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Head InjuryHead Injury
Dr Mike NoonanDr Mike Noonan
Local Experience
• Mortality from severe TBI in Australasia varies from 17.2% up to
19.6%
• This has improved from figures of around 33% in the early 1990’s
• Brain injury is the largest singe cause of death in patients surviving
to hospital
• In Australia: severe TBI 1000 patients/year. 60% die or are left
severely disabled
• In Victoria, approximately 2500 major trauma patients per year
– In hospital mortality is approximately 11%, with TBI accounting for
75% of these
Gabbe et al. 2011. www.plosone.org Hunt et al. 1995. ANZ J Surg. (65)83-86.
Gabbe et al. 2011. Ann Surg. (253)138-143. Myburgh et al. 2008. J Trauma. (64)854-862
Trauma Registry Principal Cause of Death CodeTrauma Registry Principal Cause of Death Code
all trauma deathsall trauma deaths
Principal Cause of DeathPrincipal Cause of Death 20062006 20072007 20082008 20092009
20102010
YTDYTD
GrandGrand
TotalTotal
Fatal TBI 50 74 69 59 15 267267
Complications of Injury 11 15 19 19 9 7373
Multiple Injuries 17 15 4 3 3 4242
Uncontrollable Haemorrhage 11 6 10 5 2 3434
Succumbed to co morbidities 14 14 15 22 9 7474
Other 4 3 2 6 4 1919
Hypoxia 2 1 2 1 2 88
Not Coded 17 2 2 10 9 4040
Grand TotalGrand Total 126126 130130 123123 125125 5353 557557
Head and truncal operations for multi-system
trauma 2009
ProceduresProcedures PtsPts
Head
Craniotomy 83 77
Craniectomy 37 36
Chest
Thoracotomy 35 29
ED Thoracotomy 5 5
Abdomen
Laparotomy 130 100
Laparoscopy 11 11
ED Laparotomy 1 1
Pathophysiology
Blunt TBI occurs due to:
•Direct force
•Acceleration and de-acceleration
•Sheering
Neuron damage occurs via:
•Direct damage: eg- contusion, sheering
•Raised intracranial pressure reducing cell perfusion and causing
brain herniation
6
7
CPP = MAP - ICP
8
Pressure-Volume Curve
Compensation
Point of
¬ Decompensation
Herniation
Volume of Mass
ICP
(mm Hg)
5-
10-
15-
20-
25-
30-
35-
40-
45-
50-
55-
60-
36 year old male
Mechanism:
•Pushbike with helmet into parked car
Injuries:
•Facial Injuries: epistaxis, facial lacerations.
•Head Injury: GCS: E1 V2 M5
Rx:
•O2 via Hudson mask
•Cervical hard collar
10
What now?
• Call for help
• O2 with Cx spine control
• Is the airway adequate?
• ECG/SpO2/EtCO2
• IV access with bloods:
– FBE,coag, glucose, Xmatch, ABGs
11
12
Rapid sequence intubation
• (cervical spine immobilization)
• drug administration / assistant
• Blunt rise in ICP
• cricoid pressure
• intubation
• EtCO2 32 mmHg
• keep paralyzed and sedated
What Next
13
Is there a space-occupying lesion?
14
15
Treatment Principles
• Prevention of additional (secondary) brain injury caused by brain
hypo-perfusion and hypoxia
• Includes:
– Optimisation of cerebral perfusion pressure
Fluid resuscitation and balance with inotropic support (when
appropriate)
ICP monitoring and CSF drainage
Evacuation of haematoma, decompressive craniectomy
Optimisation of ventilation
Minimisation of extracranial surgical procedures
– Decrease in the metabolic requirements of neurones
Optimisation of sedation
Control of pyrexia
Intracranial Monitoring
• The management of intracranial hypertension has become central
to the intensive care of patients with severe TBI1
1: Fakhry et al. 2004. J Trauma (56)492-500
2: Brain Trauma Foundation 2007. J Neurotrauma (24)Supplement1
Recommended:2
•Severe TBI with an abnormal CT scan
•GCS <9 with a normal CT scan and
two or more of the following:
- Age >40 years
- Motor posturing
- SBP<90mmHg
Management of Intracranial Hypertension
First tire management of intracranial hypertension is medical therapy:
Intubation and ventilation: RSI
•PCO2: aim: 35-40mmHg.
•PO2 aim: >94%
•Avoidance of high inspiratory
pressures- low PEEP (5cmH2O,
tidal vol <8ml/kg)
Blood pressure:
•Aim for CPP of >60mmHg
•MAP>80mmHg (assuming ICP
20mmHg when not measured)
•Avoid hypovolemia
•NSaline, Blood and FFP
Monitoring:
•Arterial line
•Central line
•ICP monitor
Sedation:
•Deep sedation for ICP control
•Fentanyl and Midazolam
•Propofol if required (limited to
200mg/hr or more*
Management of Intracranial Hypertension
First tire management of intracranial hypertension is medical therapy:
Monitoring:
•Arterial line
•Central line
•ICP monitor
GCS <9 and abnormal CT
GCS <9 and normal CT
with
•Age >40yrs
•Motor score <6*
•SBP<90mmHg
Patient requires intubation
and deep sedation for
extra-cranial trauma
GCS <9 and abnormal CT
GCS <9 and normal CT
with
•Age >40yrs
•Motor score <6*
•SBP<90mmHg
Patient requires intubation
and deep sedation for
extra-cranial trauma
Target: <20mmHgTarget: <20mmHg
Management of Intracranial Hypertension
Action for sustained increase in ICP:
•Ensure adequate sedation
•Vent from EVD (if available)
•Osmotherapy: bolus 20% saline (0.5ml/kg 20% hypertonic saline) –
avoiding serum Na >155mmol/L
•Reduction in PEEP (may need to increase FiO2)
•Neuromuscular blockade: boluses in preference to infusion
•Normothermia: may require active cooling
•Thipentone boluses (250mg iv) – used with EEG monitoring
Decompressive Craniectomy
• Many patients with severe TBI have intracranial hypertension that
becomes refractory to medical management
• Decompressive craniectomy is used in many neurosurgical centers
Decompressive Craniectomy
• No difference in mortality
• Worse functional outcome
at 6 months
• ICP trigger: >20mmHg for
>15min
• Similarity of study groups?
• Surgical technique
Randomised Evaluation of Surgery with
Craniectomy for Uncontrollable Elevation
in Intra-Cranial Pressure
•ICP trigger 25mmHg for 1-2 hours
•Surgical techniques differ
Current Areas of Research
POLAR
Prophylactic Hypothermia Trial to Lessen Traumatic
Brain Injury- Randomised Controlled Trial
EPO-TBI
Erythropoietin in Traumatic Brain Injury
Summary
• Management of TBI: A.B.C
• Prevent secondary brain injury
• Early identification of space-occupying lesion: urgent theatre
• Medical management of intracranial hypertension
24

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Neuro-trauma - Mike Noonan

  • 1. Head InjuryHead Injury Dr Mike NoonanDr Mike Noonan
  • 2.
  • 3. Local Experience • Mortality from severe TBI in Australasia varies from 17.2% up to 19.6% • This has improved from figures of around 33% in the early 1990’s • Brain injury is the largest singe cause of death in patients surviving to hospital • In Australia: severe TBI 1000 patients/year. 60% die or are left severely disabled • In Victoria, approximately 2500 major trauma patients per year – In hospital mortality is approximately 11%, with TBI accounting for 75% of these Gabbe et al. 2011. www.plosone.org Hunt et al. 1995. ANZ J Surg. (65)83-86. Gabbe et al. 2011. Ann Surg. (253)138-143. Myburgh et al. 2008. J Trauma. (64)854-862
  • 4. Trauma Registry Principal Cause of Death CodeTrauma Registry Principal Cause of Death Code all trauma deathsall trauma deaths Principal Cause of DeathPrincipal Cause of Death 20062006 20072007 20082008 20092009 20102010 YTDYTD GrandGrand TotalTotal Fatal TBI 50 74 69 59 15 267267 Complications of Injury 11 15 19 19 9 7373 Multiple Injuries 17 15 4 3 3 4242 Uncontrollable Haemorrhage 11 6 10 5 2 3434 Succumbed to co morbidities 14 14 15 22 9 7474 Other 4 3 2 6 4 1919 Hypoxia 2 1 2 1 2 88 Not Coded 17 2 2 10 9 4040 Grand TotalGrand Total 126126 130130 123123 125125 5353 557557
  • 5. Head and truncal operations for multi-system trauma 2009 ProceduresProcedures PtsPts Head Craniotomy 83 77 Craniectomy 37 36 Chest Thoracotomy 35 29 ED Thoracotomy 5 5 Abdomen Laparotomy 130 100 Laparoscopy 11 11 ED Laparotomy 1 1
  • 6. Pathophysiology Blunt TBI occurs due to: •Direct force •Acceleration and de-acceleration •Sheering Neuron damage occurs via: •Direct damage: eg- contusion, sheering •Raised intracranial pressure reducing cell perfusion and causing brain herniation 6
  • 7. 7 CPP = MAP - ICP
  • 8. 8 Pressure-Volume Curve Compensation Point of ¬ Decompensation Herniation Volume of Mass ICP (mm Hg) 5- 10- 15- 20- 25- 30- 35- 40- 45- 50- 55- 60-
  • 9. 36 year old male Mechanism: •Pushbike with helmet into parked car Injuries: •Facial Injuries: epistaxis, facial lacerations. •Head Injury: GCS: E1 V2 M5 Rx: •O2 via Hudson mask •Cervical hard collar
  • 10. 10 What now? • Call for help • O2 with Cx spine control • Is the airway adequate? • ECG/SpO2/EtCO2 • IV access with bloods: – FBE,coag, glucose, Xmatch, ABGs
  • 11. 11
  • 12. 12 Rapid sequence intubation • (cervical spine immobilization) • drug administration / assistant • Blunt rise in ICP • cricoid pressure • intubation • EtCO2 32 mmHg • keep paralyzed and sedated
  • 13. What Next 13 Is there a space-occupying lesion?
  • 14. 14
  • 15. 15
  • 16. Treatment Principles • Prevention of additional (secondary) brain injury caused by brain hypo-perfusion and hypoxia • Includes: – Optimisation of cerebral perfusion pressure Fluid resuscitation and balance with inotropic support (when appropriate) ICP monitoring and CSF drainage Evacuation of haematoma, decompressive craniectomy Optimisation of ventilation Minimisation of extracranial surgical procedures – Decrease in the metabolic requirements of neurones Optimisation of sedation Control of pyrexia
  • 17. Intracranial Monitoring • The management of intracranial hypertension has become central to the intensive care of patients with severe TBI1 1: Fakhry et al. 2004. J Trauma (56)492-500 2: Brain Trauma Foundation 2007. J Neurotrauma (24)Supplement1 Recommended:2 •Severe TBI with an abnormal CT scan •GCS <9 with a normal CT scan and two or more of the following: - Age >40 years - Motor posturing - SBP<90mmHg
  • 18. Management of Intracranial Hypertension First tire management of intracranial hypertension is medical therapy: Intubation and ventilation: RSI •PCO2: aim: 35-40mmHg. •PO2 aim: >94% •Avoidance of high inspiratory pressures- low PEEP (5cmH2O, tidal vol <8ml/kg) Blood pressure: •Aim for CPP of >60mmHg •MAP>80mmHg (assuming ICP 20mmHg when not measured) •Avoid hypovolemia •NSaline, Blood and FFP Monitoring: •Arterial line •Central line •ICP monitor Sedation: •Deep sedation for ICP control •Fentanyl and Midazolam •Propofol if required (limited to 200mg/hr or more*
  • 19. Management of Intracranial Hypertension First tire management of intracranial hypertension is medical therapy: Monitoring: •Arterial line •Central line •ICP monitor GCS <9 and abnormal CT GCS <9 and normal CT with •Age >40yrs •Motor score <6* •SBP<90mmHg Patient requires intubation and deep sedation for extra-cranial trauma GCS <9 and abnormal CT GCS <9 and normal CT with •Age >40yrs •Motor score <6* •SBP<90mmHg Patient requires intubation and deep sedation for extra-cranial trauma Target: <20mmHgTarget: <20mmHg
  • 20. Management of Intracranial Hypertension Action for sustained increase in ICP: •Ensure adequate sedation •Vent from EVD (if available) •Osmotherapy: bolus 20% saline (0.5ml/kg 20% hypertonic saline) – avoiding serum Na >155mmol/L •Reduction in PEEP (may need to increase FiO2) •Neuromuscular blockade: boluses in preference to infusion •Normothermia: may require active cooling •Thipentone boluses (250mg iv) – used with EEG monitoring
  • 21. Decompressive Craniectomy • Many patients with severe TBI have intracranial hypertension that becomes refractory to medical management • Decompressive craniectomy is used in many neurosurgical centers
  • 22. Decompressive Craniectomy • No difference in mortality • Worse functional outcome at 6 months • ICP trigger: >20mmHg for >15min • Similarity of study groups? • Surgical technique Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation in Intra-Cranial Pressure •ICP trigger 25mmHg for 1-2 hours •Surgical techniques differ
  • 23. Current Areas of Research POLAR Prophylactic Hypothermia Trial to Lessen Traumatic Brain Injury- Randomised Controlled Trial EPO-TBI Erythropoietin in Traumatic Brain Injury
  • 24. Summary • Management of TBI: A.B.C • Prevent secondary brain injury • Early identification of space-occupying lesion: urgent theatre • Medical management of intracranial hypertension 24

Editor's Notes

  1. Mortality from severe TBI in Australasia varies from 17.2% up to 19.6% Trauma Registry data Victoria 2001-2006
  2. 1: Fakhry et al. 2004. Guidelines that include ICP monitoring have been validated This is despite lack of randomised controlled trials 3rd Edition of the BTF Guidelines published in 2007.
  3. Propofol: associated with toxicity. Must be limited to 200mg/hr and dose reduced with therapeutic hypothermia and if used after 48/24
  4. 0.5ml/kg 20% hypertonic saline- 20-40ml dose, may increase serum Na by 2-3mmol/L Thiopentone: EEG to establish burst suppression These actions are in conjunction with consultation with treating neurosurgeon and consideration for repeat CT scan
  5. POLAR: Multi-centre prospective, randomised controlled trial: early and sustained prophylactic hypothermia in patients with severe TBI Has been used to decrease secondary brain injury following out of hospital cardiac arrest Patient recruitment commenced mid 2010. EPO: Multicentre prospective, ramdomised double-blind placebo-controlled trial Patients with moderate to severe TBI Endpoint: neurological outcome at 6 months