neurologicalMonitoring

neurologicalMonitoring - Neurological Monitoring Augusto...

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Unformatted text preview: Neurological Monitoring Augusto Torres, MD Department of Anesthesiology MetroHealth Medical Center April 2009 Outline Outline EEG SSEP MEP Transcranial Doppler Cerebral Oximetry 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 EEG Three uses perioperatively: – Identify inadequate blood flow to cerebral cortex caused by surgical/anesthetic­induced 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 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 Normal EEG: characteristic frequency (beta, then alpha) with symmetrical signals EEG EEG EEG EEG 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) Abnormal EEG Abnormal EEG EEG EEG The gold standard for intra­op EEG monitoring: continuous visual inspection of a 16­ to 32­channel 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 Anesthetic Agents and EEG Anesthetic Agents and EEG Anesthetic drugs affect frequency and amplitude of EEG waveforms Subanesthetic doses of IV and inhaled anesthetics (0.3 MAC): – Increases frontal beta activity (low voltage, high frequency) Light anesthesia (0.5 MAC): – Larger voltage, slower frequency Anesthetic Agents and EEG Anesthetic Agents and EEG General anesthesia (1 MAC): – Irregular slow activity Deeper anesthesia (1.25 MAC): – Alternating activity Very deep anesthesia (1.6 MAC): – Burst suppression eventually isoelectric Anesthetic Agents and EEG Anesthetic Agents and EEG Some agents totally suppress EEG activity (e.g. isoflurane) Some agents never produce burst suppression or an isoelectric EEG – Incapable (e.g. benzodiazipines) – Toxicity (e.g. halothane) prevents giving large enough dose Anesthetic Agents and EEG Anesthetic Agents and EEG Barbiturates, propofol, etomidate: – Initial activation, then dose­related depression, results in EEG silence – Thiopental – increasing doses will reduce oxygen requirements from neuronal activity Basal requirements (metabolic activity) reduced by hypothermia – Epileptiform activity with methohexital and etomidate in subhypnotic doses Anesthetic Agents and EEG Anesthetic Agents and EEG Ketamine: – Activates EEG at low doses (1mg/kg), slowing at higher doses – Cannot achieve electrocortical silence – Also associated with epileptiform activity in patients with epilepsy Benzodiazepines: – Produce typical EEG pattern – No burst suppression or isoelectric EEG Anesthetic Agents and EEG Anesthetic Agents and EEG Opioids – – – – Slowing of EEG No burst suppression High dose – epileptiform activity Normeperidine Nitrous oxide – Minor changes, decrease in amplitude and frontal high­frequency activity – No burst suppression Anesthetic Agents and EEG Anesthetic Agents and EEG Isoflurane, sevoflurane, desflurane: – EEG activation at low concentrations; slowing, eventually electrical silence at higher concentrations – Isoflurane Periods of suppression at 1.5 MAC Electrical silence at 2 – 2.5 MAC Anesthetic Agents and EEG Anesthetic Agents and EEG Enflurane – Seizure activity with hyperventilation and high concentrations (>1.5 MAC) Halothane – 3­4 MAC necessary for burst suppression Cardiovascular collapse Non­anesthetic Factors Affecting Non­anesthetic Factors Affecting EEG Miller et al. Surgical Cardiopulmonary bypass Occlusion of major cerebral vessel (carotid cross­clamping, aneurysm clipping) Retraction on cerebral cortex Surgically induced emboli to brain Pathophysiologic Factors Hypoxemia Hypotension Hypothermia Hypercarbia and hypocarbia Intraoperative Use of EEG Intraoperative Use of EEG EEG used to monitor for ischemia Avoid during critical periods of the case: – Changing anesthetic technique – Changing gas levels – Administering boluses of medications that affect EEG Intraoperative Use of EEG Intraoperative Use of EEG Cardiopulmonary bypass – Theoretically beneficial Embolic events with cannulation Increased risk in patients with carotid disease – Difficult to interpret EEG changes Alteration of arterial carbon dioxide tension Changes in blood pressure Hypothermia Hemodilution (anemia) Intraoperative Use of EEG Intraoperative Use of EEG Carotid endarterectomy – Well­established – 20% of patients with major EEG changes awaken with neurological deficits – Normal cerebral blood flow 50mL/100g/min – Cellular survival threatened 12mL/100g/min – EEG changes seen at 20mL/100g/min With isoflurane EEG changes not seen until 10mL/100g/min – If EEG changes noted, intervene Shunting Increase CBF Intraoperative Use of EEG Intraoperative Use of EEG Limitations to EEG for CEA – Need for experienced technician to monitor – Strokes still occur despite normal intra­op EEG Subcortical events not monitored by EEG – Not proven to reduce incidence of stroke – False positives Intraoperative Use of EEG Intraoperative Use of EEG What to do if EEG technician indicates a possible problem? – Check to see if anesthetic milieu is stable – Rule out hypoxemia, hypotension, hypothermia, hypercarbia and hypocarbia Raise the MAP, obtain ABG – See if there is a surgical reason Evoked Potentials Evoked Potentials 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 Sensory Evoked Potential Sensory Evoked Potential 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 Sensory Evoked Potential Sensory Evoked Potential Responds to injury by increased latency, decreased amplitude, ultimately disappearance Problem is response non­specific Surgical injury Hypoperfusion/ischemia Changes in anesthetic drugs Temperature changes Sensory Evoked Potentials Sensory Evoked Potentials Signals easily disrupted by background electrical activity (ECG, EMG activity of muscle movement, etc) – Baseline is essential to subsequent interpretation SSEPs SSEPs Stimulation with fine needle electrodes Stimulate median nerve – signal travels anterograde causing muscle twitch, also travels retrograde up sensory pathways along dorsal columns all the way to brain cortex SSEPs SSEPs Can measure the electrophysiologic response to nerve stimulation all the way up this pathway Monitor many waves (representing different nerves along pathway) and localization of where the neural pathway is interrupted is possible Intraoperative SSEPs Intraoperative SSEPs Neurologic pathway must be at risk and intervention must be available 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 Intraoperative SSEPs Intraoperative SSEPs Scoliosis surgery – well established – – Lessen degree of spine straightening False­negatives rare, false positives more common 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 – – – Poor correlation in thoracic aortic surgery Intraoperative SSEPs Intraoperative SSEPs 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 Intraoperative SSEPs Intraoperative SSEPs 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 Other SEP’s Other SEP’s 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 Other SEP’s Other SEP’s VEP – flash stimulation of retina assess pathway from optic n. to occipital cortex – Procedures near optic chiasm – Very sensitive to anesthetic drugs and variable signals ­ unreliable Anesthetic Agents and SEPs Anesthetic Agents and SEPs Most anesthetic drugs increase latency and decrease amplitude – Volatile agents: increase latency, decrease amplitude – Barbituates: increase in latency, 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 and SEP’s Physiologic Factors and SEP’s All of these affect SSEPs Hypotension Hyperthermia and hypothermia – Mild hypothermia (35­36 degrees) minimal effect Hypoxemia Hypercapnea Significant anemia (HCT <15%) Technical factor: poor electode­to skin­contact and high electrical impedence (eg electrocautery) Anesthetic Management Anesthetic Management Schubert “Clinical Neuroanesthesia” Stable, constant anesthetic level, especially during critical periods Response to poor signal Rule out technical factors: – Electrode impedance, radio frequency interference Cortical vs. subcortical changes Anesthetic Management Anesthetic Management Schubert “Clinical Neuroanesthesia” Rule out systemic factors: – KEY: improve neural tissue blood flow and nutrient delivery – Intravascular volume and cardiac performance optimized (crystalloid/colloid or blood) to increase oxygen­carrying capacity – optimal HCT 30% or higher – Elevate MAP – Blood gas – assure oxygenation, normocarbia to help improve collateral blood supply if hypocarbic – Consider steroids (shown to work with traumatic spinal cord injury) – Mannitol – improve microcirculatory flow and reducing interstitial cord edema Anesthetic Management Anesthetic Management Schubert “Clinical Neuroanesthesia” Rule out neurological factors – Brain and spinal cord ischemia – Pneumocephalus – Peripheral n. ischemia and compression Motor Evoked Potentials 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 Motor Evoked Potentials Evoked responses may be recorded: – Spinal cord, peripheral n., muscle itself Motor Evoked Potentials 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 Transcranial Doppler Transcranial Doppler Direct, noninvasive measurement of CBF Sound waves transmitted through thin temporal bone, contact blood, are reflected, and detected Most easily monitor middle cerebral artery Transcranial Doppler Transcranial Doppler Does not measure actual blood flow but velocity – Velocity often closely related to flow but two are not equivalent Surgical field may limit probe placement and maintenance of proper position Carotid endarterectomy – Measure adequacy of CBF during clamping Technically difficult in ~20% – Useful for detecting embolic events – How much emboli is harmful? Transcranial Doppler Transcranial Doppler CPB – Detect air or particulate emboli during cannulation, during bypass, weaning from bypass, decannulation – Significant data pending Detection of vasospasm (well­established) – Smaller area – increase in velocity (>120cm/s) Cerebral Oximetry (Near infrared Cerebral Oximetry (Near infrared spectroscopy) Measures oxygen saturation in the vascular bed of the cerebral cortex Interrogates arterial, venous, capillary blood within field – Derived saturation represents a tissue oxygen saturation measured from these three compartments Unlike pulse oximetry (requires pulsatile blood), NIRS assess the hemoglobin saturation of venous blood, which along with capillary blood, composes approximately 90% of the blood volume in tissues Believed to reflect the oxygen saturation of hemoglobin in the post extraction compartment of any particular tissue Measures tissue oxygen saturation Cerebral Oximetry (Near infrared Cerebral Oximetry (Near infrared spectroscopy) Concerns: – 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?) – High intersubject variability – Low specificity Rigamonti et al. (J Clin Anesth 2005;17:426) – Compared EEG to rSO2 in CEA in terms of predicting need to place shunt 44% sens 84% spec Conclusion Conclusion EEG is a useful modality for measuring intraoperative cerebral perfusion SSEP offers the additional advantage of measuring subcortical adverse events New techniques for neurological monitoring are being developed which need to be further evaluated and validated ...
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