Head injury management
Adapted from source
Traumatic Brain Injury
22,000-25,000/yr pts Australian
– 1,493 moderately TBI
– 1,000 severe cases of TBI
–
Qld incidence 200/100,000
National 140/100,000
1/3 trauma deaths
Traumatic Brain Injury
Assessment History
History Time & Mechanism Injury
Neuro status
– at scene (GCS Score and pupils)
– in transport
– After resuscitation
Vital signs Hypoxia and hypotension
Time of intubation presence of apnoea
Associated injuries
Age
Alcohol / drugs/s intake
Brain CT
Traumatic Brain Injury
Traumatic Brain Injury
15-13 Mild
9 – 12 Moderate
<9 Severe
Traumatic Brain Injury-GCS
Eye opening Best Motor
– Spontaneous 4 Response
– To speech 3 – Obeys 6
– To pain 2 – Localises 5
– NONE 1 – Withdraws 4
– Abnormal flexion 3
Verbal Response – Extensor response 2
– Orientated 5 – None 1
– Confused conversation 4
– Inappropriate words 3
– Incomprehensible
sounds 2
– After
– None 1 Resuscitation
Traumatic Brain Injury-GCS
Outcome
GCS 8-15 = 0.3% mortality
GCS 6-7 = 24% mortality
GCS 4-5 = 49% mortality
GCS 3 = 83% mortality
Klauber et al 1134 patients
Pathophysiology TBI
Primary insult
– Primary injury
– Secondary injury
Secondary insult
Primary insult
Primary insult
– Primary injury
– Direct damage
involves mechanical
forces
Brain : contact energy
transfer and inertia
energy transfer
Vasculature: vessel
shear and disruption
Secondary Brain injury
Ischaemia (CBF)
Excitotoxicity
(CMRO2)
Neuronal death
cascades.
Cerebral oedema
(vasogenic,
cytotoxic).
Inflammation.
Secondary insults
Independently of the primary impact
Secondary insults
Discrete processes, often iatrogenic
Secondary injury
Traumatic brain injury management
Primary injury
– Prevention
Secondary injury
– attenuate secondary injury mechanisms
– manage raised ICP
Secondary insult
– Prevent and treat secondary insults
– ABCD
Management Principles Secondary TBI
Prevent further cerebral insults
Hypoxia
Hypotension
Hyperglycaemia
Defend cerebral perfusion
Limit intracranial pressure rise
Cerebral oedema
Cerebral blood volume
CSF volume
Limit cerebral metabolic demand
Hypoxia –Traumatic Brain Injury
Apnoea accompanies most head injuries.
– Airway obstruction and aspiration major
causes of death treatable head injuries
Hypoxia is common
– PaO2 ≤ 60 mm Hg 46% admissions to the emergency department
Cerebral metabolic rate for oxygen
(CMRO2)
CMRO2
– 3.5 ml/100g/min
– 50 ml/min (20% of
total basal
requirements).
PaO2 minimal effect
on CBF until 50
mmHg
Hypoxia –Traumatic Brain Injury
Associated
– 50% mortality rate
– 50% severe disability
among survivors
Worse outcomes for
patients with TBI who
were intubated in the
field
Why ?
Intubation –TBI
Risk ICP, aspiration, and hypoxia.
IPPV increases intra thoracic pressure,
– decrease venous return impair CPP.
Sedative agents can cause hypotension
Risk of hyperventilation
Brain Trauma Foundation
Prehospital guidelines recommend
intubation
GCS scores ≤ 8
Inadequate airway
SaO2 < 90% with supplemental O2
PaCO2 TBI
PaCO2 levels emergency department
– 17%, PCO2 < 30
– 47%, PCO2 30–39
– 26%, PCO2 > 40
Target PaCO2 range of 30–39
– mortality 21%
PaCO2 < 30 or >39
– mortality 34%
PaCO2 CBF
CO2 potent cerebral
vasodilator
1 mm Hg drop in
PCO2 3% decrease
in CBF
Hyperventilation can
lead to cerebral
ischemia
Hypotension TBI
Hypotension is common.
– 8–13% severe head injury pt.
Single episode of hypotension (SBP< 90
mm Hg) X2 mortality rate
Hypotension TBI
Hypotension diff in adults to children
Other injury
Spinal cord injury
Cardiac contusion/tamponade
Tension pneumothorax
Children may be hypotensive due to blood losses
of head injury
Pressure autoregulation
In normal brain CBF
constant between MAP 50
mmHg and 150 mmHg
Nml CBF
– 50ml/100g/min
– 700 ml/min
– 14 % of the cardiac output.
Severe TBI CBF is blood
pressure dependent.
CBF TBI
Severe TBI CBF is blood pressure dependent.
Cerebral perfusion pressure (CPP)
– CPP = MAP – ICP (or CVP, whichever is the highest)
Increase in mortality and poor outcome when
CPP < 70 mmHg for a sustained period.
Pressure auto-regulation
MAP
1/3 (SBP-DBP) +DBP
CPP = MAP – ICP
ICP is 7-17 mmHg
Defend cerebral perfusion
MABP 90 mmHg
CPP = MABP – (ICP or JVP)
Avoid raised JVP or CVP
– Blood volume
– JVP obstruction
– Raised intrathoracic pressure
– Excessive PEEP
Inotropes NAdr or Adr
Position
– Nurse head up 20-30°(if spine cleared)
– C-spine collar
Avoid excessive ventilatory pressures
Pressure-Volume Curve
Herniation
60-
ICP 55-
(mm Hg) 50-
45-
40-
35-
30-
25-
20-
15- Point of
10-
Compensation Decompensation
5-
Volume of Mass
Intracranial Pressure (ICP)
10 mm Hg = Normal
> 20mm Hg = Abnormal
> 40mm Hg = Severe
Many pathologic processes affect
outcome
ICP Brain function, outcome
Normal2
CSF volume
Haematoma
Head injury1
Brain
0 20 swelling60
40 80 100 120
Intracranial pressure
Intracranial tissue volume
Limit intracranial pressure rise
Cerebral blood volume
Avoid hypertension
– CVS responses to pain, stimulation
– Analgesia & sedation associated injuries
Transfers
Procedures Intubation
Control PaCO2
– Ventilation to PaCO2 = 34 - 36 mmHg
Limit intracranial pressure rise
Cerebral oedema
– Avoid hypo Na+
– Target Na+ >135 mmol
0.9% saline
Signs of Impending Herniation
Deteriorating LOC (GCS score)
Pupillary asymmetry >1mm
Motor asymmetry
Extensor (decerebrate) posturing (M2),
Cushing’s response BP HR
Respiratory arrest
Urgent measures to lower critical ICP
Mannitol Administration
Hypertonic Saline
Hyperventilation-ICP
Hyperventilation Therapy
PaCO2 < 25 mmHg no
further reduction in CBF
HypoCO2
– shift the oxygen
dissociation curve to left
– oxygen less available to the
tissues.
Hyperventilation-ICP
Herniating patients
– goal of PaCO2 30–35 mm Hg
End-tidal PCO2 not reliable measure of PaCO2
Without cerebral herniation
– PaCO2 goal of 35 - 40 mm Hg
– Vt 10 ml/kg and 10 bpm
– Prophylactic hyperventilation worse prognosis
Hypothermia critical ICP
Admission temp (<35C) is a predictor of death in trauma
patients
Hypothermia TBI controversial
Induced therapeutic hypothermia vs accidental
hypothermia
6–7% decrease CMRO2 / 1C decrease in temp
Rewarming
TBI Management Minimise CMRO2
Sedation
– no evidence regarding superiority of any particular sedative
use short acting agents
?role NMB
Control temperature
– Brain in TBI temp 2 C degrees > core temp
– Mild hypothermia 34-35.5C
Prevent/treat seizures
– minimize CMRO2
– Phenytoin (loading dose 15mg/kg, infuse 50mg/min)
Trauma response TBI
TBI with on-scene
stabilization in the field
– better survival rates
– long-term outcomes incur
longer median
Independent of scene
time
– (113 vs 45 minutes,
respectively; p < 0.001)
– Compared with other
trauma
Trauma response TBI
Neurosurgical expertise single
most important determinant of
outcome in pts with mass
lesions
Acute subdural hematomas
mortality rate
30% if evacuation < 4hrs
90% if surgical evacuation > 4
hrs.
Trauma response TBI
Intervention of air
medical and rapid-
response teams
Pts with minimal
neurological functions
(GCS 4)
Greatest increase in
survival.
Things to Do:
Maintain mean BP > 90 mm Hg
Maintain PaCO2 approximately 35
mm Hg
Use isotonic solution for euvolemia
Frequent neurologic exams
Reassess ABC if deterioration
Things to Avoid:
Do Not Allow patient to become
hypotensive
Do Not Allow patient to become hypoxic
Do Not hyperventilate
Do Not Use hypotonic IV fluids
Do Not Paralyse before performing
complete exam (if possible )
Prognosis
Very difficult to accurately predict prognosis
within the first 24 hrs of TBI
Avoid assessments of medical futility and
possible organ donation
Allow the results of resuscitative efforts to be
evaluated
?S
Secondary injury
