3. INTRODUCTION
• Primary aim mx – minimize secondary injury by
maintaining cerebral perfusion and oxygenation
• Mech of secondary injury – triggered by secondary
insults, subtle and remain undetected by the usual
systemic physiological monitoring
• Continuous monitoring can serve 2 functions :
1) Early detection
2) Monitor therapeutic interventions
4. CNS PHYSIOLOGY
• Brain
• 2% body weight
• 15% CO
• Energetic tissue, utilize
• 3-5 mls O2/min/100gm
• 5mg glucose/min/100gm
• Brain energy
• 60% sustain synaptic function
• 40% maintain cellular integrity
5. • CBF 50ml/min/100gm
• Any disruption to CBF, produce rapid demise
to brain tissue
• The magnitude of reduce CBF and its duration
– primary determinant of ischemic injury and
neurological outcome
6. INTRACRANIAL PRESSURE
• The pathophysiology of brain injury are complex
• Major factors influencing outcome in patients with acute
brain injury are the secondary cerebral insults – hypoxia and
ischemia
• These secondary insults cause permanent neurological
damage and worsening outcome if undetected and
untreated
• The purpose of continuous brain monitoring is to detect
these insults and inform approach to treatment
• CT scan and MRI – useful info but not continuous and bed
side investigation
7. RELATIONSHIPS BETWEEN CBF AND
CHANGES IN BP, PaO2 AND PaCO2
CBF remains constant over a
range of BP but varies with
• Age – shifted to left in
newborns
• Chronic hypertension – to the
right
CBF varies linearly with PaCO2
• Doubling PaCO2 doubles CBF
• Halving PaCO2 halves CBF
CBF is affected with severe
hypoxemia
9. Primary brain damage
• Many etiologies:
• Vascular insufficiency or disruption
• Trauma
• Infection or inflammation
• Tumour
• Metabolic and nutritional derangement
10. Global brain injury
• Hypoxemia, cardiovascular insufficiency or arrest lead to
hypoxic and low or no flow states or complete
hypoperfusion of entire organ
• No potential for recruitment of collateral flow
• Recovery depend on severity and duration of insult
• After 5-6 min have permanent histological damage and
neurological deficit in survivors
• Outcome worsens significantly after 15 min
11. Focal brain injury
• Occlusion of an arterial distal to circle of willis
• Permit some collateral flow
• Dense ischaemic core with a partially perfused
surrounding penumbral zone and tissue more
salvageable and target for neuroprotection
• The time course for infarction and irreversible
damage around 30-60 mins
12. Area of ischemia and damage
• Area of infarction/ damage =
zero CBF
• Penlucida = ischemic area,
cerebral function is abolished
• CBF < 6ml/100g/min
• Penumbra = ischemic area
potential for restoration of
cerebral function
• CBF + 6-15ml/100g/min, maintain
cellular integrity but no synaptic
function
13. CBF (ml/min per 100g brain) CHANGES
50 Normal
25-30 Abnormal EEG
15-25 Loss of electrical activity (i.e;
isoelectric EEG)
10-15 Sufficient to maintain ATP to
support ionic pump funtion
≤10 Membrane failure due to a critical
loss of ATP, which causes ionic
imbalance between the cell and
the extracellular
<10 + prolonged (min) + worsened Permanent neurological
impairment due to cell death
14. Secondary brain damage
• As a sequence of primary insult
• Reflect physiological consequence of ischemia reduction in
CBF & metabolism, hydrocephalus & herniation, shift vital
structures & axonal disruption pressure effects to underlying
brain region
• Neural injury is worsen by
• Hypoxemia
• Hypercapnia
• Hyperglycemia
• Hypotension
• Hypothermia
• Anemia
• Electrolyte imbalance
15. CNS MONITORING
• General monitoring brain injury patient
include;
• Continuous IABP – ABG analysis and blood
glucose
• Pulse oxymeter
• ETCO2 – early correction of hypercapnia induce
high ICP
• CVP
• Temperature
• Clinical monitoring - GCS
16. SPECIFIC MONITORING
• Brain specific monitoring
• Pressure within the cranial cavity (ICP)
• Changes in brain oxygenation
• Metabolism (jugular venous oxygen saturation,
brain tissue monitoring)
• Cerebral hemodynamics (transcranial doppler)
• Electrical activity of the CNS
17. INTRACRANIAL PRESSURE
MONITORING
• ICP is defined as the pressure within the rigid
cranial vault relative to atmospheric pressure
• Normal ICP ranges between 5-15 mmHg
• Two components – a vasogenic (vascular)
component and a cerebrospinal fluid (CSF)
component
18. The relationship between ICP & the
volume of the skull contents
A – the compensation phase
•A large increase in volume, a little
increase in ICP
B – the pressure buffering system is
exhausted
•A small increase in volume, a large
increase in ICP
C – the steep part of the curve
•Increase ICP, reduce the CPP
profoundly
•Therefore increase MAP to maintain
CPP
19. ICP monitoring provide
• Continuous monitoring of pressure changes within the
intracranial cavity
• Acute rises in ICP occur when the compensatory mech
which control ICP (e.g, CSF production and outflow,
changes in cerebral blood flow and volume) are exhausted
• A small rise in intracranial volume results in a large rise in
ICP
• Pressure > 20mmHg are regarded as abnormal and usually
requires intervention to reduce ICP
20. Indications
• Severe head injury (GCS 3-8 • Tumour - obst hydrocephalus
following resuscitation)
• Vascular abn – AVM / aneurysm
• Abnormal CT scan – contusion, a/w obst hydrocephalus
edema, hematoma & compressed
basal cisterns • Postop on cerebral protection
• Severe head injury but has a
normal CT scan; however 2 or
more of the following findings are
present at admission:
• Age >40
• Uni or bilateral motor posturing
• Systolic hypotension ( ≤90 mmHg
21. Methods measuring ICP
• Common sites : intraventricular, intraparenchymal, subdural
and extradural
• Intraventricular drains allow direct measurement of ICP and
advantage of allowing CSF withdrawal when ICP rises
• Gold standard monitoring
• Cath inserted at lateral ventricle
• Zero reference pt at level of foramina of Monroe / ext
auditory meatus
• Insertion difficult or impossible brain swelling
• Risk of infection
• Continuous CSF drainage, measurement of ICP unreliable
22. • Intraparenchymal monitor
• Inserted through a support bolt or tunnelled
subcutaneous from burr hole either at bedside
or post craniotomy
• Common site frontal lobes
• Easy to insert
• Low risk of infection
23. • Subdural catheters are easily inserted but
measurement are unreliable and easily block
• Extradural probes are less reliable and less
specific due to uncertainty about the
relationship between ICP and pressure in the
extradural space
26. Advantages Disadvantages
Epidural catheter •Lower risk of infection •Decreased accuracy
•No transducer adjustment sensing through dura
with head movement •Unable to drain CSF
•Unable to recalibrate
or zero after placement
Subarachnoid •No penetration of brain •Unable to drain CSF
bolt /screw •Decreased risk of infection •Transducer
•Able to sample CSF repositioning with head
movement
•Direct pressure
measurement •Requires intact skull
•High pressure may
cause herniation of brain
tissue into bolt
27. Advantages Disadvantages
Ventriculostomy •CSF drainage and •Risk of intracerebral
catheter bleeding or edema along
sampling cannula track
• Direct •High risk for infection
measurement •Transducer
of pressure repositioning
with
head movement
Fiberoptic •Versatile, may be •Separate monitoring
catheter placed in ventricle or system required
subarachnoid space •Catheter relatively
• No adjustment of fragile
•Unable to recalibrate or
transducer with head rezero after placement
28. • Normal ICP 5-15 mmHg
• Active management when ICP 25-30 mmHg
• The normal ICP waveform contains 3 phases:
• P1 (percussion wave) from arterial pulsation
• P2 (rebound wave) reflects intracranial
compliance
• P3 (dicrotic wave) represent venous pulsation
29. normal ICP waveform - three peaks within
the cardiac cycle
first peak (P1) is called the percussion wave,
P2 is the tidal wave and
P3 is the dicrotic wave
30. • first peak (P1) is called the percussion wave,
• arterial pressure being transmitted from the choroid
plexus
• Arterial hypotension and hypertension affect the
amplitude of P1;
• severe hypotension causes a decrease in amplitude
whereas severe hypertension causes an increase in
amplitude
• P2 is the tidal wave and
• varies in amplitude with brain compliance and ends on
the dicrotic notch
• P3 is the dicrotic wave
• caused by closure of the aortic valve
31. ICP Wave Analysis
• Begins with understanding its shape and amplitude.
• The shape of the ICP waveform resembles the shape of the
arterial waveform.
• The amplitude, or height of the waveform, varies with changes in
physiologic state and is influenced by changes in intracranial
compliance and cerebral blood flow
• As the ICP increases due to an excess of components within the
cranial vault, the amplitude of P1, P2, and P3 all increase,
• but if the ICP continues to rise, P2 becomes more elevated than
P1 until eventually P1 may disappear within the waveform .
• This signifies a decrease in intracranial compliance and may warrant
intervention
34. ICP: b-waves II
b-
B-waves are frequent elevations (up to 50mmHg)
lasting several seconds
- Suggestive of poor intracranial compliance
35. A waves or plateau waves comprise a steep increase ICP
from normal value & persisting 5-20mins. Always
pathological and occur in reduce IC compliance. Long
lasting waves (several mins) indicative of diffuse cerebral
ischemia, and often precede herniation.
36. JUGULAR BULB OXIMETRY
• Blood from the venous sinuses of brain drains into
IJV
• Monitoring oxygen saturation in JV blood gives an
estimation the balance of global oxygen delivery
and cerebral metabolism
• Tech involves inserting a retrograde cath into IJV
and advancing cephalad
• Correct cath placement is level of mastoid process
and confirm by lateral neck x-ray
37. • Normal range SjvO2 60-75%, less than 50%
associated with worsen outcome in head injury
• Limitation - regional or small area of ischaemia
may not detected
38.
39. Physiology of jugular venous
oxygenation
• Clinical measurementof SjvO2, reflect the
balance of oxygen supply and consumption of
the brain
• SjvO2 reflects an average value from the
whole brain and cannot detect focal changes
in CBF
• Sjv02 < 55% indicates brain hypoxia
40. • Reduced SjvO2 values • Elevated SjvO2
• Vasoconstriction induced • Hyperaemic phase of TBI
by low PaCO2 • Hypercapnia induced
• Hypoxemia vasodilatation
• Anemia • Brain death (brain cells
• Insufficiency low CPP cease to extract O2)
• Inapp high CPP
41. BRAIN TISSUE OXYMETRY
• Brain tissue oxygenation can be monitored
with an oxygen sensitive microelectrode place
in brain parenchymal
• Accurate to area 15mm2 around the probe
• Aim to detect evolving brain injury before
global sign brain injury become apparent
• Critical PbrO2 ~ 1.3-7 kPa
42. MICRODIALYSIS
• Continuous monitoring of changes in brain
chemistry
• Inserted at risk tissues – next to hematoma /
brain injury
• Monitoring markers of brain ischaemia and cell
damage e.g; lactate, pyruvate, glycerol,
glutamate and glucose
• Lactate-pyruvate ratio >25 – indicate focal
ischaemia
• Glycerol elevated in TBI, seizure and secondary
brain damage
43. TRANSCRANIAL DOPPLER
ULTRASONOGRAPHY
• Non invasive monitoring – measures flow
velocities in basal cerebral arteries
• Normal MCA velocity : 60-70 cm/s
• Normal ICA velocity : 40-50 cm/s
• MCA:ICA = 1.76
• High velocity states – cerebral vasospasm or
hyperaemia
44. ELECTROPHYSIOLOGY
ELECTROENCEPHALOGRAM (EEG)
• EEG represents spontaneous electrical activity of
cerebral cortex
• Summation of excitatory and inhibitory post
synaptic potential of cortical neurons
• Not reflect activity in subcortical , cranial nerves
and spinal cord
• Important tools in investigations and
management of epilepsy and detect ischaemic
cerebral event
45. • EEG wave
• Recorded from the scalp / surface of the brain
• Summation of extracellular current fluctuations :
excitatory and inhibitory synaptic potentials
(EPSP & IPSP)
• Surface negative waves : summation of EPSP’s
• Surface positive waves : summation of IPSP’s
• EEG recorded from the scalp is attenuated and
filtered by tissues between the brain and
recording
46. Anaesthetic effects on EEG
Awake
high frequency, low amplitude
Light anesthesia
increase amplitude
slow frequency
Deep Anesthesia
Burst suppression
Isoelectric EEG
47. Goal for EEG monitoring
• To assess :
• Cerebral ischemia
• Cerebral protection
• Epilepsy surgery
49. Bispectral index scores
• Electroencephalogram (EEG) monitor display
analog score 1 to 100
• Represent patient level of awareness
• 100 – fully awake
• 65-85 – recommended for sedation
• 40-65 – general anesthesia
• 1- complete lack of brain activity
• However in comparison with MAC, BIS poorly
predicts a movement or non-movement response,
esp in the presence of opiates
• Inaccurate with ketamine
50.
51. SOMATOSENSORY EVOKED
POTENTIALS (SSEPs)
• SEP is a time locked event related, pathway
specific electroencephalographic activity
generated in response to a specific stimulus such
as electrical stimuli.
• The SSEPs recorded in response to stimulation of
the median nerve, ulnar nerve and posterior tibial
nerve monitor the integrity of the respective
pathways from the periphery to the cortex.
• Routine monitor for surgical procedure on the
spinal column with potential risk to the spinal cord
52. • As with EEG, ischemia/hypoxia leads to
depression of conduction with resultant
decrease in amplitude and increase latency of
the specific peaks
• For SSEPs, 50% reduction in amplitude from
baseline in response to a specific surgical
maneuver is generally accepted to be a
significant change warranting alteration of
surgical strategy to avert potential damage
53. • As with EEG, anesthetic agents influence cortical
evoked potentials.
• Unlike EEG, SSEPs resist the influence of intravenous
agents.
• Although the amplitude maybe slightly reduced and
the latency increased, cortical SSEPs can be recorded
• In contrast, inhalational cause a dose related decrease
in amplitude and increase in latency
• Opioids have negligible effects on SSEP.
54. MOTOR EVOKED POTENTIALS
(MEP)
• Because SSEP monitors only the integrity of the
sensory pathway, it is theoretically possible to miss an
injury specifically affecting the motor pathway but
sparing the sensory tracts.
• Thus, MEP recording was introduced to complement
SSEP recording.
• An electromyographic potential recorded over
muscles in the hand or foot in response to
depolarization of the motor cortex.
• Depolarizaton can be achieved using transcranial
magnetic or electrical stimulation.
56. INTRODUCTION
• Cerebral protection – interventions aimed to
reduce neuronal injury that instituted before
possible ischaemic / hypoxic event
• Cerebral resuscitation – interventions that
occur after such event
57. Indication for cerebral
protection
• Majority associated with high ICP:
• Cerebral oedema
• Post myocardial infarction
• Post cranial surgery
• Seizures
• Head injury
• Cerebral hypoxia
• Post cardio respiratory arrest
• Brain infection
• Space occupying lesion
58. Aims:
• Prevent further cerebral damage
• Reverse cerebral damage
• Improve cerebral functions and neurological
outcome
• Maintain of cerebral perfusion
• Maintain of systemic hemodynamics
• Maintain adequate oxygenation and ventilation
59. Methods
• Various methods to reduce intracranial
pressure
• Physiological manipulation
• Pharmacological
• Physical manipulation
60. Physiological manipulation
1) Mechanical ventilation
• To maintain PaCO2 normocapnia between 35-40
mmHg
• ICP reduced by 30% per 10mmHg reduction in CO2
• Avoid hypoxia – cytotoxic cerebral oedema
• For how long? 24-48H only
• After 48H, acute changes in hyperventilation return
to normal value owing to normalize CSF pH and
compensatory to CSF volume
• Can be repeated if needed : interval of 12-24 H in
between cerebral resuscitation
61. 2) Hypothermia
• Each 1°C reduction can reduce CMRO2 by 7%
• Aim for mild (33-34°C) to moderate (26-31°C)
hypothermia
• Avoid shivering- increase CMRO2 & CBF, may
require muscle relaxant
62. 3) Hypertension
• Aim
To limit ischemia by increasing regional CBF
To overcome regional vasospasm
Done usually with drugs - vasopressors
• During ischemia
Autoregulation is impaired
CBF is pressure dependent
• Maintain CPP 70-80 mmHg
63. Pharmacological
• Sedation and neuromuscular blockade
• IV anaesthetic agent decreased cerebral
metabolism and reduce CBF
• Propofol more potent than benzodiazepine
• Opioid min effect on cerebral metabolism and
CBF
• Routine use NMB should be avoided
• Prevent raise ICP during straining and
coughing
• Impossible to recognized the seizure
• Long term polyneuropathy and myopathy
64. • Anticonvulsant
• Severe TBI – 20% seizures
• Highest in depressed skull fractures, IC
hematoma and contusion
• Efficient in reducing of early post traumatic
seizure
• First line therapy – phenytoin ( a week duration)
65. Fluid management and
glycaemic control
• Aim fluid management provide adequate
hydration
• Hypotonic fluid (dextrose) may exacerbate
brain edema
• High plasma levels of glucose associated with
poor outcome from TBI
66. Osmotherapy
• Mannitol
• Increase plasma osmolality – withdrawal of brain
across bbb
• Reduction ICP after 20-30mins
• Need to monitor plasma osmolality, not > 320
mosmol/ml
• Hypertonic saline (5or 7.5%)
• Reduces brain water by establish osmotic gradient
across bbb
• Hypernatremia, <155 mmol/L
• Cause tissue necrosis and thrombophlebitis
67. Barbiturate coma
• Barbiturates decreases ICP – reduce CMRO2
and CBF
• Can lower ICP refractory to other measures
• Dose titrated to burst suppression on EEG
68. Physical manipulation
1) Patient position
Important for both prevention and treatment of
elevated ICP
Aim :
Allow proper cerebral venous drainage (venous return)
Maintain the head and neck elevated 30°
Maintain neutral position
Avoid obstruction to jugular vein i.e; ETT anchoring,
cervical collar
Avoid increase in intrathoracic & intraabdominal
pressure
69. Avoid ;
Excessive stimulation e.g suctioning, only do it
when necessary
Sudden movement to head
Rough handling of patient
Painful stimulation
Hyperthermia >38°C
70. Surgical intervention
1) Ventriculostomy / CSF drainage
Eg; EVD, VP shunt
1) Decompressive surgery
Decompressive craniectomy part of skull is
removed
Decompressive lobectomy brain parenchymal is
resected either from non dominant temporal or
frontal lobe
