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Advanced Principles of Anesthesia > Week 2 - Neuromuscular Disorder Anesthesia > Flashcards

Week 2 - Neuromuscular Disorder Anesthesia Flashcards

1
Q

Describe the steps of neuromuscular junction activity

A
  • Action potential spreads over terminal – voltage gated Ca channels open – allows for large quantities of Ca to diffuse to the inner terminal
  • Synaptic vesicle fusion - Ca causes fusion of synaptic vesicles with membrane of axon terminal
  • Release of ACh – ACh is contained within vesicles is released by exocytosis into synaptic cleft – Ca ions are pumped out of axon terminal
  • ACh binds to specific receptor – ACh gated ion channels, channels closed until ACh binds to 2 alpha sub units – undergo conformational change and channel opens (K+ out, Na+ and Ca+ in) – electrical potential at motor end place initiates AP (propagates along sarcolemma down T tubules and myofibrils) – muscle contraction
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2
Q

How is ACh broken down?

A

Rapidly broken down by acetylcholinesterase into Choline which is recycled to ACh and Acetate

Small amount diffuses out of synaptic space

*causes termination of the action potential

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3
Q

What is multiple sclerosis?

A

Autoimmune disorder that affects brain and spinal cord (CNS)

Damage to myelin sheath – nerve signals are disrupted and slowed or stopped = dysfunction

Caused by inflammation – generally unknown etiology

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4
Q

What does normal nerve conduction along myelinated fibers look like?

A

Nodes of Ranvier occur every 1-3 mm along myelin sheath – action potentials occur here = “Saltation”

Myelin membrane provides insulation for the nerve fiber

  • decreases capacitance which increases electrical resistance (prevents current from leaving the axon)
  • allows repolarization with minimal energy lost
  • allow conduction at high rate of velocity
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5
Q

What are the signs and symptoms of multiple sclerosis?

A
  • Vary based on location
  • Often described as “attacks” (can last for days, weeks, months)
  • Associated with periods of remission (reduced or no symptoms)
  • Overall general deterioration over time – inability of body to re-myelinate

Environmental influence: fever, sun exposure, heat and stress can trigger or even worsen “attacks”

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6
Q

How is multiple sclerosis diagnosed?

A

Thorough neuro exam

MRI and nerve function tests (evoked potentials)

LP also common – looks at immunoglobulins and presences of albumin in CSH

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7
Q

What is the treatment for multiple sclerosis?

A

No Known Cure!

Goal is to control symptoms

  • Steroids
  • Interferons
  • Methotrexate
  • Fingolimod
  • IV Ig
  • Antidepressants
  • Dantrolene
  • Amantadine for fatigue
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8
Q

What are the preop considerations for MS?

A
  • Thorough H&P
  • Detailed neurological exam and discussion of symptoms/attacks
  • Document any preop neurologic deficits
  • Preop Labs - steroids (adrenal insufficiency?), Dantrolene (liver dysfunction)
  • Stress increases MS symptoms –> Diazepam
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9
Q

What are the intraop considerations for a patient with MS?

A

GETA preferred:

  • Propofol is induction agent of choice
  • Volatile agents are safe
  • Neuromuscular agents should be used with caution (variable response to NDMRs, Avoid SUX - hyperkalemia) – increased risk of residual weakness and resp distress
  • Higher increase of invasive monitoring (autonomic dysfunction, monitor temp very carefully)
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10
Q

What are neuraxial anesthesia considerations in a patient with MS?

A
  • Relative contraindication to spinal – exacerbation of symptoms, nerve root exposed to higher concentration of drug causing local neurotoxicity
  • Epidural is ok — combination of local and opioid, reduced doses of meds required (keep infusion duration as short as possible), actually beneficial in MS pts in labor
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11
Q

What are postop considerations for a patient with MS?

A

Monitor closely due to risk of decline

  • more often associated to fever than particular anesthetic
  • respiratory weakness – higher FiO2 need and PPV?
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12
Q

What is Myasthenia Gravis?

A

Autoimmune Disease

  • Weakness of voluntary skeletal muscles – most often muscles innervated by cranial nerves (any muscle can be affected)
  • Caused by antibodies of nicotinic ACh receptors (reduced receptors, increased destruction of receptors)
  • Incidence is 20 per 100,000
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13
Q

What are signs and symptoms of Myasthenia Gravis?

A
  • Weakness with exertion (classic sign)
  • Muscle groups commonly affected = eye, mouth, throat, and limbs
  • often lead to resp muscle weakness and risk of aspiration
  • Hyperplasia of Thymus
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14
Q

What are the Osserman and Genkins Classifications of Myasthenia Gravis?

A

I - Ocular only (Ptosis and diplopia)
IIA - Generalized moderate weakness and/or bulbar dysfunction
III - Acute fulminent presentation and/or resp dysfunction
IV - Late severe generalized

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15
Q

What are the main goals of treatment for Myasthenia Gravis?

A
  • Increase neuromuscular transmission – use cholinesterase inhibitors (Edrophonium)
  • Decreasing circulating antibodies – plasmapheresis, 4-8 plasma exchanges over 1-2 weeks
  • Immunosuppressive therapy (Corticosteroids or Asathioprine)
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16
Q

What are preop considerations for Myasthenia Gravis?

A
  • Respiratory status – low vital capacity, Thymoma?, assess for resp infection
  • Cardiac status – cardiac arrhythmias (A-Fib, Sinus Brady, PVC’s, ST and T wave changes
  • History of Rheumatoid?? – C-spine films within 2 years
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17
Q

What are the GETA intraop considerations for a patient with Myasthenia Gravis?

A
  • Induction with Propofol, Thiopental, Etomidate
  • TIVA vs Inhalational (inhalational agents have neuromuscular blocking effects)
  • NDMR (avoid if possible) – utilize effects of volatiles, reduced number of ACh receptors, sensitive to nondepolarizers
  • SUX (MG pts are more resistant to SUX, use with caution)
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18
Q

What are the regional anesthesia intraop considerations for a patient with Myasthenia Gravis?

A

Regional anesthesia is preferred

  • Ester locals should be reduced or avoided in pts receiving anticholinesterase drugs
  • Regional for labor and delivery – symptom exacerbation common during pregnancy (second term labor increases due to skeletal muscle weakness)
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19
Q

What are postop considerations for a patient with Myasthenia Gravis?

A
  • Post op mechanical ventilation common due to residual weakness
  • Pain is often not adequately controlled – sensitivity to respiratory side effects of opioids
  • use of regional anesthesia for post op pain
20
Q

What is a Cholinergic Crisis?

A

Excessive ACh at neuromuscular junction

-due to inactivity or inhibition of acetylcholinesterase (via nerve gas, overdose on cholinergic agents, surgical pts)

Signs and Symptoms: increased weakness and muscarinic effects (bradycardia, excess salivation, bronchoconstriction)

21
Q

How do you determine if it is a Myasthenic Crisis or Cholinergic Crisis?

A

Give Edrophonium (anticholinesterase) – 1-10mg

If pt improves = Myasthenic Crisis
If pt condition worsens = Cholinergic crisis

22
Q

What is Eaton -Lambert Syndrome?

A

Faulty communication between nerves and muscles

  • Pre junctional alteration (decreased release of ACh)
  • Often associated with malignancy (Oat Cell Lung Cancer)
  • Affects peripheral and pelvic muscles
  • May improve with exercise (unlike MG, ACh can build up for strength to improve somewhat)
  • No improvement with anticholinesterases
  • Sensitive to NMBD - use with caution
23
Q

What is Duchenne disease?

A

Muscular Dystrophy – X linked recessive condition

  • most common severe childhood myopathy
  • occurs 1:3300 male births
  • pelvic weakness between age 2-6 followed by proximal muscle atrophy and delayed motor milestones – Gowers Sign
  • teenage years – immobility –> spinal muscle deformity (Scoliosis) –> respiratory failure due to intercostal muscle involvement –> cardiomyopathy also common
24
Q

What are preop considerations in a patient with Duchenne?

A

Evaluation is critical!

Detailed cardiac and respiratory exam

Obesity – thick hypertrophic tongue very common

Difficulty with intubation/ventilation due to scoliosis?

25
Q

What are intra op considerations for Duchenne?

A
  • Airway management (be prepared) – awake fiberoptic intubation?
  • Potential for aspiration (Na Citrate, Pepcid, Reglan?)
  • ECG changes typical – cardiomyopathy – tall R wave in lead V1, deep Q wave in lateral leads, sinus tachy and shortened PR interval common
  • Positioning problems – kyphoscoliosis/contractures of limbs
26
Q

Malignant Hyperthermia is associated with which neuromuscular disorder?

A

Duchenne

  • avoid MH triggering agents (inhalational agents/SUX)
  • TIVA

**increased risk of MH in ALS as well

27
Q

What is the concern with muscle relaxant usage in Duchenne?

A

Lead to postop respiratory weakness

Many case reports of cardiac arrest
-hyperkalemia from SUX, periop Rhabdo

28
Q

What is Guillan Barre Syndrome?

A

Autoimmune disorder characterized by acute inflammatory demyelinating disorder

  • can occur at any age, but more common between ages 30-50
  • number one cause of acute muscular weakness
  • generally preceded by infection (lung or GI) – usually minor infection
29
Q

What are signs and symptoms of Guillan Barre Syndrome?

A 
– Ascending symmetrical motor weakness (loss of reflexes in arms / legs)
– Numbness/ tingling in legs/ arms
– Tenderness or muscle pain
– Blurred vision / double vision
– Palpitations / difficulty breathing

*symptoms usually plateau within 28 days

30
Q

How do you diagnose Guillan Barre Syndrome?

A

Nerve conduction studies, EMG, PFT’s, ECG, CSF

*diagnosis by exclusion

31
Q

What is the treatment for Guillan Barre Syndrome?

A

Supportive

  • Plasmapheresis effective (takes multiple exchanges)
  • IV IG frequently part of treatment plan (may be more useful than Plasmapheresis, Pain should be treated with NSAIDs)
  • Respiratory failure may occur if intercostal muscles affected (intubation and get them through until symptoms resolve with treatment)

*Complete recovery usually within weeks

32
Q

What are the anesthetic considerations for Guillan Barre Syndrome?

A

Sensitivity to muscle relaxants

Avoid SUX due to risk of hyperkalemia due to extrajunctional receptors

May have hemodynamic variability (low BP) during acute phase

33
Q

What is Amyotrophic Lateral Sclerosis?

A

Progressive loss of upper and lower motor neurons and effects medulla

  • causes severe muscle weakness, disability, and ultimately death
  • starts with twitching of peripheral extremity – difficulty swallowing, slurred speech
  • progresses to affecting autonomic functions – breathing, BP, HR

approx 95% of case etiology is unknown

34
Q

What are the anesthetic considerations for a patient with ALS?

A
  • Spasticity of limbs (positioning problems)
  • Severe muscle weakness/ atrophy/ weight loss (deconditioning, respiratory failure, dysphagia)
  • Increased risk of MH – take precautions
  • No SUX (up regulation of ACh receptors) – causes hyperkalemia, prolonged response to NDMRs
  • Hypothermia – loss of autonomic function
35
Q

What is Parkinson’s Disease?

A

Degenerative disease of CNS
-loss of dopamine producing cells in Substantia Nigra

Symptoms (Extrapyramidal):

  • movement related – shaking, rigidity, slowness of movement, impaired walking/gait
  • later signs include behavioral and cognitive delays (dementia)
36
Q

What are the treatment options for Parkinson’s Disease?

A

Focus on managing symptoms

  • Levodopa and Dopamine agonists
  • COMT inhibitors, MAO B inhibitors, anticholinergics, Amantadine
  • over time drugs become ineffective at treating symptoms and can cause dyskinesias
  • Diet and rehabilitation are effective for some time
37
Q

What is the surgical intervention to treat Parkinson’s?

A

Deep Brain Stimulation

  • reduce motor symptoms in severe cases where drugs are ineffective
  • surgeons implant electrodes into brain – connect to generator in chest that sends electrical impulses to brain
  • not curative
  • can provide significant relief of symptoms
38
Q

What are the anesthetic considerations for a patient with Parkinson’s Disease?

A
  • Be aware of autonomic dysfunction – orthostatic HoTN, constipation, incontinence, excessive sweating
  • Respiratory dysfunction due to uncoordinated voluntary movements (rigidity and muscle weakness may be present)
  • GI stasis and increased risk for aspiration
  • Psych symptoms including delusions and hallucinations
  • Potential for drug interactions (Levodopa causes severe N/V – MAO inhibitors contraindicated in pts taking Levodopa)
  • Avoid Phenothiazine, Butyrophenone, and Reglan
39
Q

What type of anesthetic should you do for a patient with Parkinson’s Disease?

A

Regional and General OK
– Regional allows for communication w/ patient
– Avoid muscle relaxation and potential side effects
– Increased incidence of PONV w/ GA in Parkinson’s patients
– Improved pain relief and potentially decreased stress response w/ regional anesthesia
– Increased risk of pneumonia or URI in PD patients w/ GETA
– Regional and sedation do not eliminate PD symptoms – Tremor or rigidity may compromise surgeons work environment, Delicate surgery (Patient may not be able to be completely still without GETA), Surgical procedure may not be possible under regional

40
Q

What is Malignant Hyperthermia and its triggers?

A

Life threatening disorder of skeletal muscle

Triggers = succinylcholine and inhalational anesthetics

*uncommon and inherited in some families – autosomal dominant pattern

41
Q

What is the pathophysiology of malignant hyperthermia?

A

50-70% - mutation of Ryanodine receptor (type I)

  • defect in Sarcoplasmic reticulum of skeletal muscle
  • affects calcium regulation

Multiple other mutation possibilities – end result is greatly increased Calcium release (causes consumption of large amounts of ATP causing excessive heat and damage to muscle cell)

42
Q

What are the signs and symptoms of malignant hyperthermia?

A
  • Extremely high temp
  • Tachycardia
  • Increased CO2 production and O2 consumption
  • Acidosis
  • Muscle rigidity and rhabdomyolysis

*usually develop about 1 hour after exposure, but can occur later

43
Q

What lab findings will you see with malignant hyperthermia?

A 
PCO2 >60
Base excess more negative than -8
pH <7.25
K+ > 6
CK > 10,000 even without use of SUX
Myoglobin >170mcg
Urine Myoglobin >60mcg
44
Q

What are the preop considerations for malignant hyperthermia?

A
  • Family history of life threatening problem with anesthesia – High fever, unexpected death, etc
  • Family or personal history of cola colored urine after anesthetic
  • Linkage to Duchenne and other dystrophy’s

Absence of positive pt or family history doesn’t preclude the pt from having MH

45
Q

How do you treat malignant hyperthermia?

A
  • Get Help – tell surgeon what is going on – need to end the case NOW
  • Stop volatile agent
  • 100% O2 and hyperventilate
  • Dantrolene 2.5 to 10 mg/kg (each vial contains 20mg and mix in 60cc sterile water
  • Treat arrhythmias, acidosis, electrolyte abnormalities (avoid Ca channel blockers)
46
Q

What are the anesthetic considerations for intraop management of suspected malignant hyperthermia?

A
  • Standard ASA monitors
  • Prepare machine – MH specific machine? Changed bellows, tubing, etc.. Flush with 100% O2 for 30 min, tape over volatile agent slot
  • Absolutely avoid volatile agents and SUX (TIVA, local, regional all ok)
  • MH cart available outside pharmacy! (26 vials of Dantrolene in cart)
47
Q

What diagnostic testing is used to diagnose malignant hyperthermia?

A

Caffeine Halothane Test – Gold standard

  • thigh muscle biopsy - measure contractility response to caffeine, halothane, or both
  • *Negative biopsies are not definitive**

Genetic testing – performed on a limited basis (usually strong family hx)

Advanced Principles of Anesthesia (31 decks)

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