neurosurgical anesthesia Flashcards
what occupies the closed, non-expandable cranial vault?
- brain tissue (80%)
- blood (12%)
- CSF (8%)
what are challenges of craniotomy procedures?
- space-occupying lesions and increased intracranial volume in an enclosed space (increased pressure; something displaced, usu. blood)
- altered vasoreactivity and autoregulation
- control of CBF, CBV, CPP, ICP and brain swelling
- unfamiliar monitoring
- HOB away from the anesthetist
- access to airway is not readily available
- varying levels of noxious stimuli (intense at beginning and end; little in the middle)
- flow and metabolism are coupled
- blood loss and hemodynamics can change rapidly
- head ROM is fixed d/t cranial pinning
what are the varying levels of noxious stimuli during craniotomy?
- scalp, skull, dura elicit increased noxious stimuli (sawing open)
- brain tissue almost free from nociceptive nerve tissue (once in, may see a drop in BP d/t decreased stimulation)
what is cushing’s reflex?
with an increased ICP will see a reflex systemic HTN and decreased HR
*increased ICP can lead to brain damage (ischemic neurological tissue)
what is the use of epinephrine soaked gauze and what is the AI?
- used by surgeon to stop bleeding by immediate vasoconstriction where it is placed
- as it is absorbed systemically will see beta 2 effects causing systemic vasodilation and a decrease in BP
since hemodynamics can change rapidly w/ craniotomies, what is best practice?
-vasoconstrictors AND vasodilators inline and ready for immediate titration (both are hung and titrated as needed to keep hemodynamics at optimal level)
what is the anesthetic goal during craniotomies?
keep the brain “relaxed” not “tight”
describe metabolism of the brain
- glucose is the primary substrate of metabolism
- hypoglycemia worsens hypoxic injury
- metabolic rate of the brain is measured in O2 consumption
- cerebral metabolic rate of oxygen consumption (CMRO2)
what does “flow and metabolism are coupled” in the brain mean?
high brain metabolic activity causes high CBF
*flow and metabolism are proportional
how much of the CO does the brain utilize?
650-700 ml out of 5000 total of CO
*15-20% of CO
what is the average cerebral blood flow (CBF)?
avg. 50 ml/100 gm/min
* can vary from 30-300 ml/100 gm/min
what EEG changes are seen with decreases in CBF?
- less than 25 ml/100 gm/min: slowing of EEG
- 15-20 ml/100 gm/min: isoelectric EEG
- less than 10 ml/100 gm/min: irreversible injury
what parts of the brain are more sensitive to hypoxic brain injury?
- hippocampus (memory)
- cerebellum (coordination; movement)
how is cerebral perfusion pressure determined?
CPP equal to MAP-ICP or CVP (whichever is higher)
*since ICP/CVP is small, CPP essentially equal to MAP
at what MAP is CBF autoregulated?
50-150 torr
*autoregulation diminished below 50 torr
what EEG changes are seen with decreases in CPP?
- CPP less than 50 torr: EEG changes
- CPP less than 25 torr: irreversible damage
what is CBF proportional to?
PaCO2
*when Vm doubles (CO2 dropped), CBF decreases by half
how does temperature effect CBF?
CBF increases 5-7% for every 1 degree C temp
how do volatile agents affect the brain?
- all decrease cerebral vascular resistance: cerebral vascular dilation
- dose dependent impairment of autoregulation
- increases CBV, CBF, and ICP
- decrease CMRO2 and abolishes cortical activity
- *neuroprotective at high doses
with volatile agents what must be done to offset the increase in ICP?
hyperventilate
how does nitrous oxide affect the brain?
- expands closed gas spaces
- increases CBF, ICP, and CMRO2
when should N2O be avoided in craniotomies?
- presence of intracranial air such as during a recent craniotomy, repeat craniotomy or cranial trauma
- evoked potential signal is inadequate
- evidence of increased ICP
- tight brain
- *just don’t use
how do barbiturates (thiopental) affect the brain?
- decreases CBF, ICP, and CMRO2
- inhibit excitatory neurotransmitter receptors
- slowing of EEG
how does propofol affect the brain?
- dose dependent decrease in CBF, CMRO2
- isoelectric EEG at 500 mcg/kg/min
- neuroprotective
how does etomidate affect the brain?
- decreases CBF, ICP, and CMRO2
* *but can cause seizures in pts. w/ seizure history (spikes CMRO2 up; don’t want to risk)
how do opioids affect the brain?
- dose dependent decreases in CBF, CMRO2
* Demerol metabolite, normeperidine, can cause seizures
how do benzodiazepines affect the brain?
- anticonvulsants
- decreases in CBF, CMRO2
- respiratory depression limits use (increased CO2 leads to increased CBF)
how does ketamine affect the brain?
- dissociative effects
- increased ICP (more than 80%)
- increased CBF
- avoid
how do muscle relaxants affect the brain?
- depolarizers (SCh): increased ICP, CBF, CMRO2
- contraindicated in denervated muscle, CVA, motor neuron lesions
- nondepolarizers: effects are small
- anticonvulsants like Dilantin are enzyme inducers and cause and increased dosage requirement of nondepolarizers (constantly monitor nerve stimulator)
describe fluid management considerations for craniotomy
- avoid dextrose containing solutions
- limit volume of LR
- use colloid and NS for volume resuscitation
- limit hetastarch to 1-1.5 L to avoid coagulopathy
- maintain hct at 30-35%
- mild volume expansion for aneurysm clipping may help reduced vasospasm
- keep pts. isovolemic, isotonic, and isooncotic
describe monitoring including during a craniotomy
- EKG
- direct arterial BP
- ETCO2, pulse ox, ABGs
- peripheral nerve stimulation
- CVP
- body temp (usu. keep cold)
- urinary output
- EEG or SSEP
- cerebral oximetry
how do volatiles affect SSEP?
- increase in latency
- decrease in amplitude
- IV anesthetics affect SSEP less than inhaled anesthetics
how do etomidate and ketamine affect SSEP?
increase in amplitude
how do opioids affect SSEP?
no effect on amplitude
how does N2O affect SSEP?
60% N2O: decreased amplitude
-no effect on latency
how does CBF affect SSEP?
reductions in blood flow decrease SSEP
what is important to remember if pt. has SSEP monitoring?
- GA inhibits neurotransmission
- regulate hemodynamics w/ non-anesthetic agents b/c its important to maintain a constant anesthetic level throughout the procedure so they can know if changes in SSEP are d/t nerve damage
what is the purpose of EEG monitoring?
detects decreases in perfusion and ultimately ischemia based on reductions in electrical brain activity
how does the EEG detect decreases in perfusion?
- CBF for electrical failure is still higher than that needed to maintain cell integrity
- will see an EEG change before any cell damage occurs
what other factors can affect the EEG?
- hypothermia
- tumors
- anesthesia
- *crucial to maintain the same level of anesthesia throughout the surgical procedure
describe sensory evoked potentials
- assess the integrity of sensory pathway
- stimulation of peripheral nerve sends electrical signal to brain, where electrodes sense response
- damage to the pathway will display a decreased signal amplitude and an increased latency
- SSEP: median and posterior tibial nerves stimulus recorded at spinal or cortical sites
- BAEP: clicking sends auditory nerve sensory signal; indicated for surgery in posterior fossa to assess integrity of CN8
describe motor evoked potentials
- better assessment for spinal surgery b/c anterior (motor) cord is at greatest risk than posterior (sensory)
- stimulus above the surgical site via transcranial or direct stimulation of spinal cord
- electrical potentials measured below the surgical site by monitoring nerve or muscle potentials
- anesthesia affects transcranial greater than direct spinal
- MEP usefulness still under discussion
- EMG: monitors motor response to nerve stimulation; used to assess facial nerve integrity
- *avoid paralytic agents when MEP used
what are goals of induction for a craniotomy?
- smooth induction
- avoid increase in ICP or compromising CBF
- avoid HTN (increases CBF and ICP)
- avoid hypotension (decreased CPP)
- maximize venous drainage: avoid excessive neck flexion; HOB up greater than 15 degrees
- hyperventilation during apnea time or preoxygenation period
- opioids can blunt SNS outflow
- adequate muscle relaxant to prevent bucking/coughing
what are goals of emergence for a craniotomy?
- slow, smooth and controlled!!
- neurological function intact prior to extubation
- prevent straining, coughing, or bucking on ETT (increased ICP, re-bleeds, hematoma, etc)
- fentanyl
- HOB returned to machine and CRNA
- rapid awakening promotes neuro assessment
when should spontaneous breathing be re established?
prior to skin closure and pin removal
*once pins (noxious stimuli) removed, then return of spontaneous ventilation may be delayed
what categories are masses divided into based on location on the brain?
- supratentorial (cerebrum): above the tentorium
- infratentorial (cerebellum): below the tentorium (worse d/t vital respiratory and cardiac centers)
what symptoms are seen w/ supratentorial mass lesions?
- HA
- seizures
- hemiplegia
- aphasia
what symptoms are seen w/ infratentorial mass lesions?
- cerebellar dysfunction (ataxia, nystagmus)
- brain stem compression (altered mental status or altered respirations)
what are intracranial mass symptoms present based on?
- growth rate: slow typically asymptomatic; fast acute neurological deficits
- location: deficits align w/ location of masses
- ICP: intracranial HTN is common
what are common neurological symptoms usually present w/ intracranial mass?
- reduced cognitive function
- HA
- focal neurological deficits
what type of mass of majority of intracranial mass surgeries for?
supratentorial
what are AIs for mass lesions?
- all types have same anesthetic implications
- brain edema and midline shift may be evident on CT
- evaluate and document neurologic deficits (or will sue you for them)
- many times are on anticonvulsants (enzyme induction), steroids (need coverage; abnormal glucose), and diuretics (hypovolemic; abnormal electrolytes)
- present w/ HA, seizures, reduced cognitive and neuro functions, focal neuro deficits
what should be done to avoid ICP?
- avoid benzos and opioids pre-op (resp. depression leads to increased PaCO2 and increased ICP)
- raise HOB 15-30 degrees to control ICP
what are signs and symptoms of elevated ICP?
- HA
- N/V
- papilledema
- focal neuro deficits
- altered mental status (AMS)
what can contribute to poor outcomes after ischemic events?
increased blood glucose
increased brain temp
increased CPP
**neuroprotection: anesthetic induced suppression of electrocortical activity allows brain to tolerate disruption of metabolic substrate delivery
how is ICP treated?
- hyperventilation (PaCO2 30-35 mmHg)
- admin. diuretics (mannitol or Lasix)
- cerebrospinal fluid drainage if available
- avoid over hydration; target normovolemia
- elevate head; position to improve cerebral venous return; avoid neck vein compression
- intracranial pressure monitor
- optimize hemodynamics (MAP, CVP, PCWP, HR, CPP); consider antihypertensive
- corticosteroids (decadron)
- surgical decompression; consider decompressive craniectomy if hematoma is present
- cerebral vasoconstriction (thiopental, propofol)
- consider mild hypothermia
what are concerns w/ posterior fossa surgery (infratentorial)?
- vital brain stem centers in close proximity: circulatory and respiratory centers; RAS, ANS and some cranial nerves
- infratentorial masses can obstruct CSF at 4th ventricle and lead to obstructive hydrocephalus
- spontaneous ventilation is a form of monitoring respiratory center damage
- sitting position is most preferred
describe venous air embolism (VAE) risk w/ posterior fossa surgery
- increased risk w/ open venous system subatmospheric
- can occur in any position where wound is above heart
- highest incidence (over 20%) during sitting craniotomy
- dependent on volume and rate of entry
- small air bubble diffuse into pulmonary system; large air bubbles can impede pulmonary flow leading to increased RV afterload and decreased CO
- N2O enhances the air embolus
what clinical presentation is seen with VAE?
- decreased ETCO2 (flattens)
- decreased oxygen saturation
- sudden hypotension
- circulatory arrest (obstructing RV outflow)
- increased ET nitrogen d/t absorption through alveoli (nitrogen in the air that is entrained large enough to be captured on sensor in lungs)
- precordial Doppler (most sensitive non-invasive): sporadic roaring sound
- TEE (most sensitive invasive): o.25 ml air detected
- precordial stethoscope: mill wheel
describe treatment for VAE
- notify surgeon on detection (will flood surgical field w/ saline and wax bone edges to close off “open system”)
- dc N2O admin and admin 100% O2
- perform valsalva maneuver or compression of jugular veins (close pop off and give breath and hold)
- aspirate air from atrial catheter
- support BP w/ volume and vasopressors
- reposition in left lateral decubitus w/ 15 degree head down tilt if BP continues to drop
- modify anesthetic as needed to optimize hemodynamics
describe paradoxical air embolism
- air enters the systemic circulation
- patent foramen ovale (PFO) or atrial or ventricular septal defect
- PFO exists in 30-35% of population (unknown)
- further evaluation should be initiated for those suspected of having intracardiac defects (murmur)
- surgical positioning may need to be altered to lessen the risks of air entrainment (prone rather than sitting)
what is a cerebral aneurysm?
dilated intracranial arteries
-many types exist
what are complications of aneurysms
- subarachnoid hemorrhage (SAH)
- bleeding
- vasospasm (need to dilute cell mass and irritating factors)
what is the leading cause of SAH (non traumatic)?
saccular aneurysm rupture
- peak rupture age 55-60 y/o
- females greater than males
what vessels are mostly affected by aneurysms?
- internal carotid bifurcation
- anterior cerebral artery
what are signs of SAH?
- intense HA (85%)
- transient LOC (45%)
- N/V (most often seen)
what are complications of cerebral aneurysms?
- SAH
- HTN develops which can worsen SA bleed
- autoregulation impaired (dropping BP not good option)
- ECG: T and ST changes (non ischemic in origin, no adverse effect)
- 50% of previously ruptured aneurysms re-bleed w/ 80% mortality
- cerebral vasospasm (30%) 4 days post-op rupture is major cause of mortality and morbidity
when is surgical intervention usu. done w/ cerebral aneurysms?
if greater than 7mm
what are coiling procedures?
- pt. put to sleep and paralyzed
- enters through groin to fix aneurysm w/o cutting skull open
- have been successful
what correlates best w/ CPP?
BP transducer at the level of the external auditory meatus and tragus
- estimates CPP at Circle of Willis
- lower pressure than level of heart d/t vertical column and hydrostatic pressure difference
how does the distance from the heart to circle of willis compare in mmHg of pressure?
10 cmH2O equals 7.5 mmHg
describe treatment for vasospasm
- no perfusion distal to site; promote perfusion
- maintain CPP
- augment BP and CO
- admin inotropic agents (dopamine, dobutamine)
- admin Ca+ channel blockers (nimodipine, nicardipine)
- intravascular volume expansion
- hemodilution (hct less than 32%)
- correct hyponatremia
- transluminal angioplasty
- *triple H: hemodilution, hypervolemia, HTN**
describe arteriovenous malformation (AVM)
- progressively grow w/ time
- intracerebral hemorrhage (not SA)
- present at an earlier age (10-30) w/ bleeding
- HA and seizures often present
describe surgical Rx of AVMs
- if neuroradiology Rx fails, then surgical resection
- extensive blood loss compared w/ aneurysms
- hyperventilation and mannitol facilitates surgical resection of AVMs or any mass
- same techniques apply to AVM as for aneurysms
describe pituitary surgery considerations
- 20-50% are non-secretory
- hypersecretory tumors can lead to acromegaly and hyperglycemia
- difficult intubations may be a factor (enlarged facial features, laryngeal hypertrophy, enlarged tongue)
- resection is usu. transphenoidal (may be intracranial)
- cushing’s disease may be present
- diabetes insipidus may occur post-op
what are the benefits of transphenoidal resection for pituitary tumors?
- less blood loss
- less mortality and morbidity
what are presenting symptoms of cushing’s disease?
- HTN
- diabetes
- osteoporosis
- obesity
- friability of skin
what are anesthetic implications peri-op w/ transphenoidal resection?
- remember, airway is shared w/ surgeon (ETT placed to left side and secured to chin)
- upper lip free
- thorough airway assessment
- lubricate eyes to prevent fluids from entering
- avoid N2O
- *avoid hyperventilation as it causes pituitary to retract into sella, hindering resection
- *raise ETCO2 to force the pituitary into view
- be prepared for blood loss as carotid arteries lie in close proximity
describe stereotactic procedures
- usu. undertaken w/ MAC and light sedation
- uncomfortable procedures are securing the halo w/ pins and drilling a hole in the skull, both of which are performed following local anesthetic infiltration
- since halo preclude, direct laryngoscopy care must be taken not to obliterate respirations w/ sedation or compromise the pts. ability to maintain airway
- an alternate airway plan for oxygenation and ventilation should be in place
- greater airway control may be needed; fiberoptic bronchoscopy as head is in fixed position in pinned head frame
- or just intubate from the start
describe Arnold-Chiari malformation
- malformation where medulla protrudes through foramen magnum
- CSF outflow obstruction, hydrocephalus
- more common in females
- Rx: decompressive pressure relief
- AIs: same as for posterior fossa surgery
what are challenges w/ head trauma?
- other traumatic injuries accompany
- hypotension, hemodynamic instability
- pulm. contusions, 70% have hypoxemia
- assumed to have cervical spine injury
- varying degrees of consciousness
- increased ICP
- brain contusion, deceleration injuries
- hemorrhage, hematomas, epidural/subdural bleed
- airway challenges: facial fracture, full stomach
- primary neuro insult and secondary insult
- *ketamine a good choice for trauma
what are AIs w/ head trauma?
- avoid N2O
- treat HTN w/ increased agent, hyperventilation (avoid too much hyperventilation as it decreases CBF)
- treat hypotension w/ alpha agonist
- maintain CPP at 70-110 mmHg
- treat enhanced vagal tone w/ atropine
- avoid PEEP until after dura is opened b/c of increased ICP
- may have to leave intubated and paralyzed until increased ICP is resolved
