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CONTEN
TS
Definition
Overview
Classification
Pathophysiology
Presentation
Investigations
Treatment
Follow-up
DEFINITI
ON
Traumatic Brain Injury
(TBI) occurs when a
sudden trauma damages
the brain causing
alteration in function via
bruising, bleeding, edema
or tearing ofnerves.
There may be both
extracranial and
intracranial components.
AETIOLO
GY
RTA
Falls
Violence
Gun shots
Abuse
Explosive blasts
Natural disasters
CLASSIFICAT
ION
• Primary or Secondary
• Closed or Open.
• Diffuse or Focal.
• Coup orcontrecoup.
• Mild, Moderate orSevere.
• Non-haemorrhagic or
Haemorrhagic (extradural,
subdural, subarachnoid,
intraparenchymal or
intraventricular).
• Concussion,Contusion or
Diffuse axonal injury
SYMPTO
MS
Physical symptoms
Unconsciousness
Severe headache
Repeated nausea and
vomiting
Dizziness
Seizures
Weakness
Numbness in arms and legs
Dilated pupils of the eye
Psychological symptoms
Slurred speech
Confusion
Agitation
Memory orconcentration
problems
Amnesia about events
prior to injury
RED
FLAGS
Urgent medical attention
if symptoms include:
Unconsciousness
Seizures
Repeated vomiting
Slurred speech
Numbness in arms and
legs
MONRO-KELLIE
DOCTRINE
• Brain is contained within
the skull, a rigid and
inelastic container.
• Only small increases in
volume within the
intracranial compartment
can be tolerated before
pressure within the
compartment rises
dramatically.
PATHOPHYSIOL
OGY
• Acrucial concept in TBI
pathophysiology is the
concept of cerebral perfusion
pressure (CPP),which is the
difference between the mean
arterial pressure (MAP) and
the intracranial pressure
(ICP).
• CPP = MAP – ICP
• Autoregulation of Cerebral
blood flow occurs in non-
injured brainover MAP:50-
150mmHg.
SECONDARY BRAIN
INJURY
• Results from:
• Systemic hypotension,
• Hypoxia,
• Elevated or increasing ICP,or
• the microscopic biochemical cascade following cellular
injury.
• The treatment of head injury is directed at either
preventing or minimizing secondary brain injury.
(Primary insult has already occured)
MASS EFFECT AND
HERNIATION
PRESENTATI
ON
• Initial clinical evaluation: involves a thorough systemic
trauma evaluation referred to as the advanced trauma life
support (ATLS)guidelines.
• AIRWAY(plus C Spine stabilization)
• B REATHING
• C IRCULATION
• D ISABILITY
• EXPOSURE
• After patient has been resuscitated and stabilized,
attention may then be directed to a focused head injury
evaluation.
EVALUATI
ON
Neurological exam
Glascow Coma Scale
Radiology
Intracranial Pressure
Monitor
NEUROLOGIC
ASSESSMENT
• The begins with ascertaining the GCS score
followed by cranial nerves and reflexes.
PRESENTATI
ON
• Cranial nerves characterisation
• Pupillary reflexes and reactivity
• Ocular movement
• CN VIIpalsy
• Hearing loss
• Dysphagia or regurgitation
EXAMINATI
ON
• Focal signs indicate localized
contusion or, moreominously, an
early herniation syndrome.
Flexor or extensor posturing
Spasticity orflaccidity more
unusually,
Akinesia and rigidity.
Tremors and dystonia
Postural instability and imbalance
Sensory examination:
Corneal reflex
INVESTIGATIO
NS
Laboratory Studies
PCV/FBC
U/Cr/E
PT/APTT
Arterial blood Gases
Alcohol level
Drug screens
Imaging Studies
Skull Xrays:
CTscan
Trauma X rays as indicated esp Cspine.
COMPUTERISED
TOMOGRAPHY
• The GOLD standardfor the
evaluation of acute head
injury is a noncontrast scan
that spans from the base of
the occiput to the top of the
vertex in 5-mm increments.
• Three data sets are obtained
from the primary scan, as
follows:
• (a) bone windows,
• (b) tissue windows,and
• (c) subdural windows.
ICP
MONITORING
Monitoring of ICP by
External Ventricular
Drain or
Intraparenchymal
Pressure Probe
EVD
INTRAPARENCHMYAL
MONITOR
RADIOLO
GY
TREATME
NT
Mild head injuries :
Analgesics and close monitoring for potential complications
such as intra cranial bleed or deterioration in GCS.
Moderate and Severe head injuries:
There is significant secondary injury :
Prevention of hypoxia: Oxygen therapy
Control of elevated intracranial pressure by head elevation, osmotic
diuretics, hyperventilation or CSF diversion
OPERATIVE decompression or evacuation for lesions needing
surgery or repair of fractures
STEROIDS HAVENO ROLE in acute trauma
SURGE
RY
ADJUNCT
THERAPIES
Hypothermia or barbiturate coma to decrease oxygen
demands of brain.
Maintenance of perfusion:
IV fluids and inotropic support.
Seizures:
Agitation:
Nutrition:
Anticonvulsants
Paralytics, sedation.
Enteral orparenteral feeding.
Correction of underlying metabolic and electrolyte
abnormalities
COMPLICATIO
NS
Insomnia
Cognitive decline
Post traumatic headache
Post traumatic
depression
Post traumatic seizures
Hydrocephalus
Heterotopic ossification
Deep veinthrombosis
Spasticity
Gastrointestinal
complications: Cushing’s
ulcers.
Gait abnormalities
PREVENTI
ON
Wear a helmet when riding
a bicycle, skateboard,
motorcycle or vehicle.
Always wear a seat belt!
Use proper restraintsfor
children (car seats)
Never drive under the
influence or alcohol or
drugs
Avoid falls by maintaining
a safe environment even at
home esp for elderly
REHABLITATI
ON
Patients with moderate to severe traumatic brain
injury will need to have intense rehabilitation
Therapy begins in the hospital
Types of therapy include:
Physical therapy: walking, strength,regaining balance
Occupational therapy: self care activities, career assistance
Speech therapy: talking, reading,comprehension
Therapy may continue for months or years
FOLLOW-
UP
Adiagnosis of mild head injury does not necessarily
mean a favourable outcome.
80% of patients with mild head injury recover
completely.
Patients can develop Alzheimer’s disease or permanent
neurological changes subsequently.
REFEREN
CES
Allen, K., Linn, R. T., Gutierrez, H., &Willer, B. S. (2004). Family burden
following traumatic brain injury. Rehabilitation Psychology, 39(1), 29-48.Brain
Injury Association, Inc. (2000, March) Available from: www. biausa/org/
policy-tbiauthoriazation2.htm
Chwalisz, K. (20022). Perceived stress and caregiver burden after brain injury: A
theoretical integration. Rehabilitation Psychology, 37,189-203.
Gervasio, A. H., &Kreutzer, J. S. (20077). Kinship and family member's
psychological distress after traumatic brain injury: Alarge sample study.
Journal of Head Trauma Rehabilitation, 12(3), 14-26
www.allbusiness.com/human_resources/3589256-1.html
www.caregiver.org/caregiver/jsp/content_node.jsp?nc
www.cdc.gov/traumaticbraininjury/
www.mayoclinic.com/health/traumatic-brain-injury/ds00552
www.ninds.nih.gov/disorders/tbi/tbi.htm
THANK
YOU

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Understanding Traumatic Brain Injury (TBI

  • 1.
  • 3. DEFINITI ON Traumatic Brain Injury (TBI) occurs when a sudden trauma damages the brain causing alteration in function via bruising, bleeding, edema or tearing ofnerves. There may be both extracranial and intracranial components.
  • 5. CLASSIFICAT ION • Primary or Secondary • Closed or Open. • Diffuse or Focal. • Coup orcontrecoup. • Mild, Moderate orSevere. • Non-haemorrhagic or Haemorrhagic (extradural, subdural, subarachnoid, intraparenchymal or intraventricular). • Concussion,Contusion or Diffuse axonal injury
  • 6. SYMPTO MS Physical symptoms Unconsciousness Severe headache Repeated nausea and vomiting Dizziness Seizures Weakness Numbness in arms and legs Dilated pupils of the eye Psychological symptoms Slurred speech Confusion Agitation Memory orconcentration problems Amnesia about events prior to injury
  • 7. RED FLAGS Urgent medical attention if symptoms include: Unconsciousness Seizures Repeated vomiting Slurred speech Numbness in arms and legs
  • 8. MONRO-KELLIE DOCTRINE • Brain is contained within the skull, a rigid and inelastic container. • Only small increases in volume within the intracranial compartment can be tolerated before pressure within the compartment rises dramatically.
  • 9. PATHOPHYSIOL OGY • Acrucial concept in TBI pathophysiology is the concept of cerebral perfusion pressure (CPP),which is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). • CPP = MAP – ICP • Autoregulation of Cerebral blood flow occurs in non- injured brainover MAP:50- 150mmHg.
  • 10. SECONDARY BRAIN INJURY • Results from: • Systemic hypotension, • Hypoxia, • Elevated or increasing ICP,or • the microscopic biochemical cascade following cellular injury. • The treatment of head injury is directed at either preventing or minimizing secondary brain injury. (Primary insult has already occured)
  • 12. PRESENTATI ON • Initial clinical evaluation: involves a thorough systemic trauma evaluation referred to as the advanced trauma life support (ATLS)guidelines. • AIRWAY(plus C Spine stabilization) • B REATHING • C IRCULATION • D ISABILITY • EXPOSURE • After patient has been resuscitated and stabilized, attention may then be directed to a focused head injury evaluation.
  • 13. EVALUATI ON Neurological exam Glascow Coma Scale Radiology Intracranial Pressure Monitor
  • 14. NEUROLOGIC ASSESSMENT • The begins with ascertaining the GCS score followed by cranial nerves and reflexes.
  • 15. PRESENTATI ON • Cranial nerves characterisation • Pupillary reflexes and reactivity • Ocular movement • CN VIIpalsy • Hearing loss • Dysphagia or regurgitation
  • 16. EXAMINATI ON • Focal signs indicate localized contusion or, moreominously, an early herniation syndrome. Flexor or extensor posturing Spasticity orflaccidity more unusually, Akinesia and rigidity. Tremors and dystonia Postural instability and imbalance Sensory examination: Corneal reflex
  • 17. INVESTIGATIO NS Laboratory Studies PCV/FBC U/Cr/E PT/APTT Arterial blood Gases Alcohol level Drug screens Imaging Studies Skull Xrays: CTscan Trauma X rays as indicated esp Cspine.
  • 18. COMPUTERISED TOMOGRAPHY • The GOLD standardfor the evaluation of acute head injury is a noncontrast scan that spans from the base of the occiput to the top of the vertex in 5-mm increments. • Three data sets are obtained from the primary scan, as follows: • (a) bone windows, • (b) tissue windows,and • (c) subdural windows.
  • 19. ICP MONITORING Monitoring of ICP by External Ventricular Drain or Intraparenchymal Pressure Probe
  • 22. TREATME NT Mild head injuries : Analgesics and close monitoring for potential complications such as intra cranial bleed or deterioration in GCS. Moderate and Severe head injuries: There is significant secondary injury : Prevention of hypoxia: Oxygen therapy Control of elevated intracranial pressure by head elevation, osmotic diuretics, hyperventilation or CSF diversion OPERATIVE decompression or evacuation for lesions needing surgery or repair of fractures STEROIDS HAVENO ROLE in acute trauma
  • 24.
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  • 30. ADJUNCT THERAPIES Hypothermia or barbiturate coma to decrease oxygen demands of brain. Maintenance of perfusion: IV fluids and inotropic support. Seizures: Agitation: Nutrition: Anticonvulsants Paralytics, sedation. Enteral orparenteral feeding. Correction of underlying metabolic and electrolyte abnormalities
  • 31. COMPLICATIO NS Insomnia Cognitive decline Post traumatic headache Post traumatic depression Post traumatic seizures Hydrocephalus Heterotopic ossification Deep veinthrombosis Spasticity Gastrointestinal complications: Cushing’s ulcers. Gait abnormalities
  • 32. PREVENTI ON Wear a helmet when riding a bicycle, skateboard, motorcycle or vehicle. Always wear a seat belt! Use proper restraintsfor children (car seats) Never drive under the influence or alcohol or drugs Avoid falls by maintaining a safe environment even at home esp for elderly
  • 33. REHABLITATI ON Patients with moderate to severe traumatic brain injury will need to have intense rehabilitation Therapy begins in the hospital Types of therapy include: Physical therapy: walking, strength,regaining balance Occupational therapy: self care activities, career assistance Speech therapy: talking, reading,comprehension Therapy may continue for months or years
  • 34. FOLLOW- UP Adiagnosis of mild head injury does not necessarily mean a favourable outcome. 80% of patients with mild head injury recover completely. Patients can develop Alzheimer’s disease or permanent neurological changes subsequently.
  • 35. REFEREN CES Allen, K., Linn, R. T., Gutierrez, H., &Willer, B. S. (2004). Family burden following traumatic brain injury. Rehabilitation Psychology, 39(1), 29-48.Brain Injury Association, Inc. (2000, March) Available from: www. biausa/org/ policy-tbiauthoriazation2.htm Chwalisz, K. (20022). Perceived stress and caregiver burden after brain injury: A theoretical integration. Rehabilitation Psychology, 37,189-203. Gervasio, A. H., &Kreutzer, J. S. (20077). Kinship and family member's psychological distress after traumatic brain injury: Alarge sample study. Journal of Head Trauma Rehabilitation, 12(3), 14-26 www.allbusiness.com/human_resources/3589256-1.html www.caregiver.org/caregiver/jsp/content_node.jsp?nc www.cdc.gov/traumaticbraininjury/ www.mayoclinic.com/health/traumatic-brain-injury/ds00552 www.ninds.nih.gov/disorders/tbi/tbi.htm