1. NEUROTRAUMA
Nishantha Gunasekera
MBBS MS MRCS
Consultant Neurosurgeon

2.  36 year old male presented to a District Hospital ED
 He was arrested for intoxication and fighting at 0530hrs
 ? Head injury
 He was found to be difficult to rouse at 0800hrs
 CT scan of head
 Initial examination (at District Hospital)
 GCS 15/15; PEARL 3mm

7. Natasha Richardson autopsy: internal brain bleed caused death
 The official word from the New York City medical examiner's office is that
actress Natasha Richardson died from a blunt impact to the head.
 Her death was ruled an accident Thursday after an autopsy was performed.
The blunt impact caused internal brain bleeding (an epidural hematoma),
which is what killed her, the M.E.'s office reports, but it is still not clear
exactly how she injured her head.
Monday afternoon, during a private ski lesson on a beginner hill at Mont
Tremblant in Quebec, Richardson fell in the middle of the ski run and did not
appear to hit any object aside from the snow on the ground.
Afterward, 45-year-old Richardson initially appeared fine and was “lucid”,
talking, even making jokes.

8. Why is Neurotrauma
management so
important?
 Injuries to the brain, spinal cord and its
associated structures – VITAL ORGANS
 Most patients are healthy, young and the
productive people of society (MVA, accidents,
assaults, war)
 Very good outcome if managed correctly
 Very poor outcome if managed incorrectly

9. Role of Nursing in
Neurotrauma
 Correct handling of neurotrauma victims
 In-ward care is critical for good patient outcome
 Knowledge of possible injuries and their effects
vital for good management and nursing care
 Understanding the long term problems of
neurotrauma helps plan rehabilitation
 Education in prevention of neurotrauma
 Compassion for whom you care for and passion
for what you do

10. Introduction
 Head injury
 Spinal injury
 Mixed head and spinal trauma
 Initial assessment (ABCDE)
 Transport
 Primary survey (ABCDE)
 Secondary survey
 Treatment
 Rehabilitation

11. Head Injury
 Mechanism
 Forces
 Patterns of injury
 Prevention
 Primary assessment

12. Mechanism and forces

13. Transport
 Stabilize the spine
 Airway
 Oxygen
 Fluids
 Inform casualty neurosurgical unit

14. Head injury
 Primary brain damage
 Secondary brain damage
 Prevention of primary and
secondary brain damage

15. Head injury
Primary brain damage
Brain damage at the time of injury
Secondary brain damage
Damage due to effects of primary brain damage
and other physiological changes that result
Main aim of management is limitation and
reversal of secondary brain damage

16. Secondary brain
damage
 Oedema
 Hypoxia
 Hypovolaemia
 Hypoglycaemia / Hyperglycaemia
 Hyperthermia
 Seizures
 Electrolytes
 Cytokines

17. Head injury
 Intracranial pressure (ICP)
 Cerebral perfusion pressure (CPP)
 Mean arterial pressure (MAP)
 How does it alter
 Monitoring of pressures

18. Head injury
 Mechanisms of controlling ICP
 Non surgical
 Surgical

19. Head injury
 Effects of raised ICP
 Cardiovascular
 Respiratory
 Cushings reflex
 Decerebration

20. Herniation syndromes
 a) Cingulate (subfalcine)
 b) Uncal
 c) Central (transtentorial)
 d) Thru’ defects
f
 e) Tonsillar
 f ) Upward (cerebellar)

21. Clinical Stages of
Central herniation
STAGE Consciousness Respiration Pupils Occulomotor Motor
Diencephalic Altered alertness, Sighs, yawns, Small congugate, Appropriate,
lethargy, agitation later Cheyne- (1-3mm) Parinaud’s Babinski
(some), stupor, Stokes slow Geganhalten(resists)
coma
Midbrain stupor Cheyne- Mod. Dolls eyes, Decorticate,
Stokes, dilatation, Dyscongugate Decerebrate
Tachypnoea (3-5mm)
Fixed
Lower pons coma Regular, Mid Dolls eyes Flaccid, Babinski
shallow, position,
rapid (20- Fixed
40/min)
Medullary Coma 3/15 Slow, Widely
irregular, dilated,
gasps, apnea fixed

22. Clinical stages of
Uncal Herniation (Trauma)
STAGE CONSCIOUSNESS RESPIRATION PUPILS OCCULOMOTOR MOTOR
Early 3rd Alert, Normal Ipsilateral Doll’s (-), Appropriate,
Maybe Babinski
nerve oriented, dilatation dysconjugate
obeys
Late 3rd Stuporous, Sustained Fully EOO Ipsilateral
hyper-
nerve comatose ventilation
dilates (External weakness
occulomotor Kernohan’s
ophthalmoplegia) phenomenon
rarely
Midbrain Comatose Sustained Contralateral Absent Decerebrate
hyperpnea dilates, both
fixed (7mm)

23. Herniated Right Uncus

24. Head injury
 Monitoring ICP
 Clinical
 Invasive
 ICU (Nursing)

25. Head injury
 Management of specific injuries
 Minor 12-15 Observation only
 Moderate 8-11 Observation/ treatment
 Severe <8 Most need treatment
 Based on GCS
 Mechanism
 Anatomy

26. Glasgow Coma Scale
Glasgow Coma Score

27. Head Injury
 Investigations
 Skull x ray AP/lateral
 CT scan, bone window
 CT reconstruction
 MRI
When to do what investigation?

28. Head Injury
 Compound fractures
 Extra dural haemorrhage (EDH)
 Acute Subdural Haemorrhage (SDH)
 Chronic SDH
 Intracerebral Haemorrhage (ICH)
 Traumatic subarachnoid haemorrhage (SAH)
 Intraventricular haemorrhage (IVH)
 Contre-coupe injury
 DIFFUSE AXONAL INJURY (DAI)

29. NORMAL CT

30. Compound fracture

31. Compound fractures
cntd.

32. Compound
fractures cntd.

33. Compound fractures
cntd.

34. Comp. fractures
Complications

35. EDH

36. EDH

37. EDH (MRI)

38. EDH (MRI) cntd.

39. EDH (MRI) cntd.

40. ASDH

43. CSDH

44. CSDH

45. ICH

46. ICH -trauma

47. Traumatic SAH

48. IVH

49. DAI

50. Contre coup injury
 Injury directly opposite the site of impact
 Maybe an EDH with SDH on the other side
 Both have to be managed
 May need surgery for both
 Outcome may be poorer

51. Modalities of Treatment
 Mechanical
 Medical
 Surgical

52. Management
Trauma Systems
 Guides: Regionalized trauma systems
 Option: Neurosurgeons need to have a
responsive system in place
 Option: In rural setting, where no
neurosurgeon: know how to Rx extra-
dural haematoma in deteriorating pt

53. Primary survey
CLINICAL ASSESSMENT!!
 ABCDE
 GCS
 Resuscitate
 History
 Image
 Specific Treatment

54. Initial Assessment
ATLS
Airway
Breathing
Circulation
Disability
Exposure

55. Treatment
Initial Management Options
 Rapid physiologic resuscitation
 No intracranial HTN Rx unless herniation or
rapid neurologic deterioration
 Cautious hyperventilation
 Mannitol if adequate volume established
 Sedation as desired with careful monitoring (GCS)
 Short-acting neuromuscular blockade prn

56. Treatment
Resus: Blood Pressure
 Guides: Achieve SBP > 90 mm Hg
 Options: MAP > 90 mm Hg
CPP > 70 mm Hg
 Use fluid infusion to achieve above

57. Treatment
Resuscitation: Hypoxia
 Guides: PaO2 > 60 mmHg, O2 sat > 90%
 Options: Endotracheal intubation for
 GCS < 9
 Unable to maintain airway
 Persistent hypoxia

58. Secondary survey
CLICAL ASSESSMENT!!
 All injuries
 From head to toe
 Treat on priority basis
 Chest-abdomen-c spine-head- limbs
 Refer to appropriate speciality surgeon

59. Treatment
Hyperventilation
 Standards: Normal ICP, avoid sustained
pCO2 < 25 mm Hg in severe TBI
 Guides: Avoid early prophylactic
hyperventilation (pCO2 < 35 mm Hg)
 Note: During first 24 hours, cerebral
perfusion can be compromised due to low
cerebral blood flow

60. Treatment
Hyperventilation Options
 Option: Hyperventilation useful briefly
 Acute neurologic deterioration
 Longer use if intracranial HTN persists despite
other medical therapies (sedation, paralysis,
mannitol, CSF drainage)
 Option: Test for cerebral ischaemia
 Jugular venous O2 sat, AV O2 sat diff
 If sustained pCO2 < 30 mm Hg needed

61. Treatment
Hyperventilation
 Rapidly lowers ICP via vasoconstriction,
which reduces cerebral blood flow
 One RCT
 Considerable uncertainty
 Possible beneficial effect on mortality
 No proven neurologic outcome benefit

62. Treatment
Mannitol
 Guides: Controls increased ICP
 Severe TBI
 0.25 to 1.0 gr/kg body weight
 Renal problems
 Electrolyte imbalance
 Good drug in good hands

63. Treatment
Mannitol Options
 Options: Use in herniation, rapid decline
 Avoid hypovolaemia
 Keep serum osmolarity below 320mOsm
to avoid renal failure
 Achieve euvolaemia, use a Foley
 Use intermittent boluses, may be better

64. Treatment
Mannitol
 May reverse brain swelling, lower ICP
 Few eligible RCTs
 Considerable uncertainty
 May be superior:
 to pentobarbital for increased ICP
 in setting of measured increased ICP

65. Treatment
High Dose Barbiturates
 Guides: Controls increased ICP
 May be useful when maximal therapies fail
 Includes both medical and surgical Rx
 Severe TBI, salvageable
 Haemodynamically stable

66. Treatment
Barbiturates
 Lower ICP via lower cerebral metabolism
 Few eligible RCTs
 Noted hypotension in 1 of 4 patients
 May offset any beneficial ICP effects

67. Treatment
Cerebral Perfusion Pressure
 Guides: Maintain CPP at 70 mm Hg
 Reduce ICP by
 Mechanical means (position, collar)
 Medical means (mannitol, frusemide)
 Ventilation
 Surgery (drain, decompressive craniectomy)

68. Treatment
ICP Rx Algorithm
 Insert ICP monitor, maintain CPP > 70
 Ventricular drainage
 Repeat CT
 Hyperventilate to pCO2 30-35 mm hg
 Mannitol 0.25 to 1.0 gr/kg
 Second tier Rx: barbitruates, pCO2 < 30
CLINICALL ASSESSMENT!!

69. Treatment
ICP Monitoring
 Guides Useful in severe TBI (GCS < 9)
 Guides: Abnormal initial head CT
 Hematomas, contusions
 Edema, compressed basal cisterns
 All other recommendations are options

70. Treatment
ICP Monitoring: Normal CT
 Guides: ICP monitor with normal CT if
two of three noted
 Age > 40 years
 Persistent BP < 90 mm Hg
 Motor posturing

71. Treatment
ICP Monitoring Not Indicated
 Guides: Not useful with GCS > 8
 May be useful if traumatic mass lesion is
evident on head CT

72. Treatment
ICP Monitoring Technology
 Ventricular catheter (Camino catheter)
 External strain gauge
 Accurate, low-cost, reliable
 Parenchymal monitor: drifting values
 Subarachnoid, subdural, epidural:

73. Treatment
Seizure Prophylaxis
 Guides: High risk: prevent early sz
 Phenytoin, carbamazepine effective
 Reduces spikes in ICP in theory
 No difference in long-term outcome

74. Treatment
Seizure Prophylaxis, Rx
 Reduced secondary damage due to increased
metabolism, ICP, glutamate
 Six RCTs
 RR for early sz prophylaxis: 0.34
 For every 100 patients treated, 10 would remain
seizure-free for the first week
 No reduction in late seizures or outcome

75. Treatment
Steroids
 Standards: Not recommended
 No decrease in ICP
 No improved outcome
 Used with caution in our units for traumatic
brain injury

76. Treatment
Calcium Channel Blockers
 Prevent vasospasm, keep blood flow
 Four RCTs
 Considerable uncertainty
 Two RCTs, traumatic SAH, nimodipine
 Pooled OR 0.59 for death (95% CI .37-.94)
 Pooled OR 0.67 for death, disability

77. Treatment
Surgical
 Craniotomy
EDH, ASDH, ICH
 Craniotomy and removal of bone flap only
 Burr hole
 External drainage (EVD)
 Wound toilet (debridement)

78. EDH -surgery

79. EDH –surgery cntd.

80. CSDH surgery

81. CSDH surgery

82. REHABILITAION
 Starts in the ward
 Continues until the patient is back to his/her
optimum
 Multidisciplinary (nurses, physiotherapists,
relatives, doctors)
 Special equipment

83. IN WARD
NURSING
 Care of the unconscious
 MONITORING
 Nutrition (oral, nasogastric, tpn)
 Drugs
 Bed sores
 Eye, nose, mouth care
 Bladder, bowel
 Stimulation
 Mobilization
 Physiotherapy
 Education

84. Physiotherapy
 Exercise
 Chest physio
 DVT prophylaxis
 Bed sores
 Walking training
 OT
 Cognitive
 Long term management – home care with regular
supervision

86. Qs&As