Neurological Flashcards
1
Q
Cellular Processes Activated by Ischemia
A
- Cellular acidosis
- Cellular swelling (cytotoxic edema)
- Neurotoxicity
- Enzymatic activation
- Nitric oxide production
- Inflammation
- Apoptosis
- Necrosis
2
Q
Monroe Kellie
A
Cranial vault = fixed space
Blood 80%
Blood 12%
CSF 8%
3
Q
CPP
A
MAP - ICP
Normal 80-100mmHg
4
Q
CBF
A
CPP/R
Directly proportional to CPP
5
Q
Average CBF
A
50mL/100g/min
Brain average size 1500g
= 750mL/min
Receives 15% CO
6
Q
Middle Cerebral Artery
A
Carries 80% blood to the brain
7
Q
Circle of Willis
A
Provides collateral flow
8
Q
ICP
A
Normally <10mmHg
9
Q
Cerebral Autoregulation
A
Myogenic - intrinsic VSMC response in arterioles to MAP changes
Metabolic - CO2 and metabolites vasodilate and directly relax VSMC
10
Q
CSF Production
A
Adult 21mL/hr or 500mL/day
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)
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
13
Q
DCML
A
Dorsal column
Touch
Decussates high
14
Q
Spinothalamic
A
Anterolateral Originates in the spine & transmits to thalamus Pain & temperature Decussates low Signal diffuse - difficult to locate
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
16
Q
Cerebrovascular Accident (CVA)
A
Ischemic - thrombotic or embolic
Global hypoperfusion - shock or ↑ICP
Hemorrhagic - intracerebral hemorrhage
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
18
Q
Aneurysm Rupture Etiologies
A
Trauma
Inflammation
Atherosclerosis
Congenital
19
Q
Aneurysm Associated w/
A
Structural abnormalities Genetics Atherosclerosis HTN Coarctation Connective tissue disorders
20
Q
Aneurysm Rupture Characteristic Presentation
A
Sudden onset severe headache
N/V, neck stiffness, photophobia
LOC sometimes
Hypertensive, dysrhythmias, EKG abnormalities
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
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
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
24
Q
Ischemic Stroke
A
Interrupted cerebral perfusion
1° thrombotic & embolic
Vicious cycle cell hypoxia, edema, & metabolic derangements
3rd leading cause of US death
25
Ischemic Stroke Risk Factors
Increasing age
Underlying atherosclerotic disease
Previous transient ischemic attacks
Associated w/ CV disease (Afib, valve prosthesis, carotid disease, bacterial endocarditis)
26
Ischemic Stroke Anesthetic Implications
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
27
Venous (Vascular) Air Embolus Risk Factors
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
28
VAE Clinical Manifestations
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
29
VAE Detection
Consider when unexplained hypotension or sudden ↓ETCO2
SOB after central venous catheter
C/S sudden hypotension & hypoxia after delivery
30
VAE Monitoring Devices
Transesophageal echocardiography most sensitive
| ETCO2 most common & easily available
31
VAE Anesthetic Implications
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)
32
Hemorrhage CVA Common Causes
Intracranial aneurysm rupture
Intracranial bleed d/t TBI, tumors, coagulation defects, infection, HTN
Arteriovenous malformation
Subarachnoid hemorrhage (originates intra or extra-axial)
33
SAH Risk Factors
Hypertension
Diabetes
Coronary artery disease
34
Anesthetic Effects on Ischemic Brain
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
35
Ischemia Brain Anesthetic Considerations
Modest ↑BP = protective
Hypotension = DELETERIOUS
Avoid prophylactic hyperventilation ↓CO2 vasoconstriction
Hypocapnia ↓CBF ↑ischemic tissue
36
Factors that Affect CBF
```
Vasodilation:
↓PaO2
↑PaCO2
↑metabolites H+
↑cellular activity
```
↓temp ↓CMR
Viscosity inversely proportional (optimal Hct 33%)
37
CVA Autoregulation
Re-established at 4-6wks
| Compromised until inflammation gone
38
Hyperglycemia
Associated w/ ischemic cerebral injury exacerbation
Glucose → lactate via glycolysis (anaerobic) ↓pH further compromises ischemic injury
Implications on diabetes mellitus
39
Encephalopathy
General term r/t brain pathology
40
Encephalopathy S/S
Dependent on injury location
Motor cortex → cerebral palsy
Occipital lobe → blindness
Cerebral cortex → cognitive impairment
41
TBI Causes
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
42
TBI Types
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
43
TBI S/S
Altered consciousness, coma, seizures, vomiting, irritability, acute temporary cognitive decline
Children especially susceptible
44
Pediatric Differences
```
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
```
45
TBI Anesthetic Implications
```
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
```
46
Seizure Risk Factors
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)
47
Hyperthermia
↑ glutamate release (excitatory)
| Induces respiratory acidosis ↑pH
48
Hypoxia & Hypo/Hyperglycemia
Altered brain metabolism
↓GABA transmission (inhibitory)
↑neuronal excitability (glutamate)
49
Hyponatremia
Neuron swelling d/t extracellular hypo-osmolarity → cerebral edema
50
Sleep Disorders
↓seizure threshold
| Insomnia, restless leg syndrome, OSA
51
Seizure Anesthetic Implications
```
Status epilepticus = medical emergency
↑ CMR ↑O2 ↑glucose ↑ATP
Maintain airway & admin O2
Measure electrolytes, glucose, CBC, toxic drugs
Antiepileptic drugs
```
52
Intracranial Hypertension
Elevated ICP
>20mmHg
Directly associated w/ poor outcomes
53
Elevated ICP Anesthetic Implications
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
54
Elevated ICP S/S
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
55
Cushing's Triad
```
Severe ↑ICP
Hypertension - CNS ischemic response
Bradycardia - baroreflex PSNS in response to ↑BP
Irregular respiration (Cheyne-Stokes)
*Occurs prior to herniation
```
56
Elevated ICP Periop Tx
Diuretics - loop & osmotic
Hyperventilate to vasoconstrict (potentially exacerbates ischemia)
Hypothermia ↓demand ↓CMRO2
Normotensive
Fluid restriction
Goal ↓ICP w/o exacerbating ischemia & neuronal injury
57
Elevated ICP Anesthetic Implications
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
Communicating Hydrocephalus
Extraventricular
CSF flow obstruction from subarachnoid space to saggital sinus (veins) caused by neoplasm, traumatic/spontaneous hemorrhage, infection)
59
Non-Communicating Hydrocephalus
Intraventricular
CSF flow obstruction from ventricles through aqueducts to subarachnoid space
Cause usually congenital deformity of aqueducts or ventricles
60
Parkinson's Disease S/S
```
Tremor at rest
Rigidity
Bradykinesia
Postural instability
Dementia & depression
ANS dysfunction - gastric retention, inappropriate diaphoresis, orthostatic hypotention
```
61
Bradykinesia
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
Rigidity
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
Tremor
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
Parkinson's Tx
```
Levodopa
↑dopamine D1R or D2R agonists
Muscarinic receptor antagonists ↓ACh
NMDA receptor antagonists
Nicotine ↑DA release
DA antagonists exacerbate S/S
```
65
Parkinson's Anesthetic Implications
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
Alzheimer's Disease
Emergence delirium risk ↑patient mortality
Brain neurons ↓ACh
Do NOT admin anticholinergic that crosses BBB (exacerbates disease process)
67
Alzheimer's S/S
```
Memory loss
Impaired learning
Spatial disorganization
Anomia (unable to name)
Apraxia (unable to execute normal movements)
Paranoia, delusions, hallucinations
```
68
Alzheimer's Risk Factors
```
Genetic 70% non-heredity 30% familial
Functional deficit in apolipoprotein E
Chronic HTN
Head injury
Female?
Chronic TIA
```
69
Alzheimer's Clinical Manifestations
Variable onset age, intensity, & symptoms sequence
Typically develops slowly over 5yrs
Disturbances increasingly involve memory, language, personality, motor system, & intellect
70
Alzheimer's Anesthetic Implications
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
Cerebral Palsy Clinical Manifestations
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
Cerebral Palsy Anesthetic Implications
Assess baseline neurological function & patient comprehension (developmental delays)
↑seizure risk
GERD → aspiration risk
Motor issues - prolonged response to muscle relaxants
73
Spinal Cord Blood Supply
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
Artery of Adamkiewicz
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
Aortic Cross Clamp
| Hemodynamic Changes
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
Aortic Cross Clamp Risks
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
Aortic Cross Clamp
| Anesthetic Implications
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
Aortic Cross Clamp
| UNCLAMPING
↓BP (preload) ↓SVR metabolic response distal to clamp causes vasodilation
Gradually release clamp to prevent mass vasodilation
↓LVEDP ↓MVO2 ↑coronary perfusion
79
Carotid Artery Disease Causes
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
Carotid Artery Disease Treatment
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
Carotid Artery Disease Management
Control HTN, hypercholesterolemia, & diabetes
Smoking cessation
Physical activity
Anti-platelet therapy
82
Endarterectomy Surgery
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
Carotid Artery Disease PREOP
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
Carotid Artery Disease INTRAOP
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
Carotid Artery Disease POSTOP
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
Demyelinating Disorders
Multiple sclerosis
Amyotrophic lateral sclerosis (ALS or Lou Gehrig's)
Guillian Barre syndome
87
Multiple Sclerosis
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
Multiple Sclerosis S/S
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
Multiple Sclerosis Anesthetic Implications
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
Amyotrophic Lateral Sclerosis (ALS)
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
ALS Causes
Environmental - heavy metal exposure
Glutamate excitotoxicity
Oxidant stress
Hereditary component - mutation in SOD1 (powerful antioxidant)
92
ALS S/S
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
ALS Anesthetic Implications
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
Guillain Barre
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
Guillain Barre S/S
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
Guillain Barre Treatment
Anticipate dysrhythmias & autonomic instability
Tachycardia admin β blockers
Severe bradycardia - pacing
Prophylactic anticoagulation to prevent thromboembolic complications
Ileus - prokinetics
Enteral feeding
Ventilatory support
97
Guillain Barre Anesthetic Implications
Succinylcholine contraindicated d/t hyperkalemia
| Non-depolarizing neuromuscular blockers used sparingly d/t prolonged response
98
Neuromuscular Junction Disorders
Myasthenia gravis
| Lambert-Eaton myasthenic syndrome (LEMS)
99
Myasthenia Gravis
Grave muscle weakness
Chronic autoimmune neuromuscular disease
Skeletal muscle weakness to varying degrees
Antibodies block nAChR at motor endplate (post-synaptic)
↓EPP ↓APs
100
Myasthenia Gravis S/S
Muscle weakness (increases w/ exercise - fatigability)
Eye, facial, bulbar, & limb muscle weakness
Respiratory muscle weakness rare but possible postop complication
101
Myasthenia Gravis Anesthetic Implications
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
Lambert-Eaton Myasthenic Syndrome (LEMS)
Neuromuscular junction autoimmune disease
Auto-antibodies downregulate pre-synaptic VGCa2+ channels
Disorder at pre-synaptic membrane
↓ACh release → muscle weakness
Mild autonomic dysfunction
103
LEMS Anesthetic Implications
Titrate paralytic to minimum dose required
Paralytic reversal often ineffective
Admin 3,4-diaminopyridine (VGK+ channel inhibitor) postop
↑sensitivity to Succinylcholine
↑NDMR effectiveness
104
Muscular Dystrophy
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
Dystrophin
Absence → dysfunction
Progressive skeletal muscle weakness
Damage to plasma membrane (sarcolemma) resulting in muscle degeneration & necrosis
Cardiac muscle weakness → dilated cardiomyopathy → arrhythmias
106
MD Anesthesia Implications
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
Spinal Cord Anatomy
Extends from skull base to L1
Spinal cord tapers at L1-2 (conus medullaris)
Vertebral column & CSF protect nerves
108
Grey Matter
Nerve cell bodies
109
White Matter
Schwann cells (myelin sheath)
110
Spinal Cord Injury Causes
```
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
Primary Spinal Cord Injury
```
Stretching
Tearing
Compression
Penetrating
Vertebral stenosis
Tumor
Ischemia
```
112
Secondary Spinal Cord Injury
Cytokine & amino acid release from injured cells leads to inflammation, free radical formation, cellular edema, cellular apoptosis
113
Spinal Cord Shock
"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
Spinal Cord Shock S/S
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
C5-T1
Brachial plexus
116
C3-C5
Phrenic nerve
117
C5
External intercostals
118
T1-T5
Cardio-accelerator fibers (nerve axons) exit spinal cord
119
C7-L1
SNS fibers to VSMC
| T5/6 SNS innervation to splanchnic vasculature
120
S2-S4
PNS fibers
121
Acute Spinal Cord Injury Management
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
Acute (Emergent) Spinal Cord Injury
| Anesthetic Implications
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
Chronic Spinal Cord Injury
| Anesthetic Implications
Impaired musculature → impaired mobility & ventilation
Impaired mobility → osteoporosis & ↑thrombus formation
Injury above T6 susceptible to autonomic hyperreflexia
124
Spinal Cord vs. Neurogenic Shock
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
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Neurogenic Shock
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
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Scoliosis
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
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Scoliosis Anesthetic Implications
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
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Kyphoscoliosis
Posterior & lateral spine curvature
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Ankylosing Spondylitis
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
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Ankylosing Spondylitis S/S
Low back pain & stiffness (early sign mid 20yrs)
Restricted spinal motion
Reflex muscle spasms may occur
Chest movement can become restricted
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Ankylosing Spondylitis Anesthetic Implications
Consider positioning & ability to ventilate independently postop
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Spina Bifida
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
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Spina Bifida S/S
Associated w/ lumbosacral region nerves
Lower limb weakness leads to gait changes & abnormal feet positioning
Sphincter disturbance at bladder & bowel (lower motor neurons)
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Spina Bifida Anesthetic Implications
Prone position - prevent injury to eyes, brachial plexus, & abdomen
Impaired ventilation
Positioning considerations - more difficult to intubate
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Cauda Equina
Spinal nerves bundle that resemble a horse's tail
| Nerves originate in the spinal cord conus medullaris
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Cauda Equina Syndrome
Compression of nerve roots below L1 caused by spine fracture or disk herniation
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Cauda Equina Syndrome S/S
Prolonged LE weakness (motor deficits)
Variable sensorimotor & reflex dysfunction
Sexual dysfunction
Bladder & bowel dysfunction
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Cauda Equina Anesthetic Implicatinos
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
