1. Traumatic brain injury can cause extradural haemorrhage, subarachnoid haemorrhage, intracerebral haemorrhage, contusions, and diffuse axonal injury from shearing and tearing of neurons. 2. Primary brain injuries occur at the time of impact while secondary injuries develop afterwards from processes like brain swelling and inflammation. 3. Brain injuries can be mild, moderate or severe depending on factors like loss of consciousness duration. Monitoring tools like ICP, CPP, oxygenation and imaging are important for management.

1. Traumatic brain injury
Dr jigar j. mehta
Critical care consultant

3. Extradural
haemorrhage
Traumatic
Subarachnoid
Haemorrhage

4. Intracerebral Haemorrhage
• Any size, anywhere
• Initial pressure from clot
causes damage
• 2ndry injury from
products of clot
breakdown

5. Contusions
• Contusions involve cortical bruising
• Lacerations to vessels and brain
tissues causes tissue necrosis,
pulping and infarctions

6. Diffuse Axonal Injury & Concussion
• DAI is leading cause of
death disability
• Produces multiple
‘invisible’ lesions
• Diffuse nature makes it
impossible to predict
nature and extent of
injury

7. Pathophysiologic types
• Primary (occurs at time of impact, irreversible)
• Secondary (changes developing after impact, potentially
preventable)

8. Primary Effects of Brain Injury
______________________________________________________
• Injury to brain tissue at the initial site of impact and at
the second injury site (Coup & Contracoup)
• Shearing and tearing of neurons throughout the brain
disrupts communication

9. Mechanism of injury: Coup/Contracoup
______________________________________________________
Reprinted with permission from the North Carolina Department of Public Instruction

10. Shearing & Tearing of Neurons
• When an injury occurs the neurons stretch, twist or
tear.

11. Mild, Moderate, Severe
______________________________________________________
• Injuries can range from “mild” (a brief change in mental
functioning) to “severe” (extended period of
unconsciousness)
• Significant long-term disability.
• Full effects of brain injury may not be apparent until later
when the child is expected to perform more advanced skills
and to self-regulate behavior.

12. Severity of Brain Injury: Mild
______________________________________________________
• Brief or no loss of consciousness
• Signs of concussion
• Nausea and vomiting
• Headache
• Fatigue
• Dizziness
• Poor recent memory
• Unable to form new memories following the injury
(less than 1 hour)

13. Severity of Brain Injury: Moderate
______________________________________________________
• Coma less than 24 hours
• Unable to form new memories following the injury (less than
24 hours)

14. Severity of Brain Injury: Severe
_______________________________________________________
• Coma more than 24 hours
• Unable to form new memories following the injury (longer
than 24 hours)

15. No one aim need
to see surrounding

16. Systemic insult
•Hypotension
•Hypoxia
•Hyper/hypocarbia
•Hyperthermia
•Hyper/hypoglycaemia
•Electrolyte derangement
•Infection
Intracranial Insult
ICP
Seizures
Vasospasm
Infection
Other Insults
Ischaemia
Brain Swelling
Energy Failure
Inflammation
Neuronal Death
•Primary Injury
•Secondary Injury

17. Other Causes of LOC
Cerebral
Overdose
Metabolic
Alcohol

19. Indication for CT scan Brain: Adult
• GCS less than 13 at any point since the injury
• GCS equal to 13 or 14 at 2 hours after the injury
• Suspected open or depressed skull fracture
• Any sign of basal skull fracture
• Post-traumatic seizure
• Focal neurological deficit
cont….

20. Indication for CT scan Brain : Adult
•More than one episode of vomiting
•Amnesia for greater than 30 minutes of
events before impact
•If ANY LOC or amnesia in patients
• Older then 65 years
• Coagulopathy
• Dangerous mechanism of injury
• RTA as Pedestrian
• RTA: Ejected from car
• Fall from > 1meter or > 5 stairs

21. Imaging of Cx Spine: Indication
• GCS less than 15 at the time of assessment
• Paraesthesia in the extremities
• Focal neurological deficit
• Not possible to test range of movement in neck

22. Monitoring Neurological Functions
Methods of monitoring Intracranial Pressure (ICP)
• Intraventricular catheter
• Fibreoptic devices
• Strain gauge microtransducer systems
Methods of monitoring cerebral blood flow
• Transcranial doppler
Methods of monitoring cerebral oxygenation
• Jugular venous oxygen saturation
• Near-infrared spectroscopy
• Brain oxygen tension
Methods of monitoring function
• Clinical neurological assessment
• Glasgow coma scale
• Electroencephalogram (EEG)
• Electromyography

25. CSF leak
• Halo sign
• β2 transferritin or sugar
• Postural leak
• Constant dribbling
• Occasional post nasal trickle
• “Soreness” in throat

26. Initial Management of Severe Head Injury
• Undress the patient…..Completely
• A – Airway = Intubation / Tracheostomy
• B - Breathing + ventilator
• C - Circulation
• Replace lost blood volume
• Fix hypotension (< 90 mm Hg = bad)
• Fix hypoxia (< 60% SpO2 = bad)
• Hard Cervical Collar
• CT scan head (+/- body) when stable
• Primary assessment while pt is being
stabilized (includes plain spine X-Rays)

27. Points Of Interest
• Cerebral Dehydration (Anti edema measures)
• Steroids
• Seizure Prophylaxis
• Post Traumatic Amnesia
• ICP control
• Goal oriented activity

28. Cerebral
Dehydration
Therapy

29. Hypertonic Saline (3%)
Vs
Mannitol (20%)
Vs
Glycerol

30. How It Works??
•Raising plasma osmolality from
310 mOsm/kgH2O to 344 mOsm/kgH2O can
shrink the brain by 10%, with half of the
shrinkage occurring in 12 minutes.
•Mannitol also reduces blood
viscosity [SURGICAL NEUROLOGY; Andrews,RJ;
39(3):218-222 (1993)] and oxidative damage.
•0.25-2 gm/kg body weight as 15-25%
solution
•Should be given fast over 20-30 minutes to
achieve peak effect

31. Mechanism>> Osmotic???
• The ICP reduces before actual white mater
water content regresses
• When ICP is maximally reduced, there is no
significant change in white mater water
content
• ICP remains high, despite of reduction in
white mater water content by i/v albumin

33. What is Ideal??
• Glycerol can be administered orally
• Long term Rebound edema
• >20% concentration Hemolysis
• BBB actively extrudes sodium, so less chance of
rebound edema with HS
• After initial dose (n=??) of mannitol causing brain
dehydration, repeated doses exacerbates edema
When given in an equimolar, rapid,
HSD reduces intracranial pressure more
than mannitol.
[Crit Care Med. 2005 Jan ;33:196-202; discussion
15644669]

34. NO Role of
steroids in TBI
TBI

36. Post
Traumatic
Seizures

37. Seizures in TBI : A Bad Sign
• ICP
• Metabolic demands
• Risk of secondary brain
injuries
• Overall recovery is
delayed

39. Current Concept (NOT Guideline)
• Immediate onset seizure following injury does not mean
seizure disorders
• Prophylactic AED is not necessary
• Post traumatic status epilepticus is rare
• Those who did not have seizures in early 7-8 days don’t
require long term prophylaxis
• Normal scalp EEG does no rule out seizure risk

40. How to
treat Head
Injury
(SEVERE)

41. ICP
• After a brain injury the skull may become over full with
swollen brain tissue, blood or CSF
• Monroe Kellie Doctrine
• Increase in the volume of one
compartment must be offset by a decrease
in the volume of another compartment
• Total volume stays the same

42. Normal state- ICP normal

43. Compensated state- ICP normal

44. Uncompensated state- ICP Elevated
75 ml 75 ml

45. Volume-Pressure Curve

46. ICP Reducing Measures
• Sedate & Paralyse
• Ventilate to PCO2 =4.0 KPa
• Position: Head 30deg up
• Prevent Hypo/Hyperglycaemia
• Treat seizure activity
• Prevent Hyperthermia
• Minimise interventions

47. Goals Of Treatment
• CPP target > 70 mmHg
• Once stable, 60 mmHg may be adequate though
though
• pCO2 ≈ 30-35 mmHg
• ICP < 20 mmHg
• CVP ≈ 8-10 cm H2O, to titrate according to ICP
• S.Na+ ≈ 145-155 mmol/Lt

48. Indication for Ventilation
• GCS less than or equal to 8
• Loss of protective laryngeal reflexes
• Respiratory insufficiency as judged by blood gases
• PaO2 less than 9kPa
• PaCO2 greater than 6kPa
• Spontaneous hyperventilation
• Respiratory arrhythmia
• Bilateral fractured mandible
• Copious bleeding into mouth
• Seizures??

49. What to Monitor
• Admission to NCCU
• Invasive arterial line
• Radial
• ICP
• EVD catheter
• optic nerve sheath diameter
• Transcranial doppler
• Digital transducer
• Subdural catheter
• SjO2
• Right IJV
• CVP line
• Subclavian or jugular

50. Pre treatment
Before escalating vigorous medical management
• Remove any “significant” mass lesion
• Drain few ml CSF
• Jump to phase I of medical treatment

51. Phase I: General
• 200-300 head up, ensure no venous obstruction
• CPP > 70 mm Hg
• SpO2 > 97%
• Temp < 98.60 F/370 C
• SjO2 > 55%
• Sugar 80-120 gm% (4-7 mmol/Lt)
• Meds….

52. Phase I: Meds
• Phenytoin 15mg/kg if indicated
• PPI at optimum dose + Sucralfate
• Propofol 2-5 mg/kg/hr
• Fentanyl 1-2 mg/kg/hr
• Atracurium 0.5 mg/kg/hr
•

53. Phase II
• ICP > 20 and/or CPP < 60 Continue & monitor
yes
Drain CSF & assess need for CT to r/o new S.O.L.
yes
Consider to start Phase III management
no

54. Phase III
• 5% NaCl 2 ml/kg
• Repeat if Na < 155 mmol/Lt or Posm <
320
• 20% Mannitol 2ml/kg x3 or till Posm 320
• PCV, Inotrops to raise CPP > 70 mm Hg
• Daily lipid screen if on Propofol
• Reduce PaCO2 about 4 kPa if SjO2 > 55%
• EEG if suspected non-convulsive status

55. Phase IV
• Reduce temp to ≈ 33c C
• Discontinue propofol
• Jump to Phase V
• I/V anesthetics, inotrops
ICP/CPP improve
• Start Pentothal Boluses 250 mg (up to 3 gm)
• Maintain at 3-8mg/kg/hr
• Monitor EEG for burst suppression
Consider “empiric”
decompressive craniectomy

56. Monroe Kellie Doctrine

57. Herniation
• Brain tissues swell
• Transfalcine (a)
• Transtentorial (b)
• Pressure on IIIrd nerve
dilated pupil
• Foramen magnum (e)

58. Why measure ICP?
• Major cause of secondary injury
• Some evidence that keeping ICP < 20 improves outcome
• May be first indicator of something serious happening eg
clot enlarging

59. What about CPP?
• CPP: Cerebral Perfusion Pressure
• CPP = MAP – ICP
• Low perfusion causes ischaemia of brain &
secondary injury
• Aim for CPP > 60
• If low …
•Increase MAP
•Decrease ICP
………. Or both

60. How to increase BP?
• Increase fluid volume
• Use drugs
• Noradrenaline
• Dopamine

61. How to decrease ICP?
• Remove space occupying lesion
• Head-up 30° (imroves venous drainage)
• Decrease metabolism of brain
(Vasoconstriction from metabolic
autoregulation)
• Decrease brain blood volume
(Vasoconstriction from hyperventilation)
• Decrease brain water (Mannitol, hypertonic
saline)
• Decrease CSF volume (EVD)
• Open the skull to give more room
(Craniectomy)

62. Decrease Brain Metabolism
• Sedation
• Morphine, midazolam,Propofol
• Barbiturates
• Paralysis
• Stops muscle activity
• Cooling
• Effective to mild levels – 34 to 35 degrees
• Problems with infections and bleeding

63. Decrease Brain Volume
• Hyperosmotic diuresis
• Mannitol
• Hypertonic saline – in favour now
• Drain CSF
• Need ventricular catheter in place
• Raise Head of Bed/Check neck is free
• Reduces venous congestion
• Hyperventilation
• Low CO2 causes constriction of vessels
• Only use as last resort because also causes
ischaemia

64. •Major bleeding wounds means bad injury
•All patients need brain scan
•Oxygen “cures”
•Cocktail works well…Steroids… antibiotics
•Head injury means “mannitol”
•Focal lesion >>>> give Anti Epileptics…
•MRI >> CT scan
•Ventilator means “terminal event”
•Hyperventilation, “Always”