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1. Traumatic Brain Injury (TBI)
Dr Nor Hidayah Zainool Abidin
International Islamic University of Malayia
(IIUM)
Hospital Sultan Abdul Halim

2. Morbidity and mortality impact…
• leading cause of death among adult < 45 yr
and in children (1–15 yr).
• Mild TBI
– good prognosis providing treatable complications
are not missed.
– Overall mortality - 0.1% (missed intra-cranial
haemorrhage)
– around 50% of survivors have moderate or severe
disability

3.  more severe TBI
 prognosis is much worse. Approximately 30% with GCS
score <13 will ultimately die.
 Mortality for those with GCS <8 after resuscitation may
be as high as 50%.
 Patient with GCS <12 around 8% will die within the
first 6 h, 2% within the first hour.
 Long-term outcome among survivors - only around
20% will make a good recovery on the (GOS)

5. • Skull is a rigid box – fixed volume
• About 1600ml – 1700ml
SKULL
Brain
CSFBlood

6. Brain Edema
• Traumatized brain tissue and damage capillary
wall  brain edema compress vasculature
 decrease blood flow – brain ischemia
• Ischemia – arteriolar dilatation – increase
capillary pressure  cause more edema

7. • And increase 1 of the 3 components must be
compensated with a decrease of volume of
another component
SKULL
Brain
Blood CSF

8. • for a certain period of time
• A critical point – no further compensation can
occur lead to exponencial rise in ICP causing
secondary brain damage
Inrease ICP will reduce CPP
CPP = MAP –ICP

9. Cushing’s Reflex
• Increase MAP
• Falls in pulse rate
– Reflexs from increasing blood pressure
• Rise in respiratory rate
– With further ischemia, body attemp to incrase oxygenation by
increasing respiratory rate

10. Physiology of Human brain
• Normal blood flow 50-65ml/100g/min
• 750-900ml/min
• 2 % of body weight
• 15% of resting cardiac output

11. • 150 ml of skull volume occupied by CSF
• Formed at rate of 500ml/day
• Normal pressure in CSF system = 150mm H2O
(10mmHg)
• Ranging 65 mmH2O-195 mmH2O

12. Brain metabolism
• 2% of total body weight
• 15% of total body metabolism
• 7.5 times the average metabolism in non-nervous system tissue
• Most excess metabolism occur in the neuron – transport sodium
and calcium ions for proper ionic different to conduct action
potentials
• During high level of brain activity – neuronal metabolism can be as
high as 100-150%
No anaerobic activity
Neuronal activity depends on second to second delivery of O2 from the blood
Glucose delivery – not dependant on insulin

13. Types of brain injury
• the initial, mechanical forces
• in shearing and compression
of neuronal, glial, and
vascular tissue.
Primary
Damage
• further physiological insults
• may start at the time of
initial mechanical insult.
Secondary
Damage

14. Primary Damage
1. Diffuse injuries
Concussion
• Mildest form
• Temporary LOC
• Confusion
• Headache, dizziness,
nausea, ringing in the
ears
Diffuse axonal injury
• Prolonged coma
• 44% of head Injuries –
coma damage in
primarily microscopic
and scattered
throughout the brain
• Autonomic dysfunction
(high fever, sweating m
hypertension)

15. 2. Focal injuries
Extradural Hematoma
• Inner surface of the skull and
dura mater
• Caused by tear in MMA and
its braches
• Excellent prognosis if treated
• May have Lucid interval after
initial injury
Acute Subdural Hematoma
• Fall or strong deceleration
forces
• High mortality (70%)
• Seen In about 30% of TBI
• Early evacuation improves
outcome
• Poor prognosis because of
underlying brain damage
•Bruise of the brain
Shearing force of the cortex
Swelling of the brain
Unconcious for some time
Accompanied bu subpial and subarachnoid hemorhages
Intracerebral hemotoma maybe present
Contussion
Hemorrhages

16. Secondary
Insults
Hypoxia
Hypercapnia
and
hypocapnia
Hyperglycemia
Hypotension

17. Secondary Injury
1/3 of patients who die after TBI will talk or
obey commands before their death
 suggesting that the initial injury per se is not
lethal, even with diffuse axonal injury, but the
consequences are.
The secondary injury is amenable to treatment
The early management of TBI is therefore
directed towards minimizing progression of
injury

18. Risk factors for poor outcome
• Secondary insults
amenable for
intervention
– Hypotension
– Hypoxia
– Hyperglycaemia
– Hypercapnia and
hypocapnia
• Fixed risk factors - may
provide prognostic
information, but cannot
be influenced by
subsequent care.
– Mechanism of injury
– Age, gender, and genetics
– Pupillary signs
– Glasgow coma scale
– CT findings

19. Mechanism of injury
• Penetrating injuries have a worse outcome than blunt
trauma, when other factors are taken into account.
– more likely to present with a lower GCS and die early.
• Non-accidental injury in children , 5 yr is associated
with worse outcome, which may be in part because of
a higher rate of cerebral infarction in this group.
• Pedestrians & pedal cyclists fare worse > vehicle
occupants in MVA
• Ejection from the vehicle > significant intra-cranial
injury

20. Age, gender, and genetics
• The age of the patient influences both the
likelihood of TBI and the prognosis.
• TBI has a bimodal incidence distribution;
young adult males comprise the largest peak
– motor vehicle accidents
– lcohol-associated trauma
• second smaller peak in the elderly
• women > brain swelling and intra-cranial
hypertension

21. Pupillary signs
• Pupil size and reactivity can be affected by a
variety of mechanisms associated with head
injury
– Trauma to the eye
– 3rd nerve damage – at any point of its course
– Mid brain and pontine dysfunction
– Drug administration
• May provide prognostic information

22. • Pupillary constriction is mediated via a
parasympathetic pathway by the third nerve and
its nuclei in brain stem
• Third nerve palsy initially -> mydriasis then loss of
reactivity to light.
– compression of the nerve
• Unilateral  the consensual light reflex (opposite
eye constricting in response to bright light)
should still be present.
• Optic nerve injury  impair both the direct and
indirect responses
– lead to fixed or sluggish pupils, which may display
spontaneous fluctuations

23. • Bilaterally fixed pupils occur in around 20–30% of patients
with severe head injury (GCS _8) after resuscitation:
– 70–90% of these patients will have poor outcome
(vegetative or dead) when compared with around 30%
with bilaterally reactive pupils.
• Unreactive pupils are associated with the presence of
hypotension, lower GCS, and closed basal cisterns on CT.
• The underlying pathology influences the prognostic value of
unreactive pupils:
– patients with epidural haematoma fare better than those
with subdural haematoma.
• Unilaterally unreactive pupils have an outcome intermediate
between bilaterally reactive and unreactive pupils.
– Pupil asymmetry is associated with an operable mass
lesion in around 30% of patients

24. Glasgow coma scale
• The relationship between field GCS and survival is non-
linear, with a steep relationship between GCS 3 and 7,
followed by a shallower decline in mortality between GCS 8
and 15
• Relationship between field GCS and functional outcome
appears to be approximately linear
• post-resuscitation GCS vs mortality &functional outcome in
generalized TBI
– a sharp decrease in mortality as GCS increases from 3 to 8,
– a shallower decrease between 8 and 15.
• The change in GCS may also be prognostic, with
deterioration in GCS predicting the need for evacuation of
traumatic subdural haematoma.

25. CT Brain
• The incidence of abnormalities on CT
increases with severity of head injury.
– minor head injuries- 2.5–8%
– severe TBI- 68–94%
• CT brain linked to poor outcome:
– mid-line shift
– compression of the basal cisterns
– traumatic sub-arachnoid haemorrhage (SAH),

26. Marshall CT Classification

28. Secondary
Insults
Hypoxia
Hypercapnia
and
hypocapnia
Hyperglycemia
Hypotension

29. Hypotension
• hypotension were separately and additively associated
with increased mortality.
• a single episode of hypotension during the period from
injury through resuscitation  doubling of mortality
and a parallel increase in morbidity in survivors.
• The duration and number of episodes of hypotension
are correlated with mortality
The precise mechanism for the enhanced
susceptibility of the injured brain to hypotension is
not clear
but up to 90% of head-injured patients have been
found to have evidence of ischaemic damage at
autopsy

30. Hypoxia
• Association between observed early hypoxia ,
SpO2< 90% or kPa 7.9 kPa (60 mm Hg)] and
poor outcome.
• The association is not as strong as for
hypotension
• Hypoxia may be a marker of the severity of
brain or systemic injury, or it may be a
secondary insult to the at risk brain.

31. Hyperglycemia
• Severe TBI leads to a marked sympathetic and
hormonal response levels of catecholamines
inversely related to the severity of injury.
• Hyperglycaemia is common after TBI and is
associated with severity of injury
• Has poor outcome for both early mortality and
functional recovery in adults and children.
• Approximately 50% of patients present with
blood glucose >11.1 mmol l and peak levels
greater than this in the first 24 h after admission
are associated with a significantly worse mortality

32. Hypercapnia and hypocapnia
• Hypercapnia is more likely to occur in the setting of
multiple trauma
• Hypercapnia  secondary insult
– Significant association between hypercapnia and poor outcome.
• As a consequence of these findings, hyperventilation has
previously been used in the initial and ongoing
management of TBI.
• However, cerebral blood flow in the first few hours after
injury has been shown to be reduced to less than half of
normal (~25 ml 100 g min vs ~50 ml 100 g min)
• Various studies have demonstrated both physiological
derangements and worse outcome paCO2 < 4 kPa (30 mm
Hg)] if aggressive indiscriminate hyperventilation is used.

33. • Hypercapnia  cerebral vasodilatation
increase cerebral blood volume  increase
intracranial pressure (ICP)  reduce cerebral
perfusion.
• reduced cerebral blood flow and oxygen
delivery, where intracranial hypertension is
not a problem, it is possible
– that hypercapnia may be of benefit through
improvements in cerebral blood flow

34.  General principles
1. Arterial pressure maintenance
2. Mannitol
3. Ventilatory support
4. Glycaemic control
5. Imaging
6. Other injuries
7. Seizures

35.  maintenance of adequate and stable cerebral
perfusion
 adequate oxygenation
 avoidance of hyper- and hypocapnia
 avoidance of hyper- and hypoglycaemia,
 avoiding iatrogenic injury.

36.  The American guidlelines
◦ maintaining SAP >90 mm Hg and avoidance of
hypotension
◦ the severe TBI guidance advocates MAP >90 mm
Hg.
 The European guidelines
◦ SAP >120 mm Hg , MAP >90 mm Hg,
 The UK transfer guidelines
◦ MAP >80 mm Hg

37.  Preferable Isotonic solution (normal saline)
 Avoids
◦ Hartmann’s solution is hypotonic
◦ Glucose containing fluids are usually hypotonic,
lead to hyperglycaemia
 Colloids - need to deliver large volumes of
fluid and blood is not available
 Anaemia should be corrected and some
evidence exists to suggest that the optimal
haemoglobin is 100gms/l.

38.  Suggesting that administration of high dose
mannitol (1.4 g kg) is associated with
improved outcome after traumatic brain
injury.
 1.5g/kg over 20 mins
 Rapid administration cause hypotension and
transsient hyperkalaemia

39.  For patients who are able to maintain their own airway,
supplemental oxygen therapy is always recommended.
 For patients unable to maintain oxygenation or their own
airway then tracheal intubation may be required.
 Avoid Hyper- and hypocapnia
◦ The American guidance suggests a lower limit of around 4.6 kPa,
◦ The UK guidance (4.5–5.0 kPa)
◦ The EBIC guidelines suggest a lower P (4.0–5.0 kPa).
 Problem during transfer of patient
 Risk of hyperventilation during manual begging or
portable ventilator setting
 As no Et CO2 monitoring

40.  CT is the preferred modality for initial
assessment of TBI
 CT is more sensitive for SAH
 More severe TBI  a clear indication for CT of
the head.

42.  Around 5% of patients with moderate-severe
TBI  cervical spine injury
 Conversely, around 1/3 patient with cervical
spine injury suffer moderate- severe head
injury
 CT cervical spine should be carried out at the
same time

43.  Head injury is the cause of death in around
one-third of patients dying after trauma, and
major extra-cranial injuries are found in 50%
of patients with severe TBI
 significant extra-cranial injury  significantly
higher mortality for TBI patient
 Control of haemorrhage still apply for
patients with TBI to prevent hypotension

44.  Incidence of early (1 week) seizure of 4–25%.
 Various factors increase seizure risk :
◦ GCS <10
◦ cortical contusions
◦ depressed skull fracture
◦ epidural, subdural, or intracranial haematoma
◦ penetrating head wound,
◦ seizure within 24 h of injury
Risk of increase ICP

45. American
guideline
•anti-epileptics as a
treatment option to
prevent early seizures
in high-risk patients.
UK
•Not mentioned