Neuromonitoring ram gopal final
- 2. Classification of monitoring techniques: Monitors of Intracranial Pressure and Blood Flow Dynamics Intracranial Pressure Monitor Jugular Venous Oximetry Transcranial Doppler Sonography Brain Tissue Oxygen Tension Monitor Near-infrared Spectroscopy Monitors of Brain Electrical Activity Electroencephalography Evoked Potentials Sensory Evoked Potentials Visual Somatosensory Auditory Motor Evoked Potentials
- 4. 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. It is around 2-4 mmHg in neonates and infants.
- 5. Indications for ICPmonitoring 1. Head Injury Sever HI(GCS 3-8) and abnormal CT finding Severe head injury with a normal CT scan if two or more of the following features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, systolic blood pres sure < 90 mmHg. 2. Brain Tumors 3. Subarachnoid Heamorrhage 4. Hydrocephalus 5. Neuromedical conditions : stroke, and encephalitis associated with raised ICP.
- 6. Techniques of ICP monitoring
- 7. Intraventricular Catheter : via ventriculostomy The gold standard for ICP monitoring. The lateral ventricle is cannulated by a frontal, occipital, parieto-occipital or parasagittal coronal approach. The transducer is zeroed at the level of the external auditory meatus. Advantages: a) it is reliable, b) it can be used for measurement of intracranial compliance, c) ventricular catheter can also be used for draining CSF to decrease the ICP. “risks of infection and trauma to the brain during cannulation”
- 8. ICP waveforms Flow of 3 upstrokes in one wave. P1 = (Percussion wave) represents arterial pulsation P2 = (Tidal wave) represents intracranial compliance P3 = (Dicrotic wave) represents venous pulsation In normal ICP waveform P1 should have highest upstroke, P2 in between and P3 should show lowest upstroke. On eyeballing the monitor, if P2 is higher than P1 - it indicates intracranial hypertension
- 9. Icp waveform
- 10. Abnormalities of ICP wave Earliest sign of ↑ ICP – Changes in pulsatile components Prominent P1 wave The systolic BP is too high
- 11. Diminished P1 wave • If the systolic BP is too low, P1 decreases and eventually disappears, leaving only P2. • P2 and P3 are not changed by this Prominent P2 wave The intracranial compliance has decreased The mass lesion is increasing in volume
- 12. Diminished P2 and P3 waves • Hyperventilation Rounded ICP waveform • ICP critically high
- 13. Flat • EVD clogged / kinked • Patient expired
- 14. A WAVES: plateau waves indicate ICP above 40mmHg and are sustained for 5- 20min. Represent severe pathological elevation of ICP caused by changes in regional cerebral blood volume (CBV)
- 15. B WAVES: Amplitude of 20mmHg and occur at the rate of 1-2/min. as warning signs of decreased intracranial compliance and enhanced risk of intracranial hypertension.
- 16. C wave of ICP Seen in normal ICP waveform – nonpathological. Mean wave < 20 mmhg. Represent cyclic variation of SBP.
- 17. Transcranial Doppler Measures the blood flow velocity in major cerebral blood vessles. Examination carried out through the temporal window, orbital foramen or foramen magnum. MCA commonly used. Change in velocity is proportional to change in flow considering the vessel diameter is constant.
- 18. Interpretation ofwaveforms Pulsatality Index = (Peak Systolic Velocity- End Diastolic Velocity) / Mean Velocity
- 19. Clinicalapplications ofTCD 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.
- 20. Intravascular tracercompounds 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.
- 21. Monitoring of cerebral oxygenation and metabloism Brain tissue oxygenation Jugular bulb venous oximetry monitoring Microdialysis catheter Near Infrared Spectroscopy (NIRS)
- 22. Brain tissue oxygen tension monitoring A miniature Clarke’s electrode incorporated into the tip of a catheter. The catheter is placed into the brain tissue through a twist drill hole. 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. Currently under clinical investigation
- 23. Jugular venousoximetry Jugular bulb venous oxygen saturation (Sjvo2) measures the degree of oxygen extraction by the brain and represents the balance between cerebral oxygen supply and demand. The dominant jugular vein (i.e., the right for most patients) drains predominantly cortical venous blood, whereas the contralateral jugular vein drains more of the subcortical regions. Any decrease in CBF must be accompanied by a corresponding decrease in cerebral venous oxygen saturation if CMRO2 is constant.
- 24. Jugular venousoximetry A catheter placed retrograde through the internal jugular vein into the jugular bulb. The tip of the catheter must be placed above the C1-C2 vertebral bodies to avoid contamination with blood coming from the facial vein. Correct positioning of the catheter can be confirmed with a lateral skull x-ray
- 25. Indices obtained fromSjVO2 1. Jugular venous oxygen saturation (SjVO2 ) 2. Cerebral arteriovenous oxygen difference (A- VDO2 ) (the difference between arterial and jugularvenous oxygen content) and 3. Cerebral oxygen extraction(CEO2 ) (the difference between SaO2 and SjVO2 ).
- 27. Near Infra-redSpectroscopy NIRS Based on the principle of absorption of near- infrared light by chromophores in the body like oxyhaemoglobin, deoxyhaemoglobin and cytochrome aa3. Oxygenated hemoglobin, deoxygenated hemoglobin, and cytochrome aa3 have different absorption spectra (650-800 nm). The main advantage of NIRS is that it is a noninvasive method for estimating regional changes in cerebral oxygenation.
- 28. NIRS limitations Its clinical use is limited by an inability to differentiate between intracranial and extracranial changes in blood flow and oxygenation. Currently, there are no studies providing evidence that NIRS use alone can influence outcomes in adult neurocritical care.
- 29. Cerebral Microdialysis A technique for sampling the extracellular space of a tissue. This method is based on the diffusion of water-soluble substances through a semipermeable membrane. Small molecules (<20,000 D) from the extracellular fluid can diffuse across the membrane and enter the perfusate. Conversely, substances that have been added to the perfusate can diffuse across the membrane to gain entry to the tissue. The technique of cerebral microdialysis allows continuous and online monitoring of changes in brain tissue chemistry.
- 30. • The key substances measured by microdialysis can be categorized as follows: 1. Energy-related metabolites (glucose, lactate, pyruvate, adenosine, xanthine) 2. Neurotransmitters (glutamate, aspartate) 3. Markers of tissue damage and inflammation (glycerol)
- 31. Markers: Increase in Lactate/pyruvate ratio onset of ischemia. High level glycerol inadequate energy to maintain cellular integrity membrane breakdown Glutamate neuronal injury
- 32. 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 Function of brain
- 33. EEG
- 34. 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
- 35. 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
- 36. EEG Electrodes placed so that mapping system relates surface head anatomy to underlying brain cortical regions 3 parameters of t Amplitude –size or voltage of signal Frequency –number of times signal oscillates Time –duration of the sampling of the signal
- 37. 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
- 39. 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
- 40. 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. Very deep anesthesia (1.6 MAC): Burst suppression eventually isoelectric. “As the patient loses consciousness with general anesthesia, the brain waves become larger in amplitude and slower in frequency”
- 41. Halothane No
- 42. Non-anestheticFactorsAffectingEEG • 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 Pathophysiol ogic Factors 1. Hypoxemia 2. Hypotension 3. Hypothermia
- 43. Uses ofEEG 1. EEG is a gold-standard for monitoring cerebral ischaemia: during procedures associated with temporary vessel occlusion and during cardioplumonary bypass procedures. 2. In ICU : to monitor seizure activity in patients with status epilepticus under the effect of muscle relaxants. Subclinical seizures causing neurological deterioration may also be diagnosed by EEG. 3. To prognosticate the outcome of coma. 4. It is also an ancillary tool for confirmation of brain death. 5. To quantify the depth of anaesthesia. These include bispectral index and approximate entropy
- 45. Entropy
- 46. Evoked potential EVOKED POTENTIALS Evoked potentials are the electrical responses generated in the nervous system in response to a stimulus. The evoked responses are recorded from surface electrodes placed on scalp, over the spine or in the epidural space. They have much lower amplitude than the normal EEG activity. Because of their low amplitude, they are very difficult to record.
- 47. Evoked potentials of all types (sensory or motor) are described in terms of latency and amplitude. Latency is defined as the time measured from the application of the stimulus to the onset or peak (depending on convention used) of the response. The amplitude is simply the voltage of the recorded response.
- 48. Clinically significant of evoked potential Decreases in amplitude of 50% or more from baseline associated with a less than 10% prolongation in latency as clinically significant SER changes. Intraoperative changes in evoked responses, such as decreased amplitude, increased latency, or complete loss of the waveform, may result from surgical misdeed, such as retractor placement or ischemia. They may also reflect systemic changes, such as changes in the anesthetic drugs or doses, temperature, or hypoperfusion.
- 49. Sensory-Evoked Responses(SERs) SERs are electrical CNS responses to electrical, auditory, or visual stimuli. SERs are produced by stimulating a sensory system and recording the resulting electrical responses at various sites along the sensory pathway up to and including the cerebral cortex. It include: Somatosensory EP Visual EP Brain stem auditory EP
- 50. Somatosensory-Evoked Potentials SSEPs are recorded after electrical stimulation of a peripheral mixed nerve. Responses may be recorded from electrodes placed on scalp or over the spine. The common sites of stimulation include the median nerve at the wrist, the common peroneal nerve at the knee, and the posterior tibial nerve at the ankle.
- 51. Dorsal root ganglia Posterior dorsal column Medial lemiscus Contralateral thalamus Frontoparietal somatosensory cortex
- 52. Indications forSSEP 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
- 53. Limitations Motor tracts not directly monitored Posterior spinal arteries supply dorsal columns (sensory tract) Anterior spinal arteries supply anterior (motor tracts) so injury to anterior spinal arteries goes undetected. Possible to have significant motor deficit postoperatively despite normal SSEPs
- 54. Brainstem Auditory-Evoked Potentials Auditory evoked potentials are generated in response to stimulation of the tympanic membrane by audible clicks. Reflects the VIII nerve & brainstem“well-being”. useful for surgical procedures in the posterior fossa that risk hearing or structures in the upper medulla, pons, and midbrain. Most resistant to anesthetic drugs
- 55. Visual-Evoked Potentials Visual evoked potentials are generated in response to photic stimulation of the retina by flashes of light from light-emitting diodes. VEPs are the least commonly used evoked response monitoring technique intraoperatively. Most useful for testing for optic nerve function.
- 56. Effect of physiologic variables on evoked potentials Cerebral Blood Flow: Sensory evoked potentials are normal upto a CBF value of 20 mL100g–1/min. They start deteriorating when CBF decreases to 18-13 ml/100g/min. Evoked potentials cannot be obtained when CBF is below 10- 12 mL100g/min. Systemic Blood Pressure: Hypotension prolongs the conduction in the central nervous system thereby increasing the latencies of various peaks. Intracranial Pressure : Raised ICP has been shown to result in an increase in the latency and a decrease in the amplitude
- 57. Oxygen Tension: Deterioration of evoked potentials decreases to less than 40 mmHg. Haematocrit: Latencies of VEP and SSEP are increased at a haematoctrit of 10-15%. Their amplitude is decreased when the haematoctrit is less than 10%. Carbon Dioxide Tension: Extreme hypocapnia (PaCO2 < 25 mmHg) causes deterioration of evoked potentials. Temperature: Hypothermia increases the latency.
- 58. Effects of anaesthetics on evoked potentials Most anaesthetics decrease the amplitude and increase the latencies of the various peaks. Brainstem and spinal potentials are least affected. The effects of anaesthetics on evoked potentials are dose-related.
- 60. Motor EvokedPotentials Evoked responses generated by transcranial stimulation of the motor cortex. Responses to transcranial stimulation can be recorded in the epidural space, over the peripheral nerves or from evoked muscle activity(compound muscle action potentials, CAMP). Are often use in conjunction with SSEPs to assess spinal cord function during surgery. While SSEP evaluates the ascending sensory pathway mediated through the posterior spinal cord (dorsal column), TcMEP evaluates the anterior portion of the cord or descending motor pathways
- 61. • The stimulation may be electric (transcranial electric motor evoked potentials, tcEMEP) or magnetic (transcranial magnetic motor evoked potentials, tcMMEP). • Anaesthetics may have significant effects on motor evoked responses. Even low concentrations of inhalational anaesthetics may depress CMAP recording
- 63. References Millers anesthesia 8th edition Neurological monitoring. Dr. G S Rao IJA 2002;46(4) 2017 Textbook of Critical Care, 7e 39