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 Introduction
 Physiology of CNS
 Intracranial pressure
 Pathophysiology brain injury
 CNS monitoring
 Cerebral protection
 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
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
 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
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
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
PATHOPHYSIOLOGY OF BRAIN
INJURY
Primary brain damage
• Many etiologies:
• Vascular insufficiency or disruption
• Trauma
• Infection or inflammation
• Tumour
• Metabolic and nutritional derangement
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
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
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
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
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
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
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
The relationship between ICP & the
volume of the skull Acontents
– 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 B
a large increase in ICP
 C – the steep part of the
curve
 Increase ICP, reduce the
CPP profoundly
 Therefore increase MAP to
maintain CPP
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
Indications
• Severe head injury (GCS 3-8)
• Tumour - obst hydrocephalus following resuscitation)
• Vascular abn – AVM / aneurys
• 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)
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
 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
 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
Methods of intracranial
measurement
 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
 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
• 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
 The pathophysiology and management of increased
ICP is based on the Monro-Kellie doctrine.
 Cerebral blood flow is maintained through adequate
CPP, which is determined by the mean systemic
arterial pressure minus intracranial pressure
 (CPP = MAP – ICP).
 Normal CPP values 80 mm Hg for adults,
 CPP > 50–60 mm Hg for children and
 CPP > 40–50 mm Hg for infants/toddlers.
CEREBRAL PROTECTION
INTRODUCTION
• Cerebral protection – interventions aimed to reduce
neuronal injury that instituted before possible
ischaemic / hypoxic event

• Cerebral resuscitation – interventions that occur after

such event
 The pathophysiology and management of increased
ICP is based on the Monro-
 Kellie doctrine.
 Cerebral blood flow is maintained through adequate
CPP, which is determined by the mean
 systemic arterial pressure minus intracranial pressure
(CPP = MAP – ICP). Normal CPP
 values 80 mm Hg for adults, CPP > 50–60 mm Hg for
children and CPP > 40–50 mm Hg for
 infants/toddlers.
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
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
Methods
• Various methods to reduce intracranial pressure ;
• Physiological manipulation
• Pharmacological
• Physical manipulation
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
 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
Hypothermia in brain injury pt.

• Initial pilot studies showed neuroprotective effect

but later studies did not.
• Bench-to-bedside review: Hypothermia in
traumatic brain injury
Critical Care 2010, 14:204
• The use of hypothermia in patients with traumatic
brain injury may have beneficial effects in both
ICP reduction and possible neuro-protection,
supported by the Eurotherm3235Trial protocol.
 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
Avoid hypotension
Hypotension has been shown to be deleterious to the injured brain

• Hypotension can increase cerebral infarct volumes significantly and should be avoided

• In head injured patients ,a higher than normal CPP is required to maintain normal
CBF.

• Chan and colleagues have shown that CPP of about 70 mmHg is adequate in head
injured patients
(Chan KH, et al. Neurosurgery 1993;32:547-52.)

• Patients who have sustained an ischemic cerebral injury may benefit from an augmentation of
cerebral blood flow by induced hypertension (Schwarz S, et al. Stroke 2002;33:998-1004)

• Induced hypertension, with an increase in mean arterial pressure 20% above baseline
pressure, can lead to a clinical improvement in a patients with acute stroke in whom
thrombolysis is not feasible. The potential risk for hemorrhagic conversion of the stroke exists.
Rordorf G, et al. Neurology 2001;56:1210-3.

• Maintenance of an adequate MAP and CPP

MAP 70-80 mmHg
CPP >60 mm Hg
SAH induced vasospasm- SBP 180-220 mm Hg
HEMODILUTION

• Target hematocrit 30%- 35%

• Beneficial effect by
1. decreases viscosity
2. increases CBF
3. Increases oxygen delivery
-No role in stroke,
-Definitive role in vasospasm
The Lancet Neurology, Volume
2, Issue 10, 2003
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
 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)
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
Two separate studies, by Aldrete et al. and Cullen et al.,
demonstrated that treatment with phenytoin improved
neurological recovery and reversed histopathological
changes in animals subjected to complete global ischaemia.
AIdrete JA,et al. Crit Care Med 1979; 7: 466-7 I.
Cullen JP, et al. Analg 1979; 58: 165-9 Anesth.

 Artru et al. proposed that phenytoin exerts its protective

effects through slowing the release of K + from ischaemic
neurons, and by stabilization of cellular membranes.
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
Barbiturate coma
• Barbiturates decreases ICP – reduce CMRO2 and CBF
• Can lower ICP refractory to other measures
• Dose titrated to burst suppression on EEG
Barbiturates have been found to be efficacious in
the treatment of focal ischemia and can reduce
the extent of cerebral injury.
Warner DS, et L. J Cereb Blood Flow Metab 1991;11:794
802.Drummond JC. Anesthesiology 1993;78:611-3.

BARBITURATES IN HEAD TRAUMA: Barbiturates

provide a means of reducing and maintaining ICP
but not necessarily corresponds to improved
outcome.
(Ward JD, et al. J Neurosurg 1985; 62: 383-8)
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
 Head Position vs ICP & CPP

As head-up position is increased, ICP may be reduced, but beyond 30o heads-up
CPP is likely compromised. Second source: Durward, QJ, Amadner, AL, Del
Maestro, RF, et al: Cerebral and vascular responses to changes in head elevation in
patients with intracranial hypertension, J Neurosurg 59: 938, 1983.
 Avoid ;
 Excessive stimulation e.g suctioning, only do it when
necessary
 Sudden movement to head
 Rough handling of patient
 Painful stimulation
 Hyperthermia >38°C
Surgical intervention
1) Ventriculostomy / CSF drainage
- Eg; EVD, VP shunt
2) Decompressive surgery
- Decompressive craniectomy part of skull is removed
- Decompressive lobectomy brain parenchymal is
resected either from non dominant temporal or frontal
lobe
Thank you