Posterior Fossa Procedures
(Infratentorial Craniotomy)
and Neuroanesthesia Emergencies
Mani K.C Vindhya M.D
Asst Prof of Anesthesiology
Nova Southeastern University
Anesthesia for Posterior Fossa Procedures
(Infratentorial Craniotomy)
and Neuroanesthesia Emergencies
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I. Format = approach to posterior fossa case
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Preoperative concerns –
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Problem list?
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Further labs and studies?
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Optimization? (Is the patient optimal for surgery?)
 Consults?
 Further medical treatment?
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Intraoperative concerns
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Premedication
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Monitoring
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Induction
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Maintenance
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Intra-op complications (2 main complications?)
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Emergence
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Postoperative concerns – only on the long stem
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2 main complications?
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Post-op pain relief
Posterior fossa considerations
Case Presentation.
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An 18 year-old male for posterior fossa exploration and excision of
cerebellar mass lesion.
History
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headache
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nausea and vomiting
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impaired hearing
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occasional diplopia
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Physical exam
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ataxia
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severe bilateral papilledema (3/4)
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BP = 120/70 to 140/80
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weight = 65 kg
CT scan
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cerebellar mass lesion
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hydrocephalus
The neurosurgeon desires intraoperative monitoring of:
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brain stem auditory evoked potentials (BAEP's)
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facial nerve (cranial nerve VII) function
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Problem List:
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Cerebellar mass lesion with hydrocephalus
Increased ICP
Positioning -- sitting, prone, lateral, or supine
(semi-lateral)
"Full stomach" -- nausea and vomiting, increased
ICP
Intraoperative monitoring
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Brainstem auditory evoked potentials
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Facial nerve function (motor testing)
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Posterior
Fossa
Is a "closed-in" space
Bone - on sides, back, and bottom
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Tentorium - on top (Posterior fossa is "infratentorial.")
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Brain stem - in front
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Contains about 1/4 of intracranial contents
Tumors in the posterior fossa
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Children
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Intracranial neoplasms = the most common solid tumors in
childhood (about 25% of all admissions for neoplastic disease).
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Posterior fossa = the site of origin of 50 to 60% of brain tumors in
children.
Adults -- uncommon site for brain tumors
Tumors in the posterior fossa are often:
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"Benign by histology"
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"Malignant by location"
Posterior fossa tumors can compress the brain stem (pons and medulla).
CSF outflow tracts
Cardiovascular centers
Respiratory centers -- pneumotaxic center, apneustic center
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Posterior Fossa
3
dorsal respiratory group, ventral respiratory group
d. Lower cranial nerves (and functions):
V Trigeminal
Facial sensation
VI Abducens
Eye abduction
VII Facial
Facial muscles (motor)
VIII Acoustic
Hearing
IX Glossopharyngeal Gag reflex
X Vagus
Cough reflex, laryngeal muscles
XI Spinal accessory Shoulder movement
XII Hypoglossal Tongue movement
Explanation of symptoms in case
presentation
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1. Elevated intracranial pressure (ICP) triad secondary to hydrocephalus
headache, nausea (and vomiting), papil edema
2. Cerebellar involvement -- ataxia
3. Brain stem involvment
a. Hearing loss (involvement of C.N. VII )
b. Diplopia (probably involvement of C.N. VI)
Sitting Position
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Situations in which sitting position might be used are
mainly:
 Posterior fossa procedures
 Cervical laminectomy
Establish which position the surgeon desires for
posterior fossa surgery:
 Sitting
 Prone
 Lateral decubitus
 Supine (semi-lateral)
Proper positioning for a seated posterior fossa operation
 Knees at heart level
Neck not hyperflexed
Sitting Position
Advantages of the sitting position include:
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Excellent surgical access
Comfort for the surgeon
Facilitates hemostasis (decreased blood loss)
Improved venous and CSF drainage
Exposes face for monitoring response to cranial
nerve stimulation (though this can also be done
electronically)
Possible sitting position complications include:
Air embolism (venous and arterial)
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Cardiovascular instability
 Hypotension
 Venous pooling
 Cardiac arrhythmias
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Neurologic complications
 Quadriplegia
 Nerve injuries (e.g. ulnar, sciatic, lateral peroneal)
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Pneumocephalus
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Airway obstruction
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Airway swelling (head and tongue)
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Malpractice risk. The use of the sitting position for
posterior fossa neurosurgery is somewhat controversial.
Current practice is away from operating in sitting position6
No evidence that position affects outcome.
Venous air emboli can occur in any position -sitting, lateral, prone, or supine
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Relative Contraindications to Sitting Position
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Known cardiac septal defect = a "red flag"
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Patent foramen ovale (PFO)
Atrial septal defect
Ventricular septal defect
Right atrial pressure > left atrial pressure
Functioning ventriculo-atrial shunt
?? cardiac instability
?? extremes of age
Air Emboli (Venous and Arterial)
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Incidence of venous air emboli (VAE) can be as high
as 50% in neurosurgery.
Incidence of VAE depends on both monitoring and
position.10
"Bottom line" on VAE:
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More frequent in the sitting position.
BUT -- VAE can occur in any position.
Early detection and prevention with the Doppler and other
more sensitive
VAE monitoring methods have:
Decreased the occurrence of clinically significant VAE
Increased the reported incidence of VAE
Relative sensitivity of techniques to monitor for VAE
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Comments on VAE monitors
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Bubble Doppler -- still a very sensitive and practical way to detect
VAE
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Transesophageal ECHO (TEE)
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The most sensitive way to detect VAE.
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The only way to document intraoperative "paradoxical air
emboli" which have crossed to the arterial circulation, unless the
surgeon sees air bubbles in arteries!
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ECHO could be used to detect a patent foramen ovale preop.
Incidence of patent foramen ovale = about 1 in 4.
A paradoxical air embolus can occur even if a person does not have a
patent foramen ovale. Air can traverse the pulmonary circulation.
Why don't we get pre-op ECHO's for all sitting position cases?
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Expensive
The number of complications as a result of paradoxical air emboli is
actually small
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Pulmonary artery pressures (PAP)
CVP catheters:
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Have two uses regarding VAE:
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VAE detection (much less sensitive than Doppler or TEE)
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VAE aspiration (potentially life-saving in some situations)
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How do you confirm CVP catheter placement in the right atrium
(to aspirate air lock if VAE occurs)?
Length of catheter (but could be in jugular vein)
Rapid saline bolus through CVP (listen to Doppler)
PAC's (imply atrial stimulation)
PVC's (imply ventricular stimulation)
Right ventricular pressure wave on CVP (Pull catheter back into right
atrium.)
Chest X-ray
Biphasic P-wave on intracardiac electrocardiogram
Biphasic P-wave on intracardiac electrocardiogram
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Intraoperative Concerns
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Premedication?
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Thorough pre-op interview to allay anxiety.
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None ("light" sedation with benzodiazepine if at all).
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Avoid narcotics pre-op (respiratory depression, nausea and vomiting).
Monitoring Checklist -- use "routine" monitors as reminders:
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Stethoscope -- esophageal
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Precordial Doppler -- to detect venous air emboli (VAE)
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EKG -- ST segments
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Non-invasive blood pressure
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Radial A-line -- BP, paO2, paCO2 (=25-30), H&H, K+
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CVP -- follow volume status, aspirate VAE
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Temperature -- esophageal probe
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Blood warmer, Bird or Bear humidifer
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Warming/cooling blanket
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Oxygen monitor (+ volume monitor and PIP)
 Adjust ventilation according to paCO2
Pulse oximeter
End-tidal CO2 (and infrared gas analyzer)
 Useful to trend paCO2 (End-tidal CO2 < paCO2)
 Detecting VAE (decreased end-tidal CO2, increased ET
N2)
Restraints (+ twitch monitor -- muscle relaxants)
Intake and output
 Foley catheter (furosemide, mannitol)
 Maintain even I&O (Don't "run em' dry.")
 Avoid dextrose-containing solutions in IV's
Position injuries
 Ulnar or sciatic nerves (in sitting position)
 Neck not hyper-flexed or -extended
Special monitors
1. Facial nerve (C.N. VII) function
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Neurosurgeon directly stimulates facial nerve in operative field.
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Facial muscle movement is observed:
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Directly by the anesthesiologist (under drapes)
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Indirectly by electrode and monitor
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Anesthetic implication -- neuromuscular blockade must wear
off or be reversed at time of stimulation.
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2. Brainstem auditory evoked potentials or responses
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(BAEP's or BAER’s)
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Specialized form of EEG monitoring
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Background EEG activity is electronically subtracted out.
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The EEG waveform evoked by auditory stimulus (clicking
in ear) remains.
Shape of a typical BAEP = seven peaks1
– Latency = time to first peak (usually 2 msec)
– Amplitude = height of the peaks
c. The seven peaks of the BAEP are believed to correspond to
passage of a stimulus through "generators" in the auditory nerve,
brainstem and cortex.
The seven peaks of the BAEP
WAVE
PURPORTED GENERATOR
I
Extracranial auditory nerve
II
Intracranial auditory nerve and/or cochlear nucleus
III
Superior olive
IV
Lateral lemniscus
V
Inferior colliculus
VI
Thalamus
VII
Thalamocortical radiation
BAEP
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What do we look for during surgery?
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Mainly two things:
 Increase in latency (> 10%)
 Decrease in amplitude (<50%)
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These two changes could be indicative of impending
injury or ischemia in the BAEP pathway.
BAER's are barely affected by anesthetics:
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No anesthetic drug produces a change in BAER’s that
could be mistaken for a surgically induced change.
2) Etomidate decreases amplitude and increases latency (but
this is not clinically significant).
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Induction -- "typical" anesthetic regimen for intracranial procedures,
assuming airway meets good criteria (i.e. Mallampati classification):
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1. Method: "Modified" rapid sequence induction and intubation
(with cricoid pressure)
Preoxygenate and denitrogenate (100% O2 by mask with head in good
"sniffing" position)
Cricoid pressure (N&V with increased ICP)
Hyperventilate to decrease paCO2 prior to intubation
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Typical induction agents
 Propofol, etomidate, or thiopental
 suitable I.V. induction agents
 Fentanyl or sufentanil
– as narcotic analgesics to supplement
Lidocaine IV – to blunt hypertensive and ICP response to intubation d.
Neuromuscular junction blockers –rocuronium, vecuronium, or
succinylcholine (with prior defasciculating dose of non-depolarizing NMJ
blocker)
Maintenance
 1. Reasonable Maintenance Regimens for Intracranial
Neuroanesthesia (going from routine to desperate).
a. N2O + isoflurane (½%) + fentanyl
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N2O = the first agent to go if there’s brain swelling or venous
air emboli or ischemia danger (i.e. aneurysm or head trauma)
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MAC equivalents of sevoflurane or desflurane might also
be substituted for isoflurane.
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Sufentanil could be substituted for fentanyl.
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b. Isoflurane (1%) + fentanyl
c. Isoflurane (½%) + propofol + fentanyl
 ! Volatile agents are next to go if high ICP or brain swelling
 Total IV anesthetic: Propofol + fentanyl
 Barbiturate coma -- for intractible brain swelling or cerebral
 protection during aneurysm clipping (titrated to EEG burst
suppression):
 Thiopental
 Pentobarbital
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Non-depolarizing neuromuscular junction blocker
(must wear off or be reversible by time of CN VII
testing).
 Vecuronium
 Rocuronium
 Pancuronium – increases HR
 Cis-atracurium
Additional maneuvers to decrease ICP
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Intraoperative Complications -- "Emergencies in Neuroanesthesia"
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Intraoperative Air Embolus
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What should I do immediately?
 Tell the surgeon, who should flood the field.
 Discontinue N2O and give 100% O2
 Aspirate air from the CVP line
 Light neck compression
 Call for help
 Supportive measures (i.e., treat hypotension, arrhythmias)
 Try to position patient for CPR
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What else can I do? Other considerations:
 Dopamine or dobutamine? (Suggested to increase right
ventricular contractility)
 Raise CVP by fluid loading, not PEEP. PEEP would raise
CVP, but at the risk of sending a paradoxical (arterial) air
embolus through a probe-patent foramen ovale.
 Avoid the Valsalva maneuver:This increases CVP, but:
 could cause paradoxical air embolus
 causes severe hypotension
"Tight Brain" -- Think through things we can do to decrease
intracranial volume and ICP.
Airway disaster? In any anesthetic emergency, the first things to think of
are: HYPOXIA & HYPERCARBIA! (Is this a respiratory disaster?)
Furosemide and mannitol?
Dexamethasone?
Open the spinal drain or insert a ventriculostomy?
Can I hyperventilate more (to paCO2 of 25)?
Anesthetic choice?
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Muscle relaxant?
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DC N2O, switch to 100% O2?
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TIVA (total IV anesthetic) technique?
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Barbiturate coma – as a last resort
Improve venous return?
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Reverse Trendelenberg position? Elevate head of bed?
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Reposition the head? Is there venous occlusion secondary to
positioning?
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Sudden Cardiovascular Changes
a. With any sudden change in vital signs (hyper- or hypotension,
tachy- or bradycardia, cardiac arrhythmias, etc.), the first three things to
think of in this situation are:
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HYPOXIA & HYPERCARBIA! (Always first)
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SEVERE AIR EMBOLUS (Close second)
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Artifact - has BP transducer or table moved up or down?
b. Bradycardia
1)With hypertension
a) Most likely cause = Cushing response 2ndary to:
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ICP (closed skull)
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surgical retraction (open skull)
 brain stem stimulation
 traction on trigeminal nerve (CN V)
Cushing Response
Potential treatments:
 Tell surgeon.
 Propofol or pentothal bolus
 Deepen anesthesia
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Other possible causes:
 Impending brain stem herniation
(turn off spinal drain?)
 Inadvertent phenylephrine bolus
Bradycardia With hypotension
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Most likely cause = vagal stimulation
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Potential treatments:
 Tell surgeon.
Ephedrine
Atropine (or glycopyrrolate)
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Tachycardia
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With hypertension
 Most likely causes = light anesthesia or sympathetic
stimulation
 Another cause = inadvertent Ephedrine bolus
 Potential treatments = deepen anesthesia (1st),
antihypertensives (2nd)
With hypotension
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Most likely cause = hypovolemia
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Another cause = hemodynamic instability
due to sitting position
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Potential treatments:
 Replace I&O cc per cc
 Phenylephrine
Premature Ventricular Contractions (PVC's)
POTENTIAL CAUSES POTENTIAL TREATMENTS
! Hypoxia
Oxygen
! CVP catheter
Pull back catheter
in right ventricle
! Brain stem stimulation Tell surgeon
! Hypokalemia
Potassium
(due to diuresis)
! Hypomagnesemia
Magnesium
! Intrinsic disease
Lidocaine
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Emergence.
 Hypertension is frequently a problem.
 Avoid "coughing and bucking" while head is
secured. Two agents to treat coughing and
bucking are:
 Propofol
 Lidocaine
 It's desirable for the patient to awaken quickly so
neurosurgeons can obtain a neurologic
assessment.
Postoperative Concerns.
• Many potential postoperative problems are related to the
location of the surgery on or near the brain stem.
•
Cardiovascular centers - hypertension
•
Respiratory centers - respiratory depression, apnea
•
Lower cranial nerves:
VI
VII
VIII
IX
X
Abducens
Facial
Acoustic
Glosspharyngeal
Vagus
Disconjugate gaze
Facial muscle paralysis
Hearing loss
loss of gag reflex
Vocal cord paralysis