Exam 2 Flashcards
Symptoms of anterior cerebral artery
contralateral leg weakness
middle cerebral artery occlusion symptoms
contralateral hemiparesis and hemisensory deficit (face and arm more than leg
aphasia
contralateral visual field deficit
Posterior cerebral artery occlusion symptoms
contralateral visual field defect
contralateral hemiparesis
basilar artery occlusion symptoms
occulomotor deficits and/or ataxia with “crossed” sensory and motor deficits
vertebral artery occlusion symptoms
lower cranial nerve deficits and/or ataxia with crossed sensory deficits
what medication do we avoid in pituitary tumor patients
corticosteroids such as decadron
what can the administration of decadron to a pitutiary tumor patient result in
suppression of the hypothalami-pituitary-adrenal axis resulting in a false diagnosis of hypopituitarism
what level do we want CO2 at for pituitary tumor sx
normocarbia
which type of tumor has a high bleeding risk
metastatic
what are s/s increased ICP
-N/V
-alteration of LOC
-decreased reactivity of pupils
-papilledema
-bradycardia
-systemic HTN
-breathing disturbances
-ML shifts >0.5 cm on CT or MRI
-seizure
-midline shifts
-HA
What is Cushing’s triad?
hypertension
bradycardia
irregular respirations
what drugs do we avoid with increase ICP to help with monitoring
drugs that change LOC and RR
-benzos
-narcs
-antihistamines
how do we manipulate the ventilator for increased ICP
hyperventilate to prevent increased ICP and acidosis
how do increased ICP patients present to PCP
-H/As
-visual disturbances
-seizures
-Behavior changes
what labs can be altered in pts with intracranial tumors and increased ICP
Na
glucose
what drugs increase ICP
ketamine
succs
halothane
what meds do we use to induce neuro/tumor patients with
propofol
barbiturates (thiopental, mehohexital)
what make propofol and barbiturates good induction drugs for neuro/tumors
rapid induction without increased ICP
what kind of MR do we use on neuro patients
NDMR
what inhaled anesthetic do we avoid in tumor patients
N2O- expands spaces and creates bubbles, decreases immune response
-risk of air emoboli
T/F keep tumor patient serum hypo-osmolaric
F, avoid it
what is effect of hypertonic saline (3%)
pulls H20 from brain, decreases ICP
T/F give neuro patient glucose containing solutions
F, causes ischemia and worsens neuronal injury
where do we level a line for neuro patient
circle of willis/external auditory meatus
what are anesthesia consideration post-op
-complete reversal of NMBs
-blunt reaction to ETT on emergence (elevated ICP)
what must be assessed immediately during post op period
LOC
what do we do if there are new deficits post-op
STAT CT
what does prognosis of stroke depend on
time between onset of sx to intervention
what are risk factors for CVA
-HTN MOST SIGNIFICANT RISK FACTOR,
-smoking,
-high lipids,
-DM,
-ETOH
how do we manage stroke
-ASA,TPA
Airway, O2, BP, glucose, body temperature regulation
-Prevent aspiration (ETT mb needed)
T/F hmmg stroke is more deadly than ischemic stroke
T. 4x more likely to die
how may we want CO2 in hmmg CVA
normocarbic
what is the most common cause of subarachnoid hmmg
rupture of intracranial aneurism
what are risk factors for subarachnoid hmmg
HTN,
coarctation of the aorta,
polycystic kidney disease,
fibromuscular dysplasia,
cerebral aneurysms in first-degree relatives
cigarettes
cocaine
female
oral contraceptives
what are s/s unruptured aneurism
new focal deficit
HA
seizure
what are sx of hmmg
severe HA
rapid onset of photophobia
stiff neck
decreased LOC
focal neuro changes
what VS do we control to prevent aneurysm rupture
BP
what are the 3Hs of vasospasm prevention
HTN
hypervolemia
hemodilution
what is an important anesthetic intervention to prevent rupture
depth of anesthesia during periods of stimulation
what do we have in room in case of aneurism rupture
blood, fluid, pressors
what is important in ICP monitoring
get baseline preop
what lines do we want for neuro
2 PIVs
CVL
A-line
T/F have patient take deep breath with VAE
F, can cause more air to enter
how do we monitor for VAE
precordial doppler
if patient is in beach chair with VAE and symptoms what do we do
place supine and offer hemodynamic support
what drugs can we use for awake crani
precedex, remi, LMA,
what drugs do we give to treat seizures
phenytoin
valproate
gabapentin
levetiracetam
what is an anesthetic consideration for med dosage of seizure patients
increased metabolism so increased dose
what drugs lower seizure threshold
lidociane
robaxin
ketamine
demerol
methohexitol
atricurium
cisatricurium
what seizure drugs decrease the duration of NDMR
pheytoin
carbamazepine
what is a fast way to terminate seizure during surgery
cold saline on brain
what do we need to control to prevent secondary brain injuries
-systemic hypotension
-hypoxia/hypoxemia
-hypercapnia
-hyperthemia
what is normal CPP
80-100 mmHG
what kind of patient is a candidate for awake crani
therapeutic sz meds
highly motivated and informed patient
no sleep apnea, anxiety, claustrophobia
T/F hyperventilate pituitary patient to prevent increase ICP
F, will decrease ICP and casue pituitary to retract into sella
what post op complication do we watch for in pituitary sx
DI
panhypopituiarianism
what are signs of pituitary invovlement
visual disturbances (optic nerve compression)
acromegaly (htn, cardiomyopathy)
hyperglycemia
HA
amenorrhea
galactorhea
cushings disease
potential airway comprimise
what is a complication of acromegally
airway compromise so use videoscope
when do we want pituitary patient most deep
pin placement
what are s/s DI
rapid diuresis
clear and dilute urine
increased serum osmo
decreased urine osmo
when does DI present
immediate to 2 days post op
what do we use to treat DI if we cant stabalize
DDAVP
what is the highest risk of developing VAE
sitting position
what heart defect is especially dangerous for an air embolism
PFO
what can we use to detect VAE
precordial doppler used to detect millwheel murmur
what are s/s VAE
O2 desat
lat MS
wheezing
difficulty breathing
hypotension
ST changed
JVD
RHF
mill wheel murmu
what is the most accurate way to detect VAE
TEE
metastatic brain tumors have a high risk of _______________ so prepare room and patient for admin of __________
bleeding
blood
how do we manipulate the ventilator for increased ICP
hyperventilate to prevent increased ICP and acidosis
what make propofol and barbiturates good induction drugs for neuro/tumors
rapid induction without increased ICP
what kind of MR do we use on neuro patients
NDMR
what is goal CO2 when hyperventilating neuro patient
35
why is depth of anesthesia important in neuro cases
light anesthesia can result in increased ICP
what is goal of BP for neuro cases
WNL
what medications are useful in maintaining depth of anesthesia in nuero patients
-propofol,
-lidocaine,
-paralytic,
-esmolol,
-narcotic
T/F keep tumor patient lightly paralyzed
F, very paralyzed, prevent any movement during brain surgery
T/F give neuro patient glucose containing solutions
F, causes ischemia and worsens neuronal injury
what monitors do we have for neuro patient
-A-line (Level at Circle of Willis- external auditory meatus)
-ICP monitoring
-Temp and UOP monitoring
-Large IVs or CVL (can use to aspirate intracardiac venous air embolism in sitting)
-TEE to detect air embolism
-Nerve stimulator
what is risk of sitting position
VAE
what are anesthesia consideration post-op
-complete reversal of NMBs
-blunt reaction to ETT on emergence (elevated ICP)
how do we avoid SNS response to extubation
-deep
-propofol wake up
-lidocaine bolus or gtt
what can cause delayed awakening
-Hypothermia,
-residual block,
-residual sedatives (narcs/benzos),
-primary CNS event (ischemia, hematoma, or tension pneumocephalus)
what is best volatile for neuro
ISO
what drug is useful in preventing vasospasm
nimodipine
when does vasospasm normally occur
3-15 days post op
what drugs do we use to lower BP post op in CVA
esmolol/labetalol- want to prevent depth of anesthesia so we can do nuero monitor
what do we do when surgeon clamps vessel
increase BP to provide collateral flow
how do we monitor for VAE
precordial doppler
what drugs can we use for awake crani
precedex, remi,
what drugs do we give to treat seizures
phenytoin
valproate
gabapentin
levetiracetam
what is an anesthetic consideration for med dosage of seizure patients
increased metabolism so increased dose
what seizure drugs decrease the duration of NDMR
pheytoin
carbamazepine
what is anesthesia for hydrocephalus
Tailored to ICP level,
head up/neck ML,
prevent crying,
hypervent,
inhalant if ICP not severe,
(lethargic=IV easier-IV lower ICP EXCEPT Ketamine),
Anectine caution with ICP,
MR after for motionless field
what number for SSEPS is bad
50 decreased amplitude
10 increase latency
what is the optimal hct for brain sx
30
how much CO goes to brain
15-20%
how much of total body oxygen does brain consume
20%
what is CMRO2 of the brain
3-3.8ml/100g/min
SSEPs amplitude is measured in
microvolts
MEPS amplitude is measured in
global voltage
where are leads placed for sseps
peripheral nerve and scalp
what area of the spinal cord does sseps monitor
dorsal
what area of the spinal cord dose MEPS monitor
anterior
what is a significant change in meps sseps
50% amplitude
what neuro monitor monitors auditory canal, tympanic membrane, hari cells, vestibulocochlear nerve…
BAEPs
what neuro monitor is used to assess visual pathways
VEPS
what anesthetic drugs do we avoid with SSEPS
volatiles/nitrous (0.5 MAC okay)
T/F opioids affect SSEPS
false
what drugs affect MEPS
volatiles/muscle relaxers/NO2
T/F cerebral oximetry relies on pulsatile flow
false
what do we avoid with elevated ICP during induction
hypotension
sympathetic response from laryngoscopy
hypoventilation
hypercapnia
succs
what is a good medication for IV anesthesia of nuero surgery
remifentanil
what are vent parameters for neuro surgery
6-8 ml/kg TV
peak pressures <40
avoid PEEP
PCC
what is fluid management goal for neurosurgery
euvolemia
NS no LR (hypotonic)
no glucose fluids
what electrolyte changes can mannitol cause
hyponatremia
hyperkalemia
T/F use peep with brain tumors
false
what is mannitol dose
0.5-1.5 g/kg
what issues can be associated with pituitary tumors
electolyte/fluid disturbances
SIADH/DI
what can ACTH secreting tumors lead to
cushing syndrome
SIADH has increased/decreased ADH
increased
what anesthetic complication must be carefully considered with awake crani
avoid hypoventilation
avoid hypercapnia
what are specific causes for increased ICP
tumors (size, edema, obstructing CSF)
intracranial hematomas (blood in CSF can cause dysfunction in arachnoid villi and granulations)
infections (can lead to edema or obstruction of CSF reabsoprtion)
what is a common cause of hydrocephalus
aqueductal stenosis
what causes aqueductal stenosis
congenital narrowing of the cerebral aqueduct connecting the third and fourth ventricle.
Obstructive hydrocephalus may occur during infancy or it may not present until adulthood in slower progressing cases.
what is found in 1/3 of aqueductal stenosis cases
seizures
what is the treatment for aqueductal stenosis
ventricular shunting
what is anesthesia considerations for aqueductal stenosis
managing intracranial HTN and increased ICP
what are the characteristics of benign intracranial HTN (psuedotumor cerebri)
ICP >20mmHg
CSF with normal serology and cytology
no tumors
normal ventricles (normal or small ventricular system)
symptoms worse with pregnancy
symptoms of benign intracranial HTN (psudeotumor cerebri)
headache
bilateral visual disturbances
symptoms worse in pregnancy
causes of benign intracranial HTN (psudeotumor cerebri)
found in obese women with menstrual irregularities
PCOS
systemic lupus
addisons disease
hypoparathyroidism
hypervitmaninosis A
treatment of benign intracranial HTN (psudeotumor cerebri)
removal of 20-40 ml of csf from subarachnoid space via spinal needle or catheter
acetazolamide
lumboperitoneal shunt
what is normal pressure hydrocephalus
large cerebral ventricals on CT with normal or low ICP
what causes normal pressure hydrocephalus
- develops over a period of weeks to months
- mechanism is thought to be related to compensated but impaired CSF absorption from previous insult to the brain such as SAH, meningitis, TBI
what are symptoms of normal pressure hydrocephalus
dementia
gait changes
urinary incontinence
what is the treatment of normal pressure hydrocephalus
drainage of CSF via VP shunting
symptoms of supratentorial tumors
‣ Headache
‣ Seizures
‣ New deficits-hemiparesis
‣ varying degree of edema around tumors
what patients are more likely to have supratentorial tumors
more common in adults
infratentorial tumors are more common in?
children
patients with infratentorial tumors present with
obstructive hydrocephalus
ataxia
what is the treatment for infratentorial tumors
surgical resection/debulking
chemo
radiation
steroids-reduce brain swelling and edema
what patient most commonly has atrocytomas
young adults
how do patients with astrocytomas present
new onset seizures
what are types of astrocytomas (least aggressive to most aggressive)
◦ Gliomas
◦ Pilocystic astrocytomas
◦ Anaplastic astrocytoma
◦ Glioblastoma multiforme
describe gliomas
- Least aggressive astrocytic tumor
- arise from glial cells (astrocytomas, oligodendroglioma
- Typically seen in young adults with new onset seizures.
- Surgical or radiation treatment gives good prospects for symptom free long term survival.
characteristic of pilocystic astrocytoma
seen in children and young adults
slow growing
arise in cerebellum, cerebral hemispheres, hypothalamus, optic pathways
contrast enhancing well demarcated lesion with minial surrounding edema
what are symptoms of pilocystic astrocytoma
HA
balance issues
vision problems
management strategy for pilocystic astrocytoma
surgery
characteristics of anaplastic astrocytoma
- Usually evolve into glioblastoma multiforme.
- more aggressive and faster growing, can be anywhere in brain
- appear as a contrast-enhancing lesion on imaging due to disruption of the blood-brain barrier
symptoms of anaplastic astrocytoma
HA
seizure
trouble thinking
treatment for anaplastic astrocytoma
surgery
radiation
chemo
survival 3-5 years
what is the most aggressive astrocytoma
gliobastoma multiforme
symptoms of gliobastoma multiforme
HA
memory loss
personality changes
characteristics of gliobastoma multiforme
- Accounts for 30% of all primary brain tumors in adults
- imaging usually reveals a ring-enhancing lesion reflecting central necrosis and surrounding edema
-short life expectancy
treatment of gliobastoma
debulking
radiation
chemo
characteristics of oligodendroglioma
rare
* Arises from myelin-producing cells within the central nervous system
- usually frontal lobe of brain
- Account for only 6% of
primary intracranial tumors - Typically see seizures before anything is apparent on CT, calcifications within tumor are common
- Tumor consists of both oligodendrocytic and astrocytic cells.
treatment of oligodendroglioma
resection
resistant to radiation
10-15 yr survival
when does ependymoa present
early childhood and young adult
Most commonly found in the floor of the fourth ventricle; in fluid filled spaces of brain and spinal cord
symptoms of ependymoma
obstructive hydrocephalus,
headache,
nausea, vomiting,
ataxia
treatment for ependymoma
resection
radiation
what is Primitive Neurectodermal Tumor
- Believed to arise from primitive neuroectodermal cells (immature brain cells that have not formed)
- seen mostly in cerebella, cerebral hemisphere
what is a common sign of primitive neurectodermal tumors
hydrocephalus
can affect moving, thinking, coordination, balance, seizures, and behavior
what is a meningioma
- Arise from outside the brain in arachnoid cap cells
- not inside brain, but press against it
- Slow growing and can get quite large
where are meningiomas most commonly found
sagittal sinus,
falx cerebri,
cerebral convexity.
where do meningiomas get their blood supply
external carotid artery
signs of meningiomas
HA
seizures
vision problems
memory problems
movement issues
signs of pituitary tumors
blurry vision to vision loss
typically benign
what are functional pituitary tumors
hormone secreting
aka microadenomas
what are non functional pituitary tumors
not hormone secreting
aka macroadenomas
HA, vision changes from compression of optic nerve
pituitary tumors present as
◦ Panhypopituitarism
◦ Apoplexy (sudden loss of consciousness, often followed by paralysis, caused by rupture or occlusion of a blood vessel in the brain)
◦ Visual changes
‣ Opthalmoplegia: paralysis or weakness of one or more of the muscles that control eye movement
◦ Altered mental status
what is an acoustic neuroma
- Usually the result of a benign schwannoma involving the vestibular component of cranial nerve VIII within the internal auditory canal
- may compress facial nerve or brainstem if larger tumors grow out of the internal auditory canal
- slow growing
symptoms of acoustic neuromas
hearing loss
tinnitus
disequilibrium
treatment for acoustic neuromas
resection with intraoperative cranial nerve monitoring
where do most metastatic tumors come from
lungs
breast
kidney
colon
skin
if there is more than one lesion in the brain what do we expect
metastatic brain tumors
what is abnormal about metastatic brain tumors
- abnormal angiogenesis in metastatic lesions leads to more bleeding during resection than with other tumors
what vessels can be measured through the temporal bone
◦ Middle cerebral artery- most commonly monitored
◦ Anterior cerebral
◦ Anterior communicating
◦ Posterior cerebral
◦ Posterior communicating
clinical features of stroke in anterior cerebral artery
contralateral leg weakness
clinical features of stroke in middle cerebral artery
contralateral hemiparesis
hemiparesis deficit (face and arm more than leg)
aphasia
contralateral visual field deficit
clinical features of stroke in posterior cerebral artery
contralateral visual defect
contralateral hemiparesis
clinical features of stroke in basilar cerebral artery
occulomotor deficits
ataxia with “crossed” sensory and motor deficits
clinical features of stroke in vertebral artery
lower cranial nerve deficits
and/or ataxia with crossed sensory deficits
what vessels can be assessed with doppler probe at back of flexed neck
basilar
opthalmic (also over closed eyelid)
internal carotid arteries
what is normal SjVO2
55-75
what SjvO2 would suggest cerebral ischemia
<50
what would SjvO2 >75 indicate
hyperemia, impaired O2 utilization often seen in TBI
what does the dominant jugular vein drain
mostly right side in majority of patients
cortico venous blood
contralateral vein drains subcortical regions
what are perioperative uses for EEG
◦ Identify inadequate blood flow to cerebral cortex caused by surgical/anesthetic-induced reduction in flow
◦ Guide reduction of cerebral metabolism prior to induced reduction of blood flow
◦ Predict neurologic outcome after brain insult
- Other uses: identify consciousness, unconsciousness, seizure activity, stages of sleep, coma
what are 3 parameters of EEG
amplitude- size or voltage of signal
frequency- number of time signal oscillates
time-duration of the sampling of the signal
what is the gold standard for intraoperative EEG
continuous visual inspection of a 16- to 32-channel analog EEG by experienced electroencephalographer
- provides the most detailed assessment of cerebral activity
- allows for real time interpretation of ischemia and seizure activity and anesthetic depth
general anesthesia (1 MAC) and EEG
irregular slow activity
deeper anesthesia (1.25 MAC) and EEG
alternating activity
very deep anesthesia( 1.6 MAC) and EEG
burst suppression
eventually isoelectric
subanesthetic doses of IV and inhaled anesthetics and EEG (0.3 MAC)
increases frontal beta activity
low voltage, high frequency
light anesthesia (0.5 MAC) and EEG
larger voltage, slower frequency
what are surgical non anesthetic factors that affect EEG
- Cardiopulmonary bypass
- Occlusion of major cerebral vessel (carotid cross-clamping, aneurysm clipping)
- Retraction on cerebral cortex can lead to localized hypoperfusion; show regional changes
- Surgically induced emboli to brain- can cause transient or permanent EEG disturbances
