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Neurocritical care relies on monitoring cerebral functions.
Intracranial pressure monitoring may indicate high pressure in
several acute neurological conditions. Massive stroke may cause
life-threatening brain edema and occur in about 10% of patients
with supratentorial stroke. Massive brain edema usually occurs
between the second and the fifth day after stroke onset. Case
fatality rates may exceed 80%. Other neurologic conditions that
may be accompanied with increased intracranial pressure
include severe head injuries, status epilepticus, fulminant
hepatic failure, Reye’s syndrome, and metabolic
encephalopathies.
Neuro-Specific Monitoring
Accurate neurological assessment is fundamental for the
management of patients with intracranial pathology. This
consists of repeated clinical examinations (particularly GCS and
pupillary response) and the use of specific monitoring
techniques, including serial CT scans of the brain. This chapter
provides an overview of the more common monitoring
modalities found within the neurocritical care environment
Intracranial pressure monitoring may indicate high pressure in
several acute neurological conditions. Massive stroke may cause
life-threatening brain edema and occur in about 10% of patients
with supratentorial stroke. Massive brain edema usually occurs
between the second and the fifth day after stroke onset. Case
fatality rates may exceed 80%. Other neurologic conditions that
may be accompanied with increased intracranial pressure
include severe head injuries, status epilepticus, fulminant
hepatic failure, Reye’s syndrome, and metabolic
encephalopathies.
Neuro-Specific Monitoring
Accurate neurological assessment is fundamental for the
management of patients with intracranial pathology. This
consists of repeated clinical examinations (particularly GCS and
pupillary response) and the use of specific monitoring
techniques, including serial CT scans of the brain. This chapter
provides an overview of the more common monitoring
modalities found within the neurocritical care environment
In general terms, a combination of assessments is more likely
to detect change than any one specific modality. Real-time
continuous monitoring (e.g., measurement of intracranial
pressure, ICP) will provide more timely warning about adverse
events (e.g., an expanding hematoma) compared to static
assessments such as sedation holds or serial CT brain scans.
Clinical Assessment
The Glasgow Coma Scale
The Glasgow Coma Scale (GCS) provides a standardized and
internationally recognized method for evaluating a patient’s CNS
function by recording their best response to verbal and physical
stimuli. A drop of two or more GCS points (or one or more motor
points) should prompt urgent re-evaluation and a repeat CT
scan.
Eye opening is not synonymous with awareness, and can be
seen in both coma and persistent vegetative state (PVS). The
important detail is that the patients either open their eyes to a
specific command or shows ability to fix eye on a specific target
or follows a visual stimulus.
Pupillary response
Changes in pupil size and reaction may provide useful additional
information:
– Sudden unilateral fixed pupil: Compression of the third
nerve, e.g., ipsilateral uncal herniation or posterior
communicating artery aneurysm
– Unilateral miosis: Horner syndrome (consider vascular
injury)
– Bilateral miosis: Narcotics, pontine hemorrhage
– Bilateral fixed, dilated pupils: Brainstem death, massive
overdose (e.g., tricyclic antidepressants)
In the non-specialist center, neurological assessment of the
ventilated patient consists of serial CT brain scans, pupillary
to detect change than any one specific modality. Real-time
continuous monitoring (e.g., measurement of intracranial
pressure, ICP) will provide more timely warning about adverse
events (e.g., an expanding hematoma) compared to static
assessments such as sedation holds or serial CT brain scans.
Clinical Assessment
The Glasgow Coma Scale
The Glasgow Coma Scale (GCS) provides a standardized and
internationally recognized method for evaluating a patient’s CNS
function by recording their best response to verbal and physical
stimuli. A drop of two or more GCS points (or one or more motor
points) should prompt urgent re-evaluation and a repeat CT
scan.
Eye opening is not synonymous with awareness, and can be
seen in both coma and persistent vegetative state (PVS). The
important detail is that the patients either open their eyes to a
specific command or shows ability to fix eye on a specific target
or follows a visual stimulus.
Pupillary response
Changes in pupil size and reaction may provide useful additional
information:
– Sudden unilateral fixed pupil: Compression of the third
nerve, e.g., ipsilateral uncal herniation or posterior
communicating artery aneurysm
– Unilateral miosis: Horner syndrome (consider vascular
injury)
– Bilateral miosis: Narcotics, pontine hemorrhage
– Bilateral fixed, dilated pupils: Brainstem death, massive
overdose (e.g., tricyclic antidepressants)
In the non-specialist center, neurological assessment of the
ventilated patient consists of serial CT brain scans, pupillary
response, and assessment of GCS during sedation holds. A
reduction in sedation level will usually be at the suggestion of
the Regional Neurosurgical Center (RNC) and its timing will
depend upon a number of factors. Responses such as unilateral
pupillary dilatation, extensor posturing, seizures, or severe
hypertension should prompt rapid re-sedation, repeat CT scan,
and contact with the RNC. In the patient with multiple injuries,
consideration must be given to their analgesic requirements
prior to any decrease in sedation levels.
Invasive Monitoring
Cerebral perfusion pressure (CPP) reflects the pressure gradient
that drives cerebral blood flow (CBF), and hence cerebral oxygen
delivery. Measurement of intracranial pressure (ICP) allows
estimation of CPP. CPP is mean arterial pressure minus ICP.
Sufficient CPP is needed to allow CBF to meet the metabolic
requirements of the brain. An inadequate CPP may result in the
failure of autoregulation of flow to meet metabolic needs whilst
an artificially induced high CPP may result in hyperemia and
vasogenic edema, thereby worsening ICP. The CPP needs to be
assessed for each individual and other monitoring modality (e.g.,
jugular venous oximetry, brain tissue oxygenation) may be
required to assess its adequacy.
Despite its almost universal acceptance, there are no properly
controlled trials demonstrating improved outcome from either
ICP- or CPP-targeted therapy. However, in the early 1990s
Marmarou et al. showed that patients with ICP values
consistently greater than 20 mmHg suffered worse outcomes
than matched controls, and poorer outcomes have been
described in patients, whose CPP dropped below 60 mmHg
(Marmarou 1991; Juul 2000; Young 2003). As such, ICP- and CPPtargeted
therapy have become an accepted standard of care in
head injury management.
The 2007 Brain Trauma Foundation Guidelines (Brain Trauma
Foundation 2007) recommend treating ICP values above
reduction in sedation level will usually be at the suggestion of
the Regional Neurosurgical Center (RNC) and its timing will
depend upon a number of factors. Responses such as unilateral
pupillary dilatation, extensor posturing, seizures, or severe
hypertension should prompt rapid re-sedation, repeat CT scan,
and contact with the RNC. In the patient with multiple injuries,
consideration must be given to their analgesic requirements
prior to any decrease in sedation levels.
Invasive Monitoring
Cerebral perfusion pressure (CPP) reflects the pressure gradient
that drives cerebral blood flow (CBF), and hence cerebral oxygen
delivery. Measurement of intracranial pressure (ICP) allows
estimation of CPP. CPP is mean arterial pressure minus ICP.
Sufficient CPP is needed to allow CBF to meet the metabolic
requirements of the brain. An inadequate CPP may result in the
failure of autoregulation of flow to meet metabolic needs whilst
an artificially induced high CPP may result in hyperemia and
vasogenic edema, thereby worsening ICP. The CPP needs to be
assessed for each individual and other monitoring modality (e.g.,
jugular venous oximetry, brain tissue oxygenation) may be
required to assess its adequacy.
Despite its almost universal acceptance, there are no properly
controlled trials demonstrating improved outcome from either
ICP- or CPP-targeted therapy. However, in the early 1990s
Marmarou et al. showed that patients with ICP values
consistently greater than 20 mmHg suffered worse outcomes
than matched controls, and poorer outcomes have been
described in patients, whose CPP dropped below 60 mmHg
(Marmarou 1991; Juul 2000; Young 2003). As such, ICP- and CPPtargeted
therapy have become an accepted standard of care in
head injury management.
The 2007 Brain Trauma Foundation Guidelines (Brain Trauma
Foundation 2007) recommend treating ICP values above
20 mmHg and to target CPP in the range of 50-70 mmHg. Patients
with intact pressure autoregulation will tolerate higher CPP
values. Aggressive attempts to maintain CPP >70 mmHg should
be avoided because of the risk of ARDS.
Table 6.1 – ICP Values
Normal ICP <15 mmHg
Focal ischemia occurs at ICP >20 mmHg
Global ischemia occurs at ICP >50 mmHg
Usual treatment threshold is 20 mmHg
Measuring ICP
Intraventricular devices consist of a drain inserted into the
lateral ventricle via a burr hole, and connected to a pressure
transducer, manometer, or fiber optic catheter. Although
associated with a higher incidence of infection and greater
potential for brain injury during placement, this remains the
gold standard. It has the added benefit of allowing CSF drainage.
Historically, saline could be injected to assess brain compliance.
Extraventricular systems are placed in parenchymal tissue, the
subarachnoid space, or in the epidural space via a burr hole.
These can be inserted at the bedside in the ICU. These systems
are tipped with a transducer requiring calibration, and are
subject to drift (particularly after long-term placement).
Examples of extraventricular systems are the Codman and
Camino devices. These devices have a tendency to underestimate
ICP.
In general, both types of device are left in situ for as short a
time as possible to minimize the risk of introducing infection.
Prophylactic antibiotics are not generally used.
Indications for ICP monitoring
In any case of head injury, if brain CT is positive for pathology,
and the patient fulfills the criteria for use of a ventilator,
with intact pressure autoregulation will tolerate higher CPP
values. Aggressive attempts to maintain CPP >70 mmHg should
be avoided because of the risk of ARDS.
Table 6.1 – ICP Values
Normal ICP <15 mmHg
Focal ischemia occurs at ICP >20 mmHg
Global ischemia occurs at ICP >50 mmHg
Usual treatment threshold is 20 mmHg
Measuring ICP
Intraventricular devices consist of a drain inserted into the
lateral ventricle via a burr hole, and connected to a pressure
transducer, manometer, or fiber optic catheter. Although
associated with a higher incidence of infection and greater
potential for brain injury during placement, this remains the
gold standard. It has the added benefit of allowing CSF drainage.
Historically, saline could be injected to assess brain compliance.
Extraventricular systems are placed in parenchymal tissue, the
subarachnoid space, or in the epidural space via a burr hole.
These can be inserted at the bedside in the ICU. These systems
are tipped with a transducer requiring calibration, and are
subject to drift (particularly after long-term placement).
Examples of extraventricular systems are the Codman and
Camino devices. These devices have a tendency to underestimate
ICP.
In general, both types of device are left in situ for as short a
time as possible to minimize the risk of introducing infection.
Prophylactic antibiotics are not generally used.
Indications for ICP monitoring
In any case of head injury, if brain CT is positive for pathology,
and the patient fulfills the criteria for use of a ventilator,
monitoring for intracranial pressure (ICP) becomes mandatory.
More specific indications are shown in Table 6.2.
Table 6.2 – Indications for intracranial pressure (ICP) monitoring
1) Traumatic brain injury, in particular:
– Severe head injury (GCS <8)
– Focal pathology on CT brain scan
– Head injury and age >40
– Normal CT brain scan but systolic blood pressure persistently <90 mmHg
– Where other injuries and their treatment necessitate the use of sedation
or anesthesia
2) Subarachnoid hemorrhage with associated hydrocephalus
3) Hydrocephalus
4) Hypoxic brain injury, for example, after near-drowning
5) Postoperative in patients at risk of severe cerebral edema
6) Encephalopathy (e.g., in liver failure)
Coagulopathy is the primary contraindication to insertion. The
ICP device will generally be removed as soon as the patient is
awake with satisfactory neurology (GCS motor score M5 or M6)
or when physiological challenges (removal of sedation,
normalizing PaCO2) no longer produce a sustained rise in ICP.
Intracranial Pressure Waveforms and Analysis
The normal ICP waveform is a modified arterial trace and
consists of three characteristic peaks. The “percussive” P1 wave
results from arterial pressure being transmitted from the
choroid plexi, the “tidal” P2 wave varies with brain compliance,
whilst P3 represents the dicrotic notch and closure of the aortic
valve. It is important to establish the accuracy of the ICP trace
and value before initiating therapy based upon the numbers
generated. Transient sequential occlusion of the internal jugular
veins or removing the head-up tilt should produce an increase in
ICP.
More specific indications are shown in Table 6.2.
Table 6.2 – Indications for intracranial pressure (ICP) monitoring
1) Traumatic brain injury, in particular:
– Severe head injury (GCS <8)
– Focal pathology on CT brain scan
– Head injury and age >40
– Normal CT brain scan but systolic blood pressure persistently <90 mmHg
– Where other injuries and their treatment necessitate the use of sedation
or anesthesia
2) Subarachnoid hemorrhage with associated hydrocephalus
3) Hydrocephalus
4) Hypoxic brain injury, for example, after near-drowning
5) Postoperative in patients at risk of severe cerebral edema
6) Encephalopathy (e.g., in liver failure)
Coagulopathy is the primary contraindication to insertion. The
ICP device will generally be removed as soon as the patient is
awake with satisfactory neurology (GCS motor score M5 or M6)
or when physiological challenges (removal of sedation,
normalizing PaCO2) no longer produce a sustained rise in ICP.
Intracranial Pressure Waveforms and Analysis
The normal ICP waveform is a modified arterial trace and
consists of three characteristic peaks. The “percussive” P1 wave
results from arterial pressure being transmitted from the
choroid plexi, the “tidal” P2 wave varies with brain compliance,
whilst P3 represents the dicrotic notch and closure of the aortic
valve. It is important to establish the accuracy of the ICP trace
and value before initiating therapy based upon the numbers
generated. Transient sequential occlusion of the internal jugular
veins or removing the head-up tilt should produce an increase in
ICP.
The ICP waveform: The ICP waveform can be divided into
systolic and diastolic components and demonstrates cardiac and
respiratory variations.
– P1 (percussion wave): originates from pulsations in choroid
plexus, sharp peak, consistent in amplitude
– P2 (tidal wave): variable in shape, ends on dicrotic notch
– P3 (dicrotic wave): begins immediately after dicrotic notch
When ICP increases and compliance decreases, P2 and P3 elevate
causing a rounder waveform.
In addition to simple pressure measurement, if ICP is recorded
against time, a number of characteristic wave forms (Lundeberg
waves) can be seen.
– A waves: Pathological sustained plateau waves of 50-80
mmHg lasting between 5 and 10 min, possibly representing
cerebral vasodilatation and an increase in CBF response to a
low CPP.
– B waves: Small, transient waves of limited amplitude every
1-2 min representing fluctuations in cerebral blood volume.
These may be seen in normal subjects, but are indicative of
intracranial pathology when the amplitude increases above
10 mmHg.
– C waves: Small oscillations in ICP that reflect changes in
systemic arterial pressure.
With cerebral autoregulation intact, a rise in MAP produces
vasoconstriction and a fall in ICP. However, when autoregulation
fails, the circulation becomes pressure passive and changes in
systolic and diastolic components and demonstrates cardiac and
respiratory variations.
– P1 (percussion wave): originates from pulsations in choroid
plexus, sharp peak, consistent in amplitude
– P2 (tidal wave): variable in shape, ends on dicrotic notch
– P3 (dicrotic wave): begins immediately after dicrotic notch
When ICP increases and compliance decreases, P2 and P3 elevate
causing a rounder waveform.
In addition to simple pressure measurement, if ICP is recorded
against time, a number of characteristic wave forms (Lundeberg
waves) can be seen.
– A waves: Pathological sustained plateau waves of 50-80
mmHg lasting between 5 and 10 min, possibly representing
cerebral vasodilatation and an increase in CBF response to a
low CPP.
– B waves: Small, transient waves of limited amplitude every
1-2 min representing fluctuations in cerebral blood volume.
These may be seen in normal subjects, but are indicative of
intracranial pathology when the amplitude increases above
10 mmHg.
– C waves: Small oscillations in ICP that reflect changes in
systemic arterial pressure.
With cerebral autoregulation intact, a rise in MAP produces
vasoconstriction and a fall in ICP. However, when autoregulation
fails, the circulation becomes pressure passive and changes in
MAP are reflected in changes in the ICP. Continuous analysis of
MAP and ICP allows a correlation coefficient called the pressure
reactivity index to be derived (PRx). Positive values indicate
disturbed cerebral vascular reactivity, whilst negative values
indicate that reactivity remains intact (Gupta 2002).
Despite the fact that trial results have not always been
compelling, most clinicians regard the ICP monitor as an
essential tool that allows estimation of CPP (Czosnyka 2004;
Czosnyka 1996), gives early warning of developing pathology,
allows the response to therapy to be objectively measured, and
has value as a prognostic indicator (Joseph 2005).
Methods of intracranial pressure ICP measurement:
Methods for the measurement of intracranial pressure are
ventriculostomy, subdural catheter, epidural transducer, and
fiberoptic microtransducer. Ventriculostomy remains the gold
standard for monitoring ICP as it offers an accurate and reliable
means of calibration. Disadvantages include a <2% risk for
infection, a <10% risk for hemorrhage and difficulty in placing
the catheter (Clark 1989).
One of the widely used forms of ICP monitoring is the fiberoptic
or bolt ICP monitor. This method is relatively less invasive with
lower morbidity. It lacks, however therapeutic CSF drainage.
Steps to ICP bolt placement (Crutchfeld 1990):
1. ICP bolt placement takes place in the ICU or the OR
2. A small skin incision to the skull bone is made
3. The periosteum is stripped off the bone and a drill burr
hole is made to match the size of a bolt adapter. The bolt
screw is then advanced into the skull and a dilator is used
to dilate a tract in the dura for the fiberoptic probe
4. The skin is closed around the bolt
5. The fiberoptic probe is zeroed at atmospheric pressure
6. The probe is then placed through a retaining cap into the
subarachnoid space or less commonly intraparenchymally
7. Probe placement can be verified by observing ICP
waveforms
MAP and ICP allows a correlation coefficient called the pressure
reactivity index to be derived (PRx). Positive values indicate
disturbed cerebral vascular reactivity, whilst negative values
indicate that reactivity remains intact (Gupta 2002).
Despite the fact that trial results have not always been
compelling, most clinicians regard the ICP monitor as an
essential tool that allows estimation of CPP (Czosnyka 2004;
Czosnyka 1996), gives early warning of developing pathology,
allows the response to therapy to be objectively measured, and
has value as a prognostic indicator (Joseph 2005).
Methods of intracranial pressure ICP measurement:
Methods for the measurement of intracranial pressure are
ventriculostomy, subdural catheter, epidural transducer, and
fiberoptic microtransducer. Ventriculostomy remains the gold
standard for monitoring ICP as it offers an accurate and reliable
means of calibration. Disadvantages include a <2% risk for
infection, a <10% risk for hemorrhage and difficulty in placing
the catheter (Clark 1989).
One of the widely used forms of ICP monitoring is the fiberoptic
or bolt ICP monitor. This method is relatively less invasive with
lower morbidity. It lacks, however therapeutic CSF drainage.
Steps to ICP bolt placement (Crutchfeld 1990):
1. ICP bolt placement takes place in the ICU or the OR
2. A small skin incision to the skull bone is made
3. The periosteum is stripped off the bone and a drill burr
hole is made to match the size of a bolt adapter. The bolt
screw is then advanced into the skull and a dilator is used
to dilate a tract in the dura for the fiberoptic probe
4. The skin is closed around the bolt
5. The fiberoptic probe is zeroed at atmospheric pressure
6. The probe is then placed through a retaining cap into the
subarachnoid space or less commonly intraparenchymally
7. Probe placement can be verified by observing ICP
waveforms
8. The ICP monitor is then connected to the bedside
monitorFiberoptic transducers cannot be recalibrated
externally.
Table 6.3 – Comparison between fiberoptic ICP monitoring and
ventriculostomy (Andrew 2010)
Fiberoptic bolt Ventriculostomy
Accuracy Subject to shift Gold standard
Placement Relatively easy Relatively hard
Feasibility of use No recalibration Requires height adjustment
and zeroing
Clinical use Measurement only Measurement and CSF
draining
ICP measurement Focal pressure variation is a
disadvantage
Focal variation disadvantage
is less
Continuous care Lower burden Higher burden
Risk of infection Lower Increases after >5 days
ICP waveform analysis: Analysis of the relationship between
ICP waveforms and ABP waveforms, i.e., pressure reactivity
index (PRx), has been outlined (Czosnyka 1996).
1. PRx varies from low values (no correlation) to values
approaching 1.0 (strong correlation)
2. With lower BP, lower blood vessel wall tension results in an
increase in transmission of the BP waveform to the ICP
3. With elevated ICP brain compliance is reduced thus
increasing the transmission of the BP waveform
Approximate Entropy (ApEn) is a logarithmic measure of
system regularity or randomness that can be used in physiologic
systems (Pincus 1991). Reductions in ApEn imply reduced
randomness or increased order and may indicate pathology in
the cardiovascular, respiratory and endocrine systems.
Cerebral blood flow CBF measurement is feasible and may be
considered in some patients. On the other hand, cerebral tissue
metabolic demand is not currently available.
Neurocritical
monitorFiberoptic transducers cannot be recalibrated
externally.
Table 6.3 – Comparison between fiberoptic ICP monitoring and
ventriculostomy (Andrew 2010)
Fiberoptic bolt Ventriculostomy
Accuracy Subject to shift Gold standard
Placement Relatively easy Relatively hard
Feasibility of use No recalibration Requires height adjustment
and zeroing
Clinical use Measurement only Measurement and CSF
draining
ICP measurement Focal pressure variation is a
disadvantage
Focal variation disadvantage
is less
Continuous care Lower burden Higher burden
Risk of infection Lower Increases after >5 days
ICP waveform analysis: Analysis of the relationship between
ICP waveforms and ABP waveforms, i.e., pressure reactivity
index (PRx), has been outlined (Czosnyka 1996).
1. PRx varies from low values (no correlation) to values
approaching 1.0 (strong correlation)
2. With lower BP, lower blood vessel wall tension results in an
increase in transmission of the BP waveform to the ICP
3. With elevated ICP brain compliance is reduced thus
increasing the transmission of the BP waveform
Approximate Entropy (ApEn) is a logarithmic measure of
system regularity or randomness that can be used in physiologic
systems (Pincus 1991). Reductions in ApEn imply reduced
randomness or increased order and may indicate pathology in
the cardiovascular, respiratory and endocrine systems.
Cerebral blood flow CBF measurement is feasible and may be
considered in some patients. On the other hand, cerebral tissue
metabolic demand is not currently available.
Neurocritical
Indirect measures of CBF include measurement of surrogates of
cerebral tissue physiology as jugular venous oxygen saturation,
tissue oxygen tension, and microdialysis. Other indirect markers
for CBF measurement include cerebral perfusion pressure (CPP)
and less directly continuous EEG.
Jugular Venous Oximetry (SjvO2)
SjvO2 is an indicator of global oxygen extraction of the brain.
Jugular venous desaturation suggests an increase in cerebral
oxygen extraction which indirectly implies that there has been a
decrease in cerebral oxygen delivery, and hence perfusion.
The internal jugular vein drains the majority of blood from the
brain, and in most patients the right lateral sinus is larger.
Despite the fact that flow is different on the two sides, oxygen
saturations are normally very similar. This also appears to be the
case in diffuse brain injury, whilst in focal injuries there tends to
be a greater difference in the saturation of the two veins.
Jugular venous saturation can be measured using the principle
of infrared refractometry via a specially designed catheter
(Gopinath 1994). SjvO2 values are:
– 55-75% - normal
– >75% - luxury perfusion
– <54% hypoperfusion
– <40% suggests global ischemia and is associated with
increased cerebral lactate production.
Insertion of Jugular Venous Saturation Catheter: Insertion
involves retrograde cannulation of the internal jugular vein. A
pediatric pulmonary artery catheter introducer can be used
through which the fiber optic SjvO2 catheter is advanced beyond
the outlet of the common facial vein to the level of the jugular
bulb at the base of the skull. Ultrasound is often used for
accurate identification of vein position to avoid arterial
puncture, and to minimize the risk of hematoma formation
which can in turn impede venous drainage. Correct positioning
cerebral tissue physiology as jugular venous oxygen saturation,
tissue oxygen tension, and microdialysis. Other indirect markers
for CBF measurement include cerebral perfusion pressure (CPP)
and less directly continuous EEG.
Jugular Venous Oximetry (SjvO2)
SjvO2 is an indicator of global oxygen extraction of the brain.
Jugular venous desaturation suggests an increase in cerebral
oxygen extraction which indirectly implies that there has been a
decrease in cerebral oxygen delivery, and hence perfusion.
The internal jugular vein drains the majority of blood from the
brain, and in most patients the right lateral sinus is larger.
Despite the fact that flow is different on the two sides, oxygen
saturations are normally very similar. This also appears to be the
case in diffuse brain injury, whilst in focal injuries there tends to
be a greater difference in the saturation of the two veins.
Jugular venous saturation can be measured using the principle
of infrared refractometry via a specially designed catheter
(Gopinath 1994). SjvO2 values are:
– 55-75% - normal
– >75% - luxury perfusion
– <54% hypoperfusion
– <40% suggests global ischemia and is associated with
increased cerebral lactate production.
Insertion of Jugular Venous Saturation Catheter: Insertion
involves retrograde cannulation of the internal jugular vein. A
pediatric pulmonary artery catheter introducer can be used
through which the fiber optic SjvO2 catheter is advanced beyond
the outlet of the common facial vein to the level of the jugular
bulb at the base of the skull. Ultrasound is often used for
accurate identification of vein position to avoid arterial
puncture, and to minimize the risk of hematoma formation
which can in turn impede venous drainage. Correct positioning
is confirmed on a lateral neck X-ray with the catheter tip lying at
the level of the mastoid air cells.
Indications for SjvO2 Monitoring:
– Acute brain injury. An association between SjvO2
desaturation and poor neurological outcome has been
observed. Fandino showed that in traumatic head injury
SjvO2 was the only factor associated with outcome, whilst
Gopinath showed that multiple SjvO2 desaturations were
associated with an increased incidence of poor neurological
outcome compared to those who showed no desaturations
(Moppett 2004).
– Optimal CPP would appear to be at the point when further
increases in MAP do not lead to a rise in SjvO2.
– Monitoring of therapy response. If ICP and SjvO2 are both
raised, hyperemia is implied and hyperventilation is
appropriate. SjvO2 should be monitored and kept above 55%
in these circumstances, as excessive hyperventilation may
cause profound cerebral vasoconstriction and cerebral
ischemia. More recent work using PET scanning, however,
has cast some doubt on the value of SjvO2, with
hyperventilation appearing to increase ischemic brain
volume without necessarily producing a fall in jugular
venous saturation.
– To guide optimal blood pressure and PaCO2 management
during operative treatment of aneurysms following SAH.
During the operative treatment of an aneurysm,
hypertension must be avoided because of the risk of rupture
and bleeding. However, excessive reductions in blood
pressure may risk cerebral ischemia, especially in those
patients with preoperative hypertension. SjvO2 monitoring
allows the anesthetist to assess the degree to which blood
pressure can be safely lowered during the operative period.
Similarly, a low PaCO2 will cause SjvO2 desaturation.
the level of the mastoid air cells.
Indications for SjvO2 Monitoring:
– Acute brain injury. An association between SjvO2
desaturation and poor neurological outcome has been
observed. Fandino showed that in traumatic head injury
SjvO2 was the only factor associated with outcome, whilst
Gopinath showed that multiple SjvO2 desaturations were
associated with an increased incidence of poor neurological
outcome compared to those who showed no desaturations
(Moppett 2004).
– Optimal CPP would appear to be at the point when further
increases in MAP do not lead to a rise in SjvO2.
– Monitoring of therapy response. If ICP and SjvO2 are both
raised, hyperemia is implied and hyperventilation is
appropriate. SjvO2 should be monitored and kept above 55%
in these circumstances, as excessive hyperventilation may
cause profound cerebral vasoconstriction and cerebral
ischemia. More recent work using PET scanning, however,
has cast some doubt on the value of SjvO2, with
hyperventilation appearing to increase ischemic brain
volume without necessarily producing a fall in jugular
venous saturation.
– To guide optimal blood pressure and PaCO2 management
during operative treatment of aneurysms following SAH.
During the operative treatment of an aneurysm,
hypertension must be avoided because of the risk of rupture
and bleeding. However, excessive reductions in blood
pressure may risk cerebral ischemia, especially in those
patients with preoperative hypertension. SjvO2 monitoring
allows the anesthetist to assess the degree to which blood
pressure can be safely lowered during the operative period.
Similarly, a low PaCO2 will cause SjvO2 desaturation.
Problems with SjvO2 Monitoring: The major criticism of SjvO2
is that it is a measure of global oxygen delivery and does not
reflect metabolic inadequacies in focal areas of injury and hence
may miss regional areas of ischemia. Inaccuracies can occur with
catheter misplacement, contamination with extra cerebral
blood, when the catheter abuts the vessel wall, or if thrombosis
occurs around the catheter tip. Contraindications and
complications are similar to those of an IJV central line.
Interpretation of Changes in SjvO2:
If cerebral oxygen delivery is impaired, oxygen extraction
increases and SjvO2 decreases. If autoregulation is intact, CBF
increases to meet metabolic demand and SjvO2 is restored.
However, in the injured brain autoregulation is often impaired
and cerebral ischemia ensues.
– Decreased SjvO2: This implies inadequate cerebral oxygen
delivery that may be due to decreased oxygen delivery
(systemic hypoxia, anemia), decreased CBF (hypotension,
raised ICP, excessive hypocapnia or vasospasm), or increased
cerebral oxygen consumption (seizures, hyperthermia, pain)
– Increased SjvO2: This is somewhat more difficult to
interpret, and may represent either hyperemia (e.g., when
the autoregulation mechanisms are lost) or reduced oxygen
consumption (e.g., hypothermia, deep sedation, or cerebral
infarction).
– Lactate Oxygen Index: During cerebral hypoperfusion the
brain can become a net producer of lactate, with the jugular
venous lactate rising above arterial values.
Brain Tissue Oximetry
Interest in measuring brain tissue oxygenation via implantable
sensors has grown in recent years. The Licox sensor is an
implantable polarographic electrode that measures tissue
oxygen tensions. It is inserted through a compatible bolt and
ideally should be placed into the penumbral area of the injury.
Oxygen diffuses from the tissue through the catheter into an
is that it is a measure of global oxygen delivery and does not
reflect metabolic inadequacies in focal areas of injury and hence
may miss regional areas of ischemia. Inaccuracies can occur with
catheter misplacement, contamination with extra cerebral
blood, when the catheter abuts the vessel wall, or if thrombosis
occurs around the catheter tip. Contraindications and
complications are similar to those of an IJV central line.
Interpretation of Changes in SjvO2:
If cerebral oxygen delivery is impaired, oxygen extraction
increases and SjvO2 decreases. If autoregulation is intact, CBF
increases to meet metabolic demand and SjvO2 is restored.
However, in the injured brain autoregulation is often impaired
and cerebral ischemia ensues.
– Decreased SjvO2: This implies inadequate cerebral oxygen
delivery that may be due to decreased oxygen delivery
(systemic hypoxia, anemia), decreased CBF (hypotension,
raised ICP, excessive hypocapnia or vasospasm), or increased
cerebral oxygen consumption (seizures, hyperthermia, pain)
– Increased SjvO2: This is somewhat more difficult to
interpret, and may represent either hyperemia (e.g., when
the autoregulation mechanisms are lost) or reduced oxygen
consumption (e.g., hypothermia, deep sedation, or cerebral
infarction).
– Lactate Oxygen Index: During cerebral hypoperfusion the
brain can become a net producer of lactate, with the jugular
venous lactate rising above arterial values.
Brain Tissue Oximetry
Interest in measuring brain tissue oxygenation via implantable
sensors has grown in recent years. The Licox sensor is an
implantable polarographic electrode that measures tissue
oxygen tensions. It is inserted through a compatible bolt and
ideally should be placed into the penumbral area of the injury.
Oxygen diffuses from the tissue through the catheter into an
electrolyte chamber where an electrical current is generated.
Brain tissue oxygen tension is normally lower than arterial
oxygen tension (15-50 mmHg); whilst tissue CO2 is normally
higher (range 40-70 mmHg). The sensors are useful in
monitoring local changes and trends in tissue oxygenation that
might be missed by SjvO2 measurements.
At present it is primarily used in severe head injury and poorgrade
subarachnoid hemorrhage, and in conjunction with other
monitoring modalities. The technique allows a continuous
method of monitoring of regional tissue oxygenation and in
particular, monitoring areas of high ischemic risk, and is a
promising and reliable clinical tool.
Direct measures of CBF:
Measurement of injectable tracers that reach the brain after
peripheral injection using signal intensity changes.
Xenon-Enhanced CT:
In this technique xenon, a diffusible agent is used. The patient
inhales a mixture of 28% xenon and 72% oxygen for
approximately 4 minutes after baseline CT scans are obtained.
Sequential scanning of the same slices occurs during the
inhalation period. Tissue attenuation vs. time data is then
obtained. The arterial concentration is proportional to the
expired xenon concentration. Advantages are the relatively low
cost and high ease of use. The downside is a high sensitivity to
motion artifact (Andrew 2010).
SPECT (Single Photo Emission CT):
In SPECT scanning, the radioisotope technetium-99m (Tc-99m)
is combined with hexamethylpropyleneamine (HMPAO) or ethyl
cysteinate dimer.
SPECT scanning has the advantage of being easy to perform.
However, there are limitations with regards to assembly of the
compound.
MR Perfusion: “Dynamic Susceptibility Contrast Imaging” also
called “first-pass” or “bolus tracking” MR perfusion imaging is
based on rapid acquisition of MR signal intensity data from the
brain during the injection of a contrast agent. Signal intensity
Brain tissue oxygen tension is normally lower than arterial
oxygen tension (15-50 mmHg); whilst tissue CO2 is normally
higher (range 40-70 mmHg). The sensors are useful in
monitoring local changes and trends in tissue oxygenation that
might be missed by SjvO2 measurements.
At present it is primarily used in severe head injury and poorgrade
subarachnoid hemorrhage, and in conjunction with other
monitoring modalities. The technique allows a continuous
method of monitoring of regional tissue oxygenation and in
particular, monitoring areas of high ischemic risk, and is a
promising and reliable clinical tool.
Direct measures of CBF:
Measurement of injectable tracers that reach the brain after
peripheral injection using signal intensity changes.
Xenon-Enhanced CT:
In this technique xenon, a diffusible agent is used. The patient
inhales a mixture of 28% xenon and 72% oxygen for
approximately 4 minutes after baseline CT scans are obtained.
Sequential scanning of the same slices occurs during the
inhalation period. Tissue attenuation vs. time data is then
obtained. The arterial concentration is proportional to the
expired xenon concentration. Advantages are the relatively low
cost and high ease of use. The downside is a high sensitivity to
motion artifact (Andrew 2010).
SPECT (Single Photo Emission CT):
In SPECT scanning, the radioisotope technetium-99m (Tc-99m)
is combined with hexamethylpropyleneamine (HMPAO) or ethyl
cysteinate dimer.
SPECT scanning has the advantage of being easy to perform.
However, there are limitations with regards to assembly of the
compound.
MR Perfusion: “Dynamic Susceptibility Contrast Imaging” also
called “first-pass” or “bolus tracking” MR perfusion imaging is
based on rapid acquisition of MR signal intensity data from the
brain during the injection of a contrast agent. Signal intensity
Noninvasive Monitoring
Continuous measures of CBF by Transcranial Doppler
Transcranial Doppler (TCD) is a noninvasive technique that
calculates blood flow velocity in the cerebral vasculature. An
ultrasound beam is reflected back by the moving bloodstream at
a different frequency than it was transmitted (Doppler shift),
and from the Doppler equation, the velocity of blood flow (FV)
can be calculated. Changes in FV correlate well with changes in
CBF, as long as the orientation of the transducer and the vessel
diameter remain constant. It is used clinically to diagnose
vasospasm, to test cerebral autoregulation, and to detect emboli
during cardiac surgery and carotid endarterectomy (Moppett
2004).
Normal Values. From the FV waveform systolic, diastolic, and
mean velocities can be calculated. The mean FV in the middle
cerebral artery (MCA) is usually 35-90 cm/s and correlates well
with CBF. The FV can be influenced by age, being lowest at birth
(24 cm/s), highest at age 4-6 years (100 cm/s), and then declining
until the seventh decade of life (40 cm/s). FV is also 3-5% higher
in females and increases in hemodilutional states.
Technique for Insonating the Middle Cerebral Artery
(MCA): The M1 branch of the MCA is the commonest vessel to be
insonated, and is visualized through a transtemporal window
with a 2 MHz pulsed Doppler signal. The anterior and posterior
cerebral arteries can also be accessed through this window,
whilst a transorbital approach allows access to the carotid
siphon and the suboccipital route to the basilar and vertebral
arteries.
Continuous measures of CBF by Transcranial Doppler
Transcranial Doppler (TCD) is a noninvasive technique that
calculates blood flow velocity in the cerebral vasculature. An
ultrasound beam is reflected back by the moving bloodstream at
a different frequency than it was transmitted (Doppler shift),
and from the Doppler equation, the velocity of blood flow (FV)
can be calculated. Changes in FV correlate well with changes in
CBF, as long as the orientation of the transducer and the vessel
diameter remain constant. It is used clinically to diagnose
vasospasm, to test cerebral autoregulation, and to detect emboli
during cardiac surgery and carotid endarterectomy (Moppett
2004).
Normal Values. From the FV waveform systolic, diastolic, and
mean velocities can be calculated. The mean FV in the middle
cerebral artery (MCA) is usually 35-90 cm/s and correlates well
with CBF. The FV can be influenced by age, being lowest at birth
(24 cm/s), highest at age 4-6 years (100 cm/s), and then declining
until the seventh decade of life (40 cm/s). FV is also 3-5% higher
in females and increases in hemodilutional states.
Technique for Insonating the Middle Cerebral Artery
(MCA): The M1 branch of the MCA is the commonest vessel to be
insonated, and is visualized through a transtemporal window
with a 2 MHz pulsed Doppler signal. The anterior and posterior
cerebral arteries can also be accessed through this window,
whilst a transorbital approach allows access to the carotid
siphon and the suboccipital route to the basilar and vertebral
arteries.
Analysis of Doppler waveform: Analysis of the Doppler
waveform gives rise to useful derived variables as well as blood
velocity information.
– Pulsatility Index (PI): FVsys-FVdias/FVmean (normal value:
0.6-1.1). This reflects distal cerebrovascular resistance and
correlates with CPP.
– Change in CBF with arterial CO2 tension (cerebral vascular
reactivity).
Uses of TCD in Intensive Care Head Injury: Three distinct
phases have been shown in severe head injury with regard to
CBF and MCA FV.
– Phase 1 occurs on the day of injury and has a normal CBF,
normal MCA FV, and normal AVDO2.
– Phase 2 occurring 1-2 days post-injury, a hyperemic state is
encountered with an increased CBF, MCA FV and decreased
AVDO2.
– The final phase seen at days 4-15 is the vasospastic phase
and is associated with a significantly decreased CBF and
increased MCA FV. The use of TCD allows interpretation of
the dynamic physiological changes seen in severe head
injury, and in combination with other modalities allows
perfusion and oxygenation to be optimized for the
individual patient.
The highest MCA FV recorded at any stage is an independent
predictor of outcome from head injury, and the loss of
autoregulation (calculated by regression of CPP on MCA FV) has
also been shown to be a predictor of poor outcome from head
injury.
Subarachnoid Hemorrhage: Vasospasm occurs in
approximately 50% of people with subarachnoid hemorrhage
between 2-17 days post-event, and is associated with significant
morbidity and mortality. TCD may be used to detect vasospasm
by the increase in MCA FV associated with vessel narrowing.
Spasm is also assumed to be occurring when blood velocity is
waveform gives rise to useful derived variables as well as blood
velocity information.
– Pulsatility Index (PI): FVsys-FVdias/FVmean (normal value:
0.6-1.1). This reflects distal cerebrovascular resistance and
correlates with CPP.
– Change in CBF with arterial CO2 tension (cerebral vascular
reactivity).
Uses of TCD in Intensive Care Head Injury: Three distinct
phases have been shown in severe head injury with regard to
CBF and MCA FV.
– Phase 1 occurs on the day of injury and has a normal CBF,
normal MCA FV, and normal AVDO2.
– Phase 2 occurring 1-2 days post-injury, a hyperemic state is
encountered with an increased CBF, MCA FV and decreased
AVDO2.
– The final phase seen at days 4-15 is the vasospastic phase
and is associated with a significantly decreased CBF and
increased MCA FV. The use of TCD allows interpretation of
the dynamic physiological changes seen in severe head
injury, and in combination with other modalities allows
perfusion and oxygenation to be optimized for the
individual patient.
The highest MCA FV recorded at any stage is an independent
predictor of outcome from head injury, and the loss of
autoregulation (calculated by regression of CPP on MCA FV) has
also been shown to be a predictor of poor outcome from head
injury.
Subarachnoid Hemorrhage: Vasospasm occurs in
approximately 50% of people with subarachnoid hemorrhage
between 2-17 days post-event, and is associated with significant
morbidity and mortality. TCD may be used to detect vasospasm
by the increase in MCA FV associated with vessel narrowing.
Spasm is also assumed to be occurring when blood velocity is
>120 cm/s. High MCA FV is associated with worse-grade SAH,
larger blood loads on CT (assessed by Fisher Grade) and hence
worse outcome (Steiger 1994).
Near Infrared Spectroscopy
While the criticism of jugular venous oximetry is that it is
representative of global oxygen delivery, near infrared
spectroscopy (NIRS) is a noninvasive technique that measures
regional cerebral oxygenation.
Light in the near infrared wavelength (700-1,000 nm) can pass
through bone, skin, and other tissues with minimal absorption,
but is partly scattered and partly absorbed by brain tissue. The
amount of light absorbed is proportional to the concentration of
chromophobes (iron in hemoglobin, and copper in cytochromes),
and measurement of absorption at a number of wavelengths
provides an estimate of oxygenation (Owen-Reece 1999).
The probes illuminate a volume of about 8-10 ml of tissue and
are ideally suited for use in neonates because of their thin skull,
but have been used with success in adults.
Advantages of this technique are that it is non-invasive, and
provides a regional indicator of cerebral oxygenation. Its major
limitation is its inability to distinguish between intra- and extracranial
changes in blood flow.
Electrophysiological Monitoring
An electroencephalogram (EEG) is obtained using the
standardized system of electrode placement. Practically, this is
not often readily available and requires expert interpretation.
The EEG is affected by anesthetic agents and physiological
abnormalities such as hypoxia, hypoperfusion and hypercarbia.
A number of methods have been developed to simplify and
summarize the EEG data:
– Cerebral Function Monitor (CFM): This is a modified device
from a conventional EEG. It uses a single biparietal or
larger blood loads on CT (assessed by Fisher Grade) and hence
worse outcome (Steiger 1994).
Near Infrared Spectroscopy
While the criticism of jugular venous oximetry is that it is
representative of global oxygen delivery, near infrared
spectroscopy (NIRS) is a noninvasive technique that measures
regional cerebral oxygenation.
Light in the near infrared wavelength (700-1,000 nm) can pass
through bone, skin, and other tissues with minimal absorption,
but is partly scattered and partly absorbed by brain tissue. The
amount of light absorbed is proportional to the concentration of
chromophobes (iron in hemoglobin, and copper in cytochromes),
and measurement of absorption at a number of wavelengths
provides an estimate of oxygenation (Owen-Reece 1999).
The probes illuminate a volume of about 8-10 ml of tissue and
are ideally suited for use in neonates because of their thin skull,
but have been used with success in adults.
Advantages of this technique are that it is non-invasive, and
provides a regional indicator of cerebral oxygenation. Its major
limitation is its inability to distinguish between intra- and extracranial
changes in blood flow.
Electrophysiological Monitoring
An electroencephalogram (EEG) is obtained using the
standardized system of electrode placement. Practically, this is
not often readily available and requires expert interpretation.
The EEG is affected by anesthetic agents and physiological
abnormalities such as hypoxia, hypoperfusion and hypercarbia.
A number of methods have been developed to simplify and
summarize the EEG data:
– Cerebral Function Monitor (CFM): This is a modified device
from a conventional EEG. It uses a single biparietal or
bitemporal lead, and is processed to give an overall
representation of average cortical activity.
– Cerebral function analyzing monitor: Developed from the
CFM but displays information about amplitude and
frequency separately.
– Bispectral Analysis: This modification of the EEG analyzes
the phase and power between any two EEG frequencies. The
bispectral index (BIS) is a dimensionless number statistically
derived from these phased and power frequencies and
ranges from 0 to 100 (100-awake, 60-unconscious, 0-
isoelectric EEG). This technology was derived with normal
subjects and is not readily transferable to the injured brain,
but may have a use in guiding sedation and analgesia.
Spectral Edge Frequency: Compressed Spectral Array: Raw
EEG data is processed into a number of sine waves (Fourier
analysis). Power spectral analysis then investigates the
relationship between power and frequency of the sine waves
over a short time period (Epoch). The compressed spectral array
is obtained by superimposing linear plots of successive epochs to
produce a three-dimensional “hill and valley” plot. The spectral
edge frequency looks at the frequency below which a determined
power of the total power spectrum occurs. SEF90 indicates a
spectral edge frequency of 90% and is the frequency below which
90% of activity is occurring.
Continuous Electroencephalogram Monitoring: When a
comatose, critically ill patient arrives in the intensive care unit
(ICU), he is connected to a pulse oximetry monitor, ECG monitor,
respiration monitor, arterial blood pressure monitor, etc, to
provide physicians and nurses with real-time information about
cardiopulmonary physiology. Monitoring for the brain has been
unavailable to ICU staff until recently.
In comatose or sedated patients, there may be too few
examination findings that can be reliably followed to assess
worsening brain injury. Neuroimaging cannot reveal functional
changes, such as seizures and level of sedation; it provides
representation of average cortical activity.
– Cerebral function analyzing monitor: Developed from the
CFM but displays information about amplitude and
frequency separately.
– Bispectral Analysis: This modification of the EEG analyzes
the phase and power between any two EEG frequencies. The
bispectral index (BIS) is a dimensionless number statistically
derived from these phased and power frequencies and
ranges from 0 to 100 (100-awake, 60-unconscious, 0-
isoelectric EEG). This technology was derived with normal
subjects and is not readily transferable to the injured brain,
but may have a use in guiding sedation and analgesia.
Spectral Edge Frequency: Compressed Spectral Array: Raw
EEG data is processed into a number of sine waves (Fourier
analysis). Power spectral analysis then investigates the
relationship between power and frequency of the sine waves
over a short time period (Epoch). The compressed spectral array
is obtained by superimposing linear plots of successive epochs to
produce a three-dimensional “hill and valley” plot. The spectral
edge frequency looks at the frequency below which a determined
power of the total power spectrum occurs. SEF90 indicates a
spectral edge frequency of 90% and is the frequency below which
90% of activity is occurring.
Continuous Electroencephalogram Monitoring: When a
comatose, critically ill patient arrives in the intensive care unit
(ICU), he is connected to a pulse oximetry monitor, ECG monitor,
respiration monitor, arterial blood pressure monitor, etc, to
provide physicians and nurses with real-time information about
cardiopulmonary physiology. Monitoring for the brain has been
unavailable to ICU staff until recently.
In comatose or sedated patients, there may be too few
examination findings that can be reliably followed to assess
worsening brain injury. Neuroimaging cannot reveal functional
changes, such as seizures and level of sedation; it provides
information about structural brain injury often after it is
irreversible. There is great need for central nervous system
monitoring for at-risk patients, as more interventions are
becoming available to manage neurologic injury and “time is
brain”.
It is now possible to monitor and record the continuous digital
electroencephalogram, with full electrode placement, of many
critically ill patients simultaneously. Continuous EEG monitoring
(cEEG) provides real-time dynamic information about brain
function, which is especially useful when the clinical
examination is limited. Nonconvulsive seizures and
nonconvulsive status epilepticus are common in comatose
critically ill patients and can have multiple negative effects on
the injured brain.
Nonconvulsive status epilepticus (NCSE) seems to be an
important issue in stroke; NCSE is a frequent finding reaching
18% in a recent multicenter study (Kitchener 2010), thus
requiring a high degree of suspicion in an acute stroke setting to
avoid further neuronal injury and morbidity. The majority of
seizure activity in these patients cannot be detected without
cEEG. So, cEEG monitoring is mandatory to detect and guide
management of nonconvulsive status, including those that occur
following convulsive status epilepticus. In addition, it is used to
guide management of pharmacological coma sometimes used for
treatment of increased intracranial pressure. There are
emerging applications for cEEG, one of which is to detect new or
worsening brain ischemia in patients at high risk, especially
those with subarachnoid hemorrhage. As qEEG software is
continuously improving, full scalp cEEG monitoring is feasible,
and can provide continuous information about changes in brain
function in real time at the bedside and to alert clinicians to any
acute brain event, including seizures, ischemia, increasing
intracranial pressure, hemorrhage, and even systemic
abnormalities affecting the brain, such as hypoxia, hypotension,
acidosis, and others. cEEG monitoring without expert review of
the raw EEG, must not be allowed as false positives and false
irreversible. There is great need for central nervous system
monitoring for at-risk patients, as more interventions are
becoming available to manage neurologic injury and “time is
brain”.
It is now possible to monitor and record the continuous digital
electroencephalogram, with full electrode placement, of many
critically ill patients simultaneously. Continuous EEG monitoring
(cEEG) provides real-time dynamic information about brain
function, which is especially useful when the clinical
examination is limited. Nonconvulsive seizures and
nonconvulsive status epilepticus are common in comatose
critically ill patients and can have multiple negative effects on
the injured brain.
Nonconvulsive status epilepticus (NCSE) seems to be an
important issue in stroke; NCSE is a frequent finding reaching
18% in a recent multicenter study (Kitchener 2010), thus
requiring a high degree of suspicion in an acute stroke setting to
avoid further neuronal injury and morbidity. The majority of
seizure activity in these patients cannot be detected without
cEEG. So, cEEG monitoring is mandatory to detect and guide
management of nonconvulsive status, including those that occur
following convulsive status epilepticus. In addition, it is used to
guide management of pharmacological coma sometimes used for
treatment of increased intracranial pressure. There are
emerging applications for cEEG, one of which is to detect new or
worsening brain ischemia in patients at high risk, especially
those with subarachnoid hemorrhage. As qEEG software is
continuously improving, full scalp cEEG monitoring is feasible,
and can provide continuous information about changes in brain
function in real time at the bedside and to alert clinicians to any
acute brain event, including seizures, ischemia, increasing
intracranial pressure, hemorrhage, and even systemic
abnormalities affecting the brain, such as hypoxia, hypotension,
acidosis, and others. cEEG monitoring without expert review of
the raw EEG, must not be allowed as false positives and false
negatives are common. When cEEG is combined with
individualized multimodality brain monitoring, intensivists can
identify when the brain is at risk for injury or when neuronal
injury is already occurring and intervene before there is
permanent damage. We believe that cEEG has significant
potential to improve neurologic outcomes in a variety of
settings.
Application of the EEG in the ICU:
– Seizure management: Confirms the diagnosis of seizures and
identifies a focal or lateralized source of activity. It also
helps to distinguish between involuntary movements,
posturing, and eye signs that are common in intensive care
and true seizure activity.
– Nonconvulsive status epilepticus (NCSE): This represents a
state that lasts more than 30 min with clinical evidence in
alteration in mental state from normal, and seizure activity
on the EEG. Between 4 and 20% of patients with status
epilepticus have nonconvulsive episodes. NCSE is a frequent
finding in ischemic stroke reaching 18% of ischemic stroke
patients admitted to neurocritical care units.
– Metabolic suppression: Burst suppression (isoelectric EEG) is
a definable end point when pharmacological reduction of
the cerebral metabolic rate of the injured brain is required
for either neuroprotection or intractable intracranial
hypertension.
– Ensuring adequate sedation in patients who require
prolonged neuromuscular paralysis.
– Prognosis: The EEG can be of prognostic value following
brain injury, with absence of spontaneous variability being
associated with poor outcome.
individualized multimodality brain monitoring, intensivists can
identify when the brain is at risk for injury or when neuronal
injury is already occurring and intervene before there is
permanent damage. We believe that cEEG has significant
potential to improve neurologic outcomes in a variety of
settings.
Application of the EEG in the ICU:
– Seizure management: Confirms the diagnosis of seizures and
identifies a focal or lateralized source of activity. It also
helps to distinguish between involuntary movements,
posturing, and eye signs that are common in intensive care
and true seizure activity.
– Nonconvulsive status epilepticus (NCSE): This represents a
state that lasts more than 30 min with clinical evidence in
alteration in mental state from normal, and seizure activity
on the EEG. Between 4 and 20% of patients with status
epilepticus have nonconvulsive episodes. NCSE is a frequent
finding in ischemic stroke reaching 18% of ischemic stroke
patients admitted to neurocritical care units.
– Metabolic suppression: Burst suppression (isoelectric EEG) is
a definable end point when pharmacological reduction of
the cerebral metabolic rate of the injured brain is required
for either neuroprotection or intractable intracranial
hypertension.
– Ensuring adequate sedation in patients who require
prolonged neuromuscular paralysis.
– Prognosis: The EEG can be of prognostic value following
brain injury, with absence of spontaneous variability being
associated with poor outcome.
Multimodal Monitoring
In any type of brain injury, the available monitoring modalities
are prone to artifact and misinterpretation. By utilizing more
than one monitoring technique, the observer is more likely to
determine whether a genuine change in cerebral physiology has
occurred and what the most appropriate intervention should be.
For instance, in traumatic brain-injured patients we routinely
monitor ICP, processed EEG, SjvO2 and brain-tissue oxygen
tension (PbtO2), allowing us to observe both local and regional
changes in cerebral hemodynamics. General rules cannot always
be applied to individual patients, and multimodal monitoring
can allow more informed decision making such as determining
CPP thresholds or the ability of the cerebral vasculature to
autoregulate (Cecil 2011; Czosnyka 1996).
Conclusions
A wide range of monitoring techniques is available, each with
different strengths and limitations. Multimodal monitoring
using a combination of techniques can overcome some of the
limitations of the individual methods discussed. The choice of
monitoring is often guided by clinical familiarity and local
policy.
Key points:
1. Repeated clinical assessment through the Glasgow Coma
Scale (GCS) is the cornerstone of neurological evaluation.
2. Ventilated head-injured patients with intracranial
pathology on CT require ICP monitoring.
3. Invasive or non-invasive neurospecific monitoring requires
careful interpretation when assisting goal-directed
therapies.
4. Multimodal monitoring using a combination of techniques
can overcome some of the limitations of individual
methods.
In any type of brain injury, the available monitoring modalities
are prone to artifact and misinterpretation. By utilizing more
than one monitoring technique, the observer is more likely to
determine whether a genuine change in cerebral physiology has
occurred and what the most appropriate intervention should be.
For instance, in traumatic brain-injured patients we routinely
monitor ICP, processed EEG, SjvO2 and brain-tissue oxygen
tension (PbtO2), allowing us to observe both local and regional
changes in cerebral hemodynamics. General rules cannot always
be applied to individual patients, and multimodal monitoring
can allow more informed decision making such as determining
CPP thresholds or the ability of the cerebral vasculature to
autoregulate (Cecil 2011; Czosnyka 1996).
Conclusions
A wide range of monitoring techniques is available, each with
different strengths and limitations. Multimodal monitoring
using a combination of techniques can overcome some of the
limitations of the individual methods discussed. The choice of
monitoring is often guided by clinical familiarity and local
policy.
Key points:
1. Repeated clinical assessment through the Glasgow Coma
Scale (GCS) is the cornerstone of neurological evaluation.
2. Ventilated head-injured patients with intracranial
pathology on CT require ICP monitoring.
3. Invasive or non-invasive neurospecific monitoring requires
careful interpretation when assisting goal-directed
therapies.
4. Multimodal monitoring using a combination of techniques
can overcome some of the limitations of individual
methods.
See also:
Brain Trauma Foundation Guidelines 2007
www.braintrauma.org
Anaesthesia UK
www.frca.co.uk
Brain Trauma Foundation Guidelines 2007
www.braintrauma.org
Anaesthesia UK
www.frca.co.uk
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