Neuromonitoring Study Guide PDF

Neuromonitoring: ★ Goals of Neuro Anesthesia ○ Overall goal: provide sufficient oxygen and glucose to fulfill the brain's metabolic demands - "brain requires an incredible amount of oxygen and glucose; everything needs to be balanced to do so" ○ Perioperative goals: Ensure a favorable supply /...

Neuromonitoring: ★ Goals of Neuro Anesthesia ○ Overall goal: provide sufficient oxygen and glucose to fulfill the brain's metabolic demands - "brain requires an incredible amount of oxygen and glucose; everything needs to be balanced to do so" ○ Perioperative goals: Ensure a favorable supply / demand relationship How? → "most of this is going to be controlling brain hemodynamics - don't want too much bf → hyperemia" Prevent brain herniation when the skull is closed How? → "hyperventilation (immediate effect), one of the tools we use but not long lasting" Provide relaxation Why? → "NMBs and things like that so that the patient isn't moving, that were reducing their metabolism, and we're ensuring their brain is receiving enough oxygen and that the demand isn't too high" ★ Why is Neuromonitoring Important? ○ Patients with neurologic disease undergoing surgical procedures → increased risk of ischemic / hypoxic damage to the CNS Why? → "disease process or surgical procedure - because we know there is a risk we use the intra-op monitoring" ○ Intraoperative monitoring may improve patient outcomes - how? Early detection Provides info so anesthetic and surgical procedure can be tailored to patient status "In clinical you may see that it seems like a recipe, but it shouldn't be" "What if they drink a case of beer a night, you need to tailor it" ★ Routine Anesthesia Monitors ○ ECG ○ NIBP ○ FiO2 ○ EtCO2 ○ SaO2 ○ Precordial or esophageal stethoscope ★ Expanded Anesthesia Monitors ○ Arterial pressure monitoring ○ CVP monitoring ○ PA monitoring ○ Precordial doppler - "pretty specific to neuro and sitting cases" ★ 3 Categories of Neurophysiologic Monitors - said this was a test question in the past ○ Monitors of function EEG Evoked potentials - several types Electromyography ○ Monitors of blood flow - CBF and ICP - "may or may not see in the OR" Nitrous Oxide wash-in Radioactive xenon clearance Laser doppler blood flow Transcranial doppler sonography Microvascular doppler ultrasound Indocyanine green videoangiography ICP alone Intraventricular catheter - "probably the most common thing that we will see in the OR" Fiberoptic parenchymal catheter - "may see this if pt comes with it" Subarachnoid bolt Epidural catheter ○ Monitors of Metabolism Invasive → intracerebral PO2 electrode (Paratrend, Licox) Non-invasive Transcranial cerebral oximetry (near infrared spectroscopy) Jugular venous oximetry ★ Monitors of Function - EEG ○ EEG: electroencephalography - "measure difference between multiple regions of the brain" Recording of the electrical activity of the brain Produced by the pyramidal cells in the cerebral cortex - "no information at all about subcortical tissue, spinal cord, or CNs" Dependent on an adequate supply of oxygen and glucose ○ Can be monitored from the scalp and forehead using surface or needle electrodes Electrode placement - the international 10:20 system - "describes where the electrodes are placed and how they are placed; developed for not only standardization, but also consistency so that if the same patient had multiple EEGs the results should be the same" Letters: F, T, C, P, O Distance: 10% or 20% "of total front to back or left to right side of the skull" Evens - right hemisphere Odds - left hemisphere Nasion: depressed area between the eyes Inion: lowest point of the skull ○ Amplitude (height), wave shapes, and frequencies(fast or slow) Waveforms: Beta wave - 13-30 Hz: high frequency, low amplitude, dominant during awake state - "said highest amplitude in class?" Alpha wave - 9-12 Hz: medium frequency, higher amplitude, seen in occipital cortex with eyes closed while awake - "relaxation" Theta wave - 4-8 Hz: low frequency, not predominant in any condition - "GA and children during sleep" Delta wave - 0-4 Hz: very low frequency, low to high amplitude, signifies depressed functions, consistent with deep coma or can be from anesthesia, metabolic factors, or hypoxia ○ EEG Interpretation: An EEG is → a reflection of the brain's wakefulness and metabolic activity A summation of excitatory and inhibitory postsynaptic potentials of pyramidal cells Depression of the EEG → causes by a decrease in blood flow, oxygen, or glucose - "we know if there is a decrease in blood flow the other two are decreased - blood is the carrier" Awake EEG → predominantly beta activity with high frequency and low amplitude waves Hypoxia / Ischemia leads to: ○ Transient increase in beta activity ○ Slow waves (theta) with large amplitude ○ The disappearance of beta activity Delta waves with low amplitude - "remember delta represent suppression" - ischemia ○ EEG States of Awareness ○ Abnormal EEG Patterns Generalized slowing Background slowing, intermittent slowing, continuous slowing "Techs will be looking at the cause of all this" Focal or localized slow activity "Not necessarily predominant / all the way through" More severe patterns Periodic patterns - burst suppression, background suppression, electro-cerebral inactivity (ECI - "periods of pausing / no activity") ○ Ischemia / Hypoxia and EEG Interpretation Continued ischemia / hypoxia can progress to: Suppression of electrical activity → burst suppression Then → complete flat electrical silence = flat EEG Beginning of irreversible brain damage - "longer periods of no brain activity" ○ Burst Suppression What is it? - EEG pattern characterized by periods of high voltage electrical activity alternating with periods of no brain activity Causes: Anesthesia (especially in elderly - "because their metabolism is slower anyways, and then if we give them anesthesia it slows it more") Anesthetic coma - "not GA, medically induced coma" Profound hypothermia (\< 24 degrees) CPB - "because they're cooled" Hypoxic-ischemic trauma / coma Unilateral burst suppression suggests cerebral ischemia - "warrants further investigation" ○ Isoelectric EEG "Very deep coma; the space between a 'dying brain' and a 'dead brain' - used to determine brain death" ○ EEG Recording Most intraoperative machines use 2 or 4 channels "Gold standard" for EEG monitoring → 16 channels or 8 for each hemisphere Rarely done in the OR due to complexity High frequency activity / artifact filtered out - "what they're reporting" Raw EEG → waves then grouped in frequencies ○ Monitoring EEG for Surgical Procedures Carotid artery bypass - X clamp - "you won't see this every time you do these surgeries" Cerebral bypass - ECIC - "if they did studies before hand that circulation was not enough, so they plan to do a shunt to perfuse the brain during this" - "stump pressures in carotid endarterectomies instead of EEG" Cerebral aneurysm AV malformation CPB procedures - "some of the giant aneurysm surgeries they may automatically place the patient on CPB" Deliberate hypotension techniques ○ Anesthesia and the EEG As anesthesia level deepens, EEG waveforms become slower (lower frequency) and taller (higher amplitude) ○ Effects of Medications / Agents on the EEG Most IV drugs and inhalational agents Produce a dose dependent depression of the EEG - "we have to talk to the technician about what medications were using, the MAC/percentage of gas, etc." Can produce burst suppression patterns Propofol → distinct EEG changes Early stages - beta oscillations Deeper levels - synchronous alpha activity What drug is the exception? → "ketamine" Hypothermia → decreases cerebral metabolism → slowing of EEG → burst suppression ○ Anesthetic Effects on the EEG "This is an important slide to look at (below)" Epileptiform activity → sevoflurane High frequency cortical activity Ketamine - "increased high frequency activity - important because the patient may be 'deeper' than way the EEG suggests" Underestimates anesthetic depth\* Non-rapid eye movement sleep pattern Dexmedetomidine ○ EEG as a Monitor of Ischemia - "mostly a monitor of function, but also is a monitor of ischemia" Helps identify brain tissue infarction risk Development of new delta waves during anesthesia maintenance = at risk for ischemia Cerebral ischemic mimics: deep anesthesia, hypothermia, and hypocarbia ★ Monitoring Anesthetic Depth - "what we\'re really monitoring is the effect of the drug or combination of drugs that we're using" ○ Approximated by clinical signs - HR, BP, end tidal anesthetic concentration → not 100% reliable ○ Light anesthesia - risk of recall and awareness - "there are substantiated cases when the patient truly remembers - traumatic (duh)" ○ Deep anesthesia - vasomotor depression, hemodynamic changes ○ Awareness → serious complication with long term sequelae ○ BIS - first FDA approved monitor \< 60 (she has \> 60 on the slide) → decreased incidence of anesthesia awareness ★ Bispectral Index Monitoring ○ How does it work? Uses a computer algorithm to translate raw EEG data into a number range of 0-100 ○ What is the target value for GA? - 40-60 - "at 60 (or lower) there is a low probability of recall" (said twice) ○ As GA level deepens, EEG waves show lower frequency and higher amplitude ○ What drugs cause different reactions on the EEG? ○ 20-30 second lag between EEG measurement and BIS value - why is this important? → "let's say you're chugging along and you're keeping them at 60, because of the lag the patient may be more awake than that - it's important that you know that it's not 100% and to look at other things (NMB, vitals)" ○ Less accurate in children ○ Accuracy impaired by: Hypothermia Encephalopathy Electromyographic interference (e.g. increased and decreased muscle tone) How do NMBDs affect the BIS value? → "independent use of a NMB when a patient was awake it → decreased the BIS values to 40 - so it WILL decrease the BIS" Lacks reproducibility ★ Monitors of Function - Evoked Potentials ○ Sensory evoked potentials - "really just looking at sensory pathway" Time locked, event related, pathway specific EEG activity Generated in response to electrical stimulus or stimuli applied to the median nerve Can be recorded in response to stimulation of any sensory cranial or peripheral nerve Typical peaks and troughs → described by polarity and latency "not that you need to know that, but if you see it on a report" 3 common modalities used in clinical practice: SSEP - somatosensory evoked potentials ○ Monitor the integrity of the sensory pathway from the periphery to the cortex ○ Specifically, the nerve pathways responsible for feeling pressure, touch, temperature, and pain ○ Example of use: spinal cord surgery ("something rod surgeries"), carotid endarterectomy, cerebral aneurysm surgery "May also see in spinal fusions, dorsal \_\_\_\_ (where they are untangling the nerves)" ○ SSEPs can be recorded regardless of anesthetic agent used ○ Anesthetic implications / "Confounding Factors" SSEPs are resistant to the effects of IV agents Sensitive to inhalation agents - including N2O - "doesn't mean you can't use it, lower doses are needed" Inhalation agents cause a dose dependent decrease in amplitude and increase in latency The combination of N2O and inhalational agents should be avoided - why? N2O profoundly depresses the amplitude of SSEPs - "but also it supplements / adds to effect of volatiles" FYI - opioids have a negligible effect What about ketamine? - augments amplitude of SSEPs Best anesthetic technique for SSEP recording: TIVA or low dose inhalational agents of \< 0.1 MAC What medications are best avoided with SSEPs? → "inhalation agents - especially high dose" VEP - visual evoked potentials ○ Profoundly influenced by inhalation agents Potentially recordable under TIVA ○ Difficult to perform ○ Seldom used intraoperatively ○ Possible detection and prevention of perioperative ischemic optic neuropathy - "can be a silent issue that results in blindness" BAEP - brainstem auditory evoked potentials ○ Evoked potential caused by an aural stimulus which originate from relay structures in the brainstem ○ Scalp electrodes record responses to sounds ○ Sounds / clicks → ears to stimulate CN VIII ○ Observed as a reading on the EEG ○ Used in: acoustic neuroma, vertebral basilar aneurysms, other posterior fossa surgery ○ Assesses CN VIII integrity, but can reflect brainstem integrity also ○ Anesthetic Implications / Confounding Factors BAEP is resistant to the influence of anesthetic agents and can be recorded even with high dose inhalation "However in a lot of facilities they still use TIVA" ○ Motor evoked potentials 3 main types: Transcranial magnet MEP Transcranial electric MEP Direct spinal cord stimulation MEPs were originally introduced to complement SSEP recording MEP = an electromyographic potential Recorded over muscles in the hand or foot in response to depolarization of the motor cortex Monitor integrity of motor pathways of brain, spine, aorta Depolarization → achieved with transcranial magnetic or electrical stimulation Spinal cord can be stimulated directly with MEPs 2 approaches: transcranial magnetic and electrical "The only bad thing about this - when using MEPs you can't use NMBs" Anesthetic implications: Anesthetic agents profoundly influence both transcranial magnetic and electrical stimulation ○ Makes the magnetic approach unrecordable during anesthesia TIVA only for recording electrical mode MEPs can not be recorded with neuromuscular blocking agents - why? → "blocks our motor activity / motor pathways" ○ EMG - CNs V, VII, IX, X, XI, XII ○ Interpretation of Evoked Potentials Ischemia / Hypoxia of the nerve leads to: Depression of conduction of evoked potentials Seen as a decreased amplitude and increased latency of the specific peaks Hypothermia = decreased amplitude and increased latency A 50% reduction ("from baseline") in amplitude from baseline in response to surgical stimuli = significant What action should take place in this situation? ○ Technician informs the surgeon ○ Surgeon changes approach to avoid nerve damage A 10% increase in latency of SSEP signals = significant in some centers BAEP - increased latency of \> 2 milliseconds = significant ★ Monitors of Function - Electromyography (Cranial Nerve Function) ○ Operations in the posterior fossa and lower brain stem have a high potential for injury to the cranial nerves 'Also provides nerve root stimulation - makes a noise so they know they are too close" ○ What cranial nerves have motor components? → "3, 4, 5, 6, 7, 9, 10, 11, 12" Don't: 1, 2, and 8 ○ Which ones are motor only? → "3, 4, 6, 11, 12" ○ Monitoring EMG potential for motor CNs Allow for monitoring and recording the integrity of the nerves Protects against damage ★ Neural Nerve Integrity Monitoring with NIM ETTs ○ 2 types of potentials, spontaneous and evoked, can be recorded ○ With spontaneous activity - injury potential can be detected when a surgical instrument gets near the cranial nerve ○ Evoking the nerve with electrical stimulations helps identify and preserve the cranial nerve - NIM ○ During this type of monitoring NMBAs cannot be used ○ "Don't want facial drooping or voice hoarseness if you can help it - this helps prevent that" ○ "Helps prevent injury to laryngeal nerves, particularly RLN - tube captures vocal cord movement → makes a noise" ★ Monitors of CBF / ICP ○ Absolute cerebral blood flow monitors - "real time continuous perfusion" "Correlates flow velocity and flow itself" ○ Relative cerebral blood flow monitors Comparison of flow in an area with the total blood flow Laser doppler flowmetry What is it? - surface doppler probe that measures local CBF Transcranial doppler ultrasonography Limitations: Volume of tissue monitored is limited to 1 mm Requires a burr hole for insertion Use is currently limited ○ ICP monitors ★ Review of CBF: ○ Determined by: Blood viscosity Vessel length Degree of dilation of the blood vessel (radius) ○ Influenced by: CPP Body temperature\* Blood gas content Cardiac output Altitude Autoregulation and flow metabolism coupling Chemical mediators ★ Monitoring of CBF and ICP - Transcranial Doppler (TCD) ○ Measure CBF velocity in the Circle of Willis noninvasively and continuously ○ Intraoperative → middle cerebral artery measured by placing probe over zygomatic arch ○ Qualitative assessment tools for ICP ○ Detects air / particulate emboli ○ TCD Sonography Measures relative changes in CBF Provides qualitative assessment of ICP / CPP Detection of air or emboli Can be used to determine cerebral autoregulation and CO2 reactivity Cannot measure CBF ○ Clinical Intraoperative Indications for Transcranial Doppler Monitoring Carotid endarterectomy - "taking plaque out of the artery - can have microemboli break off" Detection of ischemia and / or microemboli Diagnosis and treatment of postoperative hyperperfusion syndrome - "you can have too much blood flow - hyperemia" Diagnosis and treatment of postoperative intimal flap or thrombosis - "torn piece of tissue flapping" Cardiac surgery Cerebral emboli detection during CPB Cerebral perfusion during CPB TCD monitoring for this purpose is still in evolution and the validity is unclear Closed head injury Can be used to assess autoregulation and diagnose hyperemia and vasospasm May be useful in head injured patients undergoing non-neurosurgical procedures ○ Limitations of TCD in the OR Most monitors are designed as diagnostic tools A fixation device is required → interferes with the procedure and prevents continuous, reliable recording Skill and training is required The successful transmission of ultrasound through the skull is dependent on the thickness of the skull Failure rate: 5-20% ★ Microdialysis Catheters ○ Semi-quantitative technique ○ 20 MHz probe applied directly to the surface of the vessel ○ Allows neurosurgeon to determine vessel patency and flow in the aneurysmal sac-aneurysm repair - "it's really just a surface monitor" ○ Enables sampling and collecting from the interstitial space ○ Includes monitoring of and quantifying neurotransmitters, neuropeptides, hormones, and other molecules in brain interstitial tissue fluid ★ Indocyanine Green Video Angiography ○ Qualitative technique to assess blood flow during aneurysm surgery ○ Complements the microvascular doppler ultrasound ○ Removes need to do intraoperative angiography to determine parent vessel patency and place of clips post op - "mostly done preoperatively" ○ Uses: Spinal surgery involving vascular lesions, aneurysm, and AVM repair EC-IC bypass surgeries ★ Intracranial Pressure Measurement - "more of what were involved in that others" ○ Supratentorial pressures are measured: Lateral ventricle Subarachnoid space over the convexity of the cerebral cortex ○ Remember that intracranial volume consists of: brain tissue, blood volume, and CSF volume ★ Why is Intracranial Pressure Monitoring Important in Neuroanesthesia? ○ Since intracranial components are essentially incompressible → significant increase in ICV → increased ICP "Lots of 'tempering' things we can do like hyperventilate" ○ CPP = MAP - ICP → "range: 70-80 is normal, but it can be a little higher" ○ Helps optimize CPP ○ Allows prompt treatment of increased ICP "Surgical decompression is immediate" ○ Types of ICP monitoring: Ventriculostomy Subarachnoid bolt Epidural sensory Fiberoptic intraparenchymal monitor ★ Monitors of Cerebral Oxygenation / Metabolism ○ When is the monitoring of cerebral oxygenation and metabolism useful? ○ In the setting of TBI → secondary injury → ischemia and hypoxia concerns - "may complicate or be more damaging than the primary injury" ○ Invasive monitoring Brain tissue PO2 - invasive (paratrend, Licox) Noninvasive monitoring Jugular bulb venous oximetry - not widely used in an OR setting Allows continuous or intermittent estimation of global balance between cerebral O2 demand and supply CMRO2 must remain constant for the calculation of the arteriovenous oxygen content can to estimate relative CBF Major limitation = unable to detect focal cerebral ischemia Transcranial cerebral oximetry - NIRS (near infrared spectroscopy) Measures cerebral regional oxygen saturation → chromophobes in the brain Oxyhemoglobin, deoxyhemoglobin, and cytochrome A3 Major limitations are: ○ Inter subject variability ○ Variable optical path length ○ Potential contamination from extracranial blood ○ Lack of definable threshold ★ Monitors Specific to Neuro Anesthesia ○ Precordial Doppler Used to detect presence of VAE in the sitting position Placed after the patient is placed in the operative position Right middle ⅓ sternum - usually 4th ICS RSB but where strongest heart tones are heard Placement test: 0.5 - 1 ml agitated saline is injected through a CVP catheter or peripheral IV Audible sound produced - "mill wheel murmur" Inform surgeon anytime meds are injected ★ Normal Cerebral Parameters ○ Normal CBF: 50 - 65 ml / 100 g / min ○ Normal CMRO2: 3.0 - 3.5 ml O2 / 100 g / min ○ Normal ICP: \< 20 torr ○ What 3 things determine ICP: brain tissue, blood volume, CSF ○ Normal CPP: 80 - 100 torr ("it varies - i don't care as long as it's one of the ones i\'ve said (all \>70)" ★ Critical Cerebral Parameters ○ Critical CBF \< 50 ml / 100 g / min → acidosis \< 40 ml / 100 g / min → impaired protein synthesis \< 30 ml / 100 g / min → edema \< 20 ml / 100 g / min → critical CBF ○ Critical CPP 30 - 40 torr → ischemia \< 25 torr → irreversible brain damage \< 30 torr → critical \*\* ○ Critical PaO2 \< 50 torr ○ Critical PaCO2 \< 20 torr