patient needs to be observed?
• Which patients can be send home?

• Steil IG et al. - Between 1992-2000 – 160% increase in rate of CT

• 90% - negative for clinically important injury ; 1% - neurosurgical intervention

• Guidelines :
• Canadian CT head rule by Steill et al
• New Orleans criteria by Haydel et al
CT DECISCION RULES
New Orleans Criteria—GCS 15 Canadian CT Head Rule—GCS 13–15
Headache Age 65 y

Vomiting Suspected open or depressed skull fracture

Age >60 y Any sign of basal skull fracture

Intoxication More than one episode of vomiting

Persistent antegrade amnesia Retrograde amnesia >30 min

Evidence of trauma above the clavicles Dangerous mechanism (fall >3 ft )

Seizure GCS < 15 at 2 hrs

Identification of patients who have an intracranial lesion on CT

100% sensitive, 5% specific 83% sensitive, 38% specific

Identification of patients who will need neurosurgical intervention

100% sensitive, 5% specific 100% sensitive, 37% specific

ACEP RECOMMENDATIONS
Mild TBI even if no loss of consciousness if one or more of the following is
present:
Adults with GCS score < 15
Glasgow Coma Scale score <15
at the time of evaluation
Focal neurologic findings
should undergo CT Scan
Vomiting more than two times
Moderate to severe headache
Age >65 y
Physical signs of basilar skull fracture
Coagulopathy
Dangerous mechanism of injury (e.g., fall >4 ft)
Mild TBI with loss of consciousness or amnesia if one or more of the following
is present:
Drug or alcohol intoxication
Physical evidence above the clavicles
Persistent amnesia
Post-traumatic seizures
ADMISSION & OBSERVATION

ADMISSION OBSERVATION
• New clinically significant • GCS , Pupil size & reactivity ;limb
abnormalities on imaging movements ;RR ; HR ; Temp ; SpO2
• GCS< 15 regardless of imaging • GCS half hourly 2 hrs ; 1 hrly for 4
hrs ;2 hrly there after
• Persisting symptoms
• Any e/o intoxication
• Polytrauma
• CSF leak
TREATMENT &DISPOSITION
• REST is the main stay of treatment.
• Avoid aspirin & NSAID’s after acute injury.
• Identify patients who require early interventions or who might deteriorate
overtime.
• Give thorough “concussion discharge instruction” during discharge.
• Discharge patient to a responsible individual.
• Provide instruction to both patient & relative.
• Refer to appropriate centre for evaluation & treatment.
• Formal graduated return to activity program for athletes.
RED FLAGS
• Headaches that worsen • Increasing confusion
• Look very drowsy • Neck pain
• Can’t recognise people or places • Slurred speech
• Unusual behaviour change • Weakness/numbness in arms or legs
• Seizures • Loss of consciousness
• Repeated vomiting

http://www.cdc.gov/headsup/pdfs/providers/ace_care_plan
CASE
• 19 year old male brought to ED by his friends . while he was playing football he
collided with the opponent player while heading the ball..f/b brief loss of
consciousness..
• A - patent
• B- RR – 18 , SpO2 – 98% , Air entry equal b/l
• C – BP- 110/ 70 , PR – 90/ min ,regular
• D – GCS 13 , pupils – B/L NSRL
• Secondary survey - No injuries
• Disoriented to time & place ; opens eyes only on command
THANK YOU