Neuromonitoring in anesthesia

Neuromonitoring in anesthesia

Classification of monitoring techniques:

The brain can be monitored in terms of:

Function

Cerebral blood flow (CBF) & intracranial pressure (ICP)

Brain oxygenation and metabolism

Monitoring of FUNCTION:

Electroencephalograms (EEG) Raw EEG

Computerized Processed EEG: Compressed spectral array, Density spectral array, Aperiodic analysis, Bispectral analysis (BIS)

Evoked Potential Sensory EP:

Somatosensory EP

Visual EP

Brain stem auditory EP

Motor EP:

- Transcranial magnetic MEP

- Transcranial electric MEP

- Direct spinal cord stimulation

EMG

- Cranial nerve function (V, VII, IX, X, XI, XII)

EEG

EEG

Electroencephalogram – surface recordings of the summation of excitatory and inhibitory postsynaptic potentials generated by pyramidal cells in cerebral cortex

EEG:

Measures electrical function of brain

Indirectly measures blood flow

Measures anesthetic effects

EEG

Three uses perioperatively:

Identify inadequate blood flow to cerebral cortex caused by surgical/anesthetic-induced reduction in flow

Guide reduction of cerebral metabolism prior to induced reduction of blood flow

Predict neurologic outcome after brain insult

Other uses: identify consciousness, unconsciousness, seizure activity, stages of sleep, coma

EEG

Electrodes placed so that mapping system relates surface head anatomy to underlying brain cortical regions

3 parameters of the signal: Amplitude – size or

voltage of signal Frequency – number of

times signal oscillates Time – duration of the

sampling of the signal

EEG

EEG Waves :

Beta: high freq, low amp (awake state)

Alpha: med freq, high amp (eyes closed while awake)

Theta: Low freq (not predominant)

Delta: very low freq high amp (depressed functions/deep coma

Abnormal EEG

Regional problems - asymmetry in frequency, amplitude or unpredicted patterns of such Epilepsy – high voltage spike with slow waves

Ischemia – slowing frequency with preservation of amplitude or loss of amplitude (severe)

Global problems – affects entire brain, symmetric abnormalities Anesthetic agents induce global changes similar to global

ischemia or hypoxemia (control of anesthetic technique is important

Anesthetic agents and EEG

Subanesthetic doses of inhaled anesthetics (0.3 MAC): Increases frontal beta activity (low voltage, high frequency)

Light anesthesia (0.5 MAC): Larger voltage, slower frequency

General anesthesia (1 MAC): Irregular slow activity

Deeper anesthesia (1.25 MAC): Alternating activity

Very deep anesthesia (1.6 MAC): Burst suppression eventually isoelectric

Non-anesthetic Factors Affecting EEG

Surgical

1. Cardiopulmonary bypass

2. Occlusion of major cerebral vessel (carotid cross-clamping, aneurysm clipping)

3. Retraction on cerebral cortex

4. Surgically induced emboli to brain

Pathophysiologic Factors

1. Hypoxemia

2. Hypotension

3. Hypothermia

4. Hypercarbia and hypocarbia

Uses of EEG

1. Carotid endarterectomy

2. Cerebral aneurysm surgery when temporary clipping is used.

3. Cardiopulmonary bypass procedure

4. Extracranial-intracranial bypass procedure

5. Deliberate metabolic supression for cerebral protection.

Surgery that place the brain at risk (difficulties: restricted access)

Seizure monitoring in ICU

Processed EEG

The gold standard for intra-op EEG monitoring: continuous visual inspection of a 16- to 32-channel analog EEG by experienced electroencephalographer

“Processed EEG”: methods of converting raw EEG to a plot showing voltage, frequency, and time Monitors fewer channels, less experience required Reasonable results obtained.

The common processing techniques used are time domain analysis and frequency domain analysis.

Time domain analysis

EEG is split into small epochs of a given duration, usually about 1-4 sec.

The frequency and/or amplitude information contained in each epoch is depicted graphically.

A change in the value of the variables derived form this display is expected to represent a change in the raw EEG.

Frequency domain analysis

The EEG is split into small epochs.

Each epoch is further resolved into its component sine waves and reconstructed as frequency Vs power plot by using Fourier Analysis.

Compressed Spectral Array (CSA) and Density Modulated Spectral Array (DSA)

BIS

Entropy

EVOKED POTENTIALS

Sensory Evoked Potential

Definition: electrical activity generated in response to sensory or motor stimulus

Stimulus given, then neural response is recorded at different points along pathway

Sensory evoked potential Latency – time from stimulus

to onset of SER

Amplitude – voltage of recorded response

SEP

Sensory evoked potentials Somatosensory (SSEP) Auditory (BAEP) Visual (VEP)

SSEP – produced by electrically stimulating a cranial or peripheral nerve If peripheral n. stimulated – can record proximally

along entire tract (peripheral n., spinal cord, brainstem, thalamus, cerebral cortex)

As opposed to EEG, records subcortically

SSEP

Time-locked, event related, pathway specific EEG in respones of peripheral stimulus

Monitor integrity of the pathway from periphery to the cortex

Electrical stimulator placed at median, ulnar, or posterior tibial nerves

Indications for SSEP

Indications: Scoliosis correction Spinal cord decompression and stabilization

after acute injury Brachial plexus exploration Resection of spinal cord tumor Resection of intracranial lesions involving

sensory cortex Clipping of intracranial aneurysms Carotid endarterectomy Thoracic aortic aneurysm repair

Carotid endarterectomy

Similar sensitivity has been found between SSEP and EEG

SSEP has advantage of monitoring subcortical ischemia

SSEP disadvantage do not monitor anterior portions -frontal or temporal lobes

Cerebral Aneurysm

SSEP can gauge adequacy of blood flow to anterior cerebral circulation

Evaluate effects of temporary clipping and identify unintended occlusion of perforating vessels supplying internal capsule in the aneurysm clip

Limitations

Motor tracts not directly monitored Posterior spinal arteries supply dorsal columns

Anterior spinal arteries supply anterior (motor) tracts

Possible to have significant motor deficit postoperatively despite normal SSEPs

SSEP’s generally correlate well with spinal column surgery

• Visual Evoked Potential (VEP)

Using LED goggles to create stimulus

Difficult to perform

• Brainstem Auditory Evoked Potential (BAEP)

Repetitive clicks delivered to the ear

Reflects the VIII nerve & brainstem “well-being”

AEP

Auditory (BAEP) – rapid clicks elicit responses

CN VIII, cochlear nucleus, rostral brainstem, inferior colliculus, auditory cortex

Procedures near auditory pathway and posterior fossa

Decompression of CN VII, resection of acoustic neuroma, sectioning CNVIII for intractable tinnitus

Resistant to anesthetic drugs

Limitations

Responds to injury by increased latency, decreased amplitude, ultimately disappearance

Problem is response non-specific Surgical injury

Hypoperfusion/ischemia

Changes in anesthetic drugs

Temperature changes

Signals easily disrupted by background electrical activity (ECG, EMG activity of muscle movement, etc)

Baseline is essential to subsequent interpretation

Anesthetic agents and SEP

Most anesthetic drugs increase latency and decrease amplitude

Exceptions: Nitrous oxide: latency stable, decrease

amplitude Etomidate: increases latency, increase in

amplitude Ketamine: increases amplitude Opiods: no clinically significant changes Muscle relaxants: no changes

Physiologic factors affecting SEP’s

Hypotension

Hyperthermia and hypothermia Mild hypothermia (35-36 degrees) minimal effect

Hypoxemia

Hypercapnia

Significant anemia (HCT <15%)

Technical factor: poor electode-to skin-contact and high electrical impedence (egelectrocautery)

Motor Evoked Potentials

Motor EP:

- Transcranial magnetic MEP

- Transcranial electric MEP

- Direct spinal cord stimulation

Motor Evoked Potentials

Transcranial electrical MEP monitoring

Stimulating electrodes placed on scalp overlying motor cortex

Application of electrical current produces MEP

Stimulus propagated through descending motor pathways

Motor Evoked Potentials

MEPs very sensitive to anesthetic agents Possibly due to

anesthetic depression of anterior horn cells in spinal cord

Intravenous agents produce significantly less depression

TIVA often used

No muscle relaxant

EMG

Early detection of surgically induced nerve damage and assessment of level of nerve function intra-operatively.

Active or passive.

Uses:

1. Facial nerve monitoring

2. Trigeminal nerve monitoring

3. Spinal Accessory nerve

Cerebral blood flow and ICP monitoring

Intra-cranial Pressure

The pressure inside the lateral ventricles/lumbar subarachnoid space in supine position.

The normal value of ICP is 10-15 mm Hg in adults.

Indications for ICP monitoring

1. Head Injury

2. Brain Tumors

3. Subarachnoid Heamorrhage

4. Hydrocephalus

5. Neuromedical conditions

Techniques of ICP monitoring

ICP waveforms

ICP shows a pulsatile recording with slow respiratory component superimposed on a biphasic recording synchronous with cardiac cycle.

Normally, respiratory oscillations are greater than the cardiac oscillations, but when ICP increases, arterial pulsations also assume greater amplitude

Abnormalities of ICP waveforms

A WAVES: plateau waves indicate ICP above 40mmHg and are sustained for 5-20min.

B WAVES: Amplitude of 20mmHg and occur at the rate of 1-2/min. Occur synchronus with cheyne-stokes breathing

C WAVES: no pathological significance

Transcranial Doppler

Measures the blood flow velocity in major cerebral blood vessles.

Examination carried out through the temporal window, orbital foramen or foramen magnum.

Using 2MHz probe.

MCA commonly used.

Change in velocity is proportional to change in flow considering the vessel diameter is constant.

Interpretation of waveforms

Pulsatality Index = (Peak Systolic Velocity - EndDiastolic Velocity) / Mean Velocity

Clinical applications of TCD

1. It is useful as a noninvasive monitor of CBF.

2. It is helpful to diagnose cerebral vasospasm and monitor response to therapy in patients with subarachnoid haemorrhage and head injury.

3. It is used to study autoregulation of CBF and cerebral vascular response to carbon dioxide.

4. It can be used to assess intracranial circulatory status in raised ICP.

5. It can be a useful tool to identify intraoperative cerebral embolisation during surgery on carotid artery and cardiopulmonary bypass procedures.

6. It can be used to optimise CPP and hyperventilationin patients with head injury.

Intravascular tracer compounds

Method originally described by Kety and Schmidt.

Administration of radioactive isotope of xenon-133

Measurement of radioactivity washout with gamma detectors.

Disadvantages: 1.Exposure to radioactivity

2.Cumbersome detector equipment

3.Focal areas of hypoperfusion missed

4.Snapshot of CBF not continuous monitor.

Thermal diffusion cerebral blood flow monitoring

The rate at which heat dissipates in a tissue depends on the tissue’s thermal conductive properties and the blood flow in that area.

Measurement is automatically suspended if the passive thermistor measures a brain temperature of 39.1°C.

The inability to monitor during a febrile episode may constitute a true limitation of the technique

Monitoring of cerebral oxygenation and metabloism

Monitoring of cerebral oxygenation and metabloism

Brain tissue oxygenation

Jugular bulb venous oximetry monitoring

Microdialysis catheter

Near Infrared Spectroscopy (NIRS)

Jugular venous oximetry :principle

(A-V)DO2 x CBF = CMRO2

When CMRO2 is constant, any change in CBF is associated with a reciprocal change in the cerebral arteriovenous oxygen difference.

Based on the principle of reflectance oximetry.

Jugular venous oximetry

Continuous monitoring of jugular venous oxygen saturation (SjVO2 ) is carried out by a catheter placed retrograde through the internal jugular vein intothejugular bulb.

For accurate measurement, the tip of the catheter must be within 1 cm of the jugular bulb.

Indices obtained from SjVO2

1. Jugular venous oxygen saturation (SjVO2 )

2. Cerebral arteriovenousoxygen difference (A-VDO2 ) (the difference between arterial and jugularvenousoxygen content) and

3. Cerebral oxygen extraction(CEO2 ) (the difference between SaO2

and SjVO2 ).

Interpretation of SjVO2

Interpretation of jugular venous oxygen saturation (SjvO2) Increased values: >90% indicates absolute/relative

hyperemia Reduced metabolic need comatose/brain death

Excessive flove sever hypercapnia

AVM

Normal Values: 60-70% focal ischemia?

Decreased Values: <50% increased O2 extraction,indicates a potential risk of ischemia injury Increased demand: seizure / fever

Decreased supply: decreased flow, decreased hematocrit

As ischemiaprogress to infarction: O2 consumption decreases

Near Infra-red Spectroscopy NIRS

The principle of absorption of near-infrared light by chromophores in the body like oxyhaemoglobin,deoxyhaemoglobin and cytochrome aa3.

Light in the near-infrared region (70-1000 nm) is very minimally absorbed by body tissues. It can penetrate tissues upto 8 cm.

Measure regional cerebral blood flow, cerebral blood volume, cerebral oxygen saturation and cerebral metabolism.

NIRS limitations

Inability to assess the contribution of extracranial tissue to the signal changes.

Presence of intracranial blood in the form of haematomas and contusions can interfere with the measurements.

Measures small portion of frontal cortex, contributions from non-brain sources

Temperature changes affect NIR absorption water spectrum Degree of contamination of the signal by chromophores in

the skin can be appreciable and are variable Not validated – threshold for regional oxygen saturation not

known (20% reduction from baseline?)

Tissue partial pressure oxygen monitoring:

Based on an oxygen-sensitive electrode originally described by Clark.

The diffusion of oxygen molecules through an oxygen-permeable membrane into an electrolyte solution causes an electric current that is proportional to Po2.

The catheter is placed into the brain tissue through a twist drill hole into the subcortical white matter.

Normal values for brain tissue oxygen tension are 20-40 mmHg.

In patients with cerebral ischaemia the values are 10 ± 5 mmHg as against 37 ± 12 mmHg in normal individuals

Cerebral Microdialysis

Small catheter inserted with ICP/tissue PO2

monitor

Artificial cerebrospinal fluid,equilibrates with extracellular fluid,chemical composition analysis

Markers:

○ Lactate/pyruvate ratio : onset of ischemia

○ High level glycerol: inadequate energy to maintain cellular integrity- membrane breakdown

○ Glutamate: neuronal injury and a factor in its exacerbation

Catheter placement is usually in ‘high risk’ tissue.

Uses: 1.Ischemia/trauma

2.epilepsy

3.Tumor chemistry

References

Millers anesthesia 8th edition

Neurological monitoring. Dr. G S Rao IJA 2002;46(4)

Advances in neuroanesthesia monitoring Dr. Pramod Bithal AIIMS new delhi. 2006 ISACON

GE-Datex Ohmeda Entropy monitor manual

Coviden BIS monitor users manual

ThankyouThe end