3. DEFINITION
Strictly defined as alteration in the integrity of
the head resulting from an impact.
Hence, there may be both extracranial and
intracranial components.
However, the terms traumatic brain injury and
head injury are often used interchangeably in
the medical literature.
5. OVERVIEW
• Traumatic brain injury (TBI) continues to be an
enormous public health problem, even with
modern medicine in the 21st century.
• the most common causes include motor vehicle
accidents , falls, assaults, sports-related
injuries, and penetrating trauma.
• Motor vehicle accidents account for almost half
of the TBIs,and motorcycle-related head injuries
deserve special mention in this regard.
6. OVERVIEW
• Head injury data are difficult to compare
internationally for multiple reasons, including
inconsistencies and complexities of diagnostic
coding and inclusion criteria.
• AGE: Approximately half of the patients
admitted to a hospital for head injury are aged
24 years or younger.
• SEX: Men are nearly twice as likely to be
hospitalized with a brain injury than women.
7. CLASSIFICATION
• 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
• Primary or Secondary
9. PATHOPHYSIOLOGY
• Brain is contained within the skull, a rigid and
inelastic container. Hence,only small
increases in volume within the intracranial
compartment can be tolerated before
pressure within the compartment rises
dramatically.
• V i/c = V b + V cf + V d(Monro-Kellie equation).
10. PATHOPHYSIOLOGY
• Vi/c=1,500mls,Vb=87%,Vcf=3%,Vd=10%.
• A second 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.
11. PATHOPHYSIOLOGY
• Secondary brain injury results from: Systemic
hypotension, Hypoxia, Elevated ICP, or the
biochemical changes.
• The treatment of head injury is directed at
either preventing or minimizing secondary
brain injury.
12. PRESENTATION
• Initial clinical evaluation: involves a
thorough systemic trauma evaluation
referred to as the advanced trauma life
support (ATLS) guidelines.
• After patient has been resuscitated and
stabilized, attention may then be directed to
a focused head injury evaluation.
13. PRESENTATION
• Elicit the type and mechanisms of the injury:
prognostic value.
• Altered consciousness: even a questionable
loss of consciousness can be a marker of
severe neurological injury.
• Bleeding from sites including orifices
• Seizures
• Vomiting
14. PRESENTATION
• The presence of prior head injuries.
• Remote or active drug or alcohol use: may
raise the risk of intracranial bleeding and
cloud the mental status assessment.
• Present anticoagulant therapy .
• Carefully consider past psychiatric disease
and a premorbid history of headaches.
15. PRESENTATION
• The neurologic assessment begins with
ascertaining the GCS score.
• Cranial nerves characterisation
• Pupillary reflexes
• Ocular movement
• CN VII palsy
• Hearing loss
• Dysphagia
•
16. PRESENTATION
• Motor examination:Focal signs indicate
localized contusion or, more ominously, an
early herniation syndrome.
Flexor or extensor posturing-extensive intracranial
pathology or raised intracranial pressure.
Spasticity or flaccidity more unusually,
Akinesia and rigidity.
Tremors and dystonia
Postural instability and imbalance
17. PRESENTATION
• Sensory examination: Corneal reflex
• Primitive reflexes-despite their presence in
some healthy elderly patients,they are useful
when multiple,and can correlate with
cognitive deficits.
• Bedside Cognitive Testing:n the acute
setting, attention and orientation are
important.
18. INVESTIGATIONS
Laboratory Studies
PCV/FBC
E/U/Cr
Arterial blood Gases
Alcohol level
Drug screens
Imaging Studies
Skull Xrays:largely replaced by CT
scanning.Fractures may be visible.
19. INVESTIGATIONS
• Computerised Tomography Scanning:The
standard CT scan 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.
20. INVESTIGATIONS
• Extradural haematoma-biconvex,Subdural-
crescent,Subarachnoid-filling of gyri over
convex brain surfaces.
• Magnetic Resonance Imaging:has a limited
role in the evaluation of acute head injury
because of its long acquisition times and the
difficulty in obtaining MRIs in persons who
are critically ill.It is superior to CT scan for
helping identify diffuse axonal injury (DAI)
and small intraparenchymal contusions.
21. TREATMENT
Mild head injuries :analgesics and close
monitoring for potential complications such
as intracranial bleeding.
Moderate and Severe head injuries:There is
significant secondary injury :
Prevention of hypoxia: Oxygen therapy
Control of elevated intracranial pressure.
Mannitol,hyperventilation,CSF diversion,
22. Hypothermia,Hypertonic saline,Barbiturate
coma,Decompressive craniectomies.Steroids have no
role .
Maitenance of perfusion:Ringer’s lactate,paediatric
saline,monitoring of blood pressure,vassopressors.
Seizures:anticonvulsants
Agitation:Paralytics,sedation.
Nutrition:Enteral or parenteral feeding.
Correction of
dyselectrolytaemia:Hyponatramia,Hypomagnesaese
mia.
25. FOLLOW-UP
A putative diagnosis of mild head injury does
not necessarily mean a favourable outcome.
80% of patients with mild head injury recover
completely.
Patients could develop Alzheimer’s disease
subsequently.
