Neurology Flashcards
1
Q
The most common cause of death from subarachnoid hemorrhage (SAH) is: ____. When does this risk peak?
A
initial bleeding followed by rebleeding! Rebleeding peaks within 24 hours following initial hemorrhage.
2
Q
cerebral artery vasospasm is a risk for: ____. When does vasospasm usually happen? and when does it peak? More blood?
A
asospasm, which is a risk factor for ischemia and neurologic deficit. Vasospasm typically develops by the third day and peaks within 5-10 days, and resolves by 10-14 days. More blood, more vasospasm
3
Q
What are the 4 predictors that MG patients will require prolonged intubation?
A
- Duration of disease ≥ 72 months (≥ 6 years)**greatest value
- History of a chronic respiratory disease (e.g. asthma and COPD)
- Pyridostigmine dose of > 750 mg/day
- Vital capacity < 2.9 liters
4
Q
MG: muscle weakness improved or worsened with use? MG Pathophys:
A
Worsened with use, improved with rest. Anesthetic plan: avoid neuromuscular blockers if you’re able. Short acting opioids like remifentanil are preferred. Decreased amount of ACh receptors.
5
Q
MG: which muscle relaxants are they resistant to? Which ones to give less of? What about patients on cholinesterase inhibitors?
A
Mg patients are resistant to SUX, sensitive to other blockers. n addition, patients being treated with cholinesterase inhibitors will also have a prolonged response to succinylcholine (prolonged phase I blockade) due to impaired plasma cholinesterase function.
6
Q
CPP should be maintained at:
CPP Formula:
A
50-70. Hypotension is NOT good in TBI patients Avoid going higher than 70 (could have ARDS) unless the patient is already doing that on their own.
CPP: MAP-ICP or CVP
7
Q
Hyperventilation in TBI.
A
Not recommended to go to 25 or below.
8
Q
When should intracranial pressure be treated?
Mild, moderate, and severe TBI:
A
When it goes above 20 mmHg
mild TBI is associated with a Glasgow Coma Scale (GCS) score of 13-15 and minimal to no loss of consciousness. A moderate TBI is associated with a GCS of 9-12 and a loss of consciousness of 30 minutes or more. A severe TBI is associated with a GCS of 3-8.
9
Q
What can cause a myasthenic crisis? Symptoms? tx?
A
poor disease control, stress, hyperthermia, or pulmonary infections. Clinically these patients report severe weakness and subsequently develop respiratory failure. Treatment includes cholinesterase inhibitors, corticosteroids, immunosuppressant agents, intravenous immunoglobulin (IVIG), and plasmapheresis
10
Q
Is Sux contraindicated in Cerebral palsy? CP and GI issues? CP-is it progressive?
A
NO. Succinylcholine is not contraindicated in cerebral palsy. CP patients have an increased incidence of gastroesophageal reflux and esophageal dysmotility. Pulmonary aspiration is increased in CP patients and places them at a greater risk for postoperative pulmonary complications.Cerebral palsies are non-progressive neurologic disorders. Neurologic injury occurs around the time of birth and does not progress as part of the natural disease course.
11
Q
Are people with CP resistant to benzos?
A
Baclofen is commonly prescribed to CP patients for muscle spasticity. Baclofen can cause CNS depression and potentiate other CNS depressants. Further, CP patients are more sensitive to sedative medications at baseline and are at an increased likelihood of desaturation during monitored anesthesia care.
12
Q
What is ALS?
A
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease involving both the upper and lower motor neurons and corticospinal tracts. It typically affects men between the ages of 40 and 60.Its ascending
13
Q
ALS and muscle relaxants
A
These patients are at elevated risk of forming extrajunctional acetylcholine receptors and can mount an exaggerated hyperkalemic response to succinylcholine. These patients often show a prolonged response to nondepolarizing muscle relaxants; thus careful titration is recommended.
14
Q
ALS and neuraxial anesthesia:
A
Neuraxial anesthesia is commonly avoided in patients with neuromuscular disease, and it is relatively contraindicated in patients with amyotrophic lateral sclerosis for fear of exacerbating the disease. The mechanism behind disease exacerbation is unknown.f the benefit of neuraxial anesthesia outweighs the risk of disease exacerbation, epidural anesthesia may be preferable.
15
Q
What triggers hypokalemic periodic paralysis?
Temp?
Metabolic state?
Excercise?
How does it affect the diaphragm? Inheritance pattern?
A
Published triggers include: stress, cold environment or hypothermia, carbohydrate load, infection, glucose infusion, metabolic alkalosis, alcohol, strenuous exercise, and steroids.It is diagphragm sparing and autosomal dominant.
16
Q
T/F Only hypokalemic periodic paralysis is a risk for MH.
A
FALSE. Both hypo and hyper periodic paralysis are risk factors for MH.
17
Q
Goals of TBI patients:
A
CU Management of Patients with Severe TBI: Parameters
ICP < 20 mm Hg SaO2 > 95% Glucose < 180 mg/dL
CPP 50-70 mm Hg PaCO2 35-40 mm Hg Temperature ≤ 37° C
18
Q
Name the evoked potential in terms of the LEAST to MOST sensitive to anesthesia
A
isual evoked potentials (VEP) are the MOST SENSITIVE to anesthetic technique and are rarely ever used. The evoked potentials in order from least to most sensitive to anesthetic technique are: BAEP < SSEP < MEP < VEP, (SSEP = somatosensory evoked potential, MEP = motor evoked potential). Another way to remember: BAEP are Barely affected, SSEP are Somewhat affected, MEP are Mostly affected, and VEP are Very affected.
19
Q
: Common causes of atlantoaxial instability include, but are not limited to: _____. Can lupus cause it?
A
trauma, achondroplasia, rheumatoid arthritis, and Down syndrome. Although rare, systemic lupus erythematosus can cause atlantoaxial instability due to joint laxity
20
Q
What is transmural pressure?
A
Pressure inside (MAP in case of cerebral aneurysm) - Pressure outside (ICP)
21
Q
How can aneurysms rupture if CSF is lost?
A
with loss of CSF volume, there can be an acute drop in ICP. This can lead to an increase in the transmural gradient and therefore a rupture in the aneurysm.
22
Q
Can opioids ever lead to a rupture of an aneurysm?
A
YEs, if there’s too much opioid given, and the patient hypoventilates, then you can increase CBF (due to vasodilation), and then it can rupture.
23
Q
The majority of patients with myelomeningiocele also have what neurological issue?
A
Arnold chiari and therefore hydrocephalus.The majority of patients with myelomeningocele also have Chiari II malformation, which involves herniation of the brainstem through the foramen magnum and frequently hydrocephalus secondary to blockage of the fourth ventricle.
24
Q
What is myotonic dystrophy? How is it inherited? what ar the signs?
A
Myotonic dystrophy is a group of hereditary (usually autosomal dominant) diseases resulting in persistent contracture of skeletal muscle (myotonia) following voluntary contraction or external stimulation. This occurs because, following release, calcium does not efficiently return to the sarcoplasmic reticulum and remains available for sustained muscle contraction. In addition to skeletal muscle involvement, certain types of myotonic dystrophy (including the most common, myotonia dystrophica) also affect multiple organ systems. Symptoms and associated findings include: muscle degeneration, cataracts, diabetes mellitus, thyroid dysfunction, adrenal insufficiency, gonadal atrophy, and cardiac abnormalities (e.g. conduction dysfunction, cardiomyopathy, and mitral valve prolapse). Respiratory muscle weakness can lead to a restrictive respiratory pattern and cause mild arterial hypoxemia, reduced ventilatory response to hypoxemia and hypercapnia, and ineffective coughing. Gastrointestinal muscle weakness can lead to delayed gastric emptying, intestinal hypomotility, and pharyngeal muscle weakness. Each of these can contribute to an increased risk of aspiration.
25
myotonic dystrophy triggers
shivering due to hypothermia, neostigmine, succinylcholine, and direct surgical stimulation of muscle (especially via electrocautery).
26
Treatment of myotonic crises: Do Neuromuscular blocking drugs work?
Treatment of myotonia or myotonic crises includes phenytoin, quinine, and procainamide. The drugs work by decreasing sodium influx into skeletal myocytes and delaying the return of membrane excitability following an action potential. In addition, muscle contraction may also be relieved by direct infiltration of the affected muscle with local anesthetic or administering a high concentration of volatile anesthetic (but consider that the myocardial depressant effects may not be well-tolerated). It is important to note that neuromuscular blocking drugs do NOT treat myotonia since they act at the level of the neuromuscular junction, not within the myocyte where the abnormality occurs.
27
myotonic dystrophy and nm blockade?
Dont use sux
28
SAH and EKG changes:
BOTTOM LINE: Sudden catecholamine surge caused by SAH leads to hypertension, increased left ventricular strain, and possibly direct toxic effects to the heart. These physiologic changes increase myocardial oxygen demand and can lead to subendocardial ischemia with resultant ST-T segment changes
29
Acute spinal shock-what would you see?
In acute spinal shock the cord injury causes loss of motor, sensory, and reflex activity below the lesion.
30
Hemicord injury, also called Brown-Sequard syndrome, will result in
oss of pain and temperature at the level of the lesion on the ipsilateral side and on the contralateral side for the levels below the lesion as the spinothalamic tract decussates through the anterior white commissure from levels below in an ascending fashion and thus will carry signals from the contralateral side of the body. There will also be loss of dorsal column proprioception, vibration, and touch as well as motor function on the ipsilateral side with flaccid paralysis.
31
Anterior spinal cord injury:
Anterior spinal cord injury such as seen with injury or hypoperfusion during aortic surgery will result in preservation of the dorsal column function with loss of motor function at the level and below the level of the lesion
32
Dorsal column injury:
If the dorsal column of the spinal cord is affected than loss of touch, proprioception, and vibration will occur at and below the level of the lesion on the ipsilateral side with preservation of pain, touch, and motor function.
33
The first step with acute hemodynamic changes during posterior fossa and brainstem surgery is
To alert the surgeon to stop what they are doing as they are likely in proximity to vital structures that are easily damaged.
34
Signs of VAE
Signs of venous air embolism include increase in dead space (decrease in ETCO2 with increase in PaCO2), hypotension, tachycardia, arrhythmia, and acute right ventricular failure.
35
Detection of VAE:
Detection of VAE is most sensitive with TEE but precordial Doppler is also very sensitive and less invasive.
36
If VAE occurs, what should be done? whch position should the patient be put in?
Should a VAE occur the field should be flooded with saline immediately and the circulation supported with fluid and vasopressor if needed. The patient can be repositioned into the supine position to get the head below the level of the heart, the jugular veins occluded and attempts to aspirate the air from a multiorificed central line can be done. If air lock occurs then the patient should be placed in the left lateral decubitus position. If cardiac arrest occurs, CPR can help to break up the air lock mechanically.
37
DI metabolic abnormalities and lab hallmarks:
Common presenting signs are polydipsia, polyuria (from 4-20 L/day), and hypernatremia, without hyperglycemia or glycosuria. A urine osmolality less than 200 mOsm/kg and a urine specific gravity ≤1.005 are hallmarks of diabetes insipidus.
38
Desmopressin and carbamazepine for CDI
Desmopressin is a synthetic analogue of arginine vasopressin with potent antidiuretic activity but no vasopressor activity (A). It can be administered IV or intranasally. Vasopressin may also be administered, and may be especially useful in the setting of DI and hypotension.
Carbamazepine has also been used successfully in the treatment of CDI. The mechanism of this antiepileptic drug derives from its ability to sensitize the collecting duct to circulating ADH.
39
demeclocycline and furosemide in CDI?
Demeclocycline, derived from the tetracycline class of antibiotics, is used in the treatment of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) by actually inducing diabetes insipidus (C) and reducing ADH effects in the collecting duct.
Furosemide (D) is not used in the treatment of CDI, but may be used for SIADH
40
ASIA scoring system:
look at photos, basically A is the worst and Eis the best
41
The path of stimulus to terminal recording of a (lower extremity) motor evoked potential (MEP) descends along the neuromotor pathway from
from most superior to most inferior structures: lower limb cortex, internal capsule, brainstem, corticospinal tract, peripheral nerve, and eventually the lower limb muscle (e.g., tibialis anterior).
42
Which artery in the brain supplies motor to motor cortex?
MCA
43
benefits of transcranial doppler, which artery is it measuring?
Transcranial Doppler ultrasonography is utilized during CEA to detect thromboembolic events that could potentially cause adverse neurologic outcomes. It is also used to measure blood flow velocity in the middle cerebral artery (MCA)
44
Transcranial doppler can also detect what 2 things? what is hyperperfusion syndrome after CEA?
t can also detect asymptomatic carotid artery occlusion and hyperperfusion syndrome following CEA. Hyperperfusion syndrome consists of a >100% increase in cerebral blood flow relative to the preoperative baseline. This affects 9-14% of patients and has the potential to cause postoperative neurological dysfunction which can include ipsilateral headache, focal seizures, focal deficit, ipsilateral intracerebral hemorrhage, and/or cerebral edema.
45
Cushing reflex triad:
HTN, irregular breathing< bradycardia
46
Pneumocephalus and posterior fossa surgery
Patients undergoing seated posterior fossa craniotomy or cervical spine surgery are at increased risk of developing tension pneumocephalus. Air may track superiorly and remain trapped within the higher regions of cranium. Changes in mental status, hypertension, and bradycardia may be indications of this form of increased ICP. A CT scan of the head can confirm the diagnosis. The risk of this complication may be reduced by avoiding nitrous oxide.
47
what isJugular bulb venous oxygen saturation (SjVO2)? why would it not be helpful in acute left focalized stroke?
a monitoring modality which assesses the oxygen extraction of brain tissue by following the mixed venous oxygen saturations of the jugular venous bulbs. These values represent the balance between global cerebral oxygen supply and demand. An acute left anterior cerebral artery stroke would cause focal ischemia and focal neuronal death. The SjVO2 values may be normal (55-75%) in this setting.
48
Barbituate and CMRO2? How does cerebral edema affect SjvO2?
A barbiturate infusion will cause a decrease in the global CMRO2 which decreases cerebral oxygen demand and will increase SjVO2.An increase in cerebral edema would reduce CPP by an increase in intracranial pressure (ICP). This reduction will globally affect oxygen extraction and alter the SjVO2 trend.
49
respiratory complications and MS? which muscles are weaker in MS? which lung volume does that affect?
The three most common respiratory problems in multiple sclerosis are respiratory muscle weakness, bulbar function impairment, and abnormalities of breathing control.
Aspiration, pneumonia, and acute ventilatory failure are possible complications of multiple sclerosis due to the muscle weakness and impaired cough. Both inspiratory and expiratory muscles are affected; however, the expiratory muscles are more weakened. Expiratory muscle strength is related to forced vital capacity (FVC).
50
Glasgow coma scale: Mild TBI score? Easy way to rememer?
Look at photo. mild=13 or higher.TrueLearn Insight : A mnemonic to remember which category has 4, 5, or 6 points is "eyes, vocal, motors" where the number of letters in each word corresponds to the number of points in that category
51
EEg during wakefulness: what does isoelectric eeg mean? why is burst suppressiom the main goal?
Thiopental-what does it do to CMRO2 . and CBF?
A high frequency, low amplitude pattern is present during wakefulness and arousal. An isoelectric EEG indicates cerebral silence and the maximal decrease in CMRO2.
Although an isoelectric electroencephalogram (EEG) indicates the maximal decrease in the cerebral metabolic rate of oxygen (CMRO2), the goal is a state called “burst suppression” (E). In this state, periods of isoelectric EEG are punctuated by “bursts” of EEG activity. By maintaining this state of burst suppression, one can achieve a near isoelectric EEG while being assured that regular EEG activity will resume once the medication is stopped.
hiopental also produces a proportional decrease in CMRO2 and cerebral blood flow (CBF), thereby reducing intracranial pressure (ICP) and improving cerebral perfusion. It has been suggested that barbiturates exhibit neuroprotective properties as they decrease CMRO2, act as free-radical scavengers, stabilize liposomal membranes, and exhibit excitatory amino acid receptor blockade.
52
Are TV used in MG patients to determine outcomes s/p surgery? What are the criteria?
NoCriteria that may predict the need for postoperative mechanical ventilation include:
1. Duration of disease 6+ years
2. Presence of pulmonary disease(s) unrelated to MG (e.g., COPD)
3. Vital capacity of < 2.9 L (or < 40 mL/kg)
4. Negative inspiratory force (NIF) < 20 cm H2O (e.g. 10 cm H2O)
5. Daily pyridostigmine dose > 750 mg
53
Sux vs Roc in myasthenic patients? Response to anti-cholinesterases?
Resistant to sux, need more Roc
| Good
54
Tx for tetanus?
| MOa?Transported within the axon?
Treatment for tetanus includes supportive care and administration of tetanus immunoglobulin.Tetanus acts by preventing neurotransmitter release (glycine and GABA) from inhibitory neurons in the spinal cord. The lack of inhibition causes increased muscle contractions to the point of tetanus. Botulism toxin has a similar mechanism of preventing neurotransmitter release (acetylcholine), but botulism affects the alpha motor neuron causing flaccid paralysis
It is transported within the axon
55
Carbon monoxide causes release of what?
Carbon monoxide (CO) causes endothelial cells and platelets to release nitric oxide. This does not lead to vasospasm, but rather, can cause capillary leakage and edema. It is more likely to lead to vasodilation
56
How does Carbon monoxide do bad things?
Carbon monoxide exerts its toxic effects through a variety of mechanisms including binding to hemoglobin (functional anemia and leftward shift of oxygen-Hb dissociation curve), binding to myoglobin (impaired cardiac output), effects on mitochondrial cytochrome oxidase (impaired aerobic respiration), and peroxidation of brain lipids (direct cellular damage).
TrueLearn Insight : Fetal Hb has a > 10% higher affinity for CO than adult Hb. Because of this, even mild maternal CO poisoning can lead to severe fetal CO poisoning or even death.
kim-it can cause the O2 that is attached to hang on even more tightly
57
Are auditory evoked potentials affected by volatiles?
Not really
58
what are 3 important structures in the posterior fossa?
Brainstem, cerebellum, 4th ventricle
59
Effects of brainstem manipulation:
| Cn 5, 7, 10, pons and medulla
Effect of surgical brainstem manipulation:
CN V: Hypertension, bradycardia
CN VII: Facial muscle movement
CN X: Hypotension, bradycardia
Pons, medulla: Arrhythmias, hypo/hypertension, tachycardia/bradycardia, irregular breathing pattern
60
What is Autonomic hyperreflexia? Anesthetic mgmt?
| symptoms?
Autonomic hyperreflexia is a syndrome that may occur in patients with spinal cord injuries (SCIs) above the splanchnic outflow distribution within the sympathetic nervous system (SNSAnesthetic management of patients at high risk for AH includes neuraxial anesthesia with local anesthetic and/or deep general anesthesia. Opioid-only anesthetics administered intravenously or neuraxially do not reliably prevent AH. Symptoms of AH are related to the profound vasoconstriction that occurs below the level of the lesion (e.g. headaches, hypertensive crisis, MI) and the vasodilation that occurs above the level of the SCI (e.g. diaphoresis of upper body, nasal congestion). Treatment includes fast-acting vasodilating agents such as nitroprusside, nitroglycerin, and nicardipine.
61
What type of fluids do you need to avoid in TBI?
avoid hypotonic. Use isotonic!
62
Good lidocaine dose for pre-intubation
1.5 mg/kg
63
Propofol and volatile agents and nitrous oxide, ketamine and what they do to CBF and CMRO2
Propofol decreases both CMRO2 and CBF. Volatile agents uncouple CMRO2 from CBF in a dose-dependent manner, causing a decrease in CMRO2 while increasing CBF. Nitrous oxide increases both CBF and CMRO2. Ketamine increases CBF while having a mixed effect on CMRO2.
64
Cerebral ischemia signs on SSeP?
Decreases in SSEP amplitude and increases in latency are indicative of insults to the somatosensory pathway such as cerebral ischemia.
65
Causes for post-operative vision loss after surgery:
Causes for vision loss after surgery can be divided into five groups:
1) External ocular injury (corneal abrasion or sclera injury)
2) Cortical blindness
3) Retinal ischemia
4) Ischemic optic neuritis
5) Acute glaucoma
66
The 2 most common causes of vision loss s/p spinal and cardiac surgery
Ischemic optic neuropathy and retinal artery occlusion
67
Breakdown the retinal ischemia part-like why does it happen?
Retinal ischemia can be divided into subdivisions of branch and central retinal artery occlusion. Central retinal artery occlusion decreases the blood supply to the entire retina, while branch retinal artery occlusions are localized to a specific portion of the retina. The injury is mostly unilateral (in contrast to ION).While retinal artery occlusion can be due to a multitude of factors, such as decreased blood supply to the retina and impaired venous drainage, the most common cause of perioperative retinal arterial occlusion is improper patient positioning resulting in external compression of the eye.
68
Symptoms of central retinal artery occlusion can include: and what should you do if you see these things?
unilateral vision loss, a loss of light perception, an afferent pupil defect, periorbital eyelid edema, proptosis, ptosis, parasthesias of the supraorbital region, and at times a hazy/cloudy cornea. Macular and retinal edema with cherry red spot and attenuated retinal vessels are common fundoscopic findings in patients with central retinal artery occlusion. In patients with suspected postoperative visual loss, an emergent ophthalmology consultation is warranted.
69
Can hypotension cause retinal artery occlusion?
Episodic hypotension, though a documented cause of central retinal artery ischemia, is a much rarer cause than improper patient positioning
70
What is triple H therapy? which one of the H's is dangerous?
Triple H therapy is aimed to augment cerebral blood flow for patients with cerebral vasospasm. Hypervolemia, hypertension, and hemodilution are the components. Of note, hypervolemia can cause significant morbidity such as pulmonary edema and thus is not commonly utilized. More modern therapy is aimed at inducing hypertension.
71
PFTs and elective surgery-what are the rules?
PFT is very rarely warranted in preoperative evaluation of any patient having elective surgery unless the anesthesia provider cannot elucidate whether the patient's symptoms are cardiac or pulmonary in origin. The main exception to this is if the patient is having lung reduction surgery and PFT is required to determine residual pulmonary function following resection
72
There are actually a lot of meds that can trigger contactions in myotonic dystrophy-name them
Additionally, several medications (methohexital, etomidate, propofol, neostigmine), hypothermia, shivering and mechanical or electrical stimulation may induce myotonic reactions.
73
Why is cardiac monitoring and pacing so important in myotonic dystrophy?
Cardiac monitoring is crucial and pacing equipment should be available as one-third of patients with first degree AV block will not respond to atropine and deterioration to more advanced heart block can occur rapidly
74
What tests must be done before surgery in a patient with myotonic dystrophy?
EKG, TTE, PFT-they can really have lung issues in periop periodn the perioperative period, myotonic dystrophy patients are more likely to suffer from pulmonary related complications especially when severe disease is present or they are undergoing upper abdominal procedures.
75
Eye movement in vegetative state vs eye movements in a coma
Patients in comas do not spontaneously open or voluntarily move their eyes while patients in persistent vegetative states (PVS) open and/or move their eyes though, without conscious control
76
What is preserved, and what is lost in a persistent vegetative state?
cerebral cortical function (e.g. communication, thinking, purposeful movement, etc) is lost while brainstem functions (e.g. breathing, maintaining circulation and hemodynamic stability, etc) are preserved. Non-cognitive upper brainstem functions such as eye-opening, occasional vocalizations (e.g. crying, laughing), maintaining normal sleep patterns, and spontaneous non-purposeful movements often remain intact.
77
Diff in PVS vs Coma
Look at pic (table)
| Coma is basically no to everything, and PVS is yes to some things but never purposeful
78
Blood vessels and skin changes-
as a reminder AH Below vs above lesion
Auto hyperreflexia occurs in- and refresh of AH
Vasoconstriction leads to pallor, and vasodilatikon leads to flushing
Below lesion is vasoconstriction, above lesion-vasodilation
in lesions above t12, and particularly above T5. The intense sympathetic response below the level of injury can cause acute hypertension (at least 20-40 mm Hg above baseline), reflex bradycardia, cardiac arrhythmias (e.g., premature ventricular contractions or atrial-ventricular conduction abnormalities), and myocardial infarction. The hypertension can further lead to headaches, blurred vision, retinal hemorrhage, intracranial hemorrhage, stroke, seizure, and/or cerebral edema. Additionally, the intense vasoconstriction leads to cool, dry, pale skin below the level of SCI. The reflex cutaneous vasodilation above the level of the SCI leads to nasal congestion; sweating; and warm, flushed skin on the upper extremities, shoulders, neck, and face.
79
After injury, how longb before you see effects of AH?
utonomic hyperreflexia is generally not observed until at least two weeks to six months after the spinal cord injury
80
Subarachnoid hemorrhage (SAH) most commonly occurs from
aneurysm rupture
81
Vasospasm after SAH typically occurs when? and peaks when?
Vasospasm typically occurs at 72 hours after SAH and peaks at 5-7 days.
82
Vasospasm and nimodipine:
Vasospasm is not treated by nimodipine, but it does improve outcome and decrease cerebral infarction after SAH. This is thought to be secondary to a fibrinolytic action. Nimodipine has not been shown to relieve angiographic evident vasospasm (vasospasm that has already occurred).
83
T/F: triple H therapy decreases risk of morbidity and mortality from vasospasm
FALSE. It is still used, butTriple H" therapy has not been shown to improve outcomes after SAH and has in fact proven to increase complications owing to hypervolemia.
84
A greater admission hemoglobin correlates with a decreased incidence of cerebral infarction and with improved outcomes. t/F
TRUE
85
How is becker muscular dystrophy inherited?
X linked recessive
86
Volatile anesthetics and becker and duchenne's?
They both increase the risk of rhabdomyolysis
87
Should you use solutions that contain glucose in neurosurgery? why or why not.
No,Solutions that contain glucose should be avoided in neurosurgery because they can worsen cerebral edema. Additionally, these solutions have been known to exacerbate neuronal injury.
88
What fluid is usually preferred in neurosurgery?
The use of normal saline has been preferred over other solutions because it is slightly hyperosmolar (308 mOsm/L) thus it may help attenuate cerebral edema if it is present. Hypertonic saline has also been used with favorable results as it will further decrease brain edema. Any solution that contains glucose should be avoided unless the patient is hypoglycemic because it may exacerbate neuronal injury, especially when it is hypoosmolar such as lactated Ringer solution. Hypotonic solutions should be avoided as they have the potential to lower plasma osmolality with a resultant increase in free water into the brain parenchyma
89
Osmolality of plasmalyte vs LR:
The osmolarity of Plasmalyte is 294 mOsm/L, which is iso-osmolar compared to the lactated Ringer solution, which is hypoosmolar (273 mOsm/L).
90
What does Xenon do to CMRO2, CBF, and ICP?
Xenon produces reduction in CMRO2, but increases ICP and CBF through its action at the NMDA receptor. Look at ICP chart for stuff
91
Volatiles increase ICP after one mac. T/F
True
92
Proble with hyperkalemic periodic blah blah is with what type of channel?
odium channel inactivation does not occur properly with HKPP, muscle cells are more dependent on potassium efflux for repolarization and cessation of an action potential
93
Treatment of HyperKPP? triggers of hyperkalemic?
Treatment includes decreasing serum potassium (e.g. insulin + glucose, β-agonists) along with glucose, calcium, and/or diuretics. Measures that can be utilized to prevent the onset of an attack during an anesthetic include consideration of a regional technique, use of dextrose-containing potassium-free IV fluids, maintaining normal body temperature, and decreasing serum potassium concentrations to low-normal.
Potential triggers for a HKPP episode include hyperkalemia, potassium-rich meals or exogenous potassium administration, rest after exercise, stress, metabolic acidosis, and succinylcholine use. Factors that can worsen a HKPP episode include acetylcholinesterase inhibitors, extremes of temperature, and hypoglycemia.
94
Osserman classification syndrome for myasthenia gravis:
Class I – ocular weakness alone
Class II – mild weakness in muscle groups other than ocular
Class III – moderate weakness in muscle groups other than ocular
Class IV – severe weakness in muscle groups other than ocular
Class V – intubation necessary secondary to respiratory failure
95
chart of differences between MG and myasthenic syndrome:
look at photo
96
Lambert eaton and neuromuscular blocking stuff
"Lambs are sensitive animals", Lambert-Eaton is sensitive to both types of relaxants.
97
iLDA means what?
A decrease in amplitude or increase in latency on somatosensory evoked potential recordings may indicate sensory cortex ischemia
98
Internal carotid artery stump pressures-what do they do? what do they not do?
eflect the collateral flow back-pressure in the circle of Willis originating from the contralateral carotid artery. Stump pressures are inexpensive, dynamic, and are associated with detecting hypoperfusion at pressures < 50 mm Hg. They are not used to detect emboli.
99
EEG-what is its usefulness in measuring ischemia? what can it NOT detect?
Electroencephalography (EEG) monitoring is used to monitor cerebral ischemia and for selective shunting during CEA.It is limited as it can only detect ischemic events and not thromboembolic events. It also cannot detect subcortical ischemia. Electroencephalography can also yield false-positive and false-negative results and is affected by anesthetics, changes in temperature, and changes in blood pressure.
100
Transcranial doppler-what does it detect? what can it not detect?
Transcranial Doppler (TCD) ultrasonography during CEA continually assesses mean blood flow velocity and detects microembolic events in the middle cerebral artery (MCA), thereby assisting in detection of intraoperative thromboembolic events. This modality is limited by the inability to detect global cerebral ischemia since it can only sense embolic events in the MCA.
101
Resecting an AVM at the parietal lobe-what do you want to monitor? what are concerns when resecting an AVM?
AVM resections use neuromonitoring depending on where the AVM is located. One that is located in the parietal lobe, ischemic changes would result in motor and sensory changes. Neuromonitoring should then include sensory evoked potentials (SEP) and motor evoked potentials (MEP).
AVM resections can be complicated by ischemia, hemorrhage, and cerebral edema. During the resection, the feeding arteries are clamped or ligated to assess if the patient will tolerate the increased volume of blood that is now shunted into the cerebral circulation. This can lead to cerebral edema and hemorrhage, or "occlusive hyperemia." Ischemia is the main concern during this procedure.
102
Review GCS photo-more in depth one
okay :)
103
High dose glucocorticoids in TBI?
NO.High dose glucocorticoids have been shown to increase mortality in patient with traumatic brain injury (TBI).
104
Initial tx of SIADH, how can you tell SIADH from CSW? diagnostic labs for both?
Diagnostic criteria for SIADH and CSWS include: hyponatremia, low serum osmolarity, elevated urine osmolarity, and an elevated urine sodium. SIADH is associated with a euvolemic or slightly hypervolemic state, where CSWS is associated with hypovolemia. The initial treatment for SIADH is fluid restriction with recommended intake of less than 800 mL/day.
105
When would you use hypertonic saline in SIADH?
If fluid restriction doesnt work.Other therapies include hypertonic saline, high solute intake, high salt intake, urea administration (not commonly used in the U.S.), or vasopressin receptor antagonists. Hypertonic saline is reserved for severe cases, symptomatic, refractory to fluid restriction, or in patients with subarachnoid hemorrhage. There are several oral vasopressin receptor antagonists, but conivaptan is one of the only IV formulation available. Demeclocycline or lithium may also be used for therapy of SIADH. However, both have significant potential side effects and are often not needed. Treatment for CSWS is isotonic saline.
106
Signs that show differences in loss of cerebral vs brainstem function
What is the positive apnea test?
other clinical tests for brain death?
The absence of consciousness, motor activity, and movement in response to painful stimuli indicates cessation of cerebral cortical function. The absence of pupillary, vagal, oculocephalic, oculovestibular, and respiratory reflexes indicates cessation of brainstem function. The positive apnea test indicates the absence of ventilation in response to hypercarbia. Other clinical tests for brain death include two isoelectric EEG tracings 24-hours apart and the absence of cerebral blood flow as evidenced by cerebral angiography, transcranial Doppler ultrasonography, or MRI/MRA.
107
Albumin and TBI?
A recent study (SAFE) suggests that resuscitation with albumin actually increases mortality in TBI patients.
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Bolttom line-try to just use isotonic 0.9% NS. Hypertonic isnt first line-it can be used but isnt first line
TRUE
109
So, when you go to the mountains-what do central and peripheral chemoreceptors do? what does your body do in response? Over the next 2-3 days, then what?
nitial rapid ascent to high altitudes causes arterial hypoxemia which activates the peripheral chemoreceptors. This reduces PaCO2, PCSFCO2, and H+ in the CSF. The alkaline pH of cerebrospinal fluid (CSF) blunts the central chemoreceptors, offsetting the hypoxic ventilatory drive of the peripheral chemoreceptors. Within a few minutes, a dynamic equilibrium occurs with reduced PaCO2 and PaO2. The initial hypoxemia causes shortness of breath and tachypnea resulting in hypocarbia. Other symptoms include a headache and gastrointestinal distress. Over the ensuing 2-3 days, bicarbonate is removed from the CSF in order to restore pHCSF closer to normal values.
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Peripheral O2 chemoreceptors are most sensitive to? And how do they respond?
Peripheral O2 chemoreceptors are most sensitive to reductions in PaO2 between 65 and 50 mm Hg and respond by increasing minute ventilation.
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How does acetazolamide work?
Acetazolamide (a carbonic anhydrase inhibitor) expedites bicarbonate removal from CSF by promoting its clearance in urine and increasing the bicarbonate CSF-blood gradient.-Is this so that it can have tghe help of the central chemoreceptors?
112
IIH aka pseudotumor cerebri-higher or lower incidence of PDPH? diagnosis-
Lower
dxhe diagnosis is made by finding elevated intracranial pressure with normal cerebrospinal fluid composition and no other causes elucidated for the intracranial hypertension on brain imaging. A lumbar puncture is used to confirm an elevated opening pressure (>25 cmH2O).
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acetazolamide and preggo=
no
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Pregnant women in pain with pseudotumor cerebri
Pregnant patients with idiopathic intracranial hypertension presenting for labor analgesia are an interesting dilemma. If the patient has symptoms, an intrathecal catheter may be a great option to allow for removal of CSF if symptoms worsen during labor.
115
Evoked potentials are affected by what and not affected by:
Evoked potentials are sensitive to physiologic changes including hypotension, hypothermia, hyperthermia, hypoxia, and anemia. Acid-base balance has not been shown to negatively impact SERs.
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At what blood flow do clinical neurologic findings become abnormal? how low can anesthesia make that? SSEPs not affected until ____.
Clinical neurologic findings become abnormal below a cortical blood flow of 25 ml/min/100g of brain tissue. Anesthesia may lower this critical value to as low as 15 ml/min/100g of brain tissue. Somatosensory evoked potential recordings are not affected until cortical blood flow falls below 20 ml/min/100g of brain tissue.
117
Acetazolamide and the hyper/hypo kalemic stuff:
Acetazolamide (A) is a carbonic anhydrase inhibitor that is used to prevent episodes of paralysis in both hyperkalemic and hypokalemic periodic paralysis. The mechanism for acetazolamide preventing paralysis is unknown.
118
How does spironolactone work? Spirono and hyo/hyperkal per paralysis
Spironolactone acts by competitively inhibiting aldosterone. Prevents issues in both
119
A carbohydrate load (B) can precipitate an attack in a patient with hypokalemic periodic paralysis. Why?
A carbohydrate load can precipitate an attack in a patient with hypokalemic periodic paralysis.
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Whats the channel messed up in these potassium paralysis things?
Most of the mutations of hypokalemic periodic paralysis are in a muscle calcium channel. This channel is not found in the heart or respiratory system, therefore these patients do not suffer from respiratory failure during an attack.
121
Neuromuscular blocking agents and awareness
The risk of awareness is sufficiently low if the exhaled MAC is > 0.7 with volatile inhalational agents. Several options can further help decrease this risk: premedication with benzodiazepines, avoidance of neuromuscular blockade unless necessary for the surgical procedure, and consideration of additional monitors in high-risk situations. The use of neuromuscular blocking agents significantly increases the risk of awareness.
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Awareness and TIVA?
There is an increased risk of awareness when performing total intravenous anesthesia.
123
When is steroid therapy to decrease ICP okay?
Steroid therapy to decrease ICP is effective for space-occupying lesions with surrounding edema. By decreasing the inflammation, ICP will decrease. However, this patient has an acute traumatic injury and therefore would not benefit from dexamethasone. Further, steroids have been shown to be ineffective in traumatic injury and can worsen outcomes by increasing hyperglycemia
124
Why should mannitol NOT be rapidly infused?
rapid infusion of mannitol can potentially further increase ICP which is why administration over ≥ 15 minutes is typically recommended.
125
In a patient who is normotensive, the most effective way to quickly reduce ICP is a propofol bolus.
TRUE. In a patient who is normotensive, the most effective way to quickly reduce ICP is a propofol bolus.
126
What do IV anesthetics do as far as nitrous and its increase in CBP?
The cerebral vasodilating effect of N2O is diminished when it is given in combination with intravenous anesthetics.
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Brainstem auditory evoked potentials are the best monitor for
brainstem ischemia with posterior fossa craniotomy due to proximity to the surgical site as well as the relative resistance to anesthetic used, therefore eliminating other confounding variables in ischemia evaluation.
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Methylprednisolone-is it helpful in reducing post-op hoarseness?
Methylprednisolone has not been shown to have statistical significance in reducing postoperative hoarseness due to inflammatory edema formation.
129
tell me about the course of the RLN on the right vs the left. RLN innervates all of the muscles of the larynx except_____. Damage to RLN does what to vocal cords? what if that happens unilaterally vs bilaterally?
The course of the RLN and proximity to the operative site increases its vulnerability to injury. The RLN is a branch of the vagus nerve. On the right, the RLN emerges from below the subclavian artery and passes obliquely into the right tracheoesophageal groove. On the left, the RLN loops under the arch of the aorta and then takes a longer and more vertical course into the left tracheoesophageal groove. The RLN innervates all of the muscles of the larynx except the cricothyroid, thus when damage to the RLN occurs the cricothyroid muscle is unopposed, resulting in vocal cord adduction. If this occurs unilaterally, then dysphonia can occur. Bilateral RLN injury is rare, but it can result in complete airway obstruction requiring intubation.
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What can reduce post op hoarseness? what are other reasons for post op hoarseness?
There is evidence showing that endotracheal tube cuff pressure adjustment during surgical retraction may reduce the incidence. Other etiologies may include edema, hematoma, or trauma from the intubation (arytenoid cartilage dislocation).
131
Name all of the hormones from the pituitary-anterior and posterior
Posterior: ADH and Oxytocin
Anterior: FSH, LH, ACTH, Growth Hormone, TSH, Prolactin, gonadotrolpins and Beta lipoprotein
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What is calcitriol and what does it do?
Calcitriol is used to treat hypocalcemia associated with hypoparathyroidism. The parathyroid glands are not controlled by the pituitary gland (E). Calcitriol is the active form of vitamin D, which increases gastrointestinal uptake of calcium and decreases renal calcium excretion.
133
In a prolactin secreting tumor, patients are given bromocriptine and cabergoline-why?
How do prolactinomas present in men vs women
Bromocriptine and cabergoline (A) are dopamine agonists. Dopamine is a negative feedback neurotransmitter for the production of prolactin in the anterior pituitary. The most common pituitary mass is a prolactin-secreting microadenoma. In women, this can present as amenorrhea and galactorrhea; men typically present with impotence.
134
Who knew vasopressin could be so helpful? what does it do for CPP and cerebral oxygenation? how Sway?
Vasopressin is an alternative to phenylephrine for increasing cerebral perfusion pressure. Also, vasopressin is noted to increase cerebral oxygenation, unlike phenylephrine.This effect is likely mediated by local nitric oxide release stimulated by the direct action of vasopressin on the cerebral vasculature.
135
if they say muscular dystrophy, what do you need to avoid?
avoid volatiles and sux!
136
Channels affected in hypokalemic vs HYPERkalemic periodic paralysis:
Hyperkalemic periodic paralysis is due to sodium channel mutations. Hypokalemic periodic paralysis is due to calcium channel mutations.
137
Why do you not give labetalol to patients with autonomic hyper-reflexia? How should you treat hypertension in these patients?
Patients with autonomic hyperreflexia often exhibit reflex bradycardia. Beta blocking agents would not be the best anti-hypertensive therapy.
Pharmacologic therapy should start with a vasodilator, such as nitroglycerin or (possibly) sodium nitroprusside. Nitroglycerin can be applied as an ointment to the patient's forehead then removed after the stimulus is appropriately managed. Also, intravenous ganglion blockers, hydralazine, α-adrenergic receptor blockers, calcium channel blockers, magnesium, and nitrates have all been documented as potential treatment methods.
138
Important steps when patients with AH have an attack?
he important treatment steps include removing the stimulus (e.g. temporarily stopping surgery, draining the bladder, disimpaction of bowel). The next appropriate steps include treating persistent hypertension and inducing general anesthesia.
139
What is the mechanism behind malignant hyperthermia?
mutation in ryanodine receptor causing profound calcium release from the sarcoplasmic reticulum
140
Pathophys behind Lambert Eaton syndrome
The symptoms are caused by the production of IgG antibodies to the voltage gated Ca2+ channels in the presynaptic neuron of the neuromuscular junction.his leads to decreased release of acetylcholine and therefore weakness. The weakness, however does improve with repetition because more acetylcholine is released
141
Treatment for Lambert Eaton:
Patients are treated by managing the underlying malignancy or with 3,4-diaminopyridine (amifampridine), which increases the presynaptic release of acetylcholine.
142
After a tourniquet, patient has a decrease in ETCO2 and SpO2-what happened?
A sudden decrease in EtCO2 and SpO2 after tourniquet release should raise suspicion for a pulmonary embolus from a preoperative DVT.
143
Tourniquet inflation and body temp
Tourniquet inflation also leads to a decrease in core body temperature (usually no more than 1 °C) upon deflation due to the return of cooled blood to the central circulation
144
The most common and reliable sign of cyanide toxicity is
The most common and reliable sign of cyanide toxicity is anion gap acidosis
145
Part of the physiology of brain death
Aseptic necrosis, cytotoxic edema, vasogenic
