Exam 3 Neuro Disease Flashcards
1
Q
Cerebral blood flow (CBF) is modulated by:
A
- cerebral metabolic rate
- cerebral perfusion pressure (CPP) * MAP-ICP
- arterial blood carbon dioxide (Paco2)
- arterial blood oxygen (Pao2)
- various drugs and intracranial pathologies
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2
Q
- With autoregulation, CBF is approx ____ brain tissue per minute.
- which = ____ml/min
- and is ____% of COP
A
50 mL/100g
750 ml/min
15%
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3
Q
- The intracranial & spinal vault contains ____, ____, and ____.
- The vault is enclosed by the ____ and ____.
A
- neural tissue (brain + spinal cord), blood, and CSF
- dura mater and bone
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4
Q
Under normal conditions, brain tissue, intracranial CSF, and intracranial blood have a combined volume of
A
1200-1500mL
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5
Q
at a volume of 1200-1500ml, what is a normal ICP?
A
5-15 mmhg
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6
Q
any increase in one component of intracranial volume must be offset by a decrease in another component to prevent an elevated ICP
A
monro-kellie hypothesis
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7
Q
During normal physiologic conditions, changes in one component are well compensated for by changes in other components, but eventually a point is reached where even a small change in intracranial contents results in a ____.
A
large change in ICP
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8
Q
Since ICP is one of the determinants of CPP, homeostatic mechanisms canincrease MAP to support CPP despite increases in ICP, but eventually these compensatory mechanisms can fail, resulting in ____
A
cerebral ischemia
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9
Q
The intracranial vault is considered ____
A
compartmentalized
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10
Q
Meningeal barriers separate the brain contents and include ____ and ____.
A
- falx cerebri
- tentorium cerbelli
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11
Q
what is the falx cerebri:
A
a reflection of dura that separates the two cerebral hemispheres
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12
Q
what is the tentorium cerebelli:
A
a reflection of durathat lies rostral to the cerebellum and marks the border btw the supratentorial and infratentorial spaces
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13
Q
____ in the contents of one region may cause regional increases in ICP, and in extreme instances, the contents can herniate into a different compartment
A
Increases
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14
Q
Herniation syndromes are categorized based on the ____
A
region of brain affected
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15
Q
types of herniation
A
subfalcine
transtentorial
uncal
cerebellar tonsils
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16
Q
what is SubfalcineHerniation?
A
Herniation of hemispheric contents under the falx cerebri; typically, compressing branches of theanterior cerebral artery, creating a midline shift
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17
Q
what is transtentorialHerniation?
A
- Herniation of the supratentorial contents past the tentorium cerebelli, causing brainstemcompression in a rostral to caudal direction.
- This leads to AMS, defects in gaze and ocular reflexes, hemodynamic andrespiratory compromise, and death
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18
Q
what is Uncal Herniation?
A
- a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe) herniatesoverthe tentorium cerebelli.
- This results in ipsilateral oculomotor nerve dysfunction
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19
Q
s/s of uncal herniation
A
- pupillary dilatation
- ptosis
- lateral deviation of the affected eye
- brainstem compression
- death
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20
Q
when does cerebellar tonsils herniation occur?
A
Herniation of the cerebellar tonsils can occur due to elevated infratentorial pressure, causing the cerebellarstructures to herniate through the foramen magnum
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21
Q
s/s of cerebellar tonsils herniation
A
medullary dysfunction, cardiorespiratory instability and subsequently death
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22
Q
what type of herniation is 1, 2, 3, and 4?
A
- Subfalcine
- Transtentorial
- Cerebellar contents through foramen magnum
- Traumatic event causing herniation out of cranial cavity
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23
Q
what can cause increased ICP?
A
- tumors
- intracranial hematomas
- blood in CSF
- infections
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24
Q
how can tumors increase ICP?
A
1) directly because of their size
2) indirectly by causing edema in surrounding brain tissue
3) by obstructing CSF flow, as seen with tumors involving the third ventricle
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how can intracranial hematomas increase ICP?
Intracranial hematomas cause increased ICP similar to mass lesions
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how can blood in the CSF increase ICP?
Blood in the CSF, as is seen in subarachnoid hemorrhage, may lead to obstruction of CSF reabsorption, and granulations can further exacerbate increased ICP
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how can infections increase ICP?
Infections s/a meningitis or encephalitis, can lead to edema or obstruction of CSF reabsorption
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how do you decrease ICP?
* elevation of the head
* hyperventilation
* csf drainage
* hyperosmotic drugs
* diuretics
* corticosteroids
* cerebral vasocnstricting anesthetics
* surgical decompression
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how can elevation of the head decrease ICP?
encourages jugular venous outflow
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how canhyperventiltion decrease ICP?
lowers PaC02
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how can you drain CSF to decrease ICP?
external ventricular drain (EVD)
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how canhyperosmotic drugs decrease ICP?
increase osmolarity, drawing fluid across BBB
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how can diuretics decrease ICP?
induce systemic hypovolemia
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how can corticosteroids decrease ICP?
decrease swelling and enhance the integrity of the BBB
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how can cerebral vasoconstricting anesthetics decrease ICP? what medication is an example of this?
* decrease CMR02 and CBF
* propofol
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what to know for neurological assessment
* Know the basic pathophysiology for neurological disorders
* Look at patients' history, symptoms, and baseline neuro-deficits
* Review imaging and available neurological testing results
* Review the patients' current drugs and treatments
* Evaluate the potential risks/benefits of various anesthetic options to determine the most appropriate plan of care
* Implement pre-op measures that may help optimize the patients' condition prior to anesthesia
* Provide clear pre-op documentation of the factors above, and have a rational for chosen anesthetic plan
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what are examples of genetic neurological disorders
Multiple Sclerosis
Myasthenia Gravis
Lambert Eaton Syndrome
Myasthenia Syndrome
Muscular Dystrophies
Myotonic Dystrophies
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* This is a progressive, autoimmune demyelination of central nerve fibers.
* There is an onset at age 20-40.
* Risk factors include: female, 1st deg relative, EBV, other AI disorders, smoking
* Characterized by periods of exacerbations & remissions
* Triggers: stress, elevated temps, postpartum period
* Sx: motor weakness, sensory disorders, visual impairment, autonomic instability. Sx vary b/o site of demyelination
* Tx: No cure
multiple sclerosis "MS"
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although MS has no cure it can be managed with:
* corticosteroids
* immune modulators
* targeted antibodies
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what preanesthetic considerations should be thought of with a patient with MS?
* Assess existing deficits
* If respiratory compromise, consider pulmonary function tests
* Labs: CBC, BMP, +/-LFT
* LFT if on Dantrolene & Azathioprine (bone marrow suppression, liver function impairment)
* Close attn to glucose and electrolytes as steroids may impact levels
* Consider giving pre-op steroids in anyone with long-term steroid use
* LT steroids cause adrenal suppression, so a stress-dose of steroids may be necessary for surgery
* Temperature management is critical
* Any increase in body temp can precipitate an exacerbation of MS sx
* GA, RA & PNB’s are acceptable options
* Avoid Succinylcholine as it may induce hyperkalemia
* Upregulated N-ach receptors
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What is this disease?
* Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate
* Effects skeletal muscle, not smooth or cardiac muscle
* Muscle weakness, exacerbated w/exercise
* Cranial nerves partially susceptible
* Ocular sx common-diplopia, ptosis
* Bulbar involvement → laryngeal/pharyngeal weakness→ respiratory insufficiency, aspiration rx
* Thymic-hyperplasia is common (10%)
* 90% pts improve after Thymectomy
Myasthena Gravie "MG"
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For Myasthenia Gravie "MG"
* S/S exacerbated by:
* Tx:
* S/S exacerbated by: pain, insomnia, infection, surgery
* Tx: Ach-E inhibitors (Pyridostigmine), immunosuppressive agents, steroids, plasmapheresis, IVIG
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MG preanesthetic considerations include:
* If respiratory compromise, consider pulmonary function tests
* Optimize respiratory function
* Reduce paralytic dosage to avoid prolonged muscle weakness
* Caution with opioids to avoid respiratory compromise
* Ach-E inhibitors may prolong Succs and Ester LA’s
* Labs: CBC, BMP, +/-LFT (LFT if on Azathioprine)
* Close attn to glucose and electrolytes as steroids may impact levels
* Consider pre-op steroids in anyone with long-term steroid use
* Counsel patients on the increased risk of needing post-op resp support/ventilation until fully recovered from anesthesia
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what is this disease:
* Disorder causing the development of autoantibodies against VG Calcium chnls
* Reduce Ca++ influx into the presynaptic Ca++ channels→↓Ach release @ the NMJ
* Sx similar to MG
* >60% cases are assoc w/ small cell lung carcinoma
eaton-lambert syndrome
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for eaton-lambert syndrome:
* s/s
* tx:
* Sx: progressive limb-girdle weakness, dysautonomia, oculobulbar palsy
* Tx: Selective K+ chnl blocker “3-4 diaminopyridine”, Ach-E inhibitors, immunologics (Azathioprine), steroids, plasmapheresis, IVIG
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ELS pre-anesthetic considerations include:
* Assess existing deficits
* If respiratory compromise, consider pulmonary function tests
* VERY sensitive to ND-NMB & D-NMB
* Significantly more sensitive to ND-NMB than MG patients
* Optimize respiratory function
* Extreme caution on paralytic and opioid dosing
* Counsel on risks for needing post-op resp support until fully recovered from anesthesia
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what is this disease?
* Hereditary disorder of muscle fiber degeneration c/b breakdown of the dystrophin-glycoprotein complex, leads to myonecrosis, fibrosis, and skeletal muscle mbrn permeability.
muscular dystrophy
*6 typer of MD*
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what is the most common and severe form of muscular dystrophy?
* Ducheen MD
* Occurs only in boys, onset 2-5y. Wheelchair bound by age 8-10. Avg lifespan ̴20-25y d/t cardiopulmonary complications
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for muscular dystrophy:
* S/S:
* progressive muscle wasting without motor/ sensory abnormalities
* kyphoscoliosis
* long bone fragility
* respiratory weakness
* frequent pneumonia
* EKG changes
* Elevated serum creatine kinase c/b muscle wasting
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MD preanesthetic considerations
* CBC, BMP, PFTs, consider CK
* Pre-op EKG, echocardiogram. Evaluate for cardiomyopathy
* Caution with ND-NMB’s, careful monitoring throughout
* “Hypermetabolic Syndrome” similar to MH seen with Succs & volatile anesthetics
* Hypermetabolic syndrome can lead to: rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest
* Avoid Succs & VA as they exacerbate instability of muscle membrane
* Consider low dose rocuronium and TIVA for GA
* Have MH cart with Dantrolene available
* RA preferred over GA to avoid triggers and cardiopulmonary complications
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what are the myotonic dystrophies mentioned in class?
* myotonia
* myotonic dytrophy
* myotonia congenita
* central core disease
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what is myotonia?
* prolonged contraction after muscle stimulation
* seen in several muscle disorders
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what is myotonic dystrophy? what is its s/s?
* most common myotonia. Onset 20-30’s
* Sx: muscle wasting in face, masseter, hand, pre-tibial muscles
* may also affect pharyngeal, laryngeal, diaphragmatic muscles
* cardiac conduction may be affected; 20% have MVP
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what is myotonia congenita?
* Milder form, involving the skeletal muscles
* smooth & cardiac muscles are spared
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what is central core disease? s/s? tx?
* Rare. Core muscle cells lack mitochondrial enzymes
* Sx: Proximal muscle weakness & scoliosis
* Myotonias are triggered by stress & cold temps
* Tx: No cure. Sx managed w/Quinine, Procainamide, Steroids
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pre-anesthetic considerations for myotonic dystrophies?
* Assess the extent of cardiac and pulmonary abnormalities
* Assess breath and heart sounds for abnormalities
* GI hypomotility-↑aspiration risk
* High rx of endocrine abnormalities. Look at thyroid & glucose levels
* Keep patients warm to avoid flare-ups
* **Avoid Succinylcholine b/c fasciculations trigger myotonia**
* Optimize preop respiratory status
* Caution with opioids to avoid post-op respiratory depression
* Pts are increased risk for post-op resp weakness
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what are the 3 major dementia syndromes?
Alzheimer's (70%), Vascular dementia (25%), Parkinsons (5%)
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what should you evaluate in a pateint with dementia?
* Assess baseline level of cognitive dysfunction
* Patient may not be able to give informed consent, look to medical PoA
* Investigate any advanced directives for medical decision-making
* Review basic labs and pertinent tests/imaging
* Potential aspirations rx (may be full stomach)
* Review pre-op meds, which may affect anesthetic (AchE-I, MAOI’s, psych meds)
* ↑risk for post-op delirium (consider TIVA)
* Balance opioids to meet analgesic needs w/o exacerbating delirium
* RA preferred to ↓opioid requirements
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what is this disease?
* Degeneration of dopaminergic fibers of basal ganglia
* Unknown cause; Advanced age is biggest risk factor
* Dopamine regulates (inhibits excess stimulation) the extrapyramidal motor system, which is stimulated by Ach *these motor neurons are over stimulated*
parkinsons disease
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60
what are the triad of sx in parkinsons? what are other s/s?
* Triad:
* skeletal muscle tremor, rigidity, akinesia
* Other:
* Rhythmic “pill rolling,”
* facial rigidity,
* slurred speech,
* difficulty swallowing,
* respiratory difficulty,
* depression
* dementia
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what is treatment for parkinsons?
* Levodopa (crosses BBB),
* anticholinergics,
* MAOIs (inhibit dopamine degradation)
* Deep brain stimulator
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parkinsons pre-anesthesia considerations:
* Assess severity, with special attn to degree of pulmonary compromise
* Review home meds, as many may interact with our drugs (ex. MAOIs)
* Review basic labs along w/PFT if respiratory sx
* May need EKG, Echo if indicated
* ↑aspiration risk (dysphagia, possible dementia)
* PO Levodopa must be continued to avoid unstable extreme extrapyramidal effects s/a chest wall rigidity
* Avoid Reglan, Phenothiazines, Butyrophenones
* Avoid Demerol if on MAOI
* Deep brain stimulators may need to be disabled to avoid interaction w/cautery
* If cautery used, bipolar recommended as it reduces scattering of electro-currant
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the mass effects of any tumor can cause ____ deficits.
neurologic deficits
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common s/s of brain tumors
* ↑ICP
* Papilledema
* Headache
* AMS
* Mobility impairment
* Vomiting
* Autonomic dysfunction
* Seizures
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brain tumors may be ____ or ____.
primary or metastatic
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astrocytomas are the most common CNS glial cells. What are the 4 types of astrocytomas tumors?
* gilomas
* pilocytic astrocytomas
* anaplastic astrocytomas
* glioblastoma multiforme
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what is a glioma?
* Primary tumors. Least aggressive astrocytomas
* Often found in young adults w/new onset seizures
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what is pilocyctic astrocytomas?
* Children & young adults
* Mostly benign, good outcomes if resectable
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what is anaplastic astrocytomas?
* Poorly differentiated
* Usually evolve into Glioblastoma Multiforme
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what is glioblastoma multiforme?
* Carry a high mortality
* Usually requires surgical debulking & chemo
* Life expectance is usually within weeks, even w/treatment
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what is meinigiomas?
* Usually benign. Arise from dura or arachnoid tissue
* Good prognosis w/surgical resection
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what is pituitary adenomas?
* Noncancerous, varying subtypes
* Transsphenoidal or open craniotomy for removal is usually curative
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what is acoustic neuromas?
* Usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal
* Good prognosis w/resection +/- radiation
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what is metastatic carcinomas?
* can vary widely in origin & symptoms
* Outcomes are generally less favorable
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brain tumor pre-anesthesia considerations include
* Review history & physical
* Inquire about previous therapies, presenting symptoms & neurological deficits
* Radiation damage may lead to lethargy and AMS
* Chemotherapy may also have neurological effects
* Pts are often on steroids to minimize cerebral edema
* Will need to continue steroids, monitoring glucose levels
* Anticonvulsants common (supratentorial lesions, closer to motor cortex)
* Autonomic dysfunction may manifest on EKG, labile HR & BP’s
* CBC, BMP (glucose), EKG
* CT/MRI
* Pre-op steroids & antiseizure meds per surgeon
* Mannitol often used to reduce intracranial volume & pressure
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what are the types of strokes/CVAs?
* ischemic
* hemorrhagic
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Strokes are characterized by sudden neurologic deficits resulting from:
* ischemia (88% of cases)
* hemorrhage (12% of cases)
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what is the leading cause of death and disability?
strokes
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79
how is blood supplied to the brain?
* internal carotid arteries
* verterbral arteries
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____ join on the ____ surface of the brain to form the ____ which, during ideal circumstances, provides collateral circulation to multiple areas of the brain
* internal carotid and verterbral arteries
* inferior surface
* circle of willis
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clinical features of occluded anterior cerbral artery
contralateral leg weakness
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clinical features of occluded middle cerbral artery
* controlateral hempiparesis and hemisenory deficit *face and arme > leg*
* aphasia *dominat hemisphere*
* controlateral visual field defect
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clinical features of occluded posterior cerbral artery
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clinical features of occluded penetrating arteries
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clinical features of occluded basilar artery
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clinical features of occluded verterbral artery
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____ occlusion of a vessel that supplies a region of brain resulting in cellular ischemia
Ischemic Stroke
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What is this?
* sudden focal vascular neurologic deficit that resolves within 24 hrs
Transient ischemic attack
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____ pts who experience a TIA will subsequently suffer a stroke
1/3
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* Stroke prognosis d/o the time from onset to thrombolytic intervention (____)
* If stroke suspected, a STAT non-contrast CT is needed to distinguish what?
* < 90 min
* ischemia stroke from intracerebral hemorrhage
*This distinction is important because tx of ischemic stroke is substantially different from tx of hemorrhagic stroke*
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Causes of Ischemic stroke are categorized according to the TOAST classification into 5 groups
1. Large artery atherosclerosis (e.g., carotid stenosis)
2. Small vessel occlusion (e.g., lacunar stroke)
3. Cardioaortic embolic (e.g., emboli from atrial fibrillation)
4. Other etiology (e.g., stroke due to hypercoagulable states or vasculopathies)
5. Undetermined etiology
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Ischemic CVA treatment
* ASA initally for acute ischemic stroke
* TPA if criteria is met
* thrombectomy to stent vessels and remove clots
* revascularization
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these are performed in interventional radiology (IR), allowing for angiographic assessment and radiographic guidance during administration of thrombolytics or thromb
revascualrization
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revasculatrization anesthesia considerations
* Pre-anesthetic evaluation should be concise & efficient, avoiding any delay in treatment
* Focus on baseline neuro assessment, ability to safely lay flat, and cardiovascular function
* Determine whether procedure could be done under sedation, or if a secure airway necessary
* Patients w/ischemic stroke frequently have CV risk factors, including HTN, DM, CAD, Afib, and valvular disease, that could impact vasoactive drug choices and hemodynamic goal
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hemorrhagic CVA tx
* Tx depends on severity
* Conservative tx is centered on the reduction of ICP, blood pressure control, seizure precautions, and vigilant monitoring
* Surgical treatment involves evacuation of the hematoma
* May remain intubated depending on cardiopulmonary stability
* ICU monitoring required postoperatively
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____ stroke results from bleeding inside the cranial vault that, in turn, impairs perfusion of the brain
Acute hemorrhagic
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Hemorrhagic stroke is ____ more likely to cause death than ischemic stroke
4x
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the 2 most reliable predictors of outcome are:
estimated blood volume & change in LOC
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what are the subtypes of hemorrhagic strokes and where is the location?
* intraparenchymal- blood within the brain
* epidural/ subdural/ subarachnoid hematomas- blood in the area
* intraventricular- blood in the ventricular system *usually occurs with other types of hemorrhagic strokes*
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what is this?
* New anticoagulant for thrombus=No elective cases within 3 months
* Anticoagulants for CVA prophylaxis= consult prescriber to establish protocol
* High rx pts for CVA that pause LA anticoags (Warfarin) will need SA anticoags (LMWH, IV unfractionated heparin) to bridge the gap
* Close monitoring of coagulation status is required
* If RA planned, d/c anticoagulants for sufficient time to safely perform block
cerebrovascular disease
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cerebrovascular disease preop consdierations
* Careful review of history, deficits, imaging, treatments, and co-existing diseases
* Assess orientation, pupils, bilateral grip strength, LE strength
* Ask about headaches, tinnitus, vision/memory loss, bathroom issues
* Look at route cause of CVA: Vascular disease, embolic (a-fib, prosthetic valve, right to left shunt/PFO)
* Imaging: Carotid U/S, CT/MRI head & neck, echocardiogram
* Preop EKG
* CBC, BMP, possible T & C
* Cerebral oximetry if possible
* Aline, 2 IVs and/or CVC
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Majority of ____ are not diagnosed before rupture
cerberal aneurysms
*only 1/3 aneurysm pts hav s/s before rupture
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Cerbral aneurysm:
* s/s
* risk factors
* dx
* Sx: Headache, photophobia, confusion, hemiparesis, coma
* Rx: HTN, smoking, female, oral contraceptives, cocaine use
* Dx: CT/angio, MRI, Lumbar puncture w/CSF analysis if rupture suspected
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Intervention should be performed within ____ of aneurysm rupture for best outcomes
72h
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cerebral aneurysm anesthesia considerations
* Pt may be on steroids, glucose monitoring important
* Pre-anesthesia: CT/MRI, EKG, Echo, CBC, BMP, T&C w/blood available
* BP control, mannitol? *aim is to avoid rupture*
* seizure prophylaxis
* Surgical tx: coiling, stenting, trapping/bypass (very large aneurysms)
* Neurosurgeon may be on standby in case of intra-op rupture/SAH
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Post-SAH vasospasms
* risk for vasospasm ____ post SAH
* occurs d/t
* Risk for vasospasm 3-15 days post SAH
* Free hgb triggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction
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what is triple H therapy for post-sah vasospasms?
* Hypertension
* To avoid complications of hypervolemia, HTN is the initial main treatment
* Hypervolemia
* Hemodilution
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how do you relieve post-sah vasospasms?
Interventional treatments s/a balloon dilation and direct injection of vasodilators relieve the spasm
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Pre-anesthesia interventions for post-sah vasospasms
Same as with aneurysm, although normally less-invasive
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what is the hunt and hess classification for grading aneurysm prognosis?
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what is the world federation of neurologic surgeon grading system for grading aneurysm prognosis?
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Arteriovenous Malformations “AVM”
* sx:
* dx:
* tx:
* pre-anesthesia considerations
* Sx: range from mass-effects to hemorrhage
* Majority are supratentorial
* Dx: Angiogram, MRI
* Tx: radiation, angio-guided embolization, surgical resection (higher mortality)
* Pre-anesthesia: H&P, review meds, imaging, CBC, BMP, T&C, EKG, Echo
* BP control, mannitol?, seizure prophylaxis, CVC or 2 Lg bore IV's, Aline
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what is this?
* Arterial to venous connection w/o intervening capillaries
* Creates an area of high flow, low resistance shunting
* Believed to be congenital
Arteriovenous Malformations “AVM”
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what 3 things does the spetzier martin AVM grading system look at?
1. Nidus size
2. eloquence of adjacent brain
3. pattern of venous drainage
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what are the surgical outcomes based on the spetzler martin AVM Grade:
* 1
* 2
* 3
* 4
* 5
percent of patient with no postoperative neurological deficit
* 1= 100%
* 2= 95%
* 3= 84%
* 4= 73%
* 5= 69%
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* Congenital brain abnormalities result from defects in the ____.
* Often ____
* Disease processes may be diffuse, or confined to specific ____.
* development or structure of the CNS
* hereditary
* neuronal structures
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types of congenital brain abnormalities
* Chiari Malformation
* Tuberous Sclerosis
* Von Hippel-Lindau Disease
* Neurofibromatosis
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what is chiari malformation?
Congenital displacement of the cerebellum
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what are the 4 types of chiarir malformation?
* Type 1: downward displacement of cerebellum
* Type 2 (Arnold Chiari): downward displacement of cerebellar vermis, often assoc w/myelomeningocele
* Type 3: Rare; occipital encephalocele w/downward cerebellar displacement
* Type 4: cerebellar hypoplasia w/o displacement of posterior fossa contents
* *Not compatible with life*
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what is AKA "Bourneville Disease"
and is an autosomal dominant disease causing benign hemartomas, angiofibromas, and other malformations that can occur anywhere in the body
tuberous sclerosis
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with tuberous sclerosis lesion of the brain include? and often involve co-existing tumors of ?
* cortical tumors & giant-cell astrocytomas
* face, oropharnyx, heart, lungs, liver & kidneys
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how does tuberous sclerosis often present and what anesthesia considerations must we take into account?
* Presentation likely includes mental retardation and seizure disorders
* must consider airway compromise, and cardia and/or kidney involvement
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what is an autosomal dominant disease where benign tumors of the CNS, eyes, adrenals, pancreas and kidneys occur. And it may present w/ pheochromocytoma?
von hippel-lindau disease
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what anesthsia considerations should we take into account for von hippel lindau disease?
* exaggerated HTN in pts with pheo
* NA may be limited if there is a co-exciting spinal cord tumor
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Neurofibromatosis is an autosmal dominat disease with how many types?
* 3 types:
* Type 1 (most common)
* Type 2
* Schwannomatosis (rare)
*there are numerous disease presentations*
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what are the anesthesia considerations for neurofibromatosis?
* increased ICP
* airway issues
* scoliosis
* possibility of pheochromocytoma
* Avoid NA d/t high likelihood of spinal tumors
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____ is a disorder of CSF accumulation, causing increased ICP, that results in ventricular dilatation
Hydrocephalus
*The accumulation of CSF is due to an imbalance between CSF production and absorption*
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hydrocephalus can be congenital or aquired d/t?
* meningitis
* tumors
* head injury
* stroke
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Hydrocephalus s/s
* Sx can be acute, subacute, or chronic
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treatment for hydrocephalus
* diuretics (furosemide & acetazolamide decrease CSF production) [*controversial in children*]
* lumbar puncture [temporary measure]
* surgical treatment
* Ventriculoperitoneal (VP) shunt
* endoscopic third ventriculostomy (ETV)
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what is an or endoscopic third ventriculostomy (ETV)?
catheter placed into the lateral ventricle that drains into the peritoneal space, right atrium, or more rarely the pleural space
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what is a Ventriculoperitoneal (VP) shunt?
drain placed in ventricle of the brain and empties into peritoneum
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when does shunt malfunction occure most frequently?
in the first year of placement (high failure rate)
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traumatic brain injury is categorized as ____ or ____ by using ____ to categorize the severity
* “penetrating” or “non-penetrating,” d/o breech of dura
* Severity categorized by Glasco-Coma Scale
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what is primary injury and secondary injuries?
* Primary injury: occurs at time of insult
* Secondary injuries: neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, and neurogenic shock
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when is intubation required for TBI?
* intubation required in severe TBI (GCS < 9, AW trauma, resp distress)
* mild hyperventaion to control ICP
* CT of head/neck ASAP
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anesthesia considerations for TBI?
* Pre-anesthesia: review co-morbidities, degree of injury, imaging, labs, gross neurologic exam. *Do not delay emergent surgery*
* C-spine stabilization, adequate IV access, CVC, Aline, possible uncrossmatched blood if no time for T & C
* Refrain from NGT/OGT –potential for basal skull fx
* Intra-op ISTAT labs, Pressors, Bicarb, Calcium, & Blood products
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____: transient, paroxysmal, synchronous discharge of neurons in the brain
seizure
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what can be tranisent abnormalities that can cause a seizure?
* hypoglycemia
* hyponatremia
* hyperthermia
* intoxication
*In these cases, treating the underlying cause is curative*
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____: recurrent seizures d/t congenital or acquired factors
Epilepsy
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____ drugs decrease neuronal excitability/enhance inhibition
Antiepileptic
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pre-anesthesia considerations for seizure disorders?
* Determine source of seizures (if known) and how well they are controlled. Want anti-seizure drugs on board before incision
* Review drugs and pharmacokinetic/pharmacodynamic actions
* Phenytoin, Tegretol, Barbiturates are enzyme-inducers
* Likely require higher doses of hepatically-cleared medications
*May be called to intubate post-seizure→ RSI w/cricoid pressure*
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chiari malformaion:
* sx:
* tx:
* pre-anesthesia considerations
* Sx: headache, extending to shoulders/arms, visual disturbances, ataxia
* Tx: Surgical decompression
* Pre-anesthesia: Review H&P, deficits, imaging, CBC, BMP, T&C
* May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline
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