UNIT 7 Neuro Flashcards
Name 4 types of glial cells and describe the function of each
astrocytes
- most abundant
- regulation of metabolic environment
- repair neuron after neuronal injury
ependymal cells
- concentrated in roof of 3rd/4th ventricles & SC
- form the choroid plexus, which produces CSF
oligodendrocytes
- form the myeline sheath in the CNS
- schwann cells form the myelin sheath in the PNS
microglia
- act as macrophages and phagocytize neuronal debris
list the name and function of the 4 lobes of the cerebral cortex
frontal: motor cortex
parietal: somatic sensory cortex
occipital: vision cortex
temporal: auditory and speech
- Wernicke’s area: understanding speech
- Broca’s area: motor control of speech
Name the 12 cranial nerves
1 olfactory 2 optic 3 oculomotor 4 trochlear 5 trigeminal 6 abducens 7 facial 8 Acoustic 9 glossopharyngeal 10 vagus 11 spinal accessory 12 hypoglossal
O o o to touch and feel a girl’s vagina, ah heavenly
How to know which are sensory, motor, or both:
1 Some
2 Say
3 Marry
4 Money
5 But
6 My
7 Brother
8 Says
9 Bad
10 Business
11 Marrying
12 Money
What CNs provide motor control of the eyes? How does each nerve contribute to the eye’s movement?
CN 3, 4, 6:
CN III:
- up (in, out, and straight)
- in
- down (out and straight)
CN IV
- in and down
CN VI
- out
What bedside tests are used to assess the CN?
I smell II vision III eye movement, pupil constriction IV eye movement V facial sensation (+ ant 2/3 tongue sensation) VI eye movement VII facial movement except chewing VIII hearing, balance IX posterior 1/3 tongue sensation X swallowing XI shoulder shrug XII tongue movement
Which CN resides in the CNS? What is the implication of this?
CN II is the only CN that is part of the CNS (the rest are part of the Peripheral nervous system).
This means that CN II is the only CN that is surrounded by dura and surrounded by meninges, it’s bathed in CSF!
If you accidentally inject local anesthetic into the optic nerve during eye regional block, you gave them a subarchnoid block = CNS depression and respiratory arrest!!!
What is tic douloureux? What CN contributes to this problem?
trigeminal neuralgia
CN 5
causes excruciating neuropathic pain in the face
What is Bell’s palsy? What CN contributes to this problem?
CN 7
causes ipsilateral facial paralysis
What is the function of CSF, and where is it located?
cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function.
It is located in the:
- ventricles (lateral, 3rd, and 4th)
- cisterns around the brain
- subarachnoid space in brain & SC
What regions of the brain are NOT protected by the BBB?
BBB separates the CSF from the plasma. It has tight junctions that restrict pass of large molecules & ions.
The BBB isn’t present at the chemoreceptor trigger zone, posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus
What is the normal volume and specific gravity of CSF?
volume 150mL
spec grav 1.002-1.009
Describe the production, circulation, and absorption of CSF.
CSF production: ependymal cells of the choroid plexus (of lateral ventricles), rate of 30mL/hr
need to match to image
absorption: arachnoid villi within the superior sagittal sinus (to the venous circulation)
What is the formula for CBF? what are the normal values for global, cortical, and subcortical flow?
CBF = CPP/CVR
(CVR = cerebral vascular resistance)
- global 45-55mL/100g (or 15% of CO)
- cortical 75-80mL/100g
- subcortical 20mL/100g
What are the 5 determinants of CBF? You need to know where to label it on the graph
CMRO2 CPP venous pressure PaCO2 PaO2
What is the normal value for CMRO2? What factors cause it to increase? To decrease?
3.0-3.8mL O2/100g brain tissue/min- how much O2 the brain consumes per minute
decreased by hypothermia (7%/1C), IA, propofol, etomidate, barbs peb
increased by hyperthermia, ketamine, N2O
What is the formula for CPP? What is normal?
CPP = MAP - ICP (or CVP, whichever is higher)
autoregulation via vessel diameter changes to provide a constant CPP of 50-150mmHg
- i.e. MAP needs to be higher
- autoreg is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation
What are the consequences of a CPP that exceeds the limits of autoregulation (too high and too low?)
CPP <50
- vessels are maximally dilated
- CBF becomes pressure dependent
- risk of cerebral hypoperfusion
CPP >150
- vessels are maximally constricted
- CBF becomes pressure dependent
- risk of cerebral edema & hemorrhage
list 4 conditions that reduce CPP as a function of increased venous pressure.
a high venous pressure decreased cerebral venous drainage & increases cerebral volume –> backpressure is created to the brain that reduces the arterial/venous pressure gradient (MAP-CVP)
conditions that impair drainage:
- jugular compression d/t head position
- increased intrathoracic pressure d/t cough, PEEP
- vena cava thrombosis
- vena cava syndrome
What is the relationship b/n PaCO2 and CBF? What physiologic mechanism is responsible for this?
linear
- pH of the CSF around the arterioles controls the cerebral vascular resistance
- at a PaCO2 of 40mmHg, CBF is 50mL/100g tissue/min
At what PaCO2 does maximal cerebral vasodilation occur? How about maximal cerebral vasoconstriction?
for every 1mmHg change in PaCO2, CBF will change by 1-2mL/100g tissue/min
max vasodilation occurs at PaCO2 of 80-100mmhg
max vasoconstriction occurs at PaCO2 of 25mmHg
What is the relationship b/n CMRO2 and CBF?
- things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF) –> hyperthermia, ketamine
- things that decrease CMRO2 tend to cause cerebral vasoconstriction (decreased CBF) –> hypothermia, propofol
halogenated anesthetics are an exception; they decouple the relationship: reduce CMRO2, but also cause cerebral vasodilation
- this is why TIVA is a better choice w/ intracranial hypertension
How do acidosis & alkalosis affect CBF?
resp acidosis = increased CBF
resp alkalosis = decreased CBF
met acidosis/alkalosis don’t directly affect CBF. This is because H+ doesn’t pass through the BBB. A compensatory change in MV can, however, affect CBF.
How does PaO2 affect CBF?
PaO2 <50-60mmHg causes cerebral vasodilation & increases CBF. So don’t let your patient become hypoxic and the PaO2 drop less than 50mmHg
When PaO2 is >60mmHg, it doesn’t affect CBF.
What is the normal ICP? What values are considered abnormal?
ICP is the supratentorial CSF pressure
normal = 5-15mmHg
cerebral HTN > 20mmHg
When is ICP measurement indicated? What is the gold standard for measurement?
when GCS <7
intraventricular catheter is the gold standard
other ways:
- subdural bolt
- catheter placed over the convexity of the cerebral cortex
List the s/s of intracranial HTN
HA N/V papilledema (swelling of the optic nerve) focal neurologic deficit decreased LOC seizures coma
discuss the monroe-kellie hypothesis
- if one component increases in volume, another component must decrease in order to maintain constant pressure
- remember intracranial compliance curve
What is Cushing’s triad? What is the clinical relevance of this reflex?
indicates intracranial hypertension
- HTN
- bradycardia
- irregular respirations
increased ICP –> decreased CPP w/ compensatory HTN
–> baroreceptor reflex activation
compression of medulla –> irregular respirations
name 4 areas where brain herniation can occur.
- of the cingulate gyrus under the falx
- transtenotorial
- cerebellar tonsils via the foramen magnum
- via a site of surgery or trauma
How does hyperventilation affect CBF? What is the ideal PaCO2 to achieve this effect?
CO2 dilates vessels = decreased CVR = increases CBF = increases ICP
hyperventilation causes vasoconstriction and decreases CBF = decreases ICP
lowering PaCO2 <30 increases the risk of cerebral ischemia d/t vasoconstriction & L shift of the oxyHgb dissociation curve. Don’t hyperventilate the PaCO2 below 30
How do NTG & SNP affect ICP?
cerebral vasodilators = increases CBF = increase ICP
How does head position affect ICP?
head elevation >30 degrees facilitates venous drainage away from the brain
neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP
head down positions increase CBV & ICP
How does mannitol reduce ICP? What problems can arise when mannitol is used in this way?
0.25-1g/kg increases serum osm & “pulls” water across the BBB towards the bloodstream for excretion
- if BBB is disrupted, mannitol enters the brain & promotes cerebral edema
- mannitol transiently increases blood volume, which can increase ICP & stress the failing heart bad for low EF patients
describe anterior & posterior circulation of the brain. Where do these pathways converge?
converge at the circle of willis
anterior
ICA enter skull via foramen lacerum
aorta –> carotid –> ICA –> circle of willis –> cerebral hemispheres
posterior
vertebral a enter skull via foramen magnum
aorta –> SC –> vertebral –> basilar –> posterior fossa structures & cervical SC
Describe the anatomy of the circle of willis. Need to know how to label
primary function of the circle of willis is to provide redundancy of blood flow in the brain.
If one side of the circle becomes occluded, the other side should theoretically be able to perfuse the affected areas of the brain
- Basilar artery - Posterior cerebral artery - Posterior communicating artery - Middle cerebral artery - Anterior cerebral artery - Anterior cerebral communicating artery
Which population of stroke patients should receive a thrombolytic agent?
CVA d/t thrombosis
diagnosis must be made by emergent head CT prior to administration
if tx can begin <3hrs after onset of symptoms, the pt should receive tPA
- aspirin is acceptable if tPA cannot be administered
What is the relationship b/n hyperglycemia & cerebral hypoxia?
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue & is associated w/ worse outcomes
monitor serum glucose, treat hyperglycemia, be careful administering dextrose containing IVF
in the context of cerebral aneurysm, how is transmural pressure calculated?
an increased transmural pressure predisposes the aneurysm to rupture.
transmural pressure = MAP - ICP
MAP = pressure pushing outward against the aneurysmal sac
ICP = counterpressure that pushes against it.
–> creates a tamponade effect
risk of rupture is increased by HTN and/or acute reduction in ICP
What is the most common clinical finding in a patient w/ SAH? What are the other s/s?
WHOL (worst HA of life)
others
- LOC (50%)
- neurologic deficits
- N/V
- photophobia
- fever
What is the most significant source of M&M in the patient w/ SAH?
cerebral vasospasm- due to delayed contraction of the cerebral arteries can lead to cerebral infarction
Free Hgb that is in contact w/ the outer surface of the cerebral arteries increases the risk
there is a correlation b/n amount of blood observed on CT & vasospasm incidence
What is the incidence of cerebral vasospasm? When is it most likely to occur?
25% of patients
most likely 4-9days after SAH!!!!!!!!!!!!!!!
What is the treatment for cerebral vasospasm?
triple H therapy (hypervolemia, HTN, permissive hemodilution to Hct 27-32%)
nimodipine (CCB) reduces M&M associated w/ vasospasm –> doesn’t actual reduce the spasm, but increases the collateral blood flow
during endovascular coil placement for a cerebral aneurysm, the aneurysm ruptures. What is the best treatment at this time?
- Give them protamine 1mg/100U heparin
- low/normal MAP
- adenosine to temporarily arrest the heart to see where the bleeding is
be able to calculate the Glascow coma scale
eyes (1-4)
motor (1-6)
verbal (1-5)
How do you treat the patient w/ an ICH who is on warfarin?
- FFP
- prothrombin complex concentrate
- recombinant factor 7a
vitamin K isn’t the best option for acute warfarin reversal
How do you treat the patient w/ an intracranial hemorrhage who is on clopidogrel?
We need to reverse clopidogrel with a platelet transfusion (aspirin can be reversed this way too) there is also evidence of reversal w/ recombinant factor VIIa
What are two common ways of reducing ICP that should specifically be avoided in the patient w/ a TBI?
hyperventilation- can worsen cerebral ischemia + it’s only indicated as a temp measure
steroids- worsen neurologic outcome in traumatic brain injury
Is N2O safe in the pt w/ TBI?
No
other injuries, such as pneumothorax, may only become evident after anesthetic induction & PPV
compare and contrast the 5 types of seizures.
grand mal
- generalized tonic/clonic activity
- apnea, respiratory arrest –> hypoxia
- tx: propofol, diazepam
- surgical: vagal nerve stim or rsxn of foci
focal cortical
- localized to a particular cortical region
- can be motor or sensory
- usually no LOC
absence (petit mal)
- temporary loss of awareness staring into space and blinking
- more common in children
akinetic
- temporary lost of consciousness and loss of postural tone (can result in fall & TBI)
- more common in children
status epilepticus
- seizure activity >30min or 2 grand mal w/out regaining consciousness in between
- resp arrest –> hypoxia
- tx: phenobarb, phenytoin, benzos, propofol, and even GA
What is the relationship b/n etomidate and seizures
etomidate commonly causes myoclonus. This is not associated w/ increased EEG activity in those that do not have epilepsy.
In those w/ sz disorders, etomidate (or methohexital or alfentanil) increases EEG activity and can be used to help determine location of seizure foci during cortical mapping
Describe the patho of Alzheimer’s disease
diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain
consequences:
- dysfunctional synaptic transmission (most notable at nACh neurons)
- apoptosis (programmed cell death)
What class of drugs is used to treat Alzheimer’s disease?How do they interact w/ succinylcholine?
tx is palliative & aims to restore the [ACh]; cholinesterase inhibitors (tacrine, donepezil, rivastigmine, galantamine)
cholinesterase inhibitors increase the DOA of succ, although the clinical significance is debatable
Describe the patho of Parkinson’s disease.
dopaminergic neurons in the basal ganglia are destroyed —> imbalance of DA & ACh (relative ACh increase)
this leads to suppression of corticospinal motor system + overactivity of extrapyramidal motor system
-skeletal muscle tremor
- akinesia- inability to initiate purposeful movement
- rigidity-limited movement
What drugs increase the risk of extrapyramidal s/s in the pt w/ Parkinson’s disease?
- reglan
- butyrophenones (haldol, droperidol)
- phenothiazines (promethazine)
What is the most common eye complication in the perioperative period? What is the most common cause of vision loss?
corneal abrasion
ischemic optic neuropathy = most common cause of vision loss
Describe the patho of ischemic optic neuropathy.
ischemia of the optic nerve. Most likely explanation is that venous congestion in the optic canal reduces perfusion pressure
ocular PP = MAP - intraocular pressure
central retinal & posterior ciliary arteries are at highest risk b/c they are “watershed” areas – they lack anastomoses w/ other arteries
What surgical procedure presents the most significant risk of ION? What are other procedure & patient risk factors?
spinal surgery in the prone position = most significant risk
other factors:
- prone
- use of Wilson frame = BAD
- long duration of anesthesia
- large EBL
- low colloid:crystalloid resus
- hypotension
- male
- obesity
- DM
- HTN
- smoking
- old age
- atherosclerosis
discuss the blood flow to the SC
SC is perfused by:
1) 1 anterior spinal artery (anterior 2/3 of SC)
2) 2 posterior spinal arteries (posterior 1/3 of SC)
3) 6-8 radicular arteries
What is the most important radicular artery? Which spinal segment does it typically enter the SC?
artery of Adamkiewicz
along w/ the anterior spinal artery, the artery of adamkiewicz supplies the anterior cord in the thoracolumbar region. Most commonly originates b/n T11-T12
Envision the anatomy of the SC & spinal nerve in cross section.
sensory neurons from the periphery via the dorsal nerve root
motor & autonomic neurons exit via the ventral nerve root
compare the structure & function of the dorsal column with the spinothalamic tract.
dorsal column (medial lemniscal system)
- transmits mechanoreceptor sensations (fine touch, proprioception, vibration, pressure)
- capable of 2 point discrimination (high degree of localization)
- large, myelinated, rapidly conducting fibers
- faster transmission than anterolateral system
- a “more evolved” system
anterolateral system (spinothalamic tract)
- transmits pain, temp, crude touch, tickle, itch, sexual sensation
- no 2 point discrimination
- smaller, myelinated, slower conducting fibers
- more “primitive” system
What bedside exam can assess the integrity of the corticospinal tract? How can you interpret it?
most important motor pathway (often referred to as the pyramidal tract, all others are collectively the extrapyramidal tract)
Babinski test (firm stimulus to underside of foot) yields:
- normal: downward motion of all the toes
- upper motor neuron injury: upward extension of big toe + fanning of the others = abnormal, positive test
- lower motor neuron injury: no response
contrast the presentation of upper vs. lower motor neuron injury
upper motor neurons begin in the cerebral cortex & end in the ventral horn of the SC, while the lower motor neurons begin in the ventral horn & end at the NMJ
upper motor neuron injury presents w/ hyperreflexia & spastic paralysis
lower motor neuron injury presents w/ impaired reflexes & flaccid paralysis
discuss the patho of neurogenic shock.
impairment of cardioaccelerator fibers (T1-T4) –> unopposed cardiac vagal tone –> bradycardia & decreased inotropy
decreased SNS tone –> vasodilation –> venous pooling –> decreased CO & BP
impairment of sympathetic pathways from hypothalamus to blood vessels –> inability to vasoconstrict or shiver –> hypothermia
how can you differentiate neurogenic shock from hypovolemic shock?
neurogenic: bradycardia, hypotension, hypothermia w/ pink, warm extremities d/t cutaneous vasodilation
hypovolemia: tachycardia, hypotension, cool, clammy extremities
Discuss the use of succinylcholine in the patient w/ SC injury.
avoid if >24hrs post injury
do not use for at least 6months thereafter, some books say 1yr
When does a pt w/ SC injury become at risk for autonomic hyperreflexia? What factor (other than time) contributes to this risk?
It occurs after the neurogenic shock phase ends (1-3 weeks), the body begins to mend itself in a pathologic and disorganized way, putting the pt at risk for autonomic hyperreflexia.
up to 85% of patients w/ injury >T6 will develop
List 6 situations that can precipitate autonomic hyperreflexia
sitmulation of the hollow organs (bladder, bowel, or uterus) bladder catheterization surgery (esp cysto, colonoscopy) bowel movement cutaneous stimulation childbirth
Discuss the presentation & pathophysiology of autonomic hyperreflexia.
classic presentation = HTN & bradycardia.
stimulation below the level of SCI triggers sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury –> baroreceptor activation in carotid bodies (bradycardia) –> body attempts to reduce afterload w/ vasodilation above the level of the injury.
other s/s:
- reflex vasodilation above level of SC injury –> nasal stuffiness
- HTN –> HA/blurred vision
- malignant HTN –> CVA, sz, LV failure, dysrhythmias, pulmonary edema, and/or MI, seizure, or stroke
detail the anesthetic management of the patient w/ autonomic hyperreflexia.
prevent stimulation to the area below level of injury to prevent AH!
- GA or spinal = best
- epidural not as good for laboring mother b/c doesn’t inhibit sacral nerve roots as much
- tx HTN w/ removal of stim, deepen IA, + rapid vasodilator (SNP)
- tx bradycardia w/ atropine/glyco
- avoid meds that increase HR & vasoconstrict
- avoid sux x6months
- monitor for AH closely in the immediate post-op period, when anesthesia is wearing off.
Discuss the patho of amyotrophic lateral sclerosis (Lou Gehrig’s disease)
Progressive degeneration of motor neurons in the corticospinal tract
Astrocytic gliosis replaces the affected motor neurons. Both the upper & the lower motor neurons are affected.
Etiology is unknown
- Avoid sux due to risk of hyperkalemia
- They have increased sensitivity to nondepolarizers, so decrease the dose
- upper motor produces hyperreactive responses
- ortho hypotension
- bulbar atrophy
Detail the anesthetic management of ALS
- no clear evidence that supports one technique over another
- avoid sux (hyperK+)
- increased sensitivity to NDMR: so decrease the dose
- bulbar m dysfunction increases risk of aspiration
- chest weakness decreases VC & MMV
- consider post-op mechanical ventilation
describe the patho of myasthenia gravis
autoimmune disease
IgG Ab destroy post-junctional nAChR at the NMJ
(ACh is present in sufficient quantity, the receptors just aren’t there)
–> skeletal m weakness.
Key feature is skeletal m weakness that becomes worse later in the day or that develops w/ exercise & can recover some w/ rest.
Early signs: diplopia and ptsosis
Other signs: bulbar muscle weakness of mouth and throat, dysphagia, dysarthria, difficulty handling saliva, proximal weakness
Things that make it worse:
- pregnancy
- infection
- electrolyte imbalance
- stress
- aminoglycoside antibiotics- so avoid this bc it makes them more weaker
Treat: First line treatment with oral pyridostigmine AchE. But if you overdose is it cholinergic crisis or if they’re feeling better was it myasthenia crisis? Test with Tensilon test with Edrophonium 1-2mg IV
What surgical procedure can reduce symptoms in the patient w/ myasthenia gravis?
other treatments for MG?
the thymus gland plays a key role in MG, and thymectomy
- it reduces circulating anti-AChR IgG in most patients
- surgical approach may be via median sternotomy or by the transcervical approach
Other treatments:
- Immunosuppresants like steroids cylosporine, azathioprine, mycophenolate
- Plasmapharesis- temp relief during crisis
How does myasthenia gravis affect the pregnant mother & the fetus?
in 1/3 of women, pregnancy intensifies the symptoms of MG.
Anti-AChR IgG Antibodies cross the placenta and cause weakness in 15-20% of neonates.
This can persist x2-4 weeks, which is consistent w/ the half-life of these antibioties in the neonates circulation
Neonate may require airway management.
How can you tell the difference b/n cholinergic crisis and myasthenic crisis?
Pryidostigmine (anticholinesterase) is the first line tx for MG. An OD can cause cholinergic crisis, which can include skeletal m weakness (makes differentiation difficult)
diagnosis is made by administering 1-2mg IV edrophonium (“Tensilon test”)
- if weakness is made worse, then the pt has cholinergic crisis (tx = anticholinergic)
- if weakness improves, then it was an MG exacerbation
Treat with = anticholinesterase, immunosuppression, plasmapheresis
How do patients with myasthenia gravis respond to NMB?
There less nicotinic type m receptors at the neuromuscular junction.
- They’re more resistant to Sux. give 1.5-2mg/kg. Remember pyridostigmine impairs efficacy of pseudocholinesterase and can also prolong sux
- More sensitive to nondepolarizers. If roc was used there’s a higher risk of residual blockade. REDUCE THE DOSE by 1/2-1/3
Volatile anesthetics cause skeletal m relaxation by acting in the ventral horn of the SC - in many cases this eliminates the need for NMB.
Why are patients w/ myasthenia gravis prone to aspiration?
bulbar weakness (mouth and throat) manifests as difficulty handling oral secretions –> increased risk of aspiration just like in ALS!
describe the patho of Eaton Lambert syndrome. Can you use paralytics? What is the treatment?
IgG mediated destruction of the v-gated Ca++ channel at the presynaptic nerve terminal. presynaptic!!!
When the AP depolarizes the nerve terminal, Ca++ entry into the presynaptic neuron is limited, reducing the amount of ACh that is released into the synaptic cleft. Postsynaptic nAChR is normal
- they’re sensitive to both depolarizers and non depolarizers
- Volatile anesthetics also provide enough muscle relaxation for most surgical procedures like in MG
- association with small cell lung carcinoma
- Treatment: 3,4-diaminopyridine (DAP) increases ACh release from the presynaptic nerve terminal and improves the strength of contraction.
compare and contrast myasthenic gravis to eaton-lambert syndrome in terms of patho, common comorbidities, and response to NMB
eaton-lambert
- Destroyed v-gated Ca++ channels (pre-synaptic)
- decreased ACh release
- presynaptic neuron of NMJ
- comorb: small cell lung CA
- sensitive to NMB (both)
- AChE inhibitors doesn’t improve symptoms
MG
- Fewer Nm receptor (post-synaptic)
- decreased ACh response
- comorb: thymoma
- resistant to sux, sensitive to NDMR
- AChE inhibitors improve symptoms
Describe Guillain-Barré syndrome also known as acute idiopathic polyneuritis
Common etiologies:
Treatment:
Can you use sux and roc?
Are steroids helpful?
common etiologies: campylobacter jejuni bacteria, Epstein Barr virus, and cytomegalovirus
starts like flu-like illness followed by ascending paralysis. Starts in distal extremities and ascends up
Muscle weakness: impairs ventilation and difficulty swallowing
Immunologic assault on the myelin in the peripheral nerves. Action potential can’t be conducted –> the motor endplate never receives the incoming signal
Persists for 2 weeks and ends w/ full recovery in approx 4 weeks.
Treatment: plasmapheresis like in MG, and you also give IgG. Steroids do NOT help
Avoid sux and decrease dose of nondepolarizers like in ALS!
Sensory deficits are common: parathesias, numbness, and pain
Autonomic dysfunction is common: tachy or Brady, htn or hypotension, orthostatic hypotension, diaphoresis or anhidrosis
There is an exaggerated response to indirect acting sympathomimetics due to upregulation of postjunctioanl adrenergic receptors. So avoid ephedrine
Regional is not preffered over GA
discuss the presentation of guillian-barre and can you use sux and roc?
flu-like illness usually precedes paralysis by 1-3 weeks
s/s:
- flaccid paralysis begins in the distal extremities and ascends bilat toward proximal extremities, trunk, face
- intercostal m weakness impairs ventilation
- facial, pharyngeal weakness causes dysphagia
- sensory deficits: paresthesias, numbness, +/- pain
- autonomic dysfunction is common: HR, BP, sweating abnormalities, orthostatic hypotension
Avoid sux and use less Roc!
What is familial periodic paralysis and how can the 2 variants of this disease be distinguished from each other?
two distinct disease processes that are characterized by acute episodes of skeletal m weakness that is accompanied by hypo or hyperkalemia
hypokalemia: diagnosed if skeletal m weakness follows a glucose-insulin infusion
hyperkalemia: diagnosed if skeletal m weakness follows oral K+ administration
What drugs should be avoided in the patient with each type of familial period paralysis?
How about temperature?
Familial periodic paralysis is acute episodes of skeletal muscle weakness with changes in potassium. It is not a disease with the neuromuscular junction. It’s a disorder of the skeletal muscle membrane: reduced excitability
With hypokalemic avoid:
- glucose containing solutions! AVOID D5LR because it usually follows an insulin infusion
- K+ wasting diuretics
- B2 agonists like Terbutaline
- avoid succinylcholine because this condition might be associated with MH
- it is associated with a calcium channelopathy
With hyperkalemia avoid:
- succinylcholine
- K+ containing slns (LR)
- it’s associated with a sodium channelopathy
acetazolamide is the tx for both forms bc it creates a nonanion gap acidosis, which protects against hypokalemia. It also facilitates renal K+ excretion which guards against hyperkalemia
Shorter acting nondepolarizers are best!
Avoid hypothermia for both types at all costs
What is the dysfunctional receptor in the patient w/ MH?
when T-tubule is depolarized, extracellular Ca++ enters the myocyte via the dihydropyridine receptor at the T-tubule
this activates the ryanodine receptor (RYR1) and it’s dysfunctional, which instructs the SR to release massive Ca++ into the cell. In the case of MH, it releases WAY TOO MUCH
(consumes ATP, O2, produces CO2)
cell attempts to return some Ca++ into the SR via the SERCA2 pump (in MH, this pump becomes overworked)
(consumes ATP, O2, produces CO2)
when the skeletal m consumes all of its ATP, cell membrane integrity is no longer maintained & intracellular components (myoglobin & K+) are released into the systemic circulation
MH inherited disease: disordered calcium homeostasis
list 8 consequences of too much Ca++ inside of the skeletal myocyte
- sustained muscular contraction
- accelerated metabolic rate & rapid ATP depletion
- increased O2 consumption
- increased CO2 & heat production
- mixed respiratory and lactic acidosis
- sarcolemma breaks down
- K+ & myoglobin leak into the systemic circulation
- rigidity from sustained contraction
MH is inherited disease of skeletal muscle. Exposure of halogenated activates the defective ryanodine receptor RYR1 and stimulates SR to release too calcium
list 6 conditions that are NOT definitively linked to MH
- Duchenne muscular dystrophy- due to rhabdomylolysis
- Becker muscular dystrophy
- neuroleptic malignant syndrome
- myotonia congenita or dystrophy
- osteogenesis imperfecta
what is the most sensitive indicator of MH? What is the time course of the other s/s?
MH can occur as late as 6hrs after exposure to a triggering agent.
most sensitive indicator of MH: EtCO2 rises out of proportion to MV
early:
- tachycardia
- tachypnea
- masseter spasm- jaw can’t be opened
- warm soda lime
- irregular heart rhythm
intermediate:
- cyanosis
- pt warm to touch
- irregular heart rhythm
late:
- muscle rigidity
- cola-colored urine
- coagulopathy
- irregular heart rhythm
what is the difference b/n trismus and MH? How should you proceed if the patients presents with either condition?
trismus & masseter m rigidity exist on a continuum
- trismus: tight jaw can still be opened, normal response to sux
- masseter muscle rigidity: cannot open jaw
trismus is a normal response to succinylcholine - ok to proceed w/ surgery if occurring in isolation, but may want to avoid other triggering agents.
if the pt has masseter m rigidity, assume MH until proven otherwise
- NMB will not help this since it’s occurring distal to the NMJ spasm is due to increase calcium in the myoplasm
How is dantrolene formulated? How is it prepared?
each vial contains 20mg dantrolene + 3g mannitol &
must be reconstituted w/ preservative free H2O 60 ml
Initial dose 2.5mg/kg IV
NaCl introduces additional solute which prolongs the time required for dantrolene to dissolve into the dilutent
enlist help early!!
Dantrolene can irritate the vein, also a muscle relaxant and can cause muscle weakness
How do you treat MH?
1 d/c triggering agent #2 call for help
100% FiO2 >10L/min
dantrolene 2.5mg/kg IV, repeat Q5-10mins
- hyperventilate
- correct lactic acidosis w/ bicarb
- treat hyperK+
- CaCl 5-10mg IV
- insulin 0.15U/kg + D50 1mL/kg
protect against dysrhythmias - charcoal filter to inspiratory and expiratory limb of the circuit if you have time. Vapor- clean filter needs to be changed every hour during MH crisis
- class I agents (lido, procaine)
- avoid CCB like Verapamil w/ dantro to avoid hyperK+
- maintain UOP
- IV hydration
- 0.25mg/kg mannitol
- 1mg/kg
- cool the pt until temp <38C
- cold IVF
- cold fluid lavage
- ice packs
monitor coags, avoid DIC
If at risk of MH: monitor in PACU 1-4 hours
If they actually had MH: need to go to the ICU, MH can reoccur up to 36 hours!!!!!!
describe the patho of Duchenne muscular dystrophy
dystrophin is a critical structural component of the cytoskeleton of skeletal and cardiac muscle cells. DMD- skeletal muscle myopathy with absence of dystrophin protein from X linked recessive disease, affects many males
Absence of it destabilizes the sarcolemma during muscular contraction & increases membrane permeability.
creatine kinase and myoglobin to leak through the membrane and results in elevated plasma concentration elevated labs
Calcium also freely enters the cell = inflammation, fibrous, cell death
extrajunctional receptors populate –> avoid succinylcholine
At risk for MH-like symptoms with hyperkalemia and rhabdomyolysis not true MH.
Best to use TIVA and avoid sux and volatile agents
however, there is no denervation of skeletal tissue, meaning that sensation and reflexes are intact
How does Duchenne muscular dystrophy affect cardiac function? What EKG findings might you expect?
cardiac considerations:
- degeneration of cardiac m –> decreased contractility, pap m dysfunction, mitral regurgitation, cardiomyopathy, CHF
- signs of cardiomyopathy = resting tachycardia, JVD, S3/S4 gallop
- gold standard = echo
EKG changes
- ST + short PR
- scarring of posterobasal aspect of LV manifests as increased R wave amplitude in lead 1 & deep Q waves in the limb leads
What is the Cobb angle and what is its significance?
describes the magnitude of the spinal curvature
40-50 degrees = indication for surgery
60 degrees = decreased pulmonary reserve
70 degrees = pulmonary symptoms present
100 degrees = gas exchange significantly impaired, higher risk of post-op pulmonary complications
contrast the early & late complications of scoliosis
alters thoracic geometry, which compresses the lungs & creates a restrictive ventilatory defect. One side of the thorax becomes smaller than the other
early:
- restrictive ventilatory defect (same lung volume, capacity decreases as any)
- decreased chest wall compliance
late:
- VQ mismatching
- hypoxemia
- hypercarbia (sign of impending failure)
- pHTN
- reduced response to hypercapnia
- cor pulmonale
- cardiorespiratory failure
CV changes: RV hypertrophy and mitral prolapse (most common), mitral regurgitation, and coarctation of the aorta
List 3 ways that rheumatoid arthritis affects the airway.
TMJ, cricoarytenoid joints, cervical spine are affected
- TMJ: limited mouth opening
- cricoarytenoid joints: decreased diameter of glottic opening
- cervical spine: A-O subluxation w/ flexion + limited extension
Common complication is Atlantoaxial subluxation and seperation of the antlanto-odontoid articulation
What is the most common complication of rheumatoid arthritis? What’s its clinical significance?
What are some other complications of RA?
RA: vasculitis
AO subluxation is the most common airway complication of RA
This is d/t the weakening of the transverse axial ligament, which allows the odontoid to directly compress the SC at the level of the foramen magnum.
- puts the pt at risk for quadriparesis or paralysis
- side note: pts w/ Down syndrome are also at risk for AO subluxation
Other complications:
- cricoarytenoiditis- painful swallowing airway obstruction or stridor
- restrictive lung disease - pleural effusion/ fibrosis
- aortic regurgitation
- anemia
- renal insufficiency from NSAID use
Discuss the pathophysiology of RA.
Treatment:
autoimmune disease that targets the synovial joints. There is also widespread systemic involvement d/t infiltration of immune complexes in the small & medium arteries –> vasculitis
cytokines (TNF & interleukin-1) play a central role in the pathogenesis.
Hallmark of RA: morning stiffness that improves w/ activity
joints are painful, swollen, and warm
other symptoms:
- weakness
- fatigue
- anorexia
- lymph node enlargement
using a systems approach, list the complications of RA.
Rheumatoid arthritis is characterized by symmetric polyarthropathy that affects weight-bearing joints and proximal interphalangeal and metacarpophalangeal joints. It is typically worse in the morning. In the most severe forms, every joint can be affected except for the lumbar and thoracic spine.
airway:
- TMJ synovitis
- cricoarytenoid arthritis
- AO instability
pulmonary
- pleural effusion
- restrictive pattern d/t diffuse interstitial fibrosis + costochondral involvement that limits chest wall expansion
cardiac
- pericardial effusion/tamponade
- restrictive pericarditis
- aortic regurgitation
- valvular fibrosis
- coronary artery arteritis
hematologic
- anemia
- platelet dysfunction d/t NSAIDs
renal
- renal insufficiency d/t vasculitis, NSAIds
endocrine
- adrenal insufficiency & infections d/t steroids
GI
- gastric ulcerations d/t NSAIDs, steroids
Eyes
- Sjogren’s syndrome - risk of corneal abrasion
PNS
- peripheral neuropathy d/t nerve entrapment
describe the patho of systemic lupus erythematosus.
SLE is an autoimmune disease characterized by the proliferation of antinuclear antibodies
SLE affects nearly every organ system & most consequences are the direct result of Ab-induced vasculitis and tissue destruction
- Can cause cricoarythenoiditis: hoarseness/stridor/airway obstruction, recurrent laryngeal nerve palsy is a complication, hypercoagulability
Using a systems based approach, list the complications of systemic lupus erythematosus
targets young women
most common problems are polyarthritis (generally not the spine) & dermatitis
only 33-50% develop the “butterfly rash”
airway:
- cricoarytenoiditis: hoarseness, stridor, a/w obstruction
- RLN palsy
pulmonary
- restrictive
- pHTN
- interstitial lung dz w/ impaired diffusing capacity
- pleural effusion
- recurrent PE
CV
- pericarditis
- Raynaud’s
- HTN
- conduction defects
- endocarditis
hematologic
- antiphospholipid antibodies
- hypercoagulability = risk of DVT
- anemia
- thrombocytopenia
- leukopenia
renal: nephritis w/ proteinuria
CNS: stroke
what drugs can exacerbate SLE?
occurs d/t stress or drug exposure
drug induced usually persists for several weeks-months & presents w/ mild symptoms
most common offenders (PISSED CHIMP) Pregancy Infection Surgery Stress Enalapril D-penicillamine Captopril Hydralazine- can cause tachycardia Isoniazid Methyldopa Procainamide
what is the relationship b/n SLE & antiphospholipid syndrome?
Name of treatments and anesthesia considerations for SLE
those w/ SLE are prone to developing antiphospholipid antibodies
Although aPTT is prolonged, these pts are prone to a state of hypercoagulability & thrombosis
- risk for stroke, DVT, PE
- pregnant pts are at higher risk
- Cyclophosphamide- immunosuppressent can prolong sux
Discuss the patho of myotonic dystrophy.
characterized by prolonged contracture after a voluntary contraction.
This is the result of dysfunctional Ca++ sequestration by the SR.
Contractions can be so severe that they interfere w/ ventilation & intubation
3 things increase risk of contractures:
1) sux
2) NMB reversal so consider Sugammadex
3) hypothermia = sustained contractions
Discuss the patho of Marfan syndrome.
It is an autosomal dominant trait.
It is a connective tissue disorder that’s associated w/ an elevated risk of aortic dissection, MV prolapse, mitral regurg, aortic regurgitation
Aortic dissection of the ascending aorta can extend into the pericardium, and this increases the risk of cardiac tamponade!
Becks’ triad: JVG, hypotension, muffled heart tones
spontaneous pneumo is a common complication in these patients.
Discuss the patho of Ehlers-Danlos syndrome
inherited disorder of procollagen and collagen. There are several types, but only type IV is associated w/ vascular rupture (i.e. AAA)
increased bleeding tendency d/t lack of blood vessel integrity+ coagulopathy
- avoid regional anesthesia = hematoma is a risk
- avoid IM injections
- be careful during airway management & line placement.
Pneumothorax is also a common complication; avoid high PIP!!!!!
A!
Intrathecal opioids act centrally by diffusion into the spinal cord and interact with mu receptors in the substantia gelatinosa in the dorsal horn.
Opioid receptors (mu receptors) are present in the substantia gelatinosa (A) of the dorsal horn in the spinal cord. The substantia gelatinosa comprises the cell bodies of the second-order projection neurons that ascend from the spinothalamic tract to the thalamus. These cells are densely populated with mu receptors and form the primary immediate site of action of intrathecal opioids that diffuse from the cerebrospinal fluid into the spinal cord.
Multiple sclerosis
- Demyelination disease of Central Nervous System diagnose with an MRI
- can be exacerbated by increase in temp by 1 degree
- epidural is safe, but spinal can worsen it
- Occurs after 35 years old
- Avoid SUX!
- Pregnancy is associated with a reduced incidence of exacerbation, while the postpartum period is associated with an increased risk of relapse
Structure of spinal cord:
Review DCML anatomy
Which one is continuous touch?
Which one is reading braille?
Which one is vibration?
Which one is proprioception? Ruffini
Where is a herniation most likely to occur?
Review intracranial hypertension
Dorsal column
Sensory neurons from the periphery enter the spinal cord?
Motor and autonomic neurons exit?
Laminae 1-6 reside in the dorsal grey matter. Are they sensory or motor? What about Laminae 7-9?
Laminae 1-6 in the dorsal grey matter are sensory
Laminae 7-9 in the ventral grey matter are motor
Tracts
DCML:
- transmits mechanoreceptive sensations:
fine touch, proprioception, vibration, pressure (fine degree of intensity) - capable of 2 point discrimination- high degree of localizing the stimulus
- large, myelinated, rapid conducting fibers
- transmits sensory faster than the anterolateral system
1) First order- usually A beta, enters spinal cord through dorsal root ganglion, relays sensory info from dorsal column to the medulla
2) Second order- crosses contralateral side in the medulla
3) Third order- fibers pass through internal capsule and go in the postcentral gyrus in the parietal lobe in the cerebral cortex
DC-MLS anatomy:
- Meissner’s corpuscles
- Merkel’s discs
- Ruffini’s endings
- Pacinian corpuscles
- Meissner’s corpuscles- 2 point discriminative touch and vibration. READING BRAILLE
- Merkel’s discs- continuous touch
- Ruffini’s endings- proprioception, prolonged touch and pressure
- Pacinian corpuscles- vibration
Anterolateral System Spinothalamic Tract: combo of lateral and anterior Spinothalamic tract
Transmits: pain, temperature, crude touch, tickle, itch, and sexual sensation
Has smaller myelinated and nonmyelinated slower conducting fibers
There is NO 2-point discrimination
1) First order: there is 2 nerve fibers types:
Alpha-delta fast pain, glutamate is the neurotransmitter.
C fibers slow pain, substance P is the neurotransmitter (Where as in the DCL tract, the first fiber is alpha-beta fibers)
Pain neurons synapses with the 2nd order neuron in the substantia gelatinosa Rexed Lamina 2.
Primary pain neurons can also synapse in the 2nd order neuron in the dorsal horn Laminae 1,4,5, 6.
2) Second order neuron: crosses contralateral side of the spinal cord and ascends in 2 pathways
- 1) Lateral Spinothalamic tract- pain and temperature
- 2) Anterior spinothalaic tract- crude touch and pressure
Second-order neurons synapse with third-order in the reticular activating system and thalamus
3) Third order neuron: fibers pass through internal capsule in the post central gyrus in the parietal lobe in the cerebral cortex. Many pain fibers synapse with the third order neuron in the reticular activating system and thalamus
Injury to upper motor neuron
Upper motor begins in the cerebral cortex and ends in the ventral horn of the spinal cord
Upper motor neuron injury - contralateral spastic paralysis + hyperreflexia
Ex: cerebral palsy and ALS
Can do babinski test to assess corticopinal tract: toes fanning out is abnormal
Lower motor neuron
Begins in ventral horn and ends in neuromuscular junction
SSEPs
Monitor dorsal column medial leminiscus
Loss of SSEPs during spinal fusion is most likely due to interruption of posterior spinal artery
Neurogenic shock vs. hypovolemic shock:
What is the most common site of SCI, what are some s/s? How long can it last?
What are some initial treatment for SCI?
Neurogenic shock triad: Bradycardia, hypotension, hypothermia- with pink and warm extremities
Hypovolemia shock: tachycardia, hypotension, cool and clammy. No hypothermia!
C7 is most common site of SCI. Can last 1-3 weeks. Initially leads to flaccid paralysis, loss of sensation below the level of injury, loss of bowel and bladder function occurs
After acute phase, spinal reflexes return which leads to spastic paralysis after 6 weeks
Treatments: Levo gtt to restore SVR and give volume
sux is ok first 24 hours but switch to non depolarizer
Nitroprusside works faster than hydralazine and we need to quickly treat pressure. They’re at risk of intracerebral hemorrhage
Autonomic hyperreflexia- they will Vasodilate above the level of injury and vasoconstrict below the injury
Hypertension produces bradycardia via the baroceptor reflex. You can give anticholinergics
Autonomic hyperreflexia
HTN + bradycardia
Hypertension needs to be treated ASAP or it can cause stroke, LV failure, and pulmonary edema, seizures
Other signs: nasal stuffiness, headache or blurred vision
FIRST REMOVE STIMULUS! Then deepen anesthesia, and give sodium nitroprusside, avoid sux in chronic SCI
Adding lube to the foley doesn’t prevent AH
Things that can elicit AH: stimulation of hollow organs like bladder bowel uterus, bladder catherization, surgery like cystoscopy to colonoscopy, bowel movement, childbirth
Amyotrophic lateral sclerosis
Progressive degeneration of motor neurons in the corticospinal tract in the upper and lower motor. Sensory remains intact
- upper neurons: spasticity, hyperreflexia, loss of coordination
- lower motor neuron: muscle weakness, fasciculations, and atrophy
- it begins in the hands and spreads
- Respiratory failure is the common cause of death
- Bulbar muscle weakness increases risk of aspiration
- Extrajunctional receptors at the NMJ can cause life threatening hyperkalemia
- More sensitivity to non depolarizing neuromuscular blockers so try to avoid all of them
- Riluzole is an NMDA antagonist and is the only drug that reduces mortality
- Chest weakness reduces vital capacity. Consider postoperative mechanical ventilation
Spinothalamic tracts (anterolateral system): nociceptors and free nerve endings transmit pain signals to the brain via this tract
1) 2 posterior spinal arteries perfuse the posterior 1/3 of the spinal cord
- Medial lemniscal system dorsal column
2) 1 anterior spinal artery that perfuses 2/3 of the spinal cord perfuses:
- Spinothalamic
- corticospinal
- autonomic fibers
initial treatment for spinal cord injury = Levo gtt and intravascular volume expansion
Deep hypothermic circ arrest is for neuroprotection for pts undergoing aortic arch surgery and not SCI
You want to avoid sux for pts with SCI and risk of severe Hyperkalemia 24 hours after the injury
Meissner’s corpuscles.
Reading braille requires highly sensitive mechanoreptors in the fingertips that are capable of 2-point discrimination
Evoked potentials have replaced the need for wake up tests for back surgeries
- SSEPs- monitor posterior spinal cord- dorsal column (proprioception)
- MEPs- monitor anterior spinal cord (motor)
Dens also called odontoid process= superior boney projection off the axis C2, provides pivot point that helps with head rotation
Marfan’s syndrome- aortic insufficiency
Ehlers-Danlos syndrome- bleeding into joints
Osteogenesis imperfecta- blue sclera eyes is a unique finding, connective tissue disorder, weak bones, risk of fractures! Serum thyroxine is increased and increase basal metabolic rate = hyperthermia
M.S = sensitivity to hyperthermia
Myotonic dystrophy = sustained contracture with Sux
Paget’s diease = risk of bone fracture. Excess osteoblastic osteoclastic but it causes thick, weak, bone deposits. Caused by excess parathyroid hormone or calcitonin deficiency.
Scleroderma = CREST syndrome. Excessive fibrosis in organs. Calcinosis, Raynaud’s, Esophageal hypo motility, Sclerodactyly, Telangiectasis spider veins) which increase risk of mucosal bleeding. They also have limited mouth opening from the skin fibrosis
M.S
D5W, glucose causes insulin spike and it shifts K+ into the cells and leads to exacerbation of skeletal muscle weakness
What condition is most strongly associated with CREST syndrome?
Scleroderma- risk of mucosal bleeding
Posterior circulation:
1. Subclavian artery
2. Vertebral artery enter through the foreman magnum
3. Basilar artery
4. Posterior cerebral artery
Anterior circulation:
1. Carotid artery enter through the foramen lacerum
2. Internal carotid artery
3. Middle cerebral artery
Cranial nerves
Peripheral nervous system made up of cranial and spinal nerves
Prolonged thoracic aortic cross clamp time is most likely to result in a loss of:
A. Movement
B. Proprioception
C. Bowel control
D. Sensation
Movement and bowel control
Cobb’s angle describes the magnitude of spinal curvature
Larger the angle the smaller the thoracic volume
50 degrees- indication for surgery
60 degrees- decreased pulmonary reserve
70 degrees- pulmonary symptoms begin
100 degrees- significant gas exchange impairment
