THE TIVA TRAIN - SOFA Foundation1 -10 mcgs/kg/hr (discontinue 45 to 60 mins before emergence...

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THE TIVA TRAIN Natania Axe,CRNA, MSN, BSN Holy Spirit Hospital Geisinger Affiliate Talk Rely Anticipate I ntervention Neuromonitoring Team

Transcript of THE TIVA TRAIN - SOFA Foundation1 -10 mcgs/kg/hr (discontinue 45 to 60 mins before emergence...

Page 1: THE TIVA TRAIN - SOFA Foundation1 -10 mcgs/kg/hr (discontinue 45 to 60 mins before emergence Remifential 0.1-0.5 mcg/kg/min Alfential Sufential 0.2 – 1 mcg/kg/hr (discontinue 45

THE TIVA TRAIN

Natania Axe,CRNA, MSN, BSN

Holy Spirit Hospital

Geisinger Affiliate

Talk

Rely

Anticipate

Intervention

Neuromonitoring Team

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WHAT IS TIVA

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TIVA

The exclusive use of IV

anesthetics to provide general

anesthesia.

General Anesthesia

Utilized

Hospitals settings

Ambulatory settings

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WHY A TRAIN?

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Define and describe TIVA( Total Intravenous Anesthesia) and IOM (Intraoperative

monitoring)

Identify the types of patients and/or surgeries where TIVA is indicated and IOM is

appropriate.

Discuss the advantages and disadvantages of TIVA

List the different types of TIVA regimens and their affects on IOM

Examine physiologic & pharmacologic factors that affect evoked potentials

focusing on MEPs and SSEPs.

Distinguish between physiologic & pharmacologic influences intraoperatively that

can effect evoked potentials.

Explain the importance of establishing collaboration between the surgeon,

anesthesia, and neurophyisologists to provide safe patient outcomes.

Objectives

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THE

PERSPECTIVES

• The Surgeon

• The neurophysiologist

• Anesthesia

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TIVA

A SURGEON’S PERSPECTIVE

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CLINICAL SETTING

Operating room:

Neurosurgery

Orthopedic surgery

Otolaryngology (ENT) surgery

Cardiothoracic/ Vascular surgery

Interventional Radiology (INR) surgery

Diagnostic laboratories

Nerve conduction studies

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CASE BREAKDOWN

Neurosurgery – 30%

INR – 12%

Orthopedic – 33%

Cardiothoracic/ vascular – 25%

ENT – 11%

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COMMONLY MONITORED

NEUROSURGERIES

Spinal decompressions and fusion (anterior/ posterior)

Chiari malformation decompression

Cranial base tumors

Posterior fossa tumors

Microvascular decompressions

CN VIII resection

Brachial plexus/ peripheral nerve repair

Intercranial aneurysms/ arteriovenous malformations

Spinal tumors

Spinal cord untethering

Selective dorsal root rhizotomy

Epilepsy localization and mapping

Fronto-temporal tumors

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COMMONLY MONITORED

ORTHOPEDIC SURGERIES

Instrumentation for spinal instability

Scoliosis correction

Pelvic hip arthroplasty

Spinal decompression/ fusion (anterior/ posterior)

Stabilization of odontoid/ dens fractures

Peripheral joint procedures

Heterotrophic ossification of the hip

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THE PATH FOR TIVA

The Main Stakeholder in the

Decision: Depends on what the

surgeon ultimately want or need to

perform the case.

Which Monitoring option is the most

desirable?

Spine cord integrity: sseps meps

Peripheral Nerve roots intact (EMG)

Pedicle screw

Location of surgery

Patient’s baseline (preposition

baselines)

Surgeons comfort: Safety net

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MAIN CONCERNS WITH TIVA

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THE NEUROPHYSIOLOGIST’S PERSPECTIVE

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Neurophysiological monitoring: any measure

that is used to assess the functional integrity

of the peripheral or central nervous system

either in the operating room, the intensive

care unit, or other acute care setting.

American Society of Neurophysiological

Monitoring (ASNM)

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1. Identify neural

injury

immediately

2. Define the nature

of the injury

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END GOAL:

IONM can reduce the

incidence of iatrogenic

(provider induced) and

idiopathic (randomly

induced) neurological

injuries to patients during

surgical procedures

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MOST FREQUENT

MONITORING MODALITIES

UTILIZED IN SPINAL SURGERIES

Somatosensory Evoked Potentials (SSEPs)

Motor Evoked Potentials (MEPs)

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WHAT ARE EVOKED POTENTIALS?

Evoked Potentials(Eps):

Electrophysiologic responses of the

nervous system to sensory or motor

stimulation

Stimulating leads to transmission of neural

signals so they can be recorded as EPs

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Latency

The time that elapses between a

stimulus and the response to it

measured in milliseconds

Amplitude The power of a signal. The greater

the amplitude, the greater the

energy carried

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SOMATOSENSORY EVOKED POTENTIAL

(SSEP) MONITORING

Primary sensory

pathway – Dorsal

Column Pathway

Sensory pathways are

ASCENDING. They

bring information from

the outside into the

nervous system

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SSEP PERIPHERAL STIMULATION

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Problem with SSEP monitoring:

When monitoring Dorsal

Column pathway only, no

information is gathered about

Lateral Cortical Spinal tract

and other anterior pathways

TCMEP testing provides that

information

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MOTOR EVOKED POTENTIALS

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Anatomy Primer: Transcranial

Motor Evoked Potentials

(TcMEPs)

Primary motor pathway –

corticospinal pathway

Motor pathways are

DESCENDING. They carry

information from the motor

cortex to the muscles on the

periphery

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MOTOR EVOKED POTENTIALS

Advantages

Time required for one stimulation is

very brief

Meaningful information

Information can be updated

multiple times during critical portion

of the operation

EMG

Disadvantages NMB must be minimized or avoided

Stimulation will produce movement of limb and axial muscles

Cerebral hemisphere stimulation

Activates masseter muscles

Tongue laceration, tooth fracture, mandible fracture

Contraindicated: epilepsy, cortical lesions, skull defects, increased ICP, surgically implanted intracranial devices, cardiac pacemakers or other implanted pumps

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WHAT IS SIGNIFICANT CHANGE?

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PHYSIOLOGIC EFFECTS ON

NEUROMONITORING

Altered temperature:

Hypothermia: Increase latency , decrease amplitude

Hyperthermia: Decrease amplitude by up to 15% and SEPs are

lost at 42C

Hypotension: Decrease in amplitude

Hypoxia: Decrease in amplitude

Hypocarbia: ETCO2</= 25 mmHg latency increases

Hemodilution: Isovolemic hemodilution latency increase with

hematocrit < 15% and amplitude decrease with hematocrit <7%

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PATIENT POSITIONING EFFECTS

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ADDITIONAL EP MODALITIES : EMGS

VERSUS EEGS

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EMGS : ELECTROMYOGRAPHIC

ACTIVITY

Free-run and

stimulated EMG

When peripheral nerves or

roots are at risk for

potential injury

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Electroencephalography (EEG): is the measurement of electrical activity produced by the cortex as recorded from electrodes placed on the scalp EEG is limited by the recording depth of the electrodes; usually only sensitive to electrical activity on the surface of the cortex

Electroencephalograpy

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Electroencephalography (EEG)

Helpful for any cases in which the brain is at risk

Perfusion, metabolism, epilepsy

Passive Recording

subdermal scalp electrodes (extracranial)

direct cortical strips (intracranial)

Measures significant changes in waveform

patterns

Frequency

Amplitude

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TIVA TRAIN: THE ANESTHETIC

CONSIDERATIONS

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Communication

Key to success

1. Proposed operative procedure

2. Determine what forms of IOM will employed

3.Choose an anesthetic approach

4. Have understanding of the affect of your

anesthetic recipe on IOM

5.Maintain an constant concentration

6. Be cognizant of physiologic & pharmacologic

influences intraoperatively that can effect

evoked potentials

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GENERAL ANESTHESIA

TOTAL INTRAVENOUS

ANESTHESIA

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FALSE POSITVE: PERSISTENT

LOSS OF 90% OR GREATER

OF THE AMPLITUDE OF TCE-

MEPS

0%

5%

10%

15%

20%

25%

Total Preop motor

deficit

No Preop motor

deficit

Rates of False Positive Tce-MEP Changes

Inhalational Vs. TIVA

Inhaled TIVA

The Spine Journal 2013:

Differential rates of false-

positive findings in

transcranial electric motor

evoked potential

monitoring when using

inhalational anesthesia

versus total intravenous

anesthesia during spine

surgeries

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Fentanyl

Morphine

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THE PRINCIPLES OF TIVA

Plasma Drug concentration has to be reached quickly

and maintained

A loading dose based on volume of distribution and

the initial plasma drug concentration

Following initial administration the drug is both

redistributed to tissues and eliminated

To maintain desired plasma drug concentration a

constant rate infusion(CRI) is initiated

There will be variation to the response of CRI

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THE TIVA STARTING

POINT

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Indication Induction/Initiation Maintenance

General Anesthesia

(healthy <55 yrs)

2-2.5mg/kg (40 mg

every 10 sec until onset)

100-200 mcgs/kg/min

(intermittent bolus

increments of 20-50 mg

needed)

General Anesthesia

(elderly, debilitated,

ASA III/IV)

1-1.5 mg/kg (20 every

10 sec until onset)

50-100 mcgs/kg/min

General Anesthesia

(Pediatric >3yrs)

2.5-3.5 mg/kg over 20-

30 sec

200-300 mcgs/kg/min

(1st 30 mins) 125-150

mcgs/kg/min

(remainder)

General Anesthesia

(cardiac)

0.5-1.5mg/kg (a slow

rate of approx. 20 mg

every 10 sec until onset;

avoid rapid bolus

inductions)

Primary propofol

injection w/ secondary

opioid:100-150

mcgs/kg/min

Low dose propofol

injection w/ primary

opioid: 50-100

mcgs/kg/min (no bolus)

General Anesthesia

(neuro)

1-2 mg/kg (20 mg every

10 sec until onset)

100-200 mcgs/kg/min

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NARCOTICS

Fentanyl

1 -10 mcgs/kg/hr (discontinue 45 to 60 mins before emergence

Remifential

0.1-0.5 mcg/kg/min

Alfential

Sufential

0.2 – 1 mcg/kg/hr (discontinue 45 to 60 mins before emergence)

Long Acting narcotics

Morphine

Diladid

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TOD B SLOAN

MBA, MD, PHD

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MONITORING SSEP WHEN A REDUCTION OR

ELIMINATION OF THE INHALATIONAL

AGENTS IS NEEDED

Induction: As usual (with sux or short acting NDMB)

Maintenance: propofol infusion 100-200 mcg/kg/min

Long Acting Opioid: usual up front administration (Morphine 5 to 10mg bolus before incision or Dilaudid 1-2 mg)

Opioid Infusion: Sufentanil 0.2-0.3 mcg/kg/hr; Fentanyl 4-5 mcg/kg/hr )(turn off 30-45 mins before emergence) , or remifentanil 0.2-0.3 mgs/kg/min

: NMB: As needed

Optional: if SSEP remains too small for monitoring: Ketamine infusion (.25-.5 mg/kg/hr)

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ANESTHESIA FOR SPINAL SURGERY

WITH MEP & EMG

Induction: As usual (preferable propofol since followed by infusion)

Pure TIVA: propofol infusion titrate to anes. Depth (100-200 mcg/kg/min).

Long Acting : usual up front administration (Morphine 5 to 10mg bolus

before incision or Dilaudid 1-2 mg)

Opioid Infusion: Sufentanil 0.2-0.3 mcg/kg/hr; Fentanyl 4-5 mcg/kg/hr )(turn

off 30-45 mins before emergence) , or remifentanil 0.2-0.3 mgs/kg/min

Options: Dexmeditomidine (0.2-0.3 mcg/kg/hr with propofol (starting at 100

mcg/kg/min OR Ketamine (0.25-0.5 mg/kg/hr) with propofol 100-150

mcg/kg/min.

No NMBs

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ALTERNATIVES TO PROPOFOL OR

ADJUNCTS

Ketamine

Etomidate

Dexmeditomidate

Lidiocaine

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KETAMINE ALTERNATIVE TO PROPOFOL

Drug Administration Infusion Bolus Dose

Midazolam Premed 2-4 mg

Ketamine Induction 1-2 mg/KG

Ketamine Maintenance 0.5-1/KG/HR 0.5-1mg/kg

Midazolam Maintenance 1-2 mg per HR

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PROPOFOL/KETAMINE TIVA

Drug Administration Infusion Bolus

Midazolam premed/ intraop 2-4mg

Fentanyl Premed 50-

100mcgs

25-50mcgs

Ketamine 0.25-0.5 mg/kg/hr 0.5 mg/kg/hr

Propofol Start 140-200

mcgs/kg/min

At 10 min: 100-

120 mgs/kg/min

After 2 hours 80-

120 mcgs/kg/min

**Ketamine Propofol Mix: 2mg of ketamine per 1 mL of Propofol; taper off

depending on length of case.

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KETAMINE

Advantages

Enhancing SSEP and MEP amplitudes

Meets anesthetic requirement : loss of consciousness an analgesia

Disadvantages

Elevate cerebral blood flow : contraindicated in pts with increase ICP

Postop Hallucinations( more common in adults then in pediatrics or geriatric patients

Emergence delirium

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ETOMIDATE INFUSION

Ultra short acting IV agent

No structural relationship to other IV

anesthetics, but MOA similar to

propofol

Minimal cardiac depression,

respiratory depression

Penetrates BBB quickly; reaches

peak levels after 30-60 seconds

Redistributes quickly and

metabolizes rapidly

Hemodynamic and CV stability,

lower cerebral blood flow, cerebral

metabolic rate for oxygen and ICP

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INITIAL GUIDELINE FOR ETOMIDATE

INFUSION DURING SPINE SURGERY

Drug Administration Infusion Bolus

Midazolam Premed 2-4mg

Etomidate Induction 0.2-0.3mg/KG

Etomidate Additional Load Total 0.5 mg/KG

Etomidate Maintenance 0.6 mg/KG/HR

Midazolam Maintenance 1-2 mg per HR

Remifentanil Maintenance 0.2-0.3mcgs/KG/Min

Decadron Loading Dose 10 mg

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ETOMIDATE INFUSION

Facilitate the inhibitory effects of GABA

Smaller doses cause cortical excitatory reaction can present as EEG spikes at induction, Increase SSEP and MEP amplitudes or epileptiform activity on EEG in pts with seizure history

Advantage:

no hypotension

EEG patterns marked delta waves, higher theta than with propofol and prominent alpha activity and minimal beta: easier to monitor anesthetic depth

Disadvantage:

No analgesic properties

Pain with injection

Myoclonus

Epileptiform activity in pts with sz hx

Occasional delirium

N/V

Depressed cortisol production

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DEXMEDITOMIDINE

Effects on Eps:

Suggested therapeutic levels: (0.5-0.7 mcgs/kg/hr)(compromises MEPs but

not SSEP amplitudes

With low dose Propofol 50-75mcgs/kg/min dexmeditomidine at (<0.35

mcgs/kg/hr) MEPs amplitudes not degraded

Anesthesia Regimen:

Further investigation as a propofol alternative

ICU “opioid sparing effect” for Anesthesia Opioids infusion required and

opioid boluses may be necessary

S/E: hypotension and bradycardia r/t sympatholytic properties

Contraindicated: poor cardiac reserve or heavily dependent on intact

sympathetic system

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LIDOCAINE INFUSION

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The Effects of Anesthetic

on SSEPs and MEPs (The overview)

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Agent SSEP Amplitude MEP Amplitude Comments

Propofol Decrease Decrease SSEP & MEP

usually recorded

at anesthetic

doses but MEP

may be lost at

high doses

Opioids Minimal Minimal SSEP & MEP

usually recorded

even at high

doses

Etomidate Increase at low

doses-decrease

at higher doses

Increase at low

doses- Decrease

at higher doses

Enhancement of

SSEP & MEP seen

at low doses,

depression at

very high doses

Ketamine Minimal, increase

at low doses

Minimal, increase

at low doses

Enhancement

SSEP & MEP seen

at low doses

Shils JL, Sloan TB. Intraoperative neuromonitioring. Int Anesthesiology Clin 2015;

53:53.

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Agent SSEP Amplitude MEP Amplitude Comments

Benzodiazepines Minimal at low

doses

Minimal at low

doses, prolonged

decrease at

higher doses

SSEP & MEP usually

recorded with small

doses for amnesia

Dexmedetomidine Minimal Minimal-decrease

at higher doses

SSEP & MEP usually

recorded at low doses

but MEP lost at higher

doses

Lidocaine Minimal Minimal Can be used as

intravenous

supplement in SSEP &

MEP

Shils JL, Sloan TB. Intraoperative neuromonitioring. Int Anesthesiology Clin 2015;

53;53

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NOVEL AGENTS

Carboetomidate

Fospropofol

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BENEFITS OF TIVA

Decreased PONV

IOM can be utilized; less interference with SSEP, MEP

Decrease Pollution to environment

Avoid vasodilatation, expansion of gas cavities

Occupational exposure

Avoid MH risk

Smooth emergence, less hangover

Cost Benefit

Improved surgical field (bleeding)

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DISADVANTAGE OF TIVA

Not the ideal technique

May require additional

personnel like IOM

Level of practitioner

Hypotension

Controlled substance

accounting

Set-up and use greater

workload than vaporizers

Fluid management

Blood loss

Gag reflex intact

Dependent of IV for immobility

Opioid side effects: biliary, muscle

rigidity, GI motility, pruritus

Adverse events if IV line disrupted

Depth of anesthesia

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FURTHER CONSIDERATIONS Bis Monitoring

Neurological Disability

Pediatrics

Obesity

Target controlled infusions

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TARGET CONTROLLED INFUSION (TCI)

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TCI

Patient Infusion

System Microprocessor

Software PKPD model

Alogorithms

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NEUROLOGICAL DISABILITY

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PEDIATRIC TIVA CONSIDERATION

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ADDITIONAL CHALLENGES TO

CONSIDER WITH TIVA

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OBESE PATIENTS: LARGELY

GUESSWORK????

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BRINGING IT ALL TOGETHER

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CHECKLIST OF INTRAOPERATIVE

NEUROMONITIORING CHANGES

Anesthesia

Halogenated Agents, Nitrous oxide

Added Agent

IV Agents

Bolus dose

Change infusion

Dose wearing off

Muscle relaxation change

Epidural, Intrathecal, or regional block

Shils JL, Sloan TB. Intraoperative neuromonitioring. Int Anesthesiology Clin 2015; 53:53

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CHECKLIST OF INTRAOPERATIVE

NEUROMONITIORING CHANGES

Physiology

Temperature

Whole body temperature

Local change (irrigation,

cold IV fluids)

Ventilation

Hypoxemia

Hyper or hypoventilation

Ischemia/Reduced Blood Flow

Hypotension, poor cardiac output, bleeding

Local ischemia (retractor, clip, vasospasm)

Rheology/blood volume (change HC, colloids)

Loss autoregulation (hypoxia, hypercarbia, injury)

Vascular steal/Robin Hood

Other

Raised intracranial, CSF. Or tissue pressure

Hypoglycemia, electrolyte abnormalities

Shils JL, Sloan TB. Intraoperative neuromonitioring. Int Anesthesiology

Clin 2015; 53:53

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CHECKLIST OF INTRAOPERATIVE

NEUROMONITIORING CHANGES

Positioning

Mechanical stretch/ pressure on plexus/nerves

Vascular occlusion to area

Surgical

Blunt or surgical trauma

Mechanical effect (device, retractor, pledget pressure)

Vascular occlusion to area

Applied medications surface or intravascular (lidocaine, papaverine)

Surgical stimulation

Tissue resection

Shils JL, Sloan TB. Intraoperative neuromonitioring. Int Anesthesiology Clin 2015;

53:53

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CHECKLIST OF INTRAOPERATIVE

NEUROMONITIORING CHANGES

Technical

Stimulation

Electrodes- dislodged, edema, wrong location

Recording

Electrodes-Dislodged, edema, wrong location

Poor or mismatched impedance

Electrical noise from new equipment

Myoclonus or seizures

Machine

Malfunction

Display settings changed

Testing paradigm settings changed

Shils JL, Sloan TB. Intraoperative neuromonitioring. Int Anesthesiology Clin

2015; 53:53

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REFERENCES

References

1. Bakan, Mefkur. Umutoglu, Tarik. Topus, Ufuk. Et al. (2014). Opioid- free total intravenous anesthesia with

propofol, dexmedetomidine and lidocaine infusions for laparoscopic cholecystectomy: a prospective, randomized,

double- blinded study. Revista Brasileira De Anestesiologia. Volume 65 (3): 191-199.

2. Banoub, Mark. Tetzlaff, John E. , Schubert, Armin. (2003). Pharmacologic and physiologic influences affecting

sensory evoked potentials. Anesthesiology. Volume 99, pp-716-736.

3. Breslin, D.S., Mirakhur, R.K., Reid, J.E. et al. (May 2004). Manual versus target-controlled infusions of propofol.

Anesthesia. Volume 59, Pp 1059-1063.

4. Coetzee, Johan F. (2009). Total intravenous aneaesthesia to obese patients: largely guesswork? European Society

of Anaesthesiology. Volume 26: 359-361.

5. Darnobid, Jessica A. (2015). The pharmacology of total intravenous anesthesia. International Anesthesiology

Clinics. Volume 53, pp 13-27.

• Bakan, Mefkur. Umutoglu, Tarik. Topus, Ufuk. Et al. (2014). Opioid- free total intravenous

anesthesia with propofol, dexmedetomidine and lidocaine infusions for laparoscopic

cholecystectomy: a prospective, randomized, double- blinded study. Revista Brasileira De

Anestesiologia. Volume 65 (3): 191-199.

• Banoub, Mark. Tetzlaff, John E. , Schubert, Armin. (2003). Pharmacologic and physiologic

influences affecting sensory evoked potentials. Anesthesiology. Volume 99, pp-716-736.

• Breslin, D.S., Mirakhur, R.K., Reid, J.E. et al. (May 2004). Manual versus target-controlled

infusions of propofol. Anesthesia. Volume 59, Pp 1059-1063.

• Coetzee, Johan F. (2009). Total intravenous aneaesthesia to obese patients: largely

guesswork? European Society of Anaesthesiology. Volume 26: 359-361.

• Darnobid, Jessica A. (2015). The pharmacology of total intravenous anesthesia.

International Anesthesiology Clinics. Volume 53, pp 13-27.

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• Egan, Talmage D. (June 2015). Total intravenous anesthesia versus inhalation anesthesia: a drug delivery

perspective. Journal of Cardiothoracic and Vascular Anesthesia. Volume 29 :ppS3-S6.

• MacDonald, David B., (2006). Intraoperative motor evoked potential monitoring: overview and update.

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anesthesia with desflurane versus propofol-a prospective randomized trial. Clinical Neurophysiology.

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• McCormack, Jon G. (2008). Total intravenous anaesthesia in Children. Current Anaesthesia & Critical Care.

Pp 1-6.

• Miller, Timothy E., Gan, Tong J. (2015). Total intravenous anesthesia and anesthetic outcomes. Journal of

Cardiothoracic and Vascular Anesthesia. Volume 29, pp S11-S15.

• Pajewski, Thomas N. , Arlet, Vincent., Phillips, Lawrence H. (2007). Current approach on spinal cord

monitoring: the point of view of the neurologist, the anesthesiologist and the spine surgeon. European

Spine Journal. Volume 16, pp S115-S129.

REFERENCES

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REFERENCES

• Schnider, Thomas W. (June 2015). Pharmacokinetic and pharmacodynamics concepts underpinning total

intravenous anesthesia. Journal of Cardiothoracic and Vascular Anesthesia. Volume 29, pp S7-S10.

• Sloan, Tod B., et al. (2012). Total intravenous anesthesia (TIVA) alternatives in the face of a propofol shortage.

University of Colorado. Pp. 3-9.

• Tamkus, Arvydas A. Rice, Kent S., Kim, Howard L. (2013). Differential rates of false-positive findings in

transcranial electric motor evoked potential monitoring when using inhalational anesthesia versus total

intravenous anesthesia during spine surgeries. The Spine Journal. Pp 1-7.

• Thomas, Berlet. (2015). Remifentanil versus fentanyl in total intravenous anesthesia for lumbar spine surgery: a

retrospective cohort study. Journal of Clinical Anesthesia. Volume 27, pp 391-395.

• Rozet, Irene., Metzner, Julia., Brown, Marcia. Et al. (2015). Dexmedetomidine does not affect evoked potentials

during spine surgery. Neuroscience in Anesthesiology and Perioperative Medicine. Volume 121, pp 492-500.

• Yuil,G., Simpson, Milda. (2002). An introduction to total intravenous anaesthesia. British Journal of Anaesthesia.

Volume 2, pp24-26.