Neuro Flashcards
(168 cards)
1
Q
anterior circulation to the brain
A
internal carotid artery
2
Q
posterior circulation to the brain
A
vertebral arteries
3
Q
two vertebral arteries
A
- branches of subclavian
- enter skull through foramen magnum and run along the medulla
- join in pons to form basilar artery
4
Q
basilar artery
A
branches at the midbrain into 2 posterior cerebral arteries which supply the occipital lobes of the brain
5
Q
internal carotid branches
A
- enter through the base of the skull and pass through the cavernous sinus
- divided into anterior and middle cerebral artery
6
Q
circle of willis
A
- 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)
7
Q
cerebral blood flow in adults
A
- varies with metabolic activity
- averages 750 mL/min
- about 15-20% of cardiac output
- 50 mL/100g/min
8
Q
gray matter blood flow
A
80 mL/100g/min
more blood flow here vs white matter because more activity
9
Q
white matter blood flow
A
20 mL/100g/min
10
Q
EEG cerebral impairment
A
20-25 mL/100g/min
11
Q
EEG flat
A
15-20 mL/100g/min
12
Q
EEG irreversible brain damage
A
below 10 mL/100g/min
13
Q
CBF monitoring
A
- 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)
14
Q
NIRS
A
- 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
15
Q
neuro events + NIRS
A
rSO2 < 40%
change in rSO2 of > 25% from baseline
16
Q
CPP Formula
A
CPP = MAP - ICP
*CVP must be substituted for ICP if CVP is higher
17
Q
ICP normal value
A
10-15 mmHg
18
Q
CPP normal value
A
80-100 mmHg
19
Q
CPP slowing of EEG
A
<50 mmHg
20
Q
CPP flat EEG
A
25-40 mmHg
21
Q
CPP irreversible brain damage
A
<25 mmHg
22
Q
autoregulation
A
- 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)
23
Q
myogenic response
A
intrinsic response of smooth muscle in cerebral arterioles
24
Q
metabolic response
A
- 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
25
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
26
MAP >150-160 mmHg
this can disrupt the BBB and may result in cerebral edema and hemorrhage
27
chronic hypertension and autoregulation
right shifted in patients with chronic hypertension
28
factors effecting CBF
- PaCO2
- PaO2
- temperature
- viscosity
- autonomic influences
- age
29
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)
30
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
31
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
32
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
33
PaO2 effect on CBF
- 50 to 300 mmHg little influence on CBF
| - <50 mmHg rapidly increases CBF
34
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
35
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
36
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
37
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
38
what is optimal cerebral oxygen delivery
occurs at a hematocrit of about 30%
39
autonomic influence on CBF
- SNS = vasoconstricts and decreases CBF
| - PSNS = vasodilates and increases CBF
40
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
41
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
42
which areas of the brain are most sensitive to hypoxic injury
- hippocampus
| - cerebellum
43
glucose and the brain
- glucose primary energy source
- brain glucose consumption 5 mg/100g/min
- 90% aerobically O2 metabolized
44
hypoglycemia
means brain injury
45
hyperglycemia
may exacerbate hypoxic injury
46
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
47
lipid barrier of brain what can pass
- lipid-soluble substances freely pass
- ionized molecules restricted
- large molecules restricted
48
determinants of what can pass the BBB
- size
- charge
- lipid solubility
- plasma protein binding
49
what freely crosses the BBB
- O2
- CO2
- Lipid soluble molecules (most anesthetics)
- H2O
50
what is restricted to cross the BBB
- ions (electrolytes like Na+)
- plasma proteins
- large molecules (mannitol)
51
what disrupts the BBB
- HTN
- tumor
- trauma
- stroke
- infection
- marked hypercapnia
- hypoxia
- sustained seizure
52
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)
53
how much CSF do adults make?
21 mL/hr or 500 mL/day
54
total volume of CSF
150 mL
| 1/2 in cranium and 1/2 in spinal canal
55
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
56
what inhibits production of CSF
- Carbonic anhydrase inhibitors (acetazolamide)
- corticosteroids
- spironolactone
- furosemide
- isoflurane
- vasoconstrictors
57
absorption of CSF
-translocation from arachnoid granulations into cerebral sinuses
58
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
59
cranial vault components
- brain 80%
- blood 12%
- CSF 8%
60
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
61
normal ICP
< 10 mmHg
62
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
63
> 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
64
ICP provider goals for closed crainium
- maintain CPP
| - prevent herniation
65
ICP provider goals for open cranium
- facilitate surgical access
| - reverse ongoing herniation
66
intracranial hypertension
sustained increase in ICP about 20-25 mmHg
67
causes of intracranial HTN
- expanding tissue or fluid mass
- interference with CSF absorption
- excessive CSF production
- systemic disturbances promoting edema
68
S/S increased ICP
- HA
- nausea/emesis
- papilledema
- decreased LOC
- focal neurological deficit
- seizures
- coma
- cushings triad
69
cushing's triad
- irregular respiration
- HTN
- bradycardia
70
herniation areas
- cingulate gyrus under falx cerebri
- central
- uncal (transtentorial)
- cerebellar tonsils through foramen magnum
- upward herniation of cerebellum
- transcalvarial
71
most common area of herniation
-cerebellar tonsils through foramen magnum
72
S/S cingulate gyrus herniation
-little known
73
uncal and central herniation S/S
- decrease LOC
- pupils sluggish --> fixed and dilated
- cheyne stokes respirations
- decorticate --> decerebrate posturing
74
cerebellar tonsillar herniation S/S
- no specific clinical manifestations
- arched stiff neck
- paresthesias in shoulder
- decreased LOC
- respiratory abnormalities
- pulse rate variations
75
transcalvarial herniation S/S
-may occur during surgery
76
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)
77
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
78
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
79
CBF and alpha 2 agonists
- decreases CBF up to 25-30%
| - results from reduced CMRO2 leading to a reduced CBF
80
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
81
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
82
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)
83
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
84
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
85
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
86
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
87
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
88
opioids
-minimal effects on CBF, CMR, and ICP unless increase PaCO2
89
intracranial surgeries
- craniotomy
- interventional radiology
- trauma
90
functional surgeries
- epilepsy
- movement
- pain
91
spine surgeries
- anterior
- posterior
- transoral
92
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
93
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
94
EMG
- records muscle electrical activity using needle pairs
- continuous recording
- triggered responses
- uses --> detect nerve irritation, nerve mapping, assess nerve function, monitoring cranial nerves
95
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
96
crani bag
- cleviprex
- mannitol
- keppra
- phenyl
- precedex
- epi
97
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]
98
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
99
meds to decrease ICP for crani
- decadron 10 mg
- mannitol 50-100g (or 0.25-0.5 g/kg)
- +/- lasix
100
antiepileptic meds for crani
- keppra
| - vimpat (have to order in preop because usually really hard to get)
101
antibiotics for crani
- vancomycin
| - ancef
102
analgesics for crani
- tylenol (within 30 min of wakeup)
| - narcotic (dilaudid or fentanyl)
103
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)
104
types of intracranial mass lesions
- congenital
- neoplastic (benign vs malignant)
- infections (abscess or cyst)
- vascular (hematoma or AVM)
105
typical presentation of intracranial mass lesions
- HA (50-60%)
- seizures (50-80%)
- focal neurological deficits (10-40%)
- sensory loss
- cognitive dysfunction
106
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
107
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
108
tentorium
-fold of the dura mater that separates and forms partition between the cerebrum and cerebellum
109
primary tumors
- glial cells = astrocytoma, oligodendroglioma, glioblastoma
- ependymal cells = ependymoma
- supporting tissues = meningioma, schwannoma, choroidal papilloma
110
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
111
anesthetic goals for intracranial mass lesion
- control ICP
- maintain CPP
- protect from position related injuries
- rapid emergence for neuro assessment
112
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
113
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
114
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)
115
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
116
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
117
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
118
awake-awake crani
- no infusions until closing
| - propofol bolus for pins
119
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
120
asleep crani
- TIVA if IONM or asleep motor mapping
| - GETA if no IONM
121
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
122
MRI safety hazards for personnel
- magnetic field strength
- cold hazards
- acoustic noises
123
monteris medical ("LITT")
- epilepsy
- glioblastomas
- recurrent brain metastases
- radiation necrosis
124
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
125
contents of posterior fossa
- cerebellum = movement and equilibrium
- brainstem = ANS, CV and respiratory centers, RAS, motor/sensory pathways
- CN I-XII
- large venous sinuses
126
trigeminal nerve stimulation
cushing's reflex
| bradycardia and hypertension
127
glossopharyngeal or vagus nerve stimulation
bradycardia and hypotension
128
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
129
posterior fossa periop considerations
-same considerations as intracranial lesions
130
posterior fossa positioning considerations
-may be sitting, modified lateral, or prone
131
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
132
sitting position disadvantages
- postural hypotension
- arrhythmias
- venous pooling
- pneumocephalus
- nerve injuries (ulnar, sciatic, lateral peroneal, brachial plexus)
133
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
134
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
135
VAE incidence
- potentially lethal
- mortality rate 1%
- sitting position = 25-50%
- prone, lateral, supine = 12%
136
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
137
VAE S/S
- decreased ETCO2
- decreased PaO2
- decreased SaO2
- Spontaneous ventilation
- mill-wheel murmur (late sign)
- detection of ET nitrogen
- increased PaCO2
- hypotension
- dysrhythmias
138
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
139
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
140
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
141
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)
142
chiari malformations anesthetic considerations
- position prone or sitting
- EBL - large venous sinuses
- vital sign instability due to brainstem manipulation
- postop = pain management
143
decelerations injuries
coup and contrecoup lesions
144
skull fractures
- linear = subdural or epidural hematomas
- basilar = CSF rhinorrhea, pneumocephalus, and cranial nerve palsies (battles sign, racoon/panda eyes)
- depressed = brain contusion
145
primary head injury
- biomechanical effect of forces on the brain at time of insult
- contusion
- concussion
- laceration
- hematoma
146
secondary head injury
- represents complicating process related to primary injury (minutes, hours, days after primary injury)
- intracranial hematoma, increased ICP, seizures, edema, vasospasm
147
pituitary non functioning tumors
- arise from growth of transformed cells of anterior pituitary
- generally well tolerated until 90% of gland is non-functional
148
pituitary functioning tumors
- cushings
- acromegaly
- prolactinomas
- TSH adenomas
149
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
150
unruptured aneurysm
- HA
- unsteady gait
- visual disturbances (loss, diplopia, photophobia)
- facial numbness
- pupil dilation
- drooping eyelid
- pain above or behind eye
151
ruptured aneurysm
- sudden extremely severe HA (worst of life)
- N/V
- LOC, prolonged coma
- focal neural deficits
- hydrocephalus
- seizure
- S/S increased ICP
152
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
153
rebleeding
- rebleeding following initial SAH peaks seven days post incident
- major threat during delayed surgery
- accounts for 8% of M/M
- antifibrinolytic therapy
154
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)
155
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
156
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
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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
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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
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cerebral aneurysm preinduction
- limit sedation
- a line
- 2 large bore IVs
- type and cross 2-4 units
- remember HOB turned 90-180 degrees
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cerebral aneurysm induction
- smooth induction
| - aggressive BP and HR control (narcotics, beta blockers, deepen anesthetic)
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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
162
cerebral aneurysm fluid management
- run patient dry
- expand blood volume with colloids
- have PRBCs available
- no glucose containing solutions
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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
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likely times of intraop aneurysm rupture
- dural incision
- excessive brain retraction
- aneurysm dissection
- during clipping or releasing of clip
165
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
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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)
167
cranial nerve decompression
- treats disorders of cranial nerves (trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia)
- unilateral
- usually caused by compression of a vascular structures
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cranial nerve decompression anesthetic considerations
- position = lateral, prone, supine
- monitoring = facial nerve, brainstem auditory evoked response, EMG
- anesthesia = TIVA, brain relaxation
- PONV = multimodal
