Neuro disease-Assessment Exam 3 Flashcards
1
Q
Cerebral blood flow is modulated by what?
A
- cerebral metabolic rate
- cerebral perfusion pressure (CPP) *MAP-ICP
- arterial blood carbon dioxide (PaC02)
- arterial blood oxygen (Pa02)
- various drugs and intracranial pathologies
2
Q
With auto regulation, CBF is approximately ___ ml/___g brain tissue per minute
What is this in cardiac output?
A
50 ml/100g
750 ml/min (15% of CO)
3
Q
The intracranial and spinal vault contain what?
A
neural tissue (brain + spinal cord), blood, and CSF
4
Q
What is the spinal vault enclosed by?
A
Dura mater
Bone
5
Q
Brain tissue, CSF, and intracranial blood have a combined volume of ______mL
At this volume, ICP is maintained at ______ mmhg
A
1200-1500 ml
5-15 mmhg
6
Q
What is the Monro-kellie hypothesis?
A
any increase in one component of intracranial volume must be offset by a decrease in another component to prevent an elevated ICP
- Normally, changes in one component are compensated for by changes in other components, but eventually a point is reached where even a small increase in intracranial contents results in a large increase in ICP
- Initially, when ICP increases, homeostatic mechanismsincrease MAP to maintain CPP
- In prolonged/extreme cases, compensatory mechanisms can’t keep up, cerebral ischemiaoccurs
7
Q
T/F
The intracranial vault is compartmentalized
A
True
8
Q
What are the 2 meningeal barriers, and what do they separate?
A
- Falx cerebri: a reflection of dura that separates the two cerebral hemispheres
- Tentorium cerebelli: a reflection of dura that lies rostral to the cerebellum and separates the supratentorial and infratentorial spaces
9
Q
T/F
In extreme instances, the contents can herniate into a different compartment
Herniation syndromes are categorized based on the region of brain affected
A
True
10
Q
What is subfalcine herniation?
A
Herniation against the falx cerebri; often compressing branches of theanterior cerebral artery, creating a midline shift
11
Q
What is transtentorial herniation?
A
Herniation of the supratentorial contents against the tentorium cerebelli, compressing the brainstemin a rostral to caudal direction
12
Q
Transtentorial herniation s/s
A
AMS, defects in ocular reflexes, hemodynamic andrespiratory compromise, and death
13
Q
What is uncal herniation?
A
a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli
14
Q
Uncal herniation s/s
A
ipsilateral oculomotor nerve dysfunction, pupillary dilatation, ptosis, and lateral deviation of the affected eye, brainstem compression, and death
15
Q
Herniation of the _____ ____ can occur due to elevated infratentorial pressure, causing the cerebellarstructures to herniate through the foramen magnum
s/s of this?
A
Cerebellar tonsils
- medullary dysfunction, cardiorespiratory instability and death
16
Q
What are the brain herniation examples?
A
- Subfalcine
- Transtentorial
- Cerebellar contents through foramen magnum
- Traumatic event causing herniation out of cranial cavity
17
Q
Causes of increased ICP
A
Tumors
Intracranial hematomas
Blood in CSF
Infection
18
Q
How do 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
19
Q
Intracranial hematomas cause increased ICPsimilar to ___ ______
A
Mass lesions
20
Q
Blood in the CSF, as is seen in ______ ______, may obstruct CSF reabsorption, and granulations can further exacerbate increased ICP
A
Subarachnoid hemorrhage
21
Q
Infections s/a _____ or ______, can lead to edema or obstruction of CSF reabsorption
A
Meningitis
Encephalitis
22
Q
Methods to decrease ICP
A
- Elevation of the head: encourages jugular venous outflow
- Hyperventilation: lowers PaC02
- CSF drainage: external ventricular drain (EVD)
- Hyperosmotic drugs: increase serum osmolarity, drawing fluid across BBB
- Diuretics: induce systemic hypovolemia
- Corticosteroids: decrease swelling and enhance the integrity of the BBB
- Cerebral vasoconstricting anesthetics (propofol): decrease CMR02 and CBF
Surgical decompression
23
Q
What are the genetic neuro disorders?
A
Multiple Sclerosis
Myasthenia Gravis
Lambert Eaton Syndrome
Muscular Dystrophy
Myotonic Dystrophies
24
Q
What is multiple sclerosis?
What is the onset age?
A
Progressive, autoimmune demyelination of central nerve fibers; Pts experience periods of exacerbations & remissions
Onset age 20-40
25
Risk factors of MS
Female, 1st deg relative, Epstein Barr virus, other autoimmune disorders, smoking
26
Exacerbation triggers of MS
stress, elevated temps, postpartum period
27
Symptoms of MS
Treatment?
motor weakness, sensory disorders, visual impairment, autonomic instability. Sx vary b/o site of nerve fiber demyelination
Tx: No cure
- managed with corticosteroids, immune modulators, targeted antibodies (IVIG)
28
When would you get an LFT for MS pts preop?
Why?
If on dantrolene or azathioprine
bone marrow suppression, liver function impairment
29
Preanesthetic considerations for MS pts
- Consider PFTS is resp. compromise
- Labs: CBC, BMP, LFT
- Preop steroids (stress dose) for long term use
- Temp management
- GA, RA & PNB’s are acceptable anesthetic options
- avoid succs
30
What is myasthenia gravis?
Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate
- Effects skeletal muscle, not smooth or cardiac muscle cells
- Muscle weakness, exacerbated w/exercise
31
Cranial nerves are partially susceptible in MG. What does this look like?
Ocular sx common-diplopia, ptosis
Bulbar involvement → laryngeal/pharyngeal weakness→ respiratory insufficiency, aspiration rx
32
Thymic hyperplasia is in what percent of MG pts?
What percent improves after thymectomy?
10%
90%
33
Exacerbation triggers of MG
pain, insomnia, infection, surgery
34
Treatment of MG
Ach-E inhibitors (Pyridostigmine), immunosuppressive agents, steroids, plasmapheresis, IVIG
35
MG preanesthetic considerations
- Consider PFT
- Reduce paralytic dosage to a void prolonged muscle weakness
- caution with opiods
- Ach-E inhibitors (Pyridostigmine) may prolong Succs and Ester LA’s
- CBC, BMP, LFT (if on azathioprine)
- pre op steroids if needed
- increased risk of post op vent need
36
What is eaton-lambert syndrome?
Antibodies against VG Calcium chnls
- Reduce Ca++ influx into the presynaptic Ca++ channels→↓Ach release @ the NMJ
- Sx similar to MG
37
>60% eaton-lambert cases are associated with what?
Small cell lung carcinoma
38
S/s of eaton-lambert syndrome
progressive limb-girdle weakness, dysautonomia, oculobulbar palsy
39
Treatment of eaton-lambert syndrome
3-4 diaminopyridine (K+ chnl blocker), Azathioprine, Ach-E inhibitors, steroids, plasmapheresis, IVIG
40
ELS pre-anesthetic considerations
- VERY sensitive to ND-NMB & D-NMB;
Significantly more sensitive to ND-NMB than MG patients
- optimize resp. function
- extreme caution on paralytic/opiods
- possible post of vent support
41
What is muscular dystrophy? How many types are there?
Hereditary disorder of muscle fiber degeneration c/b breakdown of the dystrophin-glycoprotein complex, leads to myonecrosis, fibrosis, and skeletal muscle mbrn permeability
6 types of MD.
42
What is Duchenne's MD?
- most common & severe form
- Occurs only in boys, onset 2-5y.
- Wheelchair bound by age 8-10.
- Avg lifespan ̴20-25y d/t cardiopulmonary complications
43
S/S of MD
progressive muscle wasting without motor/sensory abnormalities, kyphoscoliosis, long bone fragility, respiratory weakness, frequent pneumonia, EKG changes
Elevated creatine kinase c/b muscle wasting
44
MD anesthetic considerations
- CBC, BMP, PFT, CK
- eval for cardiomyopathy
- caution with ND-NMB
- hyper metabolic syndrome
- avoid succs/VA: can exacerbate instability of muscle membrane
- low dose roc and TIVA for GA
- MH cart with dantrolene
- RA preferred
45
What is hypermetabolic syndrome?
similar to MH, triggered by with Succs & VA
- can lead to: rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest
46
What is myotonia?
prolonged contraction after muscle stimulation
- seen in several muscle disorders
47
What is myotonic dystrophy?
most common myotonia. Onset 20-30’s
Sx: muscle wasting in face, masseter, hands, pre-tibial muscles
- may also affect pharyngeal, laryngeal, diaphragmatic muscles
- cardiac conduction may be affected; 20% have MVP
48
What is myotonia congenita?
Milder form, involves the skeletal muscles only
49
What are myotonic dystrophies?
Myotonia
Myotonic dystrophy
Myotonia congenita
Central core disease
50
What is central core disease?
Rare. Core muscle cells lack mitochondrial enzymes
- Sx: Proximal muscle weakness & scoliosis
51
What are myotonic dystrophies triggered by?
Treatment?
Triggered by stress & cold temps
No cure. Sx managed w/Quinine, Procainamide (antiarrhythmic), Steroids
52
Pre anesthetic considerations of myotonic dystrophies
- 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
53
What are the 3 major dementia syndromes?
Alzheimer's (70%), Vascular dementia (25%), Parkinsons (5%)
54
Dementia anesthetic considerations
-
- 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 over GA to ↓opioid requirements
55
What is Parkinsons?
Degeneration of dopaminergic fibers of basal ganglia
- Dopamine suppresses overstimulation of the extrapyramidal motor system
- motor neurons become over stimulated
Unknown cause
56
What is the biggest risk factor of Parkinson's?
Advanced age
57
Triad of symptoms in Parkinson's
Other symptoms?
skeletal muscle tremor, rigidity, akinesia
Rhythmic “pill rolling,” facial rigidity, slurred speech, difficulty swallowing, respiratory difficulty, depression & dementia
58
Treatment of Parkinson's
Levodopa (crosses BBB), anticholinergics, MAOIs (inhibit dopamine degradation), deep brain stimulator
59
Parkinsons anesthetic considerations
- Review home meds, many may interact with our drugs (ex. MAOIs)
- 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
60
Common symptoms of brain tumors
↑ICP
Papilledema
Headache
AMS
Mobility impairment
Vomiting
Autonomic dysfunction
Seizures
61
What is the most common CNS glial cell?
Astrocytes
62
What are the 4 types of astrocytomas?
Gliomas
Pilocytic astrocytoma
Anaplastic astrocytomas
Glioblastoma multiforme
63
Explain gliomas
Primary tumors, Least aggressive astrocytomas
- Often found in young adults w/new onset seizures
64
Explain Pilocyctic astrocytomas
Children & young adults
- Mostly benign, good outcomes if resectable
65
Explain Anaplastic astrocytomas
Poorly differentiated
- Usually evolve into Glioblastoma Multiforme
66
Explain Glioblastoma Multiforme
Carry a high mortality
- Usually requires surgical debulking & chemo
- Life expectance is usually within weeks, even w/treatment
67
Explain meningiomas
Usually benign. Arise from dura or arachnoid tissue
- Good prognosis w/surgical resection
68
Explain pituitary adenomas
Noncancerous, varying subtypes
- Transsphenoidal or open craniotomy for removal is usually curative
69
Explain acoustic neuromas
Usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal
- Good prognosis w/resection +/- radiation
70
Explain metastatic carcinomas
can vary widely in origin & symptoms
Outcomes are generally less favorable
71
Brain tumor anesthetic consideration
- 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
- Anticonvulsants common (supratentorial lesions, closer to motor cortex)
- Autonomic dysfunction may manifest on EKG, labile HR & BP’s
72
Ischemic vs hemorrhagic stoke picture
73
What is the leading cause of death and disability worldwide?
How are these characterized?
Strokes
ischemia (88% of cases)
hemorrhage (12% of cases)
74
Blood is supplied to the brain from what 2 things?
These vessels join on the inferior surface of the brain to form the __________, providing collateral circulation to multiple areas of the brain
internal carotid arteries
vertebral arteries
Circle of Willis
75
Picture of cerebellar vessels
76
Clinical manifestation of regional stroke chart
77
What is an ischemic stroke?
occlusion of a vessel that perfuses a region of brain, causing brain cell necrosis
78
What is a TIA?
Transient ischemic attack: sudden focal vascular neurologic deficit that resolves within 24 hrs
79
What fraction of TIA pts will subsequently suffer a stroke?
1/3
80
Causes of Ischemic stroke are categorized according to the TOAST classification into what 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
81
Ischemic CVA treatment
- PO aspirin (initial)
- tPA (IV/intra-arterial; 3-4.5 hr onset)
- revascularization (IR)
82
Pts with ischemic stroke often have CV risk factors such as what?
Why is this important?
HTN, DM, CAD, Afib, and valvular disease
Could impact vasoactive drug choices and hemodynamic goal
83
What is a Hemorrhagic CVA?
Bleeding inside the cranial vault that impairs perfusion of the brain
84
Hemorrhagic stroke is 4x more likely to cause ____ than ischemic stroke
Death
85
The 2 most reliable predictors of outcome from hemorrhagic CVA are:
Blood volume
Change in LOC
86
Subtypes of hemorrhagic strokes are defined based on what locations of blood?
- Blood within the brain: intraparenchymal hemorrhage
- Blood in the epidural space: epidural hematoma
- Blood in the subdural space: subdural hematoma
- Blood in subarachnoid space: subarachnoid hemorrhage
- Blood located in the ventricular system: intraventricular hemorrhage
87
Treatment of hemorrhagic CVA
- Conservative tx: reduction of ICP, BP control, sz precautions
- Surgical tx: Evacuation of hematoma
- ICU post op
88
Protocol for cerebrovascular disease
- New anticoagulant for thrombus=No elective cases within 3 months
- Anticoagulants for CVA prophylaxis= consult prescriber to establish protocol
- High rx pts 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
89
Cerebrovascular disease pre op consideration
- 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
- Cerebral oximetry if possible
- Aline, 2 IVs and/or CVC
90
Majority of cerebral aneurysms are _____ before rupture
Not diagnosed
91
What fraction of aneurysm pts have sx before rupture?
1/3
92
S/S of aneurysm
Headache, photophobia, confusion, hemiparesis, coma
93
Risk factors of aneurysm
HTN, smoking, female, oral contraceptives, cocaine use
94
Diagnosis of aneurysm
CT/angio, MRI, Lumbar puncture w/CSF analysis if rupture suspected
95
Intervention of aneurysm should be performed within ____ of rupture for best outcomes
72 hr
96
Pre anesthesia consideration of aneurysm
- CT/MRI, EKG, Echo, CBC, BMP, T&C w/blood available
- BP control, mannitol? *aim is to avoid rupture
- seizure prophylaxis
97
Surgical tx of aneurysms
coiling, stenting, trapping/bypass (very large aneurysms)
- Neurosurgeon may be on standby in case of intra-op rupture/SAH
98
How many days post op for SAH are you at risk for vasospasm?
3-15 days
99
What causes a post-SAH vasospasm?
Free hgb triggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction
100
Aneurysm grading for prognosis chart
Just know that we have a grading chart
101
Treamtent of POST-SAH vasospasm?
Triple H therapy (Hypertension, Hypervolemia, Hemodilution)
- To avoid complications of hypervolemia, HTN is the initial main treatment
- Interventional treatments s/a balloon dilation and direct injection of vasodilators relieve the spasm
102
What is an AVM?
Arteriovenous malformation: arterial to venous connection w/o intervening capillaries
- creates an area of high flow, low resistance shunting
- believed to be congenital
103
Symptoms of AVM
range from mass-effects to hemorrhage
- Majority are supratentorial
104
Diagnosis of AVM
Angiogram, MRI
105
Treatment of AVM
radiation, angio-guided embolization, surgical resection (higher mortality)
106
Pre anesthesia for AVM
H&P, review meds, imaging, CBC, BMP, T&C, EKG, Echo
- BP control, mannitol?, seizure prophylaxis, CVC or 2 Lg bore IV's, Aline
107
AVM grading chart
Don't need details
108
What do congenital brain abnormalities result from?
defects in the development or structure of the CNS
- Often hereditary
- Disease processes may be diffuse, or confined to specific neuronal structures
109
What are common congenital brain abnormalities?
Chiari Malformation
Tuberous Sclerosis
Von Hippel-Lindau Disease
Neurofibromatosis
110
What is a chiari malformation?
Congenital displacement of the cerebellum
- separated into 4 types
111
Explain the 4 types of chiari 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
112
Symptoms of chiari malformation
headache, extending to shoulders/arms, visual disturbances, ataxia
113
Treatment of chiari malformation
surgical decompression
114
Pre anesthesia for chiari malformation
Review H&P, deficits, imaging, CBC, BMP, T&C
- May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline
115
What is tuberous sclerosis?
AKA Bourneville disease
- Genetic disease causing benign hemartomas, angiofibromas, and other malformations that can occur anywhere in the body
116
Lesions of the brain in tuberous sclerosis include:
cortical tumors & giant-cell astrocytomas
117
Tuberous sclerosis often involves co-exisiting tumors of what?
face, oropharnyx, heart, lungs, liver & kidneys
118
Presentation of tuberous sclerosis includes:
Mental retardation
Seizure disorder
119
Anesthetic consideration of tuberous sclerosis
Airway compromise
Cardiac/kidney involvement
120
What is Von Hippel-Lindau Disease?
Genetic disease process involving formations of benign tumors of the CNS, eyes, adrenals, pancreas and kidneys
121
Von Hippel-Lindau Disease may present with what?
Pheochromocytoma
122
Important factor in Von Hippel-Lindau Disease anesthetic consideration
Exaggerated HTN (d/t pheo)
123
What is neurofibromatosis?
Separated into 3 types
- Type 1 (most common)
- Type 2
- Schwannomatosis (rare)
Numerous disease presentations
124
Anesthesia considerations for neurofibromatosis
account for increased ICP, airway issues, scoliosis, possibility of pheochromocytoma
125
What is hydrocephalus?
Excessive CSF accumulation, causing ↑ICP, leading to ventricular dilatation
- Accumulation of CSF is due to an imbalance btw CSF production and absorption
126
Hydrocephalus can be characterized into what 2 groups?
Congenital
Acquired
- meningitis
- tumors
- trauma
- stroke
127
What is treatment for hydrocephalus?
- mainly consists of diuretics (furosemide & acetazolamide decrease CSF production)
- Sx can be acute or chronic
- Serial lumbar punctures as a temporizing measure
- Ventriculoperitoneal (VP) shunt or endoscopic third ventriculostomy (ETV)
128
What is a VP shunt?
drain placed in ventricle of the brain and empties into peritoneum
129
What is an ETV?
catheter placed into the lateral ventricle that drains into the peritoneal space, right atrium, or (rarely) the pleural space
130
Shunt malfunction for hydrocephalus occurs most frequently in what year of placement?
1st year (high failure rate)
131
TBIs are categorized into what 2 groups?
What is severity categorized by?
Penetrating
Non-penetrating
- depends on breech of dura
GCS
132
What is "primary injury" and "secondary injuries" for TBI?
Primary injury: occurs at time of insult
Secondary injuries: neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, and neurogenic shock
133
____ is required in severe TBI
Intubation (GCS <9, AW trauma, resp distress)
134
______ can be used to control ICP
Mild hyperventilation
135
What is a seizure?
transient, paroxysmal, synchronous discharge of neurons in the brain
136
Seizures can be caused by transient abnormalities such as?
hypoglycemia, hyponatremia, hyperthermia, intoxication
137
Epilepsy is defined as:
recurrent seizures d/t congenital or acquired factors
138
Antiepileptic drugs decrease what?
neuronal excitability/enhance inhibition
139
What 3 seizure drugs are enzyme inducers?
Why is this important?
Phenytoin, Tegretol, Barbiturates
- Pts on these meds require higher doses of hepatically-cleared medications
