Neuro Flashcards
anterior circulation to the brain
internal carotid artery
posterior circulation to the brain
vertebral arteries
two vertebral arteries
- branches of subclavian
- enter skull through foramen magnum and run along the medulla
- join in pons to form basilar artery
basilar artery
branches at the midbrain into 2 posterior cerebral arteries which supply the occipital lobes of the brain
internal carotid branches
- enter through the base of the skull and pass through the cavernous sinus
- divided into anterior and middle cerebral artery
circle of willis
- located at base of brain and forms an anastomotic ring that includes vertebral (basilar) and internal carotid flow
- provides collateral flow if one portion becomes obstructed
- major site of aneurysm and atherosclerosis (especially MCA)
cerebral blood flow in adults
- varies with metabolic activity
- averages 750 mL/min
- about 15-20% of cardiac output
- 50 mL/100g/min
gray matter blood flow
80 mL/100g/min
more blood flow here vs white matter because more activity
white matter blood flow
20 mL/100g/min
EEG cerebral impairment
20-25 mL/100g/min
EEG flat
15-20 mL/100g/min
EEG irreversible brain damage
below 10 mL/100g/min
CBF monitoring
- transcranial doppler (TCD) = ultrasound MCA
- brain tissue oximetry = bolt with a clark electrode oxygen sensor
- intracerebral microdialysis = assesses brain tissue chemistry
- near infrared spectroscopy (NIRS)
NIRS
- receptors detect the reflected light from superficial and deep structures
- largely reflects absorption of venous hemoglobin
- NOT pulsatile arterial flow
- more of a TREND, good to put it on to go to sleep so you can get a baseline
neuro events + NIRS
rSO2 < 40%
change in rSO2 of > 25% from baseline
CPP Formula
CPP = MAP - ICP
*CVP must be substituted for ICP if CVP is higher
ICP normal value
10-15 mmHg
CPP normal value
80-100 mmHg
CPP slowing of EEG
<50 mmHg
CPP flat EEG
25-40 mmHg
CPP irreversible brain damage
<25 mmHg
autoregulation
- myogenic regulation (originating in vascular smooth muscle)
- cerebral vasculature rapidly (10-60s) adapts to changes in CPP
- increase CPP = cerebral vasoconstriction (limit CBF)
- decrease CPP = cerebral vasodilation (increase CBF)
myogenic response
intrinsic response of smooth muscle in cerebral arterioles
metabolic response
- metabolic demands determine arteriolar tone
- tissue demand > blood flow
- release of tissue metabolites causes vasodilation = increase flow
- once thought to be hydrogen ions, but likely other things too
CBF remains constant between MAP of what?
- 60-160 mmHg
- variation between patients and based on source you look at
- CBF remains constant between these MAPs, beyond these limits, blood flow becomes pressure dependent
MAP >150-160 mmHg
this can disrupt the BBB and may result in cerebral edema and hemorrhage
chronic hypertension and autoregulation
right shifted in patients with chronic hypertension
factors effecting CBF
- PaCO2
- PaO2
- temperature
- viscosity
- autonomic influences
- age
PaCO2 effect on CBF
- most important extrinsic influence on CBF
- CBF directly proportionate to PaCO2 between tensions 20-80 mmHg
- blood flows changes 1-2 mL/100g/min per 1 mmHg change in PaCO2
- immediate and secondary changes in the pH of CSF and cerebral tissue
- attenuated at PaCO2 < 25 mmHg (ceiling effect)
does HCO3- change CBF
- ions do NOT passively cross the BBB so bicarb DOES NOT acutely affect CBF
- acute metabolic acidosis has little effect on CBF
- in 24-48 hours CSF HCO3- compensates (active transport) for change in PaCO2
- effects of hypo and hypercapnia are diminished
- BOTTOM LINE = HCO3- compensation probably happens in the ICU not the OR
PaCO2 < 20 mmHg
- marked hyperventilation shifts the oxygen hemoglobin dissociation curve to the LEFT and with changes in CBF, may result in EEG changes suggestive of cerebral impairment even in normal individuals
- LEFT = LOVE
- alkalosis causes increased affinity of Hgb for O2 and therefore decreased release of O2
restoration of normal PaCO2 after surgery/hyperventilation
- acute restoration of normal PaCO2 value will result in significant CSF acidosis after sustained period of hyperventilation and hypocapnia
- CSF acidosis results in increased CBF
- increased CBF results in increased ICP
- SLOWLY increase to normal PaCO2
PaO2 effect on CBF
- 50 to 300 mmHg little influence on CBF
- <50 mmHg rapidly increases CBF
PaO2 <50-60 mmHg
- vasodilation mediated by various things
- release of neuronal nitric oxide
- open ATP dependent K+ channels
- rostral ventrolateral medulla (RVM)
- brains O2 sensor stimulation = increase CBF, but not CMRO2
rostral ventrolateral medulla
also known as the pressor area of the medulla, is a brain region that is responsible for basal and reflex control of sympathetic activity associated with cardiovascular function
temperature effect on CBF
- CBF changes 5-7% per 1 degree celcius
- CMR decreases 6-7% per 1 degree celcius
- CMRO2 decreases by 7% per 1 degree celcius
- CMRO2 decreased by decreasing temperature
viscosity effect on CBF
- hematocrit determines viscosity
- viscosity and CBF inversely proportional
- decrease in HCT decreases viscosity and increases CBF
- decrease in HCT also decreases oxygen carrying capacity
- impaired oxygen delivery to brain tissue
what is optimal cerebral oxygen delivery
occurs at a hematocrit of about 30%
autonomic influence on CBF
- SNS = vasoconstricts and decreases CBF
- PSNS = vasodilates and increases CBF
age influence on CBF
- progressive loss of neurons with aging
- loss of myelinated fibers, loss of white matter
- loss of synapses
- CBF and CMRO2 decrease by 15-20% at 80 years
CMRO2
- brain normally consumes 20% of total body oxygen
- 60% used to generate ATP
- CMRO2 is 50 mL/min
- oxygen mostly consumed in the gray matter
- interruption of cerebral perfusion = unconsious in 10 seconds
- oxygen not restored in 3-8 minutes = depletion of ATP = irreversible cellular injury
which areas of the brain are most sensitive to hypoxic injury
- hippocampus
- cerebellum
glucose and the brain
- glucose primary energy source
- brain glucose consumption 5 mg/100g/min
- 90% aerobically O2 metabolized
hypoglycemia
means brain injury
hyperglycemia
may exacerbate hypoxic injury
blood brain barrier
- PAUCITY OF PORES are responsible for the blood brain barrier
- cerebral blood vessels are unique in vasculature
- vascular endothelial cell junctions are nearly fused
lipid barrier of brain what can pass
- lipid-soluble substances freely pass
- ionized molecules restricted
- large molecules restricted
determinants of what can pass the BBB
- size
- charge
- lipid solubility
- plasma protein binding
what freely crosses the BBB
- O2
- CO2
- Lipid soluble molecules (most anesthetics)
- H2O
what is restricted to cross the BBB
- ions (electrolytes like Na+)
- plasma proteins
- large molecules (mannitol)
what disrupts the BBB
- HTN
- tumor
- trauma
- stroke
- infection
- marked hypercapnia
- hypoxia
- sustained seizure
where is CSF made
- formed in choroid plexus
- formed by ependymal cells
- involves active secretion of sodium in the choroid plexus
- result is fluid that is isotonic with the plasma (even though there is lower concentrations of potassium, bicarb and glucose)
how much CSF do adults make?
21 mL/hr or 500 mL/day
total volume of CSF
150 mL
1/2 in cranium and 1/2 in spinal canal
CSF facts
- replaced 3-4x per day
- found in cerebral ventricles and cisterns and subarachnoid space surrounding the brain and spinal cord
- protects the CNS from trauma
what inhibits production of CSF
- Carbonic anhydrase inhibitors (acetazolamide)
- corticosteroids
- spironolactone
- furosemide
- isoflurane
- vasoconstrictors
absorption of CSF
-translocation from arachnoid granulations into cerebral sinuses
monro kellie doctrine/hypothesis
- cranial compartment is incompressible and the volume inside the cranium is a fixed volume
- the cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another to prevent a rise in ICP
cranial vault components
- brain 80%
- blood 12%
- CSF 8%
ICP
- supratentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex
- small increases in volume in one component are initially well compensated
- 5-15 mmHg
normal ICP
< 10 mmHg
intracranial elastance compensatory mechanisms
- initial displacement of CSF from the cranial to spinal compartment
- an increase in CSF absorption
- a decrease in CSF production
- a decrease in total cerebral blood volume
> 20 mmHg ICP
- anything over 20 mmHg for greater than 5 mins creates ISSUES
- a point is eventually reached at which further increases produce precipitous rises in ICP
ICP provider goals for closed crainium
- maintain CPP
- prevent herniation
ICP provider goals for open cranium
- facilitate surgical access
- reverse ongoing herniation
intracranial hypertension
sustained increase in ICP about 20-25 mmHg
causes of intracranial HTN
- expanding tissue or fluid mass
- interference with CSF absorption
- excessive CSF production
- systemic disturbances promoting edema
S/S increased ICP
- HA
- nausea/emesis
- papilledema
- decreased LOC
- focal neurological deficit
- seizures
- coma
- cushings triad
cushing’s triad
- irregular respiration
- HTN
- bradycardia
herniation areas
- cingulate gyrus under falx cerebri
- central
- uncal (transtentorial)
- cerebellar tonsils through foramen magnum
- upward herniation of cerebellum
- transcalvarial
most common area of herniation
-cerebellar tonsils through foramen magnum
S/S cingulate gyrus herniation
-little known
uncal and central herniation S/S
- decrease LOC
- pupils sluggish –> fixed and dilated
- cheyne stokes respirations
- decorticate –> decerebrate posturing
cerebellar tonsillar herniation S/S
- no specific clinical manifestations
- arched stiff neck
- paresthesias in shoulder
- decreased LOC
- respiratory abnormalities
- pulse rate variations
transcalvarial herniation S/S
-may occur during surgery
treatment of intracrainial HTN
- brain tissue = surgical removal of mass (lobectomy or removal of bone flap)
- CSF = no effective pharmacological manipulation, only practical management is drain
- Fluid = steroids, osmotics/diuretics
- blood = most amenable to rapid alteration; decrease arterial flow or increase venous drainage with patient position
- reduction of PaCO2 (to no less than 23-35 mmHg
- CMR suppression with barbiturates, propofol and hypothermia)
nitrous oxide effect on brain
- 34x more soluble than nitrogen in blood
- increases CMRO2, CBF, CBV, and ICP (more dramatic change if sole agent)
- sympathoadrenal stimulating effect
- second stage arousal phenomenon
- increase is attenuated by barbiturates, benzos, narcotics, and propofol
- intracranial tumors with 66% N2O increased ICP 13 mmHg to 40 mmHg
CBF and alpha 1 agonists
- bolus may transiently (2-5 min) change CBF and cerebral SaO2
- continous infusion has little effect on CBF and cerebral SaO2
- does not have adverse effect on brain
CBF and alpha 2 agonists
- decreases CBF up to 25-30%
- results from reduced CMRO2 leading to a reduced CBF
CBF and beta agonist
- small dose = little effect on CBF
- large doses + physical stress leads to increase in CMRO2 and CBF
- large dose increases MAP
- may increase CMRO2 and CBF up to 20%
- beta 1 receptor mediated effects
- response exaggerated with BBB defect
antagonists effects on CBF
- b blockers –> little to no effect on CBF and CMRO2
- ACE-inhibitors and ARBs –> little to no effect on CBF and CMRO2, autoregulation maintained
barbiturates effect on brain
- dose dependent reduction in CBF and CMR until isoelectric EEG
- maximum reductions in CBF and CMR of nearly 50% (flat EEG)
- highly effective in lowering ICP
- robin hood (reverse steal effect) –> CBF redistributed from normal to ischemic areas of brain
- CMR decreased more than CBF
- anticonvulsant (all except methohexital which is used for ECT)
benzodiazepines effect on brain
- dose-dependent reduction in CMR and CBF
- greater reduction in CMR and CBF than narcs
- less reduction than barbiturates, propofol or etomidate
- moderate reduction in CBF
- midaz is benzo of choice in neuro due to short half life
- may prolong emergence so consider this when there is need for post-op neuro exam
- anitconvulsant
propofol + brain
- dose dependent reduction in CBF and CMR
- decrease in CBF may exceed that in metabolic rate
- anticonvulsant
- short elimination half-life neuroanesthesia
- commonly used for maintenance of anesthesia in patients with or at risk of intracranial HTN
- most common induction agent for neuroanesthesia
etomidate + brain
- decreases CMR, CBF and ICP
- myoclonic movements on induction, but not associated with seizure activity on the EEG
- has been used to treat seizures, but not a first choice anticonvulsant
- small dose can activate seizure foci in patient with epilepsy
ketamine + brain
- only IV anesthetic that dilates cerebral vasculature and increases CBF
- can potentially increase ICP markedly if decreased intracrainial compliance
- selective activation of certain areas (limbic and reticular) is particularly offset by depression of other areas (somatosensory and auditory)
- CMR does not change (debated)
- ketamine as sole agent can increase ICP
NMDA Antagonist
- functionally dissociates the thalamus from the limbic cortex
- thalamus - relays sensory impulses from the reticular activating system to the cerebral cortex
- limbic cortex - involved with awareness of sensation
- increases HR, BP, CO, and secretions
- analgesic, hallucinogenic effects
- NMDA antagonism in brain injury patient may be protective against neuronal cell death
opioids
-minimal effects on CBF, CMR, and ICP unless increase PaCO2
intracranial surgeries
- craniotomy
- interventional radiology
- trauma
functional surgeries
- epilepsy
- movement
- pain
spine surgeries
- anterior
- posterior
- transoral
MEP
- motor evoked potentials
- used in surgeries where motor tract is at risk
- direct and scalp electrodes
- more sensitive to ischemia than SSEP by 15 minutes and degree detection
- difficult to obtain due to pre-existing conditions or anesthetic conditions
SSEP
- most commonly monitored
- stimulation of peripheral sensory nerve
- mapping in spinal cord and sensory cortex
- ischemia detection in cortical tissue
- reduce risk of spinal cord/brainstem
- mechanical or ischemic insults
- does have some motor but not as specific as MEPs, may not sense deficits as sensitively
- hyperthermia - suppresses amplitude
- hypothermia - increases latency
EMG
- records muscle electrical activity using needle pairs
- continuous recording
- triggered responses
- uses –> detect nerve irritation, nerve mapping, assess nerve function, monitoring cranial nerves
stereotactic neurosurgery
- applies rules of geometry to radiologic images to allow for precise localization within the brain, provides up to 1mm accuracy
- less invasive intracranial surgery
- small markers (fudicials) affixed to scalp and forehead
- IMPORTANT fudicials do not move
- in OR patient’s head is appropriate positioned and the locations of the fudicials are entered into a computer
- computer calculates the position of the pointer with respect to the patient and display images front he scan on the monitor
- smaller brain biopsies may be done under local/MAC
- GETA for larger resections
crani bag
- cleviprex
- mannitol
- keppra
- phenyl
- precedex
- epi
drips for crani
- propofol 40-100 mcg/kg/min [max 40 mcg/kg/min for asleep motor mapping and awake crani]
- remifentanil 0.2 mcg/kg/min [titrate up as needed]
- phenylephrine 0.2 mcg/kg/min [titrate up as needed]
induction meds for crani
- fentanyl
- propopfol
- rocuronium (not always redosed, but may redose for aneurysm or pituitary tumor because those surgeries are VERY stimulating)
- sometimes succ if performing MEPs RIGHT away
meds to decrease ICP for crani
- decadron 10 mg
- mannitol 50-100g (or 0.25-0.5 g/kg)
- +/- lasix
antiepileptic meds for crani
- keppra
- vimpat (have to order in preop because usually really hard to get)
antibiotics for crani
- vancomycin
- ancef
analgesics for crani
- tylenol (within 30 min of wakeup)
- narcotic (dilaudid or fentanyl)
specific drugs for awake crani
- caffeine (adenosine receptor antagonist; CNS stimulant, 60 mg in 3 mL)
- physostigmine (anticholinesterase; crosses BBB; antagonizes CNS depressants; 0.5-1 mg/kg Q2-10min)
types of intracranial mass lesions
- congenital
- neoplastic (benign vs malignant)
- infections (abscess or cyst)
- vascular (hematoma or AVM)
typical presentation of intracranial mass lesions
- HA (50-60%)
- seizures (50-80%)
- focal neurological deficits (10-40%)
- sensory loss
- cognitive dysfunction
supratentorial intracranial mass lesions
- seizures, hemiplegia, aphasia
- fronta - personality changes, increased risk taking, difficulty speaking
- parietal - sensory problems
- temporal - problems with memory, speech perception, and language skills
- occipital - difficulty recognizing objects, an inability to identify colors, and trouble recognizing words
infratentorial/posterior fossa intracranial mass lesions
- cerebellar dysfunction - ataxia/poor balance, nystagmus, dysarthria, cannot perform rapid alternating movements, loss of muscle coordination
- brainstem compression - cranial nerve palsy, altered LOC, abnormal respiration
- edema, obstructive hydrocephalus at fourth ventricle
tentorium
-fold of the dura mater that separates and forms partition between the cerebrum and cerebellum
primary tumors
- glial cells = astrocytoma, oligodendroglioma, glioblastoma
- ependymal cells = ependymoma
- supporting tissues = meningioma, schwannoma, choroidal papilloma
major considerations for intracranial mass lesion
- tumor location = determines position, EBL, risk for hemodynamic changes intraoperatively
- growth rate and size = slow growing tumors are often asymptomatic
- ICP elevated
anesthetic goals for intracranial mass lesion
- control ICP
- maintain CPP
- protect from position related injuries
- rapid emergence for neuro assessment
monitoring for intracranial mass lesion
- standard monitors
- arterial line
- foley
- +/- central line
- PNS - do not monitor on hemiplegic side because you may end up overdosing paralytics
- +/- ventric for ICP monitoring (zero at external auditory meatus)
- possible IONM
positioning for intracranial mass lesion
- anticipate turning HOB 90-180 degrees
- insure ability to access all vital equipment
- adequate IV line extension
- long breathing circuit
- PNS often on LEs
- HOB often elevated 10-15 degrees
- patient may be supine, lateral, prone or sitting (sitting falling out of favor)
- anticipate sympathetic response with placement of mayfield head pins
preop for intracranial mass lesion
- determine presence of elevated ICP
- document LOC and neuro deficits
- review PMH and general health status
- review med regime (esp anticonvulsants, diuretics)
- review lab findings
- review radiological studies
- premedication (avoid benzos and narcs; continue corticosteroids and anticonvulsants)
intraoperative for intracranial mass lesion
- maintenace = no preferred anesthetic technique, hyperventilation, avoid excessive PEEP (<10)
- fluid management = glucose free crystalloids or colloids; replace blood loss with blood/colloids
- ICP control = EVD/lumbar drain, increases in cerebral blood flow
emergence for intracranial mass lesion
- must be slow and controlled, straining or bucking can cause ICH or worsen cerebral edema
- aggressive BP management (SBP <140 or <160); risk for hemorrhage or stroke, clevidipine, labetalol, esmolol
- surgical team will do neuro exam immediately after extubation, prior to OR departure
postoperative for intracranial mass lesion
- admit to ICU for obs
- transport with HOB elevated (30 degrees)
- manage HTN
- O2 for transport
- minimal pain post crani
- observe for seizures, neuro deficits, or increased ICP
awake-awake crani
- no infusions until closing
- propofol bolus for pins
asleep-awake crani
- start under GA with LMA or ETT
- wake the patient up once tumor is exposed
- propofol drip 40 mcg/kg/min ABW
- remi drip 0.2-0.4 mcg/kg/min IBW
asleep crani
- TIVA if IONM or asleep motor mapping
- GETA if no IONM
why are awake craniotomies done?
- used for epilepsy surgery and resection of tumors in frontal lobes and temporal lobes when speech and motor are to assessed intraop
- patient considerations = airway, temperature, anxiety
- asleep with LMA for exposure
- awake for cortical mapping and tumor resection
- sedated for iMRI (to evaluate the resection)
- when tumor resection complete use appropriate anesthetic to keep comfortable
MRI safety hazards for personnel
- magnetic field strength
- cold hazards
- acoustic noises
monteris medical (“LITT”)
- epilepsy
- glioblastomas
- recurrent brain metastases
- radiation necrosis
MR Thermography
- uses phase change to calculate real time (8 second delay) temperature data at and around probe
- thermal dose confirmed in real time using bio thermodynamic theory
- basically burns the tumor or eliptogenic focus
contents of posterior fossa
- cerebellum = movement and equilibrium
- brainstem = ANS, CV and respiratory centers, RAS, motor/sensory pathways
- CN I-XII
- large venous sinuses
trigeminal nerve stimulation
cushing’s reflex
bradycardia and hypertension
glossopharyngeal or vagus nerve stimulation
bradycardia and hypotension
brainstem injuries
- respiratory centers may be damaged and necessitate mechanical ventilation postoperatively
- tumors around glossopharyngeal and vagus nerves may impair gag reflex and increase risk of aspiration
- CN IX, X, and XI control pharynx and larynx
posterior fossa periop considerations
-same considerations as intracranial lesions
posterior fossa positioning considerations
-may be sitting, modified lateral, or prone
sitting position advantages
- improved surgical exposure
- less retraction and tissue damage
- less bleeding
- less cranial nerve damage
- better resection of lesion
- access to airway, chest, extremities
sitting position disadvantages
- postural hypotension
- arrhythmias
- venous pooling
- pneumocephalus
- nerve injuries (ulnar, sciatic, lateral peroneal, brachial plexus)
Pneumocephalus
- open dura –> CSF leak –> air enters –> VAE
- after dural closure, air can act as a mass lesion as CSF reaccumulates
- usually resolves spontaneously
- tension pneumocephalus - burr holes to relieve
- symptoms include delayed awakening, HA, lethargy, confusion
- if using N2O discontinue before dural closure
VAE when does it happen
- pressure in a vein is subatmospheric
- level of incision is > 5 cm higher than heart
- patients with PFO can have air enter circulation
VAE incidence
- potentially lethal
- mortality rate 1%
- sitting position = 25-50%
- prone, lateral, supine = 12%
paradoxical air embolism
- air enters L side of heart and travels to systemic circulation
- occurs when right heart pressure is greater than left
- common in patients with PFO
VAE S/S
- decreased ETCO2
- decreased PaO2
- decreased SaO2
- Spontaneous ventilation
- mill-wheel murmur (late sign)
- detection of ET nitrogen
- increased PaCO2
- hypotension
- dysrhythmias
monitoring for VAE
- capnography
- CVP/PA line
- precordial doppler
- DO NOT rely on one monitor to diagnose VAE, use monitors with different sensitivities to confirm
monitors for VAE from greatest to least sensitivity
- TEE (5-10x more sensitive than doppler, detects 0.25 mL of air)
- precordial doppler
- ETCO2 (decreases with 15-25 mL of air)
- PAP (increases with 20-25 mL of air)
- CVP
- PaCO2
- MAP
VAE treatment
- 100% O2, discontinue N2O
- notify surgeon to flood the field or pack wound
- call for HELP
- aspirate from CVP line with stopcock and 30-60 cc syringe
- volume load
- inotropes/vasopressors
- Jugular vein compression (valsalva)
- PEEP
- position patient in durant (L lateral decubitus with slight trendelenburg)
- CPR if necessary
craniocervical decompression (chiari malformation)
- cerebellum protrudes through foramen magnum
- compresses brainstem and cervical spinal cord
- types I-IV
- syringomyelia (CSF abnormally located in spinal cord)
chiari malformations anesthetic considerations
- position prone or sitting
- EBL - large venous sinuses
- vital sign instability due to brainstem manipulation
- postop = pain management
decelerations injuries
coup and contrecoup lesions
skull fractures
- linear = subdural or epidural hematomas
- basilar = CSF rhinorrhea, pneumocephalus, and cranial nerve palsies (battles sign, racoon/panda eyes)
- depressed = brain contusion
primary head injury
- biomechanical effect of forces on the brain at time of insult
- contusion
- concussion
- laceration
- hematoma
secondary head injury
- represents complicating process related to primary injury (minutes, hours, days after primary injury)
- intracranial hematoma, increased ICP, seizures, edema, vasospasm
pituitary non functioning tumors
- arise from growth of transformed cells of anterior pituitary
- generally well tolerated until 90% of gland is non-functional
pituitary functioning tumors
- cushings
- acromegaly
- prolactinomas
- TSH adenomas
cerebral aneurysm
- leading cause of non-traumatic intracranial hemorrhage
- incidence of cerebral aneurysm is 2% in north america
- commonly located in anterior circle of willis
- aneurysm fills with blood and can rupture, spilling blood into the subarachnoid space, creating a subarachnoid hemorrhage
- can lead to permanent brain damage, disability or death
unruptured aneurysm
- HA
- unsteady gait
- visual disturbances (loss, diplopia, photophobia)
- facial numbness
- pupil dilation
- drooping eyelid
- pain above or behind eye
ruptured aneurysm
- sudden extremely severe HA (worst of life)
- N/V
- LOC, prolonged coma
- focal neural deficits
- hydrocephalus
- seizure
- S/S increased ICP
vasospams
- causes ischemia or infarction
- exact mechanism not known
- accounts for 14% M/M
- digital subtraction angiography is the gold standard for diagnosis (not detectable until 72 hours after SAH)
- clinically significant occurrence (20-30%)
- calcium channel blockers
rebleeding
- rebleeding following initial SAH peaks seven days post incident
- major threat during delayed surgery
- accounts for 8% of M/M
- antifibrinolytic therapy
vasopasm treatment
- triple H therapy (goal is to treat ischemia with an increased CPP)
- hypertension (SBP 160-200 mmHg)
- hemodilution (Hct ~33% provides balance between O2 carrying capacity and viscosity)
- hypervolemia (aggressive IV infusion of colloids and crystalloids for CVP >10 mmhg or PCWP 12-20 mmHg)
interventional radiology endovascular coiling
- GETA with complete muscle paralysis
- control CPP
- minimal narcotic needs since minimally invasive
- aline preferred
- minimal to no blood loss
- heparin may be used for ACT 200-250
- same post op concerns with clipping
aneurysm coiling
- guglieimi detachable coil inserted into aneurysm
- standard arteriogram is performed to locate aneurysm
- catheter is passed often through femoral vessels and coil is advanced
- advantages - shorter stay, less anesthetic requirements, uncomplicated positioning, minimally invasive
- complications –> aneurysm rupture/subarachnoid hemorrhage, vasopasm, CVA, incomplete coiling
cerebral aneurysm operating room
- most commonly treated by microsurgical clip ligation
- crani approach, parent vessel giving rise to aneurysm is identified
- aneurysm neck is isolated and clip is placed across the neck, excluding it from circulation
- deep circulatory arrest may be necessary with giant aneurysm
cerebral aneurysm intraoperative management
- maintain optimum CPP
- decrease CPP rapidly if rupture occurs during surgical clipping
- maintain transmural pressure (MAP-ICP)
- decreased intracranial volume (blood and tissue); provide slack brain
- minimize CMRO2
cerebral aneurysm preinduction
- limit sedation
- a line
- 2 large bore IVs
- type and cross 2-4 units
- remember HOB turned 90-180 degrees
cerebral aneurysm induction
- smooth induction
- aggressive BP and HR control (narcotics, beta blockers, deepen anesthetic)
cerebral aneurysm maintenance
- may use TIVA or anesthetic gases
- temporary occlusion of a cerebral artery
- maintain BP 15-20% below baseline to prevent vasospasm, decrease EBL and allow for better exposure and visualization
- employ methods for cerebral protection and to reduce ICP if necessary
cerebral aneurysm fluid management
- run patient dry
- expand blood volume with colloids
- have PRBCs available
- no glucose containing solutions
cerebral aneurysm control of BP
- control of BP is critical to successful outcome of case
- increased BP = increased TMP across aneurysmal wall = rupture of aneurysm
- surgeon may ask for temporary increase in MAP to 80-100 mmHg to provide for collateral flow if a feeder vessel is clamped for a short period to allow for clipping of aneurysm
- post clipping, MAP usually kept 80-100 mmHg
likely times of intraop aneurysm rupture
- dural incision
- excessive brain retraction
- aneurysm dissection
- during clipping or releasing of clip
treatment of intraop aneurysm rupture
- immediate, aggressive fluid resuscitation and replacement of blood loss
- propofol bolus for brain production, to decrease MAP, and decrease blood loss
- decrease MAP to 40-50 mmHg (clevidipine, labetalol, esmolol)
- surgeon may apply temporary clip on parent vessel to control bleeding, restore BP after clipping to improve collateral flow
AVM
- congential abnormality that involves direct connection from an artery to a vein nidus without a pressure modulating capillary bed
- most common presentation intracranial hemorrhage
- treatment includes intravascular embolization, surgical excision, or radiation
- preop considerations are same as with aneurysm
- potential for significant blood loss is much higher (upwards of 3L)
cranial nerve decompression
- treats disorders of cranial nerves (trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia)
- unilateral
- usually caused by compression of a vascular structures
cranial nerve decompression anesthetic considerations
- position = lateral, prone, supine
- monitoring = facial nerve, brainstem auditory evoked response, EMG
- anesthesia = TIVA, brain relaxation
- PONV = multimodal
