Traumatic brain injury (TBI) is a leading cause of disability globally. The document outlines the epidemiology, anatomy, pathophysiology, classification and prognosis of TBI. It defines TBI as damage to the brain from traumatic force. TBI can be open or closed injuries and classification is based on the mechanism of injury. The anatomy of the scalp, skull and brain are described in detail. Complications from TBI like increased intracranial pressure and herniation are explained. Outcome depends on the severity assessed using the Glasgow Coma Scale.

1. TRAUMATIC BRAIN
INJURY
SURG SLT ET DANS
MEDICAL OFFICER
ICU NNRH OJO

2. Outline
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Introduction/Definition
Epidemiology
Relevant anatomy and physiology
Aetiology
Classification
Pathophysiology
Prognosis
References

3. Introduction
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Head injury is defined as damage to the brain, skull,
scalp or any other structure of the head as a result of
a traumatic insult.
While the term ‘head injury’ is most often associated
with traumatic brain injury (TBI), head injuries also
involves injury to the bones, muscles, blood vessels, skin,
and other structures of the head.
Head injury is one of the major reasons for emergency
treatment and is associated with high mortality and
disability.
It is commonly caused by road traffic accidents (RTAs)
Detection and classification of severity is difficult,
making prognosis poor

4. Epidemiology
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Traumatic brain injury (TBI) is a leading cause of disability in all regions of the globe. 4
million people experience head trauma annually.
The global incidence rate of TBI is estimated at 200 per 100 000 people per year;
however, this rate is uncertain and a likely underestimate.
Severe head injury is the most frequent cause of trauma death (75-80% mortality)
In one study, Accident and Emergency Department (A&E) incidence rate was put at
2710 per 100,000 per year in our environment, far higher than the A&E figures of 453
and 394 per 100,000 per year for UK and US, respectively.
Incidence in Lagos state is about 450/100000 per year.
At Risk population:
Males 15-24
Infants
Young Children
Elderly
Low income individuals
Unmarried individuals
Individuals with a history of substance abuse
Individuals who have suffered a previous TBI

5. Anatomy and physiology
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SCALP
Highly vascularised
Protected by hair
Made up of 5 layers:
Skin
Connective tissue (dense)
Aponeurotic layer
Loose connective tissue
Periosteum of the skull
Blood vessels are found in the dense connective tissue layer.
Accounts for inability of the vessels to constrict when
lacerated and thus makes the scalp prone to profuse
bleeding

6. Anatomy and physiology
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SKULL
Bony structure that covers and protects the brain
Composed of eight bones separated by sutures:
- Frontal
- Parietal (2)
- Occipital
- Temporal (2)
- Sphenoid
- Ethmoid
Temporal bone has three processes
- Mastoid
- Styloid
- Zygomatic

8. Anatomy and physiology
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Brain
Weighs about 1.5 kg (apprx. 2
% of the total body mass)
Composed of neurons, glial
cells and blood vessels
It is supplied by a network of
vessels called the ‘circle of
Willis’
It takes about 20-22% of the
cardiac output and uses 20 %
of total blood glucose supply.

9. Anatomy and physiology
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The brain has 4 lobes: frontal,
parietal, temporal, occipital
Has 4 ventricles: lateral
(right and left), third and
fourth ventricle
Between the skull and the
brain are the meninges (dura
mater, arachnoid membrane,
pia mater)
Divided into 4 parts:
cerebrum, diencephalon
(thalamus, hypothalamus),
brainstem (midbrain, pons,
medulla oblongata), and
cerebellum

10. Anatomy and physiology
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Cranial volume fixed
Brain (80%)
Blood vessels & blood (12%)
CSF (8%)
Increase in volume of one component compensates by decrease of
another
Inability to compensate = increased ICP
Compensating for intracranial pressure
Compress venous blood vessels
Reduction in free CSF
Brain herniation

11. Anatomy and physiology
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Factors affecting ICP
Intracranial vasculature
Cerebral Edema
Systemic Blood Pressure
Low BP = Poor Cerebral Perfusion
High BP = Increased ICP
Reduced respiratory efficiency (hypoventilation)
Carbon Dioxide
Fever
Pain
Head posture
Agitation

12. Anatomy and physiology
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Role of Carbon Dioxide
Increase of CO2 in CSF
Cerebral Vasodilation
Encourage blood flow
Reduce hypercarbia
Reduce hypoxia
Contributes to ICP
Reduced levels of CO2 in CSF
Cerebral vasoconstriction
Results in cerebral anoxia

13. Aetiology of head injuries
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Mostly caused by RTAs
Domestic falls
Assault
Sports-related injuries
Recreational accidents
Firearm- related injury
Gunshot to the head
Stab injuries

14. Classification of head injury
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Based on brain
communication with
external environment
Closed - Skull not
compromised
and brain not exposed
(dura mater intact)
Open - Skull compromised
and brain exposed (dura
mater breeched)

15. Classification of head injury
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4.
Based on mechanism:
- Blunt Injury
Baseball injury
Motor vehicle collisions
Assaults
Falls
- Crush injury
- Penetrating
Bullet or missile (gunshots, explosions)
Sharp non-missile (stabbing)

16. Classification of head injury
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Classification based on anatomy
Scalp Injuries
Cranial Injuries
Brain Injuries

17. Scalp injuries
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Contusions
Lacerations
Avulsions
Hemorrhage

18. Scalp injuries
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Bleeds briskly due to high
vascularity
Shock: children and adult with
underlying pathology

19. Cranial Injury
• Trauma must be extreme to fracture

20. Cranial Injury
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Basal Skull
Unprotected
Spaces weaken
structure
Relatively
easier to fracture
Basal Skull Fracture Signs
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Battle’s sign
Racoon eyes
Bleeding from external orifices (eyes,
ears, nose)
CSF leakage (dura tear leading to CSF
drainage through an external
passageway)
- CSF otorrhea (ear)
- CSF rhinorrhea (nose)
- CSF orbitorrhea (eye)

21. Cranial Injury
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Battle’s sign
Retroauricular Ecchymosis
Associated with fracture of
auditory canal and lower
areas of skull
Racoon eyes
Bilateral Periorbital
Ecchymosis
Associated with orbital
fractures

22. Basilar Skull Fracture
Battle’s sign Raccoon eyes
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Head Trauma -

23. Cranial Injury
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Basilar Skull
Fracture
May tear dura
Permit CSF to drain
through an external
passageway
May mediate rise of
ICP
Evaluate for “Target”
or “Halo” sign

24. Crainial Injuries
Penetrating trauma
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Head Trauma -
Bullet fragments

25. Brain injury
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The National Head Injury Foundation defines brain
injuries as “a traumatic insult to the brain capable of
producing physical, intellectual, emotional, social and
vocational changes.”
Classification:
Direct
Primary injury caused by forces of trauma
Most primary injuries are from blunt trauma or
from movement of brain inside skull
Indirect
Secondary injury caused by factors resulting
from the primary injury

26. Brain injury
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Direct brain injury
Immediate damage
due to force
Fixed at time of injury
Coup force
Injury at site of
impact
Contrecoup force
Injury on opposite side
from impact

27. Brain injury
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Direct Brain Injury Categories:
Focal
Occur at a specific location in brain
Cerebral Contusion
Intracranial Hemorrhage
Epidural hematoma
Subdural hematoma
Intracerebral Hemorrhage
Diffuse
Pathology distributed throughout brain
Concussion
Moderate Diffuse Axonal Injury
Severe Diffuse Axonal Injury

28. Focal Brain Injury
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Cerebral Contusion
Blunt trauma to local brain tissue
Capillary bleeding into brain tissue
Common with blunt head trauma
Results from Coup-countercoup injury
There is bruising of brain tissue leading to rapid
and severe swelling.
There is prolonged unconsciousness and
confusion and amnesia is profound.

29. Brain Injuries
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Cerebral contusion
Bruising of brain tissue
Swelling may be rapid and severe
Level of consciousness
Prolonged unconsciousness,
profound confusion or amnesia
Associated symptoms
Focal neurological signs
May have personality changes
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Head Trauma -

30. Focal Brain Injury
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Intracranial Hemorrhage
Epidural Hematoma
Bleeding between dura
mater and skull
Involves arteries
Middle meningeal artery
most common
Rapid bleeding & reduction
of oxygen to tissues
Herniates brain toward
foramen magnum

31. Focal Brain Injury
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Acute epidural hematoma
Bleeding is arterial in
origin and temporal
fracture is common.
Onset is minutes to hours.
There is initial loss of
consciousness followed by
“lucid interval”.
There is associated
ipsilateral dilated fixed
pupil, signs of increasing
ICP, contralateral paralysis,
and death.

32. Focal Brain Injury
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Subdural Hematoma
Bleeding within meninges
Beneath dura mater &
within subarachnoid space
Above pia mater
Slow bleeding
Superior saggital sinus
Signs progress over several
days with slow deterioration
in mentation.

33. Focal Brain Injury
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Acute subdural hematoma
Bleeding is venous in origin.
Onset of bleeding is hours
to days.
There is fluctuations in
consciousness with
associated headaches and
focal neurologic signs.
Common among alcoholics,
elderly and those taking
anticoagulants.

34. Focal Brain Injury
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Intracerebral hemorrhage
Bleeding could be arterial or venous
and surgery is not often helpful
There is rupture within the brain
Alterations in level of consciousness
is common.
Associated symptoms vary with
region and degree of hemorrhage,
and is similar to that of stroke
(headache and vomiting).
The signs and symptoms worsen
over time.

35. •
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Types
Concussion
Moderate Diffuse Axonal Injury
Severe Diffuse Axonal Injury

36. Diffuse Brain Injury
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Concussion
Mild form of Diffuse Axonal Injury (DAI)
Nerve dysfunction without visible structural anatomic injury
to the brain
Level of consciousness
Variable period of unconsciousness or confusion
Followed by return to normal consciousness
Transient episode of
Confusion, Disorientation, Event amnesia
Momentary loss of consciousness manifesting as Retrograde
short-term amnesia
May repeat questions over and over
Associated symptoms
Dizziness, headache, ringing in ears, and/or nausea

37. Diffuse Brain Injury
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Diffuse axonal injury
Usually as a result of severe blunt trauma - Most
common injury from severe blunt head trauma
Diffuse injury
Generalized edema
No structural lesion
Associated symptoms
Unconscious
No focal deficits

38. Diffuse Brain Injury
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Moderate Diffuse Axonal Injury
Same mechanism as concussion
Additional: Minute bruising of brain tissue
Unconsciousness
May exist with a basilar skull fracture
Signs & Symptoms
Unconsciousness or Persistent confusion
Loss of concentration, disorientation
Retrograde & Antegrade amnesia
Visual and sensory disturbances
Mood or Personality changes

39. Diffuse Brain Injury
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Severe Diffuse Axonal Injury
Brainstem Injury
Significant mechanical disruption of nerve cells
Cerebral hemispheres and brainstem
High mortality rate
Signs & Symptoms
Prolonged unconsciousness
Cushing’s reflex
Decorticate or Decerebrate posturing

40. Extremity Posturing
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Decorticate
Arms flexed
and legs extended
Decerebrate
Arms extended
and legs extended
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Head Trauma -

41. Indirect Brain Injury
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Due to response to primary injury
Results from hypoxia
or decreased perfusion
Develops over hours
Can be prevented by proper management of
primary injuries

42. Indirect Brain Injury
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Indirect brain injury
Results from hypoxia
or decreased perfusion
Response to primary injury
Develops over hours
Management
Good prehospital care can help prevent
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Head Trauma -

43. Pathophysiology of head injury

44. Pathophysiology of head injury
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Increased intracranial pressure
Compresses brain tissue
Compromises blood supply
Herniates brainstem
Signs & Symptoms
Upper Brainstem
Vomiting
Altered mental status
Pupillary dilation
Medulla Oblongata
Respiratory
Cardiovascular
Blood Pressure disturbances

45. Effect of Traumatic Brain Injury on
Age
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TBI may interact negatively with aging in at least 2 ways:
Recovery after TBI is more limited for older than younger survivors;
Older individuals who have suffered a TBI are at higher risk for progressive
cognitive decline.
First, advanced age at the time of injury may result in less complete recovery
compared to younger persons with comparable injuries. While the mechanisms of this
phenomenon are not known, it may be due simply to less capacity for compensation
or reduced cognitive reserves, with increasing age.
Prospective, longitudinal outcome studies are required to determine whether
functional outcomes of TBI improve more slowly, or even decline, among older
individuals over time.
‘In patients with TBI, an increasing age is significantly associated with unfavorable
outcome at 6 months, in stepwise manner centered on a threshold of 40 years,
independent of other prognostic factors.” – Dhandapani et al.
“The study reaffirms that outcome of head injury worsens with advancing age and
indicates that severity of head injury and higher frequency of multi-system
trauma may contribute to worse outcome in older patients.” – Odebode et al.
MORTALITY IN TBI – The highest mortality rate (32.8 cases per 100,000) is found in
persons aged 15 – 24 years. The mortality rate in patients who are elderly (65 years
or older) is about 31.4 individuals per 100,000 people.

46. Prognosis
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Prognosis depends on the severity of the
injury
This can be assessed using the Glasgow coma
outcome scale

47. Prognosis
• Glasgow coma outcome scale
Score Description
1 Death
2 Persistent vegetative state: patient exhibits no obvious cortical
function
3 Severe disability(conscious but disabled): patient depend upon others
for daily support due to mental or physical disability or both
4 Moderate disability(disabled but independent): Patient is
independent as far as daily life is concerned. The disabilities found
include varying degrees of dysphagia, hemiparesis, or ataxia, as well
as intellectual and memory deficits and personality changes
5 Good recovery: resumption of normal activity even though there may
be minor neurological or psychological deficits

48. THANK YOU FOR LISTENING

49. References
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Principles and Practice of Surgery
Nelson Essentials of Pediatrics
Bailey and Love’s Short Practice of Surgery
MedlinePlus Medical Encyclopedia
Medscape
Lye CL, Shores EA. Traumatic brain injury as a risk factor for Alzheimer's
Disease: a review. Neuropsychology Rev. 2000;10:115–29. [PubMed] [Google
Scholar] [Ref list]
BMJ JOURNALS
Traumatic Brain Injury in the Accident and Emergency Department of a
Tertiary Hospital in Nigeria - J.K.C. Emejulu, C.M. Isiguzo, C.E. Agbasoga, C.N.
Ogbuagu. Department of Surgery, Nnamdi Azikiwe University Teaching Hospital,
Nnewi, Anambra State, South East NIGERIA.
Dhandapani S, Manju D, Sharma B, Mahapatra A. Prognostic significance of
age in traumatic brain injury. J Neurosci Rural Pract. 2012 May;3(2):131-5.
doi: 10.4103/0976-3147.98208. PMID: 22865961; PMCID: PMC3409980.

51. MANAGEMENT OF TBI
SURG SLT LO MAJOLAGBE

52. OUTLINE
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Introduction
Clinical features
Investigations
Management
Patient Monitoring
Diagnosis
Complications
Conclusion
References

53. INTRODUCTION
• TBI is defined as a non degenerative, non
congenital insult to the brain from an
external mechanical force, possibly leading
to a permanent or temporary impairment of
cognition, physical and psychosocial
functions with an associated diminished or
altered state of consciousness.

54. INTRODUCTION
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It is often used synonymously with head
injury which may not be associated with
neurological deficits.
National Head Injury Foundation
“A traumatic insult to the brain capable of
producing physical, intellectual, emotional, social
and vocational changes.”

55. THE MULTI-TRAUMATIZED
PATIENT

56. 5
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Head Trauma -
CLINICAL FEATURES / PRESENTATIONS

57. HEAD TRAUMA
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Open
Skull compromised
and brain exposed
Closed
Skull not compromised
and brain not exposed
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Head Trauma -

58. SCALP INJURY
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Contusions
Lacerations
Avulsions
Significant Hemorrhage

59. ECCHYMOSIS
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Basal Skull Fracture Signs
Battle’s Signs
Retroauricular Ecchymosis
Associated with fracture of
auditory canal and lower
areas of skull
Raccoon Eyes
Bilateral Periorbital
Ecchymosis
Associated with orbital
fractures

60. BASILAR SKULL FRACTURE
Battle’s sign Raccoon eyes
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Head Trauma -

61. BASILAR SKULL FRACTURE
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Basilar Skull
Fracture
May tear dura
Permit CSF to
drain through
an external
passageway

62. SIGNS & SYMPTOMS OF BRAIN INJURY
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Altered Mental Status
Altered orientation
Alteration in
personality
Amnesia
Retrograde
Antegrade
Cushing’s Reflex
Increased BP
Bradycardia
Erratic respirations
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Vomiting
Without nausea
Projectile
Body temperature
changes
Changes in pupil
reactivity
Decorticate posturing

63. SIGNS & SYMPTOMS OF BRAIN INJURY
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Frontal Lobe Injury
Alterations in personality
Occipital Lobe Injury
Visual disturbances
Cortical Disruption
Reduce mental status or Amnesia
Retrograde
Unable to recall events before injury
Antegrade
Unable to recall events after trauma
“Repetitive Questioning”
Focal Deficits
Hemiplegia, Weakness or Seizures

64. SIGNS & SYMPTOMS OF BRAIN INJURY
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Upper Brainstem Compression
Increasing blood pressure
Reflex bradycardia
Vagus nerve stimulation
Cheyne-Stokes respirations
Pupils become small and reactive
Decorticate posturing
Neural pathway disruption

65. SIGNS & SYMPTOMS OF BRAIN INJURY
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Middle Brainstem Compression
Widening pulse pressure
Increasing bradycardia
CNS Hyperventilation
Deep and Rapid
Bilateral pupil sluggishness or
inactivity
Decerebrate posturing

66. SIGNS & SYMPTOMS OF BRAIN INJURY
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Lower Brainstem Injury
Pupils dilated and unreactive
Ataxic respirations
Erratic with no pattern
Irregular and erratic pulse rate
Hypotension
Loss of response to painful stimuli

67. INVESTIGATIONS
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Plain films (X- ray) of the skull
Computer tomography (CT) scan (non-contrast)
Magnetic Resonance Imaging (MRI)
Carotid angiography
Electroencephalography
Echoencephalography
Exploratory burr hole craniotomy

68. INVESTIGATIONS -
Lateral Cervical Spine X-
ray

69. INVESTIGATIONS -
Skull XRAYS

70. INVESTIGATIONS – CRANIAL CTS SCANS

71. MANAGEMENT PROTOCOL
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Primary survey and Resuscitation
Airway Maintenance and C-spine protection
Breathing
Circulation and control of Hemorrhage
Rapid Neurologic Survey
Exposure-Remove all clothes

72. MANAGEMENT PROTOCOL
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Secondary Survey
Detailed Systemic Examination
Xrays: Chest, spine
CT Scan
Other Xrays
Laboratory Tests
Tetanus Immunization

73. MANAGEMENT PROTOCOL
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Definitive Care
Immediate, early initial intervention which focus on
detection of primary injury and prevention and
treatment of secondary injury.
Focus of management:
Prevent elevated ICP
Avoid hypotension (show to increase morbidity and
mortality)
Minimize cerebral metabolic rate of O2 consumption

74. Factors that decrease cerebral
oxygen supply
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Anemia
Hypoxemia
Systemic hypotension
Low cardiac output
Elevated intracranial pressure

75. Factors that increase cerebral oxygen
demand
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Seizure
Fever
Agitation
Pain
Excitatory neurotransmitters

76. MANAGEMENT PROTOCOL IN ICU
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It can be classified on the basis of neurological assessment using Glasgow Coma
Score into, mild (13/15), moderate (9-12/15) and severe (3-8/15).
Moderate to severe TBI often require admission to the Intensive care unit (ICU).

77. MANAGEMENT PROTOCOL IN ICU
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Severe traumatic brain injury (TBI) is currently managed
in the intensive care unit with a combined medical-surgical
approach. Treatment aims to prevent additional brain
damage and to optimize conditions for brain recovery.
The goal of ICU management of TBI is the prevention of
secondary brain injuries such as hypotension, hypercapnia,
hypertension, hypo/hyperglycemia and hyperthermia

78. MANAGEMENT PROTOCOL IN ICU

79. MANAGEMENT
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TIME IS CRITICAL
Intracranial Hemorrhage
Progressing Edema
Increased ICP (5 to 15mmhg – 7.5 to 20cmH2O)
CPP = MAP – ICP (60 to 80mmhg)
Cerebral Hypoxia
Permanent Damage

80. MANAGEMENT
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For unconscious patients: Airway maintenance with
endotracheal intubation in cases of respiratory distress
Tracheostomy in anticipated long periods of
unconsciousness
Assist ventilation
High-flow oxygen
One breath every 6–8 seconds
SpO2 >95%
Maintain EtCO2 at 35 mmHg
Fluid administration for traumatic brain injury, GCS <9
Titrate to 110–120 mmHg systolic with or without penetrating
hemorrhage to maintain Cerebral perfusion pressure (60 to
80mmhg).

81. MANAGEMENT
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Hyperventila
tion : Indications
for hyperventilation
TBI GCS <9 with decerebrate posturing
TBI GCS <9 with dilated or nonreactive pupils
TBI initial GCS <9, then drops >2 points
Age group Physiologic respiratory rate Hyperventilation respiratory rate
Adult 8–10 per minute 20 per minute
Children 15 per minute 25 per minute
Infants 20 per minute 30 per minute
If signs resolve, stop hyperventilation.
Capnography
Maintain EtCO <30
mmHg, but >25 mmHg

82. MEDICAL THERAPY
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Anticonvulsants(5-15% post-traumatic
Seizures)
Immediate, Early(first wk), Late Seizures
Prophylaxis beneficial in first week
Risk factors for late seizures: early seizures, depressed
skull fractures and intracranial haematoma
Mannitol
Lasix
Barbiturates
Steroids

83. SURGICAL THERAPY
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Wound debridement
Surgical evacuation of Intracranial
haematoma and contusions
Elevation of compound depressed fracture
Repair of Venous sinus injuries
Decompressive craniectomy for patients
with raised intracranial pressure

84. MONITORING
• Monitoring of patients with severe TBI is essential for the
guidance and optimization of therapy. The rationale of
monitoring is early detection and diagnosis of secondary
brain insults, both systemic and intracranial. Therefore,
monitoring of patients with severe TBI must comprise both
general and specific neurologic monitoring.

85. MONITORING
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Mental State examination – COMJS
GCS
Pupillary reflex
ICP monitoring (Intraventricular – EVD)
Brain tissue oxygen tension monitor (PbtO2) – delivery and consumption
Vital signs
ABG
O2 saturation
Capnography
Temperature
Blood sugar
FOUR SCORE

86. •
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Reactive: ICP increasing
Nonreactive (altered LOC):
increased ICP
PUPILLARY REFLEX
Both dilated
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Nonreactive: brainstem
Reactive
Unilaterally dilated
8
6
Head Trauma -
Eyelid closure
• Slow: cranial nerve III

87. PUPILLARY REFLEX

88. PUPILLARY REFLEX

89. GLASGOW COMA SCALE
Suspect severe brain injury GCS
<9
8
9
Head Trauma -
*Decorticate posturing to pain
**Decerebrate posturing to pain

90. EXTREMITY POSTURING
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Decorticate
Arms flexed
and legs extended
Decerebrate
Arms extended
and legs extended
9
0
Head Trauma -

91. GLASGOW COMA SCALE
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Sum of the Scores in the 3 categories
Best Score 15
Worst Score 3
Score is related to severity
Score is related to outcome

92. INCREASING ICP
9
2
Head Trauma -
Vital Sign with Increasing ICP
1. Respiration Increase, decrease, irregular
2. Pulse Decrease
3. BP Increase, widening pulse
pressure
• CUSHING’S TRIAD

93. FOUR SCORE

94. FOUR SCORE

95. General intensive care activities
• Prior to suctioning the patient through the endotracheal
tube (ETT), preoxygenation with a fraction of inspired
oxygen (FiO2) = 1.0, and administration of additional
sedation are recommended to avoid desaturation and
sudden increase in the ICP. Suctioning ETT must be brief
and atraumatic.

96. General intensive care activities
•
•
•
Similar to other patients in the intensive care, TBI
victims should receive the usual daily care as
follows:
- Raising head of bed to 30° - 45°: that would
reduce ICP and improves CPP [125]; and lower the
risk of ventilator-associated pneumonia (VAP).
- Keeping the head and neck of the patient in a
neutral position: this would improve cerebral
venous drainage and reduce ICP.

97. General intensive care activities
•
•
•
- Avoiding compression of internal or external
jugular veins with tight cervical collar or tight
tape fixation of the endotracheal tube that would
impede cerebral venous drainage and result in an
increase in the ICP.
- Turning the patient regularly and frequently
with careful observation of the ICP
- Providing eye care, mouth and skin hygiene

98. General intensive care activities
•
•
•
- Implementing all evidence-based bundles for
prevention of infection including VAP and central
line bundle .
- Administrating a bowel regimen to avoid
constipation and increase of intra-abdominal
pressure and ICP.
- Performing physiotherapy

99. DIAGNOSIS
•
•
•
•
•
•
•
•
History taking
Mechanism of injury
Loss of consciousness or amnesia
Level of consciousness at scene and on transfer
Evidence of seizures
Probable hypoxia or hypotension
Pre-existing medical conditions
Medications (especially anticoagulants)
Illicit drugs and alcohol

100. DIAGNOSIS
•
•
•
•
•
•
•
Examination
General
Close examination of the skull for external
evidence of injury
Check for pallor-suggestion for bleeding
Check mouth odour for alcohol,
acetone(suggestive of uncontrolled DM),
mousy(hepatic failure), urea( uraemia).
Level of consciousness using the GCS
Ears and nose- bleeding or CSF leakage
(suggestive basal skull fracture)

101. COMPLICATIONS
•
•
•
–
–
•
Personality changes - Frontal
lobe injury
Visual disturbances - Occipital
lobe injury
Altered mental status
Retrograde amnesia
Antegrade amnesia
Focal deficit- hemiplegia,
weakness or seizures

102. COMPLICATIONS
•








Cerebral herniation syndrome
Brain forced downward
CSF flow obstructed, pressure on brainstem
Level of consciousness
Decreasing, rapid progression to coma
Associated symptoms
Ipsilateral pupil dilatation, out-downward deviation
Contralateral paralysis or decerebrate posturing
Respiratory arrest, death

103. COMPLICATIONS
•
•
•
•
•
•
Cranial nerve injuries
Cerebral oedema
Cerebral abscess
Post traumatic epilepsy
Post traumatic headaches
Infection - Meningitis

104. GLASGOW COMA SCALE
•
•
•
•
•
•
•
•
•
Good Recovery: 5
Return to pre-injury level of function
Moderate Disability : 4
Diminished level of function but Cares for self
Severe Disability : 3
Unable to care for self
Vegetative State : 2
No awareness of self or environment
Death : 1

105. FOLLOW UP
• In-patient rehabilitation follow up is
important especially for moderate - severe
head injury.

106. CONCLUSION
•
•
•
•
Head injury is one of the major reasons for
emergency treatment and is associated with
high mortality and disability
It is commonly caused by road traffic
accidents(RTAs)
Time is critical in the management of head injuries.
Requires continuous monitoring & evaluation and follow up.

108. NURSING MANAGEMENT OF A PATIENT
WITH TRAUMATIC BRAIN INJURY
SMSN TIMOTHY RM
INTENSIVE CARE UNIT (ICU),
NIGERIAN NAVY REFERENCE
HOSPITAL, OJO, LAGOS.

109. Introduction
• It is estimated that between 750 000 and one
million individuals with head injuries attend
accident and emergency (A&E) departments in
the UK every year. Approximately 150 000 to 200
000 are admitted to hospital and, of these, 5%
require admission to a neurosurgical unit (Flint,
1997).

110. Nursing Management in Critical Care
• The critical-care nurse needs to be
alert to the potential problems that
may be encountered by the brain-
injured patient, who may be at risk of
sudden deterioration at any time. This
involves taking an holistic view of the
patient.

111. 1. Respiratory care:
•
•
Hypoxia after head injury is common for a number
of reasons:
inadequate airway clearance leading to poor tidal
volumes, associated chest trauma and aspiration
and hypermetabolic state post-injury, which will
increase tissue oxygen.

112. Haemodynamic/fluid management:
• The minimum monitoring required for a critically
head-injured patient should include continuous
arterial blood pressure monitoring (rather than
non-invasive methods in order to enable
measurement of CPP), core body temperature,
respiration rate and pattern and continuous ECG.

113. Temperature control:
•
•
In head-injured patients with hypoxia and ensuing
ischaemia, the oxygen demand of brain tissue
escalates (Chambers, 1999). The brain’s metabolic
rate increases by approximately 7% for each degree
centigrade increase in temperature(Johnson, 1999).
This elevated metabolism increases cerebral blood
volume, thereby increasing ICP (Hickey, 1997). There
may also be damage to the temperatureregulating
centre in the hypothalamus, which may cause body
temperature to fluctuate (Wong, 2000).

114. Positioning:
•
•
Positions that restrict venous drainage from
the brain through the internal jugular vein
may cause a significant rise in ICP (Johnson,
1999).
In a comprehensive review of the literature,
Beitel (1998) found that elevation of the
head from 15 to 30 degrees was associated
with a mean decrease in ICP in all patients.

115. Nutritional support:
•
•
Severe head injury is associated with a hypermetabolic
state with, in some cases, the metabolic rate increasing by
as much as 40 to 100% (Hinds and Watson, 1996).
It is therefore important to begin feeding as early as
possible, preferably enterally. The feeding tube should
always be passed via the orogastric route in head-injured
patients, unless a basal skull fracture has been definitively
ruled out (Withington, 1997).

116. Other Nursing Interventions include;
•
•
•
•
•
•
•
•
•
•
a. Maintaining the airway
b. Protecting the patient.
c. Providing mouth care.
d. Maintaining skin and joint integrity.
e. Preserving corneal integrity
f. Preventing urinary retention
g. Promoting bowel function
h. Providing sensory stimulation
i. Check Nose and Ear for CSF leak.
j. Administrator medications as prescribed.

117. SIGNS OF RAISED INTRACRANIAL PRESSURE (ICP)
•
•
•
•
•
•
•
•
•
•
•
•
* Headache
* Nausea
* vomiting
* Increased blood pressure
* Decreased mental abilities
* Confusion
* Double vision
* Pupils that don’t respond to changes in light
* Shallow breathing
* Seizures
* Loss of consciousness
* Coma

118. Conclusion
•
•
Nursing care of the head-injured patient can present many
challenges for the critical care nurse and, as a consequence,
a thorough knowledge of the dynamics of ICP and the
factors associated with its increase is required (Johnson,
1999).
Thank you for listening.

119. REFERENCES
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•
•
•
•
•
•
•
•
1. Brunner, L. S., Suddarth, D. S., Smeltzer, S. C. O., & Bare, B. G. (2004). Brunner &
Suddarth's textbook of medical-surgical nursing (10th ed.). Philadelphia: Lippincott
Williams & Wilkins.
2. Understanding Increased Intracranial Pressure Medically reviewed by Susan W. Lee,
DO
— Written by Elea Carey and Rachael Zimlich, RN, BSN on February 28, 2022,
available
on https://www.healthline.com/health/increased-intracranial-pressure
2. Shaikh F, Waseem M, Boling AM. Head Trauma (Nursing) [Updated 2022 May 15]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
Available
on https://www.ncbi.nlm.nih.gov/books/NBK568699/