TRAUMATIC BRAIN INJURY

Traumatic Brain Injury

1. TRAUMATIC BRAIN INJURY
STRATEGIES AND RATIONALE TO DECREASE
SECONDARY BRAIN INJURY
PRESENTER - DR YOGESH RATHOD
MODERATOR – DR SHALINI NAIR

2. TRAUMATIC BRAIN INJURY
Consists of two types of injuries:-
Primary Brain injury is the damage sustained as a direct result of the impact on the skull and
intracranial contents.
Secondary brain injury refers to the changes that evolve over a period of time (from hours to days)
after the primary brain injury.
It includes an entire cascade of cellular, chemical, tissue, or blood vessel changes in the brain that
contribute to further destruction of brain tissue.

3. PATHOPHYSIOLOGY
Primary brain Injury — heterogenous.
Common mechanisms
direct impact
rapid acceleration/deceleration
penetrating injury
blast waves.
External mechanical force damage results in
focal contusions and hematomas
shearing of white matter tracts (diffuse axonal injury)
cerebral edema and swelling.

4. Secondary brain Injury
These mechanisms include:
Neurotransmitter-mediated excitotoxicity (e.g. glutamate), free-radical injury to cell membranes
Electrolyte imbalances
Mitochondrial dysfunction
Inflammatory responses
Apoptosis
Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury
Current clinical approaches to the management of TBI center around primary and secondary brain injury
concepts.

5. INTRACRANIAL SECONDARY BRAIN DAMAGE
Hemorrhage
Extradural
Subdural
Intracerebral
Intraventricular
Subarachnoid
Swelling
Venous congestion/hyperemia
Edema
Vasogenic
Cytotoxic
Interstitial
Infection
Meningitis
Brain abscess

6. EXTRACRANIAL SECONDARY BRAIN
DAMAGE
 Hypoxia
 Hypotension
 Hyponatremia
 Hyperthermia
 Hypoglycemia

7. LIBERATION OF
CHEMICALS
(EAAs, PAF & Free
Radicals of O2)
DISRUPTION OF BBB
EDEMA
NEURAL DEATH
CONTINUATION OF
VICIOUS CYCLE
Neurotoxic cascades
ISCHAEMIA
AND
REPERFUSION
INJURY

8. Calcium channel disturbance
Local tissue damage  EAAs  NMDA glutamate receptors of calcium channels in the surroundings
cells  massive influx of Ca++ ions  metabolic failure of the cells and cellular edema.
Oxygen free radical production
Cellular metabolic failure  free radicals of oxygen + PAF  free radical generation and the
destruction of super oxide dismutase  damaged cells and blood vessels  Ischemia and vascular
damage  arachidonic acid cascade  prostaglandin, prostacyclin leukotrienes release with free
radical generation  further vascular damage  increase in vascular permeability and vasogenic
oedema  further brain swelling & raised ICP, a decrease in CPP and more global ischaemia.

9. Hematoma formation
Exrtadural hematomalocal ischemia, a shift of midline structures and possible fatal brainstem
damage
Subdural and subarachnoid hemotoma  local compression and swelling of the brain substance
and an increase in ICP
Blood in the subarachnoid space can cause vasospasm and further aggravate cerebral ischemia.

10. Respiratory failure
LOC accompanied by a period of central apnea and can lead to severe hypoxia.
Aspiration of vomit can cause further injury to lungs impairing ventilation.
Any hypoxia will aggravate cerebral ischemia and increases cerebral blood flow and cerebral blood
volume, thus increasing ICP.
Thus any degree of respiratory failure is particularly hazardous for the patient with head injury.
Blood Loss
CPP = MAP – ICP
Raised ICP + fall in MAP  cerebral ischaemia.
Hypotension from blood loss is not uncommon in multiple injuries and should be strenuously avoided
and corrected. Blood loss can lead to anemia and make cerebral ischemia more likely

11. Infection and Seizure
A major source of concern .
Any patient with a CSF leak or air in the intracranial cavity and open fracture of the skull
should be given an appropriate prophylactic antibiotic regimen
Epileptic seizures
Early epilepsy is most likely to be associated with intracranial haematoma and depressed skull
fracture. If the seizures are not controlled, they can cause cerebral hypoxia

12. STRATEGIES AND RECOMMENDATIONS FOR
TRAUMATIC BRAIN INJURY

13. TREATMENT RECOMMENDATIONS
Decompressive craniectomy
Bifrontal DC is not recommended to improve outcomes. But reduces ICP and minimizes days in the
ICU.
A large fronto-temporo-parietal DC (not less than 12 x 15 cm or 15 cm diameter) is recommended
over a small FTP DC for reduced mortality and improved neurologic outcomes.
Ventilation therapies
Prolonged prophylactic hyperventilation with PaCO2 of 25 mm Hg is not recommended.
Hyperventilation is recommended as a temporizing measure for the reduction of elevated ICP.
Hyperventilation avoided during the first 24 h when CBF often is reduced critically.
If hyperventilation is used, SjO2 or BtpO2 measurements are recommended to monitor oxygen
delivery.

14. Prophylactic hypothermia
Early (within 2.5 h), short-term (48 h post-injury), prophylactic hypothermia is not recommended to
improve outcomes in patients with diffuse injury.
Hyperosmolar therapy
Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg body weight. Arterial hypotension
(systolic blood pressure ,90 mm Hg) should be avoided.
Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or
progressive neurologic deterioration not attributable to extracranial causes.
Cerebrospinal fluid drainage
An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP
burden more effectively than intermittent use.
Use of CSF drainage to lower ICP in patients with an initial GCS of 6 or lower during the first 12 h after
injury may be considered.

15. Anesthetics, analgesics, and sedatives
Barbiturates for burst suppression in EEG as prophylaxis against development of intracranial HTN not
recommended.
High-dose barbiturate recommended to control elevated refractory ICP. Hemodynamic stability essential.
Propofol is recommended for the control of ICP, but not recommended for improvement in mortality or 6-
month outcomes. Caution is required as high-dose propofol can produce significant morbidity.
Steroids
Not recommended for improving outcome or reducing ICP. Rather high dose methylpred was a/w increased
mortality and is contraindicated.
Nutrition
Feeding patients to attain basal caloric replacement at least by the 5th day and at most by the 7th day
recommended to decrease mortality.

16. Infection prophylaxis
Early trach recommended to reduce mechanical ventilation days if overall benefit outweighs the complications. No
evidence that early trach reduces mortality or the rate of nosocomial pneumonia.
PI oral care is not recommended to reduce VAP and may cause an increased risk of ARDS.
Antimicrobial-impregnated catheters may be considered during EVD to prevent infections.
DVT Prophylaxis
LMWH or low-dose unfractionated heparin may be used in combination with mechanical prophylaxis. But an
increased risk for expansion of ICH.
Compression stockings + pharmacologic prophylaxis may be beneficial.
Insufficient evidence to support recommendations regarding the preferred agent, dose, or timing of pharmacologic
prophylaxis for DVT.
Seizure prophylaxis
Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS.
Phenytoin is recommended to decrease the incidence of early PTS (within 7 d of injury), when the overall benefit
outweighs the complications. However, early PTS have not been associated with worse outcomes.
Insufficient evidence to recommend levetiracetam over phenytoin regarding efficacy in preventing early PTS and
toxicity.

17. MISCELLANEOUS
Antagonists or blockers of the NMDA glutamate receptor (dizocilpine) have been successful in
preventing brain injury in animals.
Nimodipine have also been shown to have some brain protective effects.
Ketamine is an NMDA receptor antagonist that has been shown to improve neurological
outcome in a rat brain injury model, but no practical value in a clinical settings.
Nitric oxide  production of free radicals (by blocking nitric oxide synthase, outcome is
improved)
Antagonists to PAF and leucocytes antibody treatment may also limit secondary brain injury.

18. Intracranial pressure monitoring
Management of severe TBI patients using information from ICP monitoring is recommended to reduce in hospital
and 2-week post-injury mortality.
Monitored in all salvageable patients with a TBI (GCS 3-8 after resuscitation) and an abnormal CT scans.
Indicated in patients with severe TBI with a normal CT scan if >2 OR 2 of the following features are noted at
admission:
age >40 years,
unilateral or bilateral motor posturing, or
SBP <90 mm Hg.
Advanced cerebral monitoring
Jugular bulb monitoring of AVDO2 may be considered important parameter to reduce mortality and improve
outcomes at 3 and 6 mo post-injury.
Cerebral perfusion pressure monitoring
Management of severe TBI patients using guidelines-based recommendations for CPP monitoring is
recommended to decrease 2-wk mortality.
MONITORING RECOMMENDATIONS

19. Blood pressure thresholds - Maintaining SBP at >100 mm Hg OR equal for patients 50 to 69 years old
or at >110 mm Hg or equal or above for patients 15 to 49 or >70 years old may be considered to
decrease mortality and improve outcomes.
Intracranial pressure thresholds - Treating ICP >22 mm Hg is recommended because values above this
level are associated with increased mortality. A combination of ICP values and clinical and brain CT
findings may be used to make management decisions.
Cerebral perfusion pressure thresholds - The recommended target CPP value for survival and
favorable outcomes is between 60 and 70 mm Hg. Whether 60 or 70 mm Hg is the minimum optimal
CPP threshold is unclear and may depend upon the autoregulatory status of the patient. Avoiding
aggressive attempts to maintain CPP >70 mm Hg with fluids and pressors may be considered because
of the risk of adult respiratory failure.
Advanced cerebral monitoring thresholds - Jugular venous saturation of <50% may be a threshold to
avoid in order to reduce mortality and improve outcomes.
THRESHOLD RECOMMENDATIONS

20. Diffuse axonal injury
CT scan of the brain
showing diffuse axonal
injury (DAI). Note the deep
shearing-type injury in or
near the white matter of
the left internal capsule
(arrow).

21. Frontal cerebral contusion
CT scan of the brain
depicting cerebral
contusions. The basal
frontal areas (as shown)
are particularly
susceptible.

22. Traumatic epidural hematoma
CT scan demonstrating a
right epidural hematoma
(EDH, arrow). Note the
lenticular shape.

23. Traumatic subdural hematoma
CT scan showing a left acute
subdural hematoma (SDH, arrow).
Subdural hematomas are typically
crescent-shape. In this case the
SDH is causing significant mass
effect and shift of midline
structures to the right.

24. Perimesencephalic
nonaneurysmal subarachnoid
hemorrhage
Head CT of three different patients
demonstrating subarachnoid
hemorrhage in the characteristic
pattern of perimesencephalic
hemorrhage with blood in the
interpeduncular and ambient
cisterns.

25. Intracerebral Hemorrhage
CT obtained less than six hours
from symptom onset in a patient
with spontaneous acute
intracerebral hemorrhage. The CT
scan shows a hyperdense
hemorrhage predominantly in the
left frontal lobe.

26. SUMMARY
TBI encompasses a broad range of pathologic injuries of varying clinical severity.
TBI is universally categorized as mild, moderate, and severe based on GCS.
The pathophysiology of TBI includes primary and secondary brain injury.
The pathoanatomical sequelae of primary TBI include intra- and extra parenchymal hemorrhages and
DAI.
Secondary TBI results from a cascade of molecular injury mechanisms and can be exacerbated by
modifiable systemic events such as hypotension, hypoxia, fever, and seizures
Surgical treatment of primary brain injury lesions is central to the initial management.
Likewise, the identification, prevention, and treatment of secondary brain injury is the principle
focus of neurointensive care management.

27. NO QUESTIONS! JUST SELF HELP!
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