Neurological Flashcards
Cellular Processes Activated by Ischemia
- Cellular acidosis
- Cellular swelling (cytotoxic edema)
- Neurotoxicity
- Enzymatic activation
- Nitric oxide production
- Inflammation
- Apoptosis
- Necrosis
Monroe Kellie
Cranial vault = fixed space
Blood 80%
Blood 12%
CSF 8%
CPP
MAP - ICP
Normal 80-100mmHg
CBF
CPP/R
Directly proportional to CPP
Average CBF
50mL/100g/min
Brain average size 1500g
= 750mL/min
Receives 15% CO
Middle Cerebral Artery
Carries 80% blood to the brain
Circle of Willis
Provides collateral flow
ICP
Normally <10mmHg
Cerebral Autoregulation
Myogenic - intrinsic VSMC response in arterioles to MAP changes
Metabolic - CO2 and metabolites vasodilate and directly relax VSMC
CSF Production
Adult 21mL/hr or 500mL/day
CSF Flow
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)
CSF Function
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
DCML
Dorsal column
Touch
Decussates high
Spinothalamic
Anterolateral Originates in the spine & transmits to thalamus Pain & temperature Decussates low Signal diffuse - difficult to locate
Cerebral Edema Types
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
Cerebrovascular Accident (CVA)
Ischemic - thrombotic or embolic
Global hypoperfusion - shock or ↑ICP
Hemorrhagic - intracerebral hemorrhage
Intracerebral Bleed Associated w/
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
Aneurysm Rupture Etiologies
Trauma
Inflammation
Atherosclerosis
Congenital
Aneurysm Associated w/
Structural abnormalities Genetics Atherosclerosis HTN Coarctation Connective tissue disorders
Aneurysm Rupture Characteristic Presentation
Sudden onset severe headache
N/V, neck stiffness, photophobia
LOC sometimes
Hypertensive, dysrhythmias, EKG abnormalities
Aneurysm Rupture M&M Associated w/
Neurologic ischemia from vasospasm & elevated ICP
Cardiopulmonary arrhythmias, myocardial injury, pulmonary edema
Electrolyte abnormalities hypomagnesemia, - kalemia, -natremia
Common Aneurysm Locations
Anterior cerebral artery 40%
Posterior communicating artery 25%
Middle cerebral artery 25%
Only 10% aneurysms develop in the vertebrobasilar system
AVM Anesthetic Implications
Intraop bleeding can occur during AVM surgery
Deliberate hypotension to ↓blood loss but consider ischemia and venous thrombosis
Avoid ↑venous pressure
Ischemic Stroke
Interrupted cerebral perfusion
1° thrombotic & embolic
Vicious cycle cell hypoxia, edema, & metabolic derangements
3rd leading cause of US death
Ischemic Stroke Risk Factors
Increasing age
Underlying atherosclerotic disease
Previous transient ischemic attacks
Associated w/ CV disease (Afib, valve prosthesis, carotid disease, bacterial endocarditis)
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
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
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
VAE Detection
Consider when unexplained hypotension or sudden ↓ETCO2
SOB after central venous catheter
C/S sudden hypotension & hypoxia after delivery
VAE Monitoring Devices
Transesophageal echocardiography most sensitive
ETCO2 most common & easily available
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)
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)
SAH Risk Factors
Hypertension
Diabetes
Coronary artery disease
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
Ischemia Brain Anesthetic Considerations
Modest ↑BP = protective
Hypotension = DELETERIOUS
Avoid prophylactic hyperventilation ↓CO2 vasoconstriction
Hypocapnia ↓CBF ↑ischemic tissue
Factors that Affect CBF
Vasodilation:
↓PaO2
↑PaCO2
↑metabolites H+
↑cellular activity
↓temp ↓CMR
Viscosity inversely proportional (optimal Hct 33%)
CVA Autoregulation
Re-established at 4-6wks
Compromised until inflammation gone
Hyperglycemia
Associated w/ ischemic cerebral injury exacerbation
Glucose → lactate via glycolysis (anaerobic) ↓pH further compromises ischemic injury
Implications on diabetes mellitus
Encephalopathy
General term r/t brain pathology
Encephalopathy S/S
Dependent on injury location
Motor cortex → cerebral palsy
Occipital lobe → blindness
Cerebral cortex → cognitive impairment
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
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
TBI S/S
Altered consciousness, coma, seizures, vomiting, irritability, acute temporary cognitive decline
Children especially susceptible
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
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
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)
Hyperthermia
↑ glutamate release (excitatory)
Induces respiratory acidosis ↑pH
Hypoxia & Hypo/Hyperglycemia
Altered brain metabolism
↓GABA transmission (inhibitory)
↑neuronal excitability (glutamate)
Hyponatremia
Neuron swelling d/t extracellular hypo-osmolarity → cerebral edema
Sleep Disorders
↓seizure threshold
Insomnia, restless leg syndrome, OSA
Seizure Anesthetic Implications
Status epilepticus = medical emergency ↑ CMR ↑O2 ↑glucose ↑ATP Maintain airway & admin O2 Measure electrolytes, glucose, CBC, toxic drugs Antiepileptic drugs
Intracranial Hypertension
Elevated ICP
>20mmHg
Directly associated w/ poor outcomes
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
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
Cushing’s Triad
Severe ↑ICP Hypertension - CNS ischemic response Bradycardia - baroreflex PSNS in response to ↑BP Irregular respiration (Cheyne-Stokes) *Occurs prior to herniation
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
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
Communicating Hydrocephalus
Extraventricular
CSF flow obstruction from subarachnoid space to saggital sinus (veins) caused by neoplasm, traumatic/spontaneous hemorrhage, infection)
Non-Communicating Hydrocephalus
Intraventricular
CSF flow obstruction from ventricles through aqueducts to subarachnoid space
Cause usually congenital deformity of aqueducts or ventricles
Parkinson’s Disease S/S
Tremor at rest Rigidity Bradykinesia Postural instability Dementia & depression ANS dysfunction - gastric retention, inappropriate diaphoresis, orthostatic hypotention
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
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)
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
Parkinson’s Tx
Levodopa ↑dopamine D1R or D2R agonists Muscarinic receptor antagonists ↓ACh NMDA receptor antagonists Nicotine ↑DA release DA antagonists exacerbate S/S
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
Alzheimer’s Disease
Emergence delirium risk ↑patient mortality
Brain neurons ↓ACh
Do NOT admin anticholinergic that crosses BBB (exacerbates disease process)
Alzheimer’s S/S
Memory loss Impaired learning Spatial disorganization Anomia (unable to name) Apraxia (unable to execute normal movements) Paranoia, delusions, hallucinations
Alzheimer’s Risk Factors
Genetic 70% non-heredity 30% familial Functional deficit in apolipoprotein E Chronic HTN Head injury Female? Chronic TIA
Alzheimer’s Clinical Manifestations
Variable onset age, intensity, & symptoms sequence
Typically develops slowly over 5yrs
Disturbances increasingly involve memory, language, personality, motor system, & intellect
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
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
Cerebral Palsy Anesthetic Implications
Assess baseline neurological function & patient comprehension (developmental delays)
↑seizure risk
GERD → aspiration risk
Motor issues - prolonged response to muscle relaxants
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
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
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
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
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
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
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
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
Carotid Artery Disease Management
Control HTN, hypercholesterolemia, & diabetes
Smoking cessation
Physical activity
Anti-platelet therapy
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
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
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
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)
Demyelinating Disorders
Multiple sclerosis
Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s)
Guillian Barre syndome
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
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
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
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
ALS Causes
Environmental - heavy metal exposure
Glutamate excitotoxicity
Oxidant stress
Hereditary component - mutation in SOD1 (powerful antioxidant)
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
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
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
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
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
Guillain Barre Anesthetic Implications
Succinylcholine contraindicated d/t hyperkalemia
Non-depolarizing neuromuscular blockers used sparingly d/t prolonged response
Neuromuscular Junction Disorders
Myasthenia gravis
Lambert-Eaton myasthenic syndrome (LEMS)
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
Myasthenia Gravis S/S
Muscle weakness (increases w/ exercise - fatigability)
Eye, facial, bulbar, & limb muscle weakness
Respiratory muscle weakness rare but possible postop complication
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
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
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
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
Dystrophin
Absence → dysfunction
Progressive skeletal muscle weakness
Damage to plasma membrane (sarcolemma) resulting in muscle degeneration & necrosis
Cardiac muscle weakness → dilated cardiomyopathy → arrhythmias
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
Spinal Cord Anatomy
Extends from skull base to L1
Spinal cord tapers at L1-2 (conus medullaris)
Vertebral column & CSF protect nerves
Grey Matter
Nerve cell bodies
White Matter
Schwann cells (myelin sheath)
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
Primary Spinal Cord Injury
Stretching Tearing Compression Penetrating Vertebral stenosis Tumor Ischemia
Secondary Spinal Cord Injury
Cytokine & amino acid release from injured cells leads to inflammation, free radical formation, cellular edema, cellular apoptosis
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
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)
C5-T1
Brachial plexus
C3-C5
Phrenic nerve
C5
External intercostals
T1-T5
Cardio-accelerator fibers (nerve axons) exit spinal cord
C7-L1
SNS fibers to VSMC
T5/6 SNS innervation to splanchnic vasculature
S2-S4
PNS fibers
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
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
Chronic Spinal Cord Injury
Anesthetic Implications
Impaired musculature → impaired mobility & ventilation
Impaired mobility → osteoporosis & ↑thrombus formation
Injury above T6 susceptible to autonomic hyperreflexia
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
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
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
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
Kyphoscoliosis
Posterior & lateral spine curvature
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
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
Ankylosing Spondylitis Anesthetic Implications
Consider positioning & ability to ventilate independently postop
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
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)
Spina Bifida Anesthetic Implications
Prone position - prevent injury to eyes, brachial plexus, & abdomen
Impaired ventilation
Positioning considerations - more difficult to intubate
Cauda Equina
Spinal nerves bundle that resemble a horse’s tail
Nerves originate in the spinal cord conus medullaris
Cauda Equina Syndrome
Compression of nerve roots below L1 caused by spine fracture or disk herniation
Cauda Equina Syndrome S/S
Prolonged LE weakness (motor deficits)
Variable sensorimotor & reflex dysfunction
Sexual dysfunction
Bladder & bowel dysfunction
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
