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AS - N932 Advanced Pathology > Neurological > Flashcards

Neurological Flashcards

1
Q

Cellular Processes Activated by Ischemia

A
  1. Cellular acidosis
  2. Cellular swelling (cytotoxic edema)
  3. Neurotoxicity
  4. Enzymatic activation
  5. Nitric oxide production
  6. Inflammation
  7. Apoptosis
  8. Necrosis
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2
Q

Monroe Kellie

A

Cranial vault = fixed space
Blood 80%
Blood 12%
CSF 8%

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3
Q

CPP

A

MAP - ICP

Normal 80-100mmHg

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4
Q

CBF

A

CPP/R

Directly proportional to CPP

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5
Q

Average CBF

A

50mL/100g/min
Brain average size 1500g
= 750mL/min
Receives 15% CO

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6
Q

Middle Cerebral Artery

A

Carries 80% blood to the brain

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7
Q

Circle of Willis

A

Provides collateral flow

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8
Q

ICP

A

Normally <10mmHg

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9
Q

Cerebral Autoregulation

A

Myogenic - intrinsic VSMC response in arterioles to MAP changes
Metabolic - CO2 and metabolites vasodilate and directly relax VSMC

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10
Q

CSF Production

A

Adult 21mL/hr or 500mL/day

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11
Q

CSF Flow

A

Produced by choroid plexuses of the lateral ventricles & secreted by the ependymal cells of the choroid plexus
Lateral ventricles via Foramen of Monro → 3rd ventricle via Aqueduct of Sylvius → 4th ventricle → subarachnoid space via Foramen of Magendie → circulates around brain & spinal cord → empty via arachnoid villi (valves)

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12
Q

CSF Function

A 
Removes catabolites or toxins
Distributes neurotransmitters to neurons
Brain ISF homeostasis
Development
Nutritive effects
Pressure equilibrium - responds to fluctuations caused by volume changes in 3 compartments w/in rigid skull
Protect CNS from trauma
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13
Q

DCML

A

Dorsal column
Touch
Decussates high

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14
Q

Spinothalamic

A 
Anterolateral
Originates in the spine & transmits to thalamus
Pain & temperature
Decussates low
Signal diffuse - difficult to locate
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15
Q

Cerebral Edema Types

A

Increased fluid content = life-threatening condition that develops in response to inflammation reaction
Causes: cerebral trauma, cerebral infarction, hemorrhage, abscess, tumor, allergy, sepsis, hypoxia, & other toxic or metabolic factors
-Cytotoxic
-Vasogenic (damage to endothelial cells impairs BBB)
-Hydrostatic
-Osmotic
-Interstitial

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16
Q

Cerebrovascular Accident (CVA)

A

Ischemic - thrombotic or embolic
Global hypoperfusion - shock or ↑ICP
Hemorrhagic - intracerebral hemorrhage

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17
Q

Intracerebral Bleed Associated w/

A

Hypertension
Anticoagulation therapy or other coagulopathy
Drug & alcohol abuse
Neoplasia (tumors)
Amyloid angiopathy - amyloid (insoluble fibrous protein aggregate) deposits in cerebral vessel walls predisposes to leak (microvascular) bleeding
Infection

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18
Q

Aneurysm Rupture Etiologies

A

Trauma
Inflammation
Atherosclerosis
Congenital

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19
Q

Aneurysm Associated w/

A 
Structural abnormalities
Genetics
Atherosclerosis
HTN
Coarctation 
Connective tissue disorders
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20
Q

Aneurysm Rupture Characteristic Presentation

A

Sudden onset severe headache
N/V, neck stiffness, photophobia
LOC sometimes
Hypertensive, dysrhythmias, EKG abnormalities

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21
Q

Aneurysm Rupture M&M Associated w/

A

Neurologic ischemia from vasospasm & elevated ICP
Cardiopulmonary arrhythmias, myocardial injury, pulmonary edema
Electrolyte abnormalities hypomagnesemia, - kalemia, -natremia

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22
Q

Common Aneurysm Locations

A

Anterior cerebral artery 40%
Posterior communicating artery 25%
Middle cerebral artery 25%
Only 10% aneurysms develop in the vertebrobasilar system

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23
Q

AVM Anesthetic Implications

A

Intraop bleeding can occur during AVM surgery
Deliberate hypotension to ↓blood loss but consider ischemia and venous thrombosis
Avoid ↑venous pressure

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24
Q

Ischemic Stroke

A

Interrupted cerebral perfusion
1° thrombotic & embolic
Vicious cycle cell hypoxia, edema, & metabolic derangements
3rd leading cause of US death

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25
Q

Ischemic Stroke Risk Factors

A

Increasing age
Underlying atherosclerotic disease
Previous transient ischemic attacks
Associated w/ CV disease (Afib, valve prosthesis, carotid disease, bacterial endocarditis)

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26
Q

Ischemic Stroke Anesthetic Implications

A

Surgery especially CV potential stroke trigger
Patients at risk for stroke - diabetes, HTN, & coagulation therapy
Previous stroke patients - impaired cerebral autoregulation (monitor BP)
Monitor neural function during surgery

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27
Q

Venous (Vascular) Air Embolus Risk Factors

A

Operative site >5cm above R atrium
Numerous large, non-compressed venous channels in the surgical field
Pressure gradient >5cmH2O
Barotrauma to chest causes alveolar rupture into small vein & capillaries
During insertion & removal central venous catheter

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28
Q

VAE Clinical Manifestations

A

Varies according to air nature, volume, & speed entrainment into circulation
Affects CV, respiratory, & CNS
Chest pain, brady or tachy arrythmias, ↑filling pressure, ST segment changes
Dyspnea, tachypnea, “gasp” reflex, hypoxemia, hypercarbia
↓CO → cerebral hypoperfusion; direct paradoxical cerebral embolism via PFO

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29
Q

VAE Detection

A

Consider when unexplained hypotension or sudden ↓ETCO2
SOB after central venous catheter
C/S sudden hypotension & hypoxia after delivery

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30
Q

VAE Monitoring Devices

A

Transesophageal echocardiography most sensitive

ETCO2 most common & easily available

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31
Q

VAE Anesthetic Implications

A

Neurosurgery that requires sitting position = HIGH risk
S/S periop VAE directly proportional to rate and volume air entry
↑pulmonary artery pressure evident before arterial blood gas changes occur
PFO contraindicated w/ sitting surgical position
Elevate venous pressure to prevent VAE
Do NOT admin N2O (venodilator)

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32
Q

Hemorrhage CVA Common Causes

A

Intracranial aneurysm rupture
Intracranial bleed d/t TBI, tumors, coagulation defects, infection, HTN
Arteriovenous malformation
Subarachnoid hemorrhage (originates intra or extra-axial)

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33
Q

SAH Risk Factors

A

Hypertension
Diabetes
Coronary artery disease

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34
Q

Anesthetic Effects on Ischemic Brain

A

Anesthesia ↑CBF ↓CMR neuroprotective effect
Barbiturates - reverse steal effect treat focal ischemia & EEG burst suppression
Volatile anesthetics - vasodilation delays but does not prevent neuronal cell death; steal effect
Propofol - only protective for mild ischemia
Ketamine - neuroprotective effect limited use d/t neuropsychiatric side effects → emergence delirium
Etomidate - ↑incidence brain injury after admin

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35
Q

Ischemia Brain Anesthetic Considerations

A

Modest ↑BP = protective
Hypotension = DELETERIOUS
Avoid prophylactic hyperventilation ↓CO2 vasoconstriction
Hypocapnia ↓CBF ↑ischemic tissue

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36
Q

Factors that Affect CBF

A 
Vasodilation:
     ↓PaO2 
     ↑PaCO2
     ↑metabolites H+
     ↑cellular activity

↓temp ↓CMR
Viscosity inversely proportional (optimal Hct 33%)

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37
Q

CVA Autoregulation

A

Re-established at 4-6wks

Compromised until inflammation gone

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38
Q

Hyperglycemia

A

Associated w/ ischemic cerebral injury exacerbation
Glucose → lactate via glycolysis (anaerobic) ↓pH further compromises ischemic injury
Implications on diabetes mellitus

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39
Q

Encephalopathy

A

General term r/t brain pathology

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40
Q

Encephalopathy S/S

A

Dependent on injury location
Motor cortex → cerebral palsy
Occipital lobe → blindness
Cerebral cortex → cognitive impairment

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41
Q

TBI Causes

A

Contusion or deceleration
Trauma causes neural, glial, and/or vascular injury
Cell injury - release inflammatory factors
Vascular injury - capillary leak & edema → extradural or subdural hematoma or intracerebral hemorrhage

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42
Q

TBI Types

A

Extradural hematoma - usually arterial bleeding source & potentially lead to herniation d/t compression
Subdural hematoma - torn bridging vein or venous sinus ↑ICP potentially lead to herniation
Intracerebral bleed - small blood vessel trauma (shearing or penetration), ↑ICP & brain compression, cerebral edema

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43
Q

TBI S/S

A

Altered consciousness, coma, seizures, vomiting, irritability, acute temporary cognitive decline
Children especially susceptible

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44
Q

Pediatric Differences

A 
Larger head & thinner cranial bone
Less reserve d/t ↓myelinated neurons more vulnerable to cerebral edema & damage
↑CMR for oxygen & glucose
↓BP less reserve capacity
↑intracranial compliance
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45
Q

TBI Anesthetic Implications

A 
Treatment directed at preventing secondary brain injury d/t systemic hypotension
Hyperthermia exacerbated brain injury
GCS best outcome indicator
Monitor fluids glucose concentration
Goal optimize CPP w/o ↑ICP
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46
Q

Seizure Risk Factors

A

Genetic idiopathic
Predisposition associated w/ DiGeorge Syndrome, hypoparathyroid, hypocalcemia
Tumor, trauma, infection, or fever
Subarachnoid hemorrhage or stroke damage
Metabolic origin - fever, uremia, hypoxemia, hyperglycemia, hyponatremia
Hypoxia or hyperventilation (respiratory alkalosis)
Drugs or alcohol overdose/withdrawal
Fatigue or stress
Extensive sensory stimuli
HYPOCALCEMIA (Ca2+ stabilizes VGNa+ channels)

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47
Q

Hyperthermia

A

↑ glutamate release (excitatory)

Induces respiratory acidosis ↑pH

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48
Q

Hypoxia & Hypo/Hyperglycemia

A

Altered brain metabolism
↓GABA transmission (inhibitory)
↑neuronal excitability (glutamate)

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49
Q

Hyponatremia

A

Neuron swelling d/t extracellular hypo-osmolarity → cerebral edema

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50
Q

Sleep Disorders

A

↓seizure threshold

Insomnia, restless leg syndrome, OSA

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51
Q

Seizure Anesthetic Implications

A 
Status epilepticus = medical emergency
↑ CMR ↑O2 ↑glucose ↑ATP
Maintain airway & admin O2
Measure electrolytes, glucose, CBC, toxic drugs
Antiepileptic drugs
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52
Q

Intracranial Hypertension

A

Elevated ICP
>20mmHg
Directly associated w/ poor outcomes

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53
Q

Elevated ICP Anesthetic Implications

A

Monitor cerebral edema & prevent blockade CSF outflow
Assess baseline neurologic function prior to surgery
Hemorrhagic events do NOT admin Mannitol prior to craniotomy (compression applies pressure to prevent continued bleeding)
Loop diuretics & corticosteroids are considered safe

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54
Q

Elevated ICP S/S

A

Headache, N/V, paresthesias, somnolence, visual/auditory disturbances, mental changes, HTN, bradycardia, periodic breathing, seizures, midline shift >0.5cm
Cranial nerve impairment indicates pressure on the brain stem - pupillary dilation, blurred vision, inability to adduct & abduct eye
Escalating S/S focal neurological deficits, apathy, ↓LOC, seizures, coma, Cushing’s triad

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55
Q

Cushing’s Triad

A 
Severe ↑ICP
Hypertension - CNS ischemic response
Bradycardia - baroreflex PSNS in response to ↑BP
Irregular respiration (Cheyne-Stokes)
*Occurs prior to herniation
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56
Q

Elevated ICP Periop Tx

A

Diuretics - loop & osmotic
Hyperventilate to vasoconstrict (potentially exacerbates ischemia)
Hypothermia ↓demand ↓CMRO2
Normotensive
Fluid restriction
Goal ↓ICP w/o exacerbating ischemia & neuronal injury

57
Q

Elevated ICP Anesthetic Implications

A

Subarachnoid screw to measure ICP
Head tilt 15-30° to help venous drainage
Propofol & mild hyperventilation during induction (PaCO2 30-35mmHg)
Prevent coughing ↑Ppl during intubation & w/ neuromuscular agents
PEEP ↑Ppl

58
Q

Communicating Hydrocephalus

A

Extraventricular
CSF flow obstruction from subarachnoid space to saggital sinus (veins) caused by neoplasm, traumatic/spontaneous hemorrhage, infection)

59
Q

Non-Communicating Hydrocephalus

A

Intraventricular
CSF flow obstruction from ventricles through aqueducts to subarachnoid space
Cause usually congenital deformity of aqueducts or ventricles

60
Q

Parkinson’s Disease S/S

A 
Tremor at rest
Rigidity
Bradykinesia
Postural instability
Dementia & depression
ANS dysfunction - gastric retention, inappropriate diaphoresis, orthostatic hypotention
61
Q

Bradykinesia

A

Slow skeletal muscle movement including mastication & deglutition (aspiration risk)
Involves loss substantia nigra dopamine neurons
Tonic inhibitory impulses are sent to motor relay station present in thalamus thereby ↓movement
Balanced by DA neurons in sustantia nigra to ↓inhibition ↑ movement
Dopamine neurons destroyed in Parkinson’s therefore patient’s movements remain inhibited
Impaired initiation of movement = cardinal PD feature

62
Q

Rigidity

A

Involuntary skeletal muscle contraction resulting in ↑resting muscle tone
Involve nigrostriatal pathways
Normally substantia nigra limits skeletal muscle tone (not flaccid) ↓DA neurons allows ↑skeletal muscle tone unchecked or not tempered → rigidity & impedes active & passive limb movements
PD patients ↑risk opioid-induced rigidity (opioid agonists inhibit DA)

63
Q

Tremor

A

Impaired or unstable sensory-motor feedback loop exaggerates natural limb oscillation
Tremor at rest, goes away during active movements
Pathology distinct from bradykinesia & rigidity does NOT involved nigrostriatal pathway or dopamine
Basal ganglia initiate removes via cortico-cerebellar circuit

64
Q

Parkinson’s Tx

A 
Levodopa
↑dopamine D1R or D2R agonists
Muscarinic receptor antagonists ↓ACh
NMDA receptor antagonists
Nicotine ↑DA release
DA antagonists exacerbate S/S
65
Q

Parkinson’s Anesthetic Implications

A

Dopamine antagonists exacerbate symptoms (Reglan, Phenergan, Droperidol)
Respiratory - abnormal upper airway control & function, aspiration pneumonia risk, risk post-extubation laryngospasm and/or postop respiratory failure
CV - prone to hypotension (DA acts centrally & peripherally to cause vasodilation); avoid Halothane (sensitizes heart to catecholamines)
Other considerations
-Regional anesthesia preferred
-Continue L-dopa
-NMBD response
-Rigidity w/ opioids

66
Q

Alzheimer’s Disease

A

Emergence delirium risk ↑patient mortality
Brain neurons ↓ACh
Do NOT admin anticholinergic that crosses BBB (exacerbates disease process)

67
Q

Alzheimer’s S/S

A 
Memory loss
Impaired learning
Spatial disorganization
Anomia (unable to name)
Apraxia (unable to execute normal movements)
Paranoia, delusions, hallucinations
68
Q

Alzheimer’s Risk Factors

A 
Genetic 70% non-heredity 30% familial 
Functional deficit in apolipoprotein E
Chronic HTN
Head injury
Female?
Chronic TIA
69
Q

Alzheimer’s Clinical Manifestations

A

Variable onset age, intensity, & symptoms sequence
Typically develops slowly over 5yrs
Disturbances increasingly involve memory, language, personality, motor system, & intellect

70
Q

Alzheimer’s Anesthetic Implications

A

Consent potentially an issue; legal surrogate
Patience required while educating & calming patient
General anesthesia worsen cognitive impairment → emergence delirium (usually subsides w/in 45min after awakening) associated w/ Ketamine, Sevo, & Des
Avoid sedation → postop delirium & confusion
Delirium - mental state alternation characterized by changes to arousal, attention, orientation, & intellectual function
Uncooperative patients - regional anesthesia complicated
↓reserves in pulmonary, cardiac, & neurological function
AChEi ↑ACh
Glycopyrrolate anticholinergic does NOT cross BBB

71
Q

Cerebral Palsy Clinical Manifestations

A

Impaired gestational neural development
Basal ganglia & extrapyramidal tract damage → dyskinetic cerebral palsy
Poor fine motor coordination; jerky movements
Cerebral cortical damage → spastic cerebral palsy
↑muscle tone, exaggerated deep tendon reflexes, contractures, & scoliosis
Developmental delay, sensory abnormality, seizure risk

72
Q

Cerebral Palsy Anesthetic Implications

A

Assess baseline neurological function & patient comprehension (developmental delays)
↑seizure risk
GERD → aspiration risk
Motor issues - prolonged response to muscle relaxants

73
Q

Spinal Cord Blood Supply

A

Two blood supplies - vertical & segmental (both stem from the aorta)

Vertical

  • Anterior & posterior spinal arteries
  • R/L anterior arteries branch from R/L vertebral arteries & fuse to form 1 anterior spinal artery (x1)
  • R/L posterior vertebral arteries branch to form R & L posterior spinal artery (x2)

Segmental

  • Horizontal spinal blood supply
  • Provide additional blood supply to some, but not all spinal cord levels
  • Spinal cord susceptible to ischemia w/o segmental artery supply
74
Q

Artery of Adamkiewicz

A

Largest & most important segmental (or radicular) medullary artery
Major blood supply to lumbar & sacral cord
Arises from L posterior intercostal artery at 9th to 12th intercostal artery
Ischemia → urinary/fecal incontinence and/or impaired LE motor function
Cross clamp near artery of Adamkiewicz then SC blood flow significantly impaired & dependent on anterior/posterior spinal arteries alone

75
Q

Aortic Cross Clamp

Hemodynamic Changes

A

Veins distal to clamp empty → myogenic constriction → blood shifts to heart ↑BP (preload)
↓renal blood flow ↑catecholamines → ANGII release ↑SVR
Impairs spinal cord blood flow

76
Q

Aortic Cross Clamp Risks

A

Myocardial ischemia/infarct
↑afterload d/t ↑preload ↑SVR → ↑MVO2
When clamp placed initially transient ↑LVEDP ↓coronary blood flow
CAD patients at higher risk d/t ↓autoregulation response → coronary ischemia risk

77
Q

Aortic Cross Clamp

Anesthetic Implications

A

Distal tissue perfusion depends on aortic pressure proximal to clamp & collateral circulation
Maintain proximal aortic pressure as heart tolerates to minimize ischemic injury
↑duration aortic occlusion associated w/ worse morbidity & mortality

78
Q

Aortic Cross Clamp

UNCLAMPING

A

↓BP (preload) ↓SVR metabolic response distal to clamp causes vasodilation
Gradually release clamp to prevent mass vasodilation
↓LVEDP ↓MVO2 ↑coronary perfusion

79
Q

Carotid Artery Disease Causes

A

Atherosclerosis in carotid artery
Narrowing reduces blood flow
Clot forms on cracked or ruptured plaque further narrows artery lumen
Plaque fragment breaks from carotid & travels to smaller vessel → occlusion ↓CBF
RISK FOR ISCHEMIC STROKE

80
Q

Carotid Artery Disease Treatment

A

Carotid Endarterectomy
Incision along neck accessing carotid artery & plaques are removed
Artery patched using vein & stitched
OR eversion carotid endarterectomy → cut carotid artery, turn inside out, remove plaque, reattach artery
Regional or general anesthesia
Carotid artery cross-clamping occurs

81
Q

Carotid Artery Disease Management

A

Control HTN, hypercholesterolemia, & diabetes
Smoking cessation
Physical activity
Anti-platelet therapy

82
Q

Endarterectomy Surgery

A

Reduces stroke risk as compared to medical management
Significantly ↑risk periop MI
-Venous stasis on same side as clamp
-Additional stress on heart to provide enough collateral blood flow
-Pro-inflammatory surgery

83
Q

Carotid Artery Disease PREOP

A

Evaluate CV disease history
Atherosclerotic plaque present in carotid commonly have atherosclerosis in coronary vessels as well
Hypertensive patients adjust MAP goals accordingly to ensure adequate CBF
CBF dependent on collateral circulation

84
Q

Carotid Artery Disease INTRAOP

A

Extreme head rotation → compresses artery ↓CBF
Risk cerebral & coronary ischemia intraop
Balance hemodynamics to maintain CBF but prevent additional MVO2
Stroke history → impaired cerebral autoregulation
Monitor neurological function
EEG to assess cerebral ischemia
Carotid plaque typically at carotid bifurcation (baroreceptors - impact on hemodynamics)
Vasopressors & vasodilators readily available

85
Q

Carotid Artery Disease POSTOP

A

Monitor cardiac, neurologic, & ventilatory complications
Cardiac - HTN, hypotension, MI
Neurologic - assess stroke-like symptoms
Ventilatory - carotid body denervation reduces response to hypoxemia (paired w/ narcotic CNS depression)

86
Q

Demyelinating Disorders

A

Multiple sclerosis
Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s)
Guillian Barre syndome

87
Q

Multiple Sclerosis

A

Chronic degenerative disease
Affects all CNS neuron types (somatic motor & sensory, autonomic, cognition)
Autoimmune - T cells attack CNS myelin protein
Predominantly occurs in females
↓CNS dendrites & axons
Permanent dysfunction occurs when axon destroyed

88
Q

Multiple Sclerosis S/S

A

Fatigue, parasthesias, unsteady gait, muscle weakness & atrophy, respiratory insufficiency, ANS dysfunction

Brain demyelination - seizures, spasticity, emotional lability, visual loss, dysarthria, dysphagia, cognitive dysfunction
Spinal cord lesions - parasthesias, limb weakness, bladder & bowel symptoms
Brain stem lesions - autonomic dysfunction & abnormal ventilatory drive

89
Q

Multiple Sclerosis Anesthetic Implications

A

Stress associated w/ anesthesia potentially worsens symptoms
Avoid spinal cord anesthesia
Minimal adverse effects w/ epidural & other regional effects (neuraxial anesthesia safe unless active flare up present)
Possible altered CV responses
Avoid Succinylcholine d/t hyperkalemia (nAChR upregulation)
Prevent hyperthermia - slows conduction (↑temp blocks nerve conduction in demyelinated fibers)
Cardiac arrhythmia & neurogenic bladder/bowel when ANS involved

90
Q

Amyotrophic Lateral Sclerosis (ALS)

A

Lou Gehrig’s
Amyotrophic - lower motor neuron symptoms d/t ventral (anterior) horn neuron destruction
Lateral sclerosis - scars lateral cortic-spinal tracts w/ upper motor neuron S/S
Progressive, degenerative motor disease involving upper & lower motor neurons
ONLY somatic motor neurons involved (not sensory or ANS)
Cognition & sensation intact
Cranial nerve III, IV, & VI nuclei spared (motor & eye movement)
Usually begins after 4th decade w/ peak occurrence age 50
Affects male > female

91
Q

ALS Causes

A

Environmental - heavy metal exposure
Glutamate excitotoxicity
Oxidant stress
Hereditary component - mutation in SOD1 (powerful antioxidant)

92
Q

ALS S/S

A

Lower motor neuron:

  • Flaccid paresis → muscle weakness, atrophy, hypotonia → paralysis (plegia)
  • More likely to result in permanent paralysis

Upper motor neuron:

  • Spastic paresis → stiff & tight muscles causing movement weakness patterns
  • More likely to be repaired

Muscle atrophy, fasciculations, difficulty swallowing, dysarthria, & dysphonia
Sensory, autonomic, & cognitive functions preserved

93
Q

ALS Anesthetic Implications

A

Succinylcholine contraindicated d/t hyperkalemia - lower motor neuron disease ↑nAChR (upregulation)
Non-depolarizing neuromuscular blockers used sparingly d/t prolonged response
Progressive respiratory muscle weakness, aspiration risk, difficult mechanical ventilation weaning

94
Q

Guillain Barre

A

Acute inflammatory demyelinating polyneuropathy
Peripheral nerve immune disorder PNS neurons impaired - all sensory & motor (both somatic & autonomic)
CNS neurons not affected (cognition preserved)
Antibodies attack Schwann cells resulting in myelin sheath destruction
↓neuromuscular impulses
Peak disability 10-14days
Recovery in weeks to months
Most patients recover w/ minimal to no residual effects

95
Q

Guillain Barre S/S

A

Progressive muscle weakness
Areflexia
Cranial nerve & autonomic involvement
Parasthesias “pins & needles”
Elevated CSF protein
Sensory action potentials low-amplitude or absent
Respiratory muscle failure requiring ventilation
Pulmonary aspiration
ANS demyelination - sinus tachycardia, bradyarrhythmia from vagal stimulation, postural hypotension, excessive sweating, ileus

96
Q

Guillain Barre Treatment

A

Anticipate dysrhythmias & autonomic instability
Tachycardia admin β blockers
Severe bradycardia - pacing
Prophylactic anticoagulation to prevent thromboembolic complications
Ileus - prokinetics
Enteral feeding
Ventilatory support

97
Q

Guillain Barre Anesthetic Implications

A

Succinylcholine contraindicated d/t hyperkalemia

Non-depolarizing neuromuscular blockers used sparingly d/t prolonged response

98
Q

Neuromuscular Junction Disorders

A

Myasthenia gravis

Lambert-Eaton myasthenic syndrome (LEMS)

99
Q

Myasthenia Gravis

A

Grave muscle weakness
Chronic autoimmune neuromuscular disease
Skeletal muscle weakness to varying degrees
Antibodies block nAChR at motor endplate (post-synaptic)
↓EPP ↓APs

100
Q

Myasthenia Gravis S/S

A

Muscle weakness (increases w/ exercise - fatigability)
Eye, facial, bulbar, & limb muscle weakness
Respiratory muscle weakness rare but possible postop complication

101
Q

Myasthenia Gravis Anesthetic Implications

A

Depends on disease severity
Avoid sedative premedication → respiratory compromise
Hold AChEi
-Decreased requirement in postop period
-Prolong Succinylcholine action & ↑NMBD requirement
Induction & maintenance
-↑sensitivity to NMB
-Relatively resistant to Succinylcholine
-Extreme sensitivity to non-depolarizing (faster onset & prolonged action)
Postop
-Monitor respiratory function
-Potentially require mechanical ventilation
-Restart AChEi as patient starts to mobilize

102
Q

Lambert-Eaton Myasthenic Syndrome (LEMS)

A

Neuromuscular junction autoimmune disease
Auto-antibodies downregulate pre-synaptic VGCa2+ channels
Disorder at pre-synaptic membrane
↓ACh release → muscle weakness
Mild autonomic dysfunction

103
Q

LEMS Anesthetic Implications

A

Titrate paralytic to minimum dose required
Paralytic reversal often ineffective
Admin 3,4-diaminopyridine (VGK+ channel inhibitor) postop
↑sensitivity to Succinylcholine
↑NDMR effectiveness

104
Q

Muscular Dystrophy

A

Muscle fiber defect (absence dystrophin protein in skeletal & cardiac muscle leads to weakness)
Inherited disease - recessive trait
Males at increased risk
Dystrophin - cytoplasmic protein, sarcolemma structural protein, protein complex that connects cytoskeleton muscle fiber to surrounding extracellular matrix via cell membrane
-Tethering protein that connects skeletal muscle cell to cytoskeleton to extracellular matric to develop tension
-Necessary for nAChR regulation at NMJ

105
Q

Dystrophin

A

Absence → dysfunction
Progressive skeletal muscle weakness
Damage to plasma membrane (sarcolemma) resulting in muscle degeneration & necrosis
Cardiac muscle weakness → dilated cardiomyopathy → arrhythmias

106
Q

MD Anesthesia Implications

A

Risks:

  • Acute respiratory depression
  • Upper airway obstruction, hypoventilation, atelectasis, respiratory failure, & difficulty weaning from mechanical ventilation
  • Heart failure or arrhythmia
  • Rhabdomyolysis
  • Hyperkalemic cardiac arrest w/ Succinylcholine (contraindicated)
  • Short-acting NDMR recommended
  • Chronic cortico therapy slows disease progression
107
Q

Spinal Cord Anatomy

A

Extends from skull base to L1
Spinal cord tapers at L1-2 (conus medullaris)
Vertebral column & CSF protect nerves

108
Q

Grey Matter

A

Nerve cell bodies

109
Q

White Matter

A

Schwann cells (myelin sheath)

110
Q

Spinal Cord Injury Causes

A 
Age 16-30yo
M > F (3:1)
MVA 55%
Sports 18%
Penetrating 15%
Acceleration/deceleration forces
Injuries most commonly at C1-2, C4-7, T1-L2 (most mobile portions of the vertebral column)
Children especially susceptible to trauma
111
Q

Primary Spinal Cord Injury

A 
Stretching
Tearing
Compression
Penetrating
Vertebral stenosis
Tumor 
Ischemia
112
Q

Secondary Spinal Cord Injury

A

Cytokine & amino acid release from injured cells leads to inflammation, free radical formation, cellular edema, cellular apoptosis

113
Q

Spinal Cord Shock

A

“Stunning”
Temporary loss or depression all neurological activity below the spinal cord lesion level
Loss CNS influence on peripheral neurons (decentralization) → PNS dysfunction (flaccid paralysis, no spinal reflexes, & loss SNS tone)
Includes somatic sensory & motor neurons, ANS neurons, & all spinal cord reflex activity
Spinal cord reflex arcs above injury level may also be severely depressed
Onset variable - hours
Resolution - weeks to months (depending on definition)
Over time PNS neurons adapt to lack of CNS input & spinal reflexes return despite spinal cord transection

114
Q

Spinal Cord Shock S/S

A

Absent somatic (flaccid paralysis) & autonomic (hypotension) reflexes
Injury at or above C4/5 requires ventilation support
Hypotension, loss compensatory reflexes (especially tone above T1), profound bradycardia when unopposed PSNS
Bladder & bowel atony, paralytic ileus, gastric distension, & urinary retention
Inability to control temperature (no sweating paired w/ cutaneous vasodilation)

115
Q

C5-T1

A

Brachial plexus

116
Q

C3-C5

A

Phrenic nerve

117
Q

C5

A

External intercostals

118
Q

T1-T5

A

Cardio-accelerator fibers (nerve axons) exit spinal cord

119
Q

C7-L1

A

SNS fibers to VSMC

T5/6 SNS innervation to splanchnic vasculature

120
Q

S2-S4

A

PNS fibers

121
Q

Acute Spinal Cord Injury Management

A

Immobilize the injury
Check for other injuries (TBI or chest trauma)
Support respiration/ventilation
Hypoxia & hypotension exacerbate spinal cord injury & TBI d/t ischemia
Treat hypoxia & hypotension

122
Q

Acute (Emergent) Spinal Cord Injury

Anesthetic Implications

A

Spinal shock or stunning may occur → loss SNS tone to vessels & heart
Injury at or above C3-5 → mechanical ventilation
Injury at or above T1-4 → cardiac innervation compromised
Choose NDMR w/ sympathomimetic properties
Stabilize the neck especially during intubation
Add crystalloid to promote spinal cord perfusion

123
Q

Chronic Spinal Cord Injury

Anesthetic Implications

A

Impaired musculature → impaired mobility & ventilation
Impaired mobility → osteoporosis & ↑thrombus formation
Injury above T6 susceptible to autonomic hyperreflexia

124
Q

Spinal Cord vs. Neurogenic Shock

A

Spinal cord injury may lead to spinal cord shock “stunning”
-Flaccid paralysis
-Absent spinal reflexes
Spinal cord shock does NOT always lead to systemic shock
Lesion/injury above T6 the susceptible to autonomic hyperreflexia
Neurogenic shock - profound hypotension & bradycardia
Both shock types present w/ ↓SNS activity

125
Q

Neurogenic Shock

A

Profound hypotension & bradycardia d/t lack SNS tone
SNS lacking bc spinal SNS neurons loss excitation from VMC & other higher brain centers
SNS “decentralized” → dysfunctional
Decentralization may also occur d/t VMC inhibition (i.e. opioid overdose)
Spinal cord lesion at T6 then neurogenic SYSTEMIC shock will likely result

126
Q

Scoliosis

A

Lateral rotational spine curvature
Structural d/t spine itself
-Compromises alveolar ventilation ↓lung volume
Non-structural - rotation d/t other reasons (i.e. pain, posture, leg discrepancy)
Muscles, ligaments, & soft tissues become shortened on concave side
Overtime causes vertebral column & rib deformities
Higher the compressive forces ↑deformity as result

127
Q

Scoliosis Anesthetic Implications

A

Not associated w/ sensory or motor deficit
Respiratory dysfunction - reduced alveolar function → impaired mechanical ventilation
Associated w/ ↑risk mitral valve prolapse, ↑pulmonary resistance, & pulmonary hypertension
Spinal curvature impact on spinal anesthesia needle location

128
Q

Kyphoscoliosis

A

Posterior & lateral spine curvature

129
Q

Ankylosing Spondylitis

A

Chronic inflammatory joint disease
Inflammation at various regions w/in joint - primarily vertebral joints → leads to joint remodeling
Stiffening and/or spinal & sacroillac joints fusion
Genetic predisposition
Autoimmune disease attacks antigens on cartilage

130
Q

Ankylosing Spondylitis S/S

A

Low back pain & stiffness (early sign mid 20yrs)
Restricted spinal motion
Reflex muscle spasms may occur
Chest movement can become restricted

131
Q

Ankylosing Spondylitis Anesthetic Implications

A

Consider positioning & ability to ventilate independently postop

132
Q

Spina Bifida

A

Congenital disorder characterized by neural tube closure defect
Neural tube surgically closed in the neonatal period
Vertebral laminae remain unfused, most often at the lumbosacral level
Not serious neurological dysfunction except those associated w/ the lumbosacral region

133
Q

Spina Bifida S/S

A

Associated w/ lumbosacral region nerves
Lower limb weakness leads to gait changes & abnormal feet positioning
Sphincter disturbance at bladder & bowel (lower motor neurons)

134
Q

Spina Bifida Anesthetic Implications

A

Prone position - prevent injury to eyes, brachial plexus, & abdomen
Impaired ventilation
Positioning considerations - more difficult to intubate

135
Q

Cauda Equina

A

Spinal nerves bundle that resemble a horse’s tail

Nerves originate in the spinal cord conus medullaris

136
Q

Cauda Equina Syndrome

A

Compression of nerve roots below L1 caused by spine fracture or disk herniation

137
Q

Cauda Equina Syndrome S/S

A

Prolonged LE weakness (motor deficits)
Variable sensorimotor & reflex dysfunction
Sexual dysfunction
Bladder & bowel dysfunction

138
Q

Cauda Equina Anesthetic Implicatinos

A

Spinal anesthesia caused by pooling of hyperbaric local anesthetic can trigger cauda equina syndrome
Avoid 5% lidocaine to reduce risk of anesthesia-induced cauda equina syndrome

AS - N932 Advanced Pathology (8 decks)

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