1. Asst Prof of Anesthesiology Nova Southeastern University
Posterior Fossa Procedures (Infratentorial Craniotomy) and Neuroanesthesia Emergencies
Mani K.C Vindhya M.D
Asst Prof of Anesthesiology
Nova Southeastern University

2. Anesthesia for Posterior Fossa Procedures (Infratentorial Craniotomy) and Neuroanesthesia Emergencies
I. Format = approach to posterior fossa case
Preoperative concerns –
Problem list?
Further labs and studies?
Optimization? (Is the patient optimal for surgery?)
Consults?
Further medical treatment?
Intraoperative concerns
Premedication
Monitoring
Induction
Maintenance
Intra-op complications (2 main complications?)
Emergence
Postoperative concerns – only on the long stem
2 main complications?
Post-op pain relief

3. Posterior fossa considerations
Case Presentation.
An 18 year-old male for posterior fossa exploration and excision of cerebellar mass lesion.
History
headache
nausea and vomiting
impaired hearing
occasional diplopia
Physical exam
ataxia
severe bilateral papilledema (3/4)
BP = 120/70 to 140/80
weight = 65 kg
CT scan
cerebellar mass lesion
hydrocephalus
The neurosurgeon desires intraoperative monitoring of:
brain stem auditory evoked potentials (BAEP's)
facial nerve (cranial nerve VII) function

4. Problem List: Cerebellar mass lesion with hydrocephalus Increased ICP
Positioning -- sitting, prone, lateral, or supine (semi-lateral)
"Full stomach" -- nausea and vomiting, increased ICP
Intraoperative monitoring
Brainstem auditory evoked potentials
Facial nerve function (motor testing)

5. Posterior Fossa Is a "closed-in" space
Bone - on sides, back, and bottom
Tentorium - on top (Posterior fossa is "infratentorial.")
Brain stem - in front
Contains about 1/4 of intracranial contents
Tumors in the posterior fossa
Children
Intracranial neoplasms = the most common solid tumors in
childhood (about 25% of all admissions for neoplastic disease).
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:
"Benign by histology"
"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

6. Posterior Fossa

7. Explanation of symptoms in case presentation

8. Sitting Position
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

9. Sitting Position

10. Advantages of the sitting position include:
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)

11. Possible sitting position complications include:
Air embolism (venous and arterial)
Cardiovascular instability
Hypotension
Venous pooling
Cardiac arrhythmias
Neurologic complications
Quadriplegia
Nerve injuries (e.g. ulnar, sciatic, lateral peroneal)
Pneumocephalus
Airway obstruction
Airway swelling (head and tongue)
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

12. Relative Contraindications to Sitting Position
Known cardiac septal defect = a "red flag"
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

13. Air Emboli (Venous and Arterial)
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:
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

14. Relative sensitivity of techniques to monitor for VAE

15. Comments on VAE monitors
Bubble Doppler -- still a very sensitive and practical way to detect VAE
Transesophageal ECHO (TEE)
The most sensitive way to detect VAE.
The only way to document intraoperative "paradoxical air emboli" which have crossed to the arterial circulation, unless the surgeon sees air bubbles in arteries!
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?
Expensive
The number of complications as a result of paradoxical air emboli is actually small

16. Pulmonary artery pressures (PAP)
CVP catheters:
Have two uses regarding VAE:
VAE detection (much less sensitive than Doppler or TEE)
VAE aspiration (potentially life-saving in some situations)
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

17. Biphasic P-wave on intracardiac electrocardiogram

18. Intraoperative Concerns
Premedication?
Thorough pre-op interview to allay anxiety.
None ("light" sedation with benzodiazepine if at all).
Avoid narcotics pre-op (respiratory depression, nausea and vomiting).
Monitoring Checklist -- use "routine" monitors as reminders:
Stethoscope -- esophageal
Precordial Doppler -- to detect venous air emboli (VAE)
EKG -- ST segments
Non-invasive blood pressure
Radial A-line -- BP, paO2, paCO2 (=25-30), H&H, K+
CVP -- follow volume status, aspirate VAE
Temperature -- esophageal probe
Blood warmer, Bird or Bear humidifer
Warming/cooling blanket

19. 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

20. Special monitors
1. Facial nerve (C.N. VII) function
Neurosurgeon directly stimulates facial nerve in operative field.
Facial muscle movement is observed:
Directly by the anesthesiologist (under drapes)
Indirectly by electrode and monitor
Anesthetic implication -- neuromuscular blockade must wear off or be reversed at time of stimulation.
2. Brainstem auditory evoked potentials or responses
(BAEP's or BAER’s)
Specialized form of EEG monitoring
Background EEG activity is electronically subtracted out.
The EEG waveform evoked by auditory stimulus (clicking in ear) remains.

21. 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.

22. The seven peaks of the BAEP

23. BAEP

24. What do we look for during surgery?
Mainly two things:
Increase in latency (> 10%)
Decrease in amplitude (<50%)
These two changes could be indicative of impending injury or ischemia in the BAEP pathway.
BAER's are barely affected by anesthetics:
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).

25. Induction -- "typical" anesthetic regimen for intracranial procedures, assuming airway meets good criteria (i.e. Mallampati classification):
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
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)

26. Maintenance
1. Reasonable Maintenance Regimens for Intracranial Neuroanesthesia (going from routine to desperate).
a. N2O + isoflurane (½%) + fentanyl
N2O = the first agent to go if there’s brain swelling or venous air emboli or ischemia danger (i.e. aneurysm or head trauma)
MAC equivalents of sevoflurane or desflurane might also be substituted for isoflurane.
Sufentanil could be substituted for fentanyl.
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

27. 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

28. Intraoperative Complications -- "Emergencies in Neuroanesthesia"
Intraoperative Air Embolus
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
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

29. "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?
Muscle relaxant?
DC N2O, switch to 100% O2?
TIVA (total IV anesthetic) technique?
Barbiturate coma – as a last resort
Improve venous return?
Reverse Trendelenberg position? Elevate head of bed?
Reposition the head? Is there venous occlusion secondary to positioning?

30. 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:
HYPOXIA & HYPERCARBIA! (Always first)
SEVERE AIR EMBOLUS (Close second)
Artifact - has BP transducer or table moved up or down?
b. Bradycardia
1)With hypertension
a) Most likely cause = Cushing response 2ndary to:
ICP (closed skull)
surgical retraction (open skull)
brain stem stimulation
traction on trigeminal nerve (CN V)

31. Cushing Response

32. Potential treatments:
Tell surgeon.
Propofol or pentothal bolus
Deepen anesthesia
Other possible causes:
Impending brain stem herniation
(turn off spinal drain?)
Inadvertent phenylephrine bolus
Bradycardia With hypotension
Most likely cause = vagal stimulation
Ephedrine
Atropine (or glycopyrrolate)

33. Tachycardia
With hypertension
Most likely causes = light anesthesia or sympathetic stimulation
Another cause = inadvertent Ephedrine bolus
Potential treatments = deepen anesthesia (1st), antihypertensives (2nd)
With hypotension
Most likely cause = hypovolemia
Another cause = hemodynamic instability
due to sitting position
Potential treatments:
Replace I&O cc per cc
Phenylephrine

34. Premature Ventricular Contractions (PVC's)

35. 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.

36. 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: