Neuro Monitoring & Complications Flashcards

1
Q

What is the purpose of Neuromonitoring?

A

Way to protect nerves during surgeries with increased risk of injury potential.
-Electroencepholagram
-Motor Evoked Potentials
-Somatosensory evoked potentials
-Electromyography
-Brainstem Auditory Evoked Potentials
-Visual Evoked potentials

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2
Q

What are the effects of anesthesia on EEG?

A

-Most anesthetics inhibit neuronal activity
-EEG requires 50% of the total oxygen consumed in the brain
-Changes in EEG patterns are similar with ischemia and deep anesthesia
-Baseline EEG, repeat after induction and before surgery start
-Communication with NM tech about changes in anesthetic depth to eliminate false positive EEG patterns
-Drug induced burst suppression can be cerebral protective
-Volatile anesthetics are dose dependent in how they reduce CMRO2
-Used for supratentorial tumors, aneurysms, Carotid, surgeries on aorta

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3
Q

What do Somatosensory Evoked Potentials monitor?

A

Monitor the function of the brain and spinal cord during certain surgeries.
-Evoked means the neuro monitor tech gives a stimulus to check recordings
-Do not make abrupt changes in anesthetic during periods of risk.
-Good communication is critical with Monitoring technician.

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4
Q

Describe Anesthetic Management during SSEPs?

A

-Inhalation agents can decrease amplitude and increase latency of EPs.
-Use 0.5 MAC isoflurane and then TIVA. Any more than that will affect neuromonitoring.
-No abrupt changes in anesthetic. Communicate with NM tech.

Nagelhout:
-Volatile anesthetics and N2O depress the SSEP waveform in a dose-dependent manner. Avoiding abrupt changes in inhaled gas concentration and bolus injection of hypnotic drugs during periods of risk minimizes difficulties in determining whether waveform changes are due to surgical manipulation. Furthermore, a concentration of less than 1 MAC of volatile anesthetics is recommended when monitoring SSEPs.

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5
Q

What surgeries use neuromonitoring?

A

-Surgeries involving the spine, repair of intracranial aneurysm, craniotomy for tumors

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6
Q

What will alter the SSEP reading?

A

If there is posterior cord or brain ischemia- transmission of action potentials through the posterior cord and brain is diminished, thereby reducing the intensity and delaying the arrival of the action potential that reaches the cerebral cortex.
-The SSEP reading will be altered.
(!!!)

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7
Q

Which spinal tract is measured by SSEPs?

A

-Cuneatus and Gracilis Tracts (Touch, pressure, Vibration)
-Posterior Dorsal Cord
-Integrity of this area/tracts assessed by SSEP Monitoring
-Remember SAD=sensory/afferent/dorsal
-Tibial nerve stimulated: Carried up on the ipsilateral side of cord until they cross over in brainstem to the contralateral thalamus up to primary cerebral cortex where Cuneatus and Gracilis tracts lie.
-Direct Route! Early peak of the wave. Recording leads are over these tracts.

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8
Q

What is the Indirect Route monitored by SSEPs?

A

-Reticular activating system is considered the Indirect route.
-When it goes through this tract it spreads throughout the cortex.
-All recording electrodes can pick up.
-Anesthesia effects the Reticular activating System.
-This is the system that keeps you awake.
-Coma is the complete loss of the Reticular Activating System.
-Seen as the Late peak of the wave.

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9
Q

What do Motor Evoked Potentials monitor?

A

-Assess anterior lateral spinal cord containing the corticospinal tract
-Useful during surgeries that could have compromise to anterior cord, spine cases, aneurysm repair, thoracoabdominal repairs

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10
Q

What is Anesthetic Management of Motor Evoked Potentials?

A

-Avoid Muscle Relaxants
-TIVA is the best
-Avoid high MAC of volatile. Discuss with Neuro monitor tech.
-0.5 MAC is usually okay
-Always get a baseline before surgery.
-If you use MR for induction they will want to know when it’s worn off so they can run a set of baseline motors before surgery

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11
Q

How do we monitor SSEPs?

A

-Stimulus given through the tibial, ulnar or median nerve usually bilaterally. Tiny needles that are taped in place.
-The critical recording electrodes are placed midline to record tibial nerve evoked potentials and laterally for ulnar and median nerve evoked potentials.
-Sensory evoked potentials: the stimulating electrodes are placed peripherally and detecting electrodes are placed centrally.
-Remember the homunculus? The toes, feet, leg are in the longitudinal fissure. In the center of the brain. That’s where the primary electrode for measuring if you stimulate the tibial nerve.
-If the median/ulnar nerve is stimulated, the primary electrode for recording is on the lateral side.

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12
Q

What is the major reason for monitoring SSEPs?

A

To detect Ischemia (!!)

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13
Q

What is Latency?

A

The time it takes for the action potential to traverse the peripheral nerves, cord and inner brain and cerebral cortex.

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14
Q

What is Amplitude?

A

Magnitude or size of the evoked potential.

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15
Q

What changes in Amplitude and Latency indicate ischemia?

A

-50% decrease in Amplitude
-10% increase in Latency

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16
Q

If during spine surgery the SSEP decreases and the latency increases where is the damage happening in the spinal cord?

A

Posterior Cord

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17
Q

How sensitive are SSEPs to anesthetics?

A

Somewhat Sensitive

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18
Q

What is Electromyography (EMG)?

A

Continuous assessment of cranial and peripheral nerves, not a measure of ischemia.
-No Muscle Relaxants.
-Otherwise, anesthesia has no effect
-Ex: Nims tube for thyroid, ACDF, acoustic neuroma or any surgery that could damage facial nerves

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19
Q

What do Brainstem Auditory (BAEP) monitor?

A

-Auditory pathway CN VIII
-Clicks in the ear, used in peds for diagnosing hearing issues
-Used in acoustic neuroma surgery,
-B = barely sensitive to anesthetics

20
Q

What do Visual (VEP)s monitor?

A

-Cranial nerve II- difficult to obtain
-Very sensitive to anesthetics
-Pituitary , retro-orbital or occipital lesions

21
Q

How does Hydrocephalus occur?

A

-CSF is made in the choroid plexus.
-CSF is made in the lateral, 3rd, and 4th ventricles.
-All 4 ventricles are connected by narrow passages. If there is a blockage in one of the passages or in the flow of CSF, it will accumulate in the ventricles and enlarge them.
-Enlarged ventricles push the brain against the rigid cranium and can cause an increase in intracranial pressure.
-CSF then flows to the subarachnoid space, creating a fluid cushion around the brain and spinal cord.
-It is then reabsorbed multiple times a day and the process continues.
-When there is an issue in any of these steps and pressure or volume is increased, it is called hydrocephalus.

-Congenital issues: Arnold-chiari malformation, Dandy Walker Syndrome.

22
Q

What is Normal Pressure Hydrocephalus?

A

-There is still an accumulation of CSF.
-However, it does not cause an increase in Intracranial pressure.
-However, there is a triad of symptoms first named by a Dr. Hakims in 1964:
1) disturbance in gait
2) confusion or dementia
3) impaired bladder control

23
Q

What is Non-Communicating Hydrocephalus?

A

There is a blockage somewhere.
-One of the most common causes is a narrowing of the aqueduct of Sylvius, mass occupying tumors, blood clots in the drainage system, inflammatory conditions like meningitis, encephalitis.

24
Q

What is Communicating Hydrocephalus?

A

There is no blockage found.
-There is inadequate reabsorption of CSF.
-Often there is thickening of the arachnoid around the base of the brain.
-These patients can also get a shunt to help with volume of CSF.

25
Q

What is the treatment for Hydrocephalus?

A

Shunt procedure:
-Diversion procedure used to drain CSF from one or both lateral ventricles or the 4th ventricle.
-Pt will be in supine position with head turned and a burr hole drilled to place the catheter.
-The catheters have a one- way valve that is set to a predetermined pressure for drainage.

-VA shunt-drains into right atrium via the IJ or EJ. Higher incidence of venous air embolism.
-VP shunt- Ventricular Peritoneal (VP) shunt more common

26
Q

What is the Anesthetic Management of a Shunt procedure?

A

-If Emergent: treat as if they have increased ICP
-Stable or revision?
-GETA and table turned 90 degrees.
-In the VP shunt the whole body may be exposed. Warm blankets/air warmer needed
-Tunneling the catheter is very stimulating.
-Increase your anesthetic with short acting anesthesia. After tunneling they will close incisions and be done with the case!

27
Q

What is Benign Intracranial Hypertension?

A

Pseudotumor Cerebri: >20 mmHg ICP, visual disturbances, and Headaches.
-No tumors, no masses, normal CSF, asymptomatic
-May require a drain or spinal tap to pull off CSF 20-40 mL
-NO EPIDURAL ANESTHESIA (due to high volume of anesthetic needed for epidural anesthesia)

28
Q

What is a Cerebral Aneurysm?

A

-Abnormal dilations of cerebral arteries. High flow low resistance
-Occur anywhere in Circle of Willis, most of the time in the middle cerebral system.
-Aneurysms develop ~35-60 years old.
-Median age for rupture is 50 years old
-First choice of treatment is neuro interventional radiology for coiling or clipping

29
Q

What is the number one cause of subarachnoid hemorrhage?

A

Rupture of a Cerebral Aneurysm.
-80% of SAH are from
a ruptured aneurysm.

30
Q

What is an Epidural Hemorrhage?

A

-Emergency!
-If Arterial: middle meningeal artery
-Trauma to skull- common in temporal region.
-If Venous: usually from fractured skull- common in peds
-loss of consciousness, period of lucidity, then deterioration

31
Q

What is a Subdural Hemorrhage?

A

-Bleeding in arachnoid space-blood vessels are torn. -Common in elderly because of brain shrinkage and stretching of vessels.
-Blunt trauma or can happen spontaneously.

32
Q

What is a Subarachnoid Hemorrhage?

A

Traumatic or nontraumatic, from aneurysm or arteriovenous malformation
-Worst headache of life! Dizzy n/v, diplopia

33
Q

What is an Intraparenchymal Hemorrhage?

A

Bleeding into the brain tissue itself.
-AVM, tumor, coagulopathy, cerebral vascular disease, hemorrhagic stroke
-Stroke symptoms

34
Q

What are the Cardio-pulmonary S/Sx of Intracranial Hemorrhage?

A

-Arrhythmias
-Changes in EKG: ST changes, presence of U wave, prolongation of QT interval
-hypertension
-pneumonia
-neurogenic pulmonary edema
-atelectasis

35
Q

What are the Metabolic S/Sx of Intracranial Hemorrhage?

A

SIADH
DI
Hyperthermia
Cerebral edema
Coagulopathies

36
Q

What are the Neurologic S/Sx of Intracranial Hemorrhage?

A

Headache
Decreased LOC
Vasospasm with cerebral ischemia and cerebral edema

37
Q

What is the Treatment for Intracranial Hemorrhage?

A

-Interventional Radiology- coiling or occlusion of arteries is preferred treatment
-Surgical clipping and Evaluation
-Watch and Wait: Depends on the underlying cause/size (Ex: Subdurals)

38
Q

How should you control BP with Intracranial Hemorrhage?

A

Patients are usually hypertensive.
-Low Blood pressure: prevent rupture until clipping.
-Risk: hypoperfusion
-Normotensive or slightly high to maintain perfusion: 120-150 systolic
-Esmolol, nicardipine, neo drips, lebatolol IVP readily available
-Blood available or in room

39
Q

What are complications associated with Intracranial Hemorrhage?

A

-Stroke with deficits
-Bleeding/ rebleeding
-Seizures and Death
-Vasospasm

40
Q

What is the timeline for Vasospasm occurrence and peak?

A

Vasospasm in 4-12 days and peaks day 6-7

41
Q

What is Anesthetic Mgmt of Neuro Angio Embolization and Coiling?

A

Used for Vascular lesions and tumors- stop blood supply

Anesthetic management:
-Avoiding rupture (hemodynamic, ICP control and blood pressure control.
-Should be able to drop BP fast if there is rupture
-During surgery you want to maintain CPP, decrease CMRO2
-Minimizing cerebral edema
-Art line, big bore IV’s
-Blood in room or available

42
Q

What is Vasospasm?

A

Vasospasm is contraction of a vessel or group of vessels that cause prolonged decrease in blood flow and ischemia.
-Peak time is day 6-7.
-Major cause of morbidity and mortality
-Interventional NeuroRadiology- inject papaverine into spasm
-Transcranial doppler and brain tissue oxygen monitoring to guide therapy
-If inadequate response to Nimodipine: Triple H therapy (Hypervolemia, hemodilution and hypertension)

43
Q

What is the Treatment for Vasospasm?

A

Prevention and Treatment with Nimodipine.
-This is only Calcium Channel Blocker proven to decrease morbidity and mortality

44
Q

What is an Arterial-Vein Malformation?

A

-AVM are a connection from artery to vein without a capillary bed
-Large changes in pressure which may lead to rupture, seizures, deficits
-May be dealt with in angiography with embolization or surgically

45
Q

What are considerations for Post-removal or Correction of an AVM?

A

-Surrounding blood vessels may chronically dilate for perfusion and now they can experience flows and pressures they aren’t used to.
-Post hyperemia can lead to cerebral edema
-Careful blood pressure control.
-Lebatolol, esmolol, lidocaine to blunt coughing
-Smooth induction/emergence.
-No coughing. Deep extubation. Suction. Can spray cords with lidocaine.