Head Injury; mechanism, presentation, pathophysiology, investigations, scoring system and management.

2. CONTENTS
 Definition
 Overview
 Classification
 Pathophysiology
 Presentation
 Investigations
 Treatment
 Follow-up

3. DEFINITION
Traumatic Brain Injury
(TBI) occurs when a
sudden trauma damages
the brain causing
alteration in function via
bruising, bleeding, edema
or tearing of nerves.
There may be both
extracranial and
intracranial components.

4. AETIOLOGY
 RTA
 Falls
 Violence
 Gun shots
 Abuse
 Explosive blasts
 Natural disasters

5. CLASSIFICATION
• Primary or Secondary
• Closed or Open.
• Diffuse or Focal.
• Coup or contrecoup.
• Mild, Moderate or Severe.
• Non-haemorrhagic or
Haemorrhagic (extradural,
subdural, subarachnoid,
intraparenchymal or
intraventricular).
• Concussion,Contusion or
Diffuse axonal injury

6. SYMPTOMS
 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 or concentration
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. PATHOPHYSIOLOGY
• A crucial 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 brain over 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)

11. MASS EFFECT AND HERNIATION

12. PRESENTATION
• Initial clinical evaluation: involves a thorough systemic
trauma evaluation referred to as the advanced trauma life
support (ATLS) guidelines.
• A IRWAY (plus C Spine stabilization)
• B REATHING
• C IRCULATION
• D ISABILITY
• E XPOSURE
• After patient has been resuscitated and stabilized,
attention may then be directed to a focused head injury
evaluation.

13. EVALUATION
 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. PRESENTATION
• Cranial nerves characterisation
• Pupillary reflexes and reactivity
• Ocular movement
• CN VII palsy
• Hearing loss
• Dysphagia or regurgitation

16. EXAMINATION
• Focal signs indicate localized
contusion or, more ominously, an
early herniation syndrome.
 Flexor or extensor posturing
 Spasticity or flaccidity more
unusually,
 Akinesia and rigidity.
 Tremors and dystonia
 Postural instability and imbalance
 Sensory examination:
 Corneal reflex

17. INVESTIGATIONS
 Laboratory Studies
 PCV/FBC
 U/Cr/E
 PT/APTT
 Arterial blood Gases
 Alcohol level
 Drug screens
 Imaging Studies
 Skull Xrays:
 CT scan
 Trauma X rays as indicated esp C spine.

18. COMPUTERISED TOMOGRAPHY
• The GOLD standard for 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

20. EVD
INTRA PARENCHMYAL
MONITOR

21. RADIOLOGY

22. TREATMENT
 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 HAVE NO ROLE in acute trauma

23. SURGERY

30. ADJUNCT THERAPIES
 Hypothermia or barbiturate coma to decrease oxygen
demands of brain.
 Maintenance of perfusion:
 IV fluids and inotropic support.
 Seizures: Anticonvulsants
 Agitation: Paralytics, sedation.
 Nutrition: Enteral or parenteral feeding.
 Correction of underlying metabolic and electrolyte
abnormalities

31. COMPLICATIONS
 Insomnia
 Cognitive decline
 Post traumatic headache
 Post traumatic
depression
 Post traumatic seizures
 Hydrocephalus
 Heterotopic ossification
 Deep vein thrombosis
 Spasticity
 Gastrointestinal
complications: Cushing’s
ulcers.
 Gait abnormalities

32. PREVENTION
 Wear a helmet when riding
a bicycle, skateboard,
motorcycle or vehicle.
 Always wear a seat belt!
 Use proper restraints for
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. REHABLITATION
 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
 A diagnosis 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. REFERENCES
 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: A large 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

36. THANK YOU