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APEX-Neuro > NEURO-musculoskeletal dz > Flashcards

NEURO-musculoskeletal dz Flashcards

1
Q

What is the pathology of myasthenia gravis

A

Autoimmune dz

IgG antibodies destroy post-junctional nicotinic, ACh receptors at the NMJ

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2
Q

What is deficient in patients with myasthenia gravis

A

Nicotinic receptors

There is plenty of ACh

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3
Q

What is a key feature of myasthenia gravis

A

Skeletal muscle weakness that becomes WORSE LATER in the day or with exercise
Periods of rest allow skeletal muscle function recovery

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4
Q

Which organ plays a key role in myasthenia gravis

A

Thymus gland

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5
Q

What are 5 symptoms of myasthenia gravis

A
  1. Diplopia
  2. Ptosis
  3. Bulbar muscle weakness (dysphagia, dysarthria)
  4. Dyspnea on exertion
  5. Proximal muscle weakness
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6
Q

What are 5 situations that exacerbate myasthenia gravis symptoms

A
  1. Pregnancy
  2. Infection
  3. Electrolyte abnormalities
  4. Surgical and psychological stress
  5. Aminoglycoside abx
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7
Q

How does myasthenia gravis affect a neonate

A

Anti-AchR IgG antibodies cross the placenta and cause weakness in up to 20% of neonates for 2 - 4 weeks

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8
Q

Considerations for neonates of parturients with myasthenia gravis

A

Neonate may require airway mgmt

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9
Q

What is the first line medication used for myasthenia gravis

A

Anticholinesterases

-Pyridostigmine

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10
Q

How can the cause of acute weakness for a patient with myasthenia gravis who is taking pyridostigmine be determined

A

Give edrophonium 1 - 2 mg IV

  • If weakness worsens, pt has cholinergic crisis
  • I muscle strength improves, the patient has myasthenic crisis
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11
Q

A patient has increased weakness when edrophonium is given to determine the cause of myasthenia weakness while taking pyridostigmine. Why is weakness worsening and what should be given

A

Patient has anticholinergic crisis caused by increased ACh at the NMJ in the presence of an anticholinesterase

Patient should be given an anticholinergic medication

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12
Q

What medications are used for immunosuppression in myasthenia gravis

A

corticosteroids
cyclosporine
azathioprine
mycophenolate

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13
Q

Surgical procedure indicated for pts with myasthenia gravis

A

Thymectomy = reduces circulating anti-AchR IgG

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14
Q

Additional treatment for myasthenia gravis

A

Plasmapheresis can provide relief during myasthenic crisis before thymectomy

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15
Q

What test is used to distinguish between cholinergic crisis and myasthenic crisis

A

Tensilon test (edrophonium 1-2 mg IV)

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16
Q

How are patients with myasthenia gravis affected by nondepolarizing and depolarizing NMBD

A 
Nondepolarizer = INCREASED sensitivity
Depolarizers = DECREASED sensitivity (resistant)
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17
Q

Why do patients with myasthenia gravis have altered responses to NMB drugs

A

D/t fewer nicotinic receptors (type-m) at the NMJ

  • resistant to succinylcholine
  • increased sensitivity to nondepolarizers
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18
Q

How should the dose for nondepolarizing NMBD be adjusted in patients with myasthenia gravis

A

Potency is increased

Reduce dose by 1/2 or 1/3 and monitor response with nerve stimulator

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19
Q

How should the dose for succinylcholine be adjusted in patients with myasthenia gravis

A

Potency decreased

If RSI is required, increase dose to 1.5 - 2.0 mg/kg

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20
Q

How does pyridostigmine use in patients with myasthenia gravis affect succinylcholine metabolism

A

Pseudocholinesterase efficacy is impaired

Succs duration is prolonged

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21
Q

In myasthenia gravis pts, what is a primary postoperative concern

A

If NMB drugs was used, there’s a higher risk of residual neuromuscular blockade

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22
Q

What are postoperative patients with myasthenia gravis at increased risk for

A

Pulmonary aspiration d/t bulbar muscle weakness

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23
Q

What are 5 factors that increase the risk of postoperative mechanical ventilation in myasthenia gravis pts

A
  1. Dz duration >6 years
  2. Daily pyridostigmine >750 mg/day
  3. Vital capacity <2.9 L
  4. COPD
  5. Surgical procedure: median sternotomy > transcervical thymectomy
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24
Q

What is Eaton-Lambert syndrome

A

Disorder of NMJ resulting in skeletal muscle weakness

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25
Q

Other names for Eaton-Lambert syndrome

A
  1. Myasthenic syndrome

2. Lamber-eaton myasthenic syndrome (LEMS)

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26
Q

Causes of Eaton-Lamber Syndrome

A

IgG-mediated destruction of presynaptic voltage-gated

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27
Q

Pathophysiology of Eaton-Lambert Syndrome

A

Presynaptic VG Ca++ channels action is limited, reducing the amount of Ach that is released into the synaptic cleft

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28
Q

What is the difference between myasthenia gravis and Eaton-Lamber syndrome

A

MG = deficient post-synaptic nicotinic receptors d/t destruction. Normal Ach quantity

ELS = deficient Ach d/t presynaptic VG Ca++ channel destruction. Normal nicotinic Ach receptor quantity

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29
Q

How does Eaton-Lambert weakness present

A

Proximal muscle weakness

Generally worse in the morning, better throughout the day as Ach concentration increases

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30
Q

Pulmonary consequences of Eaton-Lambert Syndrome

A

Respiratory musculature and diaphragm become weak

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31
Q

3 Additional Eaton-Lambert Syndrome symptoms, aside from weakness

A
  1. Autonomic nervous system dysfunction causes orthostatic HoTN
  2. Slowed gastric motility
  3. Urinary retention
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32
Q

What is the primary treatment for Eaton-Lambert Syndrome

MOA

A

3,4-diaminopyridine (DAP)

MOA = increases Ach release from presynaptic nerve terminal and improves contraction strength

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33
Q

Are anticholinesterases used for Eaton-Lamber Syndrome? Why or why not?

A

NO they are not helpful

because it does not increase Ach release

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34
Q

How are pts with Eaton-Lamber Syndrome affected by NMBD

A

They are sensitive to BOTH succinylcholine and nondepolarizers

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35
Q

How should doses for neuromuscular blockers be adjusted in patients with Eaton-Lambert Syndrome

A

Doses should be reduced for both succinylcholine and nondepolarizers

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36
Q

How does Eton-Lamber Syndrome affect the dosing of NMB reversal

A

Reversal with anticholinesterases may be inadequate despite proper dosing

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37
Q

What condition is associated with Eaton-Lambert Syndrome

A

60% of ELS pts have small-cell carcinoma of the lung (oat-cell carcinoma)

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38
Q

A patient with lung cancer is undergoing mediastinoscopy. What associated condition could they possibly have that affects the anesthetic

A

Eaton-Lambert syndrome

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39
Q

What is Guillain-Barre Syndrome

A

An acute idiopathic polyneuritis

Characterized by an assault on myelin in the peripheral nerves

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40
Q

What is the pathophysiology of Guillain-Barre Syndrome

A

The action potential can’t be conducted so the motor endplate never receives the incoming signal

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41
Q

What is the clinical presentation of Guillain-Barre Syndrome

A

Preceded by flu-like illness by 1-3 weeks
GBS persists for ~2 weeks
Full recovery in ~4 wks

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42
Q

What are the 3 most common etiologies of GBS

A
  1. Campylobacter jejuni bacteria
  2. Epstein-Barr Virus
  3. Cytomegalovirus
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43
Q

How does weakness progress in patients with Guillain-Barre Sundrome

A
  1. Flaccid paralysis begins in the distal extremities

2. Ascends bilaterally towards the proximal extremities, trunk, and face

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44
Q

How are the upper airway and ventilation affected by Guillain-Barre Syndrome

A

Intercostal muscle weakness impairs ventilation

Facial and pharyngeal weakness causes difficulty swallowing

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45
Q

What additional sensory deficits accompany Guillain-Barre Syndrome

A

Paresthesias
Numbness
Pain

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46
Q

How is autonomic function affected by Guillain-Barre Syndrome

A

Dysfunction is common

  • Tachy or brady
  • HTN or HoTN
  • Diaphoresis or anhidrosis
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47
Q

What is the treatment for Guillain-Barre Syndrome

A

Plasmapheresis and IV IgG

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48
Q

Which 2 medication classes have no improvement on Guillain-Barre

A
  1. Steroids

2. Interferon

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49
Q

What are the 3 major anesthetic concerns in the patient with Guillain-Barre

A
  1. Skeletal muscle denervation
  2. Impaired ventilation
  3. Autonomic dysfunction
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50
Q

Which NMB drug should be avoided in Guillain-Barre and why

A

Succinylcholine

Risk for hyperkalemia from proliferation of extrajunctional Ach receptors

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51
Q

How are patients with Guillain-Barre affected by depolarizing NMB drugs

A

Increased sensitivity

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52
Q

Why is aspiration risk increased in Guillain-Barre

A

Facial and pharyngeal muscle weakness causes difficulty swallowing and protecting airway, increasing the risk of aspiration

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53
Q

Postoperative considerations in the Guillain-Barre patient

A

May require mechanical ventilation

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54
Q

What type of monitoring may be necessary in patients with Guillain-Barre and why

A

Arterial-line BP

Pts with autonomic dysfunction are at risk for hemodynamic instability

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55
Q

Describe the response a patient with Guillain-Barre can have to indirect-acting sympathomimetics

A

Exaggerated response d/t upregulation of postjunctional adrenergic receptor

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56
Q

What vascular complication are patients with GBS at risk for

A

DVT

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57
Q

Are steroids used in GBS

A

No, steroids aren’t useful

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58
Q

What is another name of Guillain-Barre Syndrome

A

Acute idiopathic polyneuritis

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59
Q

What is familial periodic paralysis

A

Paralysis characterized by acute episode of skeletal muscle weakness accompanied by changes in serum potassium concentration

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60
Q

What are the 2 variants of familial periodic paralysis

A

Hypokalemia

Hyperkalemia

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61
Q

How does familial periodic paralysis differ from other neuromuscular diseases

A
  1. It’s a disorder of the skeletal muscle membrane (reduced excitability)
  2. It’s not a dz of the NMJ
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62
Q

What abnormality is hypokalemic periodic paralysis associated with

A

Ca++ channelopathy

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63
Q

What ion channel abnormality is hyperkalemic periodic paralysis associated with

A

Na+ channelopathy

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64
Q

How is hypokalemic periodic paralysis diagnosed

A

Skeletal muscle weakness following glucose-insulin infusion which decreases serum K+

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65
Q

how is hyperkalemic periodic paralysis diagnosed

A

Skeletal muscle weakness following oral K+ administration which increases serum K+

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66
Q

What is the treatment for familial periodic paralysis

A

Acetazolamide for both forms of the disease

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67
Q

What is the mechanism of acetazolamide action when treating familial period paralysis

A

It creates a non-anion gap acidosis, which protects against hypokalemia

Facilitates K+ excretion, which guards against hyperkalemia

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68
Q

What are intraoperative anesthetic considerations for patients with familial period paralysis

A
  1. Avoid hypothermia at all cost (even during CPB)

2. Monitor serum K+

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69
Q

What 4 medications should be avoided in hypokalemic period paralysis

A
  1. Glucose containing solutions
  2. Potassium wasting diuretics
  3. Beta-2 agonist
  4. Succinylcholine
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70
Q

What 2 medications should be avoided in hyperkalemic periodic paralysis

A

Succinylcholine

K+ containing solutions (LR)

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71
Q

Which neuromuscular blocking drugs are safe for use in hypokalemia and hyperkalemic periodic paralysis

A

Succinylcholine should be avoided, especially in hyperkalemic periodic paralysis

nondepolarizing drugs are safe, in lower doses

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72
Q

What are 2 classes of drugs that induce malignant hyperthermia

A
  1. Halogenated anesthetics

2. Depolarizing NMBD

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73
Q

What is malignant hyperthermia

A

Disease of skeletal muscle, characterized by disordered calcium homeostasis

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74
Q

What is the pathophysiology of malignant hyperthermia

A
  1. Ca++ Enters the cell and activates the defective ryanodine receptor
  2. The sarcoplasmic reticulum releases too much Ca++ into the cell
  3. Increased Ca++ engages with contractile elements
  4. Increased Ca++ needs to be returned to SR via SERCA2 pumps
  5. This process uses a lot of ATP and O2
  6. Increased CO2 production plus K+ and myoglobin waste is released
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75
Q

What are 7 consequences of increased intracellular Ca++ in the myocyte

A
  1. Rigidity from sustained contraction
  2. Accelerated metabolic rate and depletion of ATP
  3. Increased O2 consumption
  4. Increased CO2 and heat production
  5. Mixed respiratory and lactic acidosis
  6. Sarcolemma breaks down
  7. Potassium and myoglobin leak into the systemic circulation
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76
Q

What are 3 co-existing diseases associated with MH

A
  1. King-Denborough syndrome
  2. Central core disease
  3. Multiminicore disease
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77
Q

Are patients with Duchenne muscular dystrophy at risk for MH

A

No
An MH-like syndrome is associated with Duchenne MD but it is due to rhabdomyolysis
MD pts have normal RyR1 receptors
Dantrolene does not treat the condition

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78
Q

What are risk factors of MH

A
  1. Geography
  2. Male sex
  3. Youth
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79
Q

What is the most sensitive indicator of MH

A

EtCO2 that rises out of proportion to minute ventilation

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80
Q

When does MH occur

A

Up to 6 hours after exposure to a triggering agent

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81
Q

What are 5 early signs of MH

A
  1. Tachycardia
  2. Tachypnea
  3. Masseter spasm
  4. Warm soda lime
  5. Irregular heart rhythm
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82
Q

What are 5 late signs of MH

A
  1. Muscle rigidity
  2. Cola-colored urine
  3. Coagulopathy
  4. Irregular heart rhythm
  5. Overt hyperthermia
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83
Q

What is the definition of masseter muscle rigidity

A

A tight jaw that cannot be opened

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84
Q

How is masseter muscle rigidity affected by NMB drugs

A

Spasm is due to increased Ca++ in myoplasm

Since the site of action is distal to the NMJ, a NMB will not relax the jaw

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85
Q

What is the gold standard for diagnosing MH

A

Caffeine-halothane contracture test, which requires a live muscle biopsy sample

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86
Q

What are possible differential diagnoses to consider apart from MH

A
  1. Thyroid storm
  2. Malignant neuroleptic syndrome
  3. Sepsis
  4. Pheochromocytoma
  5. Serotonergic syndrome
  6. Metastatic carcinoid
  7. Cocaine intoxication
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87
Q

What are preventative measures taken in the OR prior to an MH pt

A
  1. Anesthesia machine must be flushed with high flow O2 for 100 minutes
  2. All external parts should be removed and replaced
  3. Vaporizers should be removed
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88
Q

What 10 interventions are warranted when MH is suspected

A
  1. Discontinue triggering agent
  2. Initiate TIVA
  3. Call for help and notify surgeon to stop
  4. Hyperventilate w/ 100% FiO2 at 10 L/min
  5. Apply charcoal filters to inspiratory and expiratory ports
  6. Exchange circuit and reservoir bag
  7. Give dantrolene
  8. Cool patient
  9. Treat acidosis
  10. Maintain UO 2 mL/kg/hr
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89
Q

What is the dose for dantrolene

A

2.5 mg/kg IV q 5-10 minutes

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90
Q

What are the 2 MOAs of Dantrolene

A
  1. Reduces Ca++ release from RyR1 receptor in skeletal myocyte
  2. Prevents Ca++ entry INTO myocyte, which reduces the stimulus of Ca-induced Ca++ release
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91
Q

How is dantrolene supplied

A

As 20 mg vial with 3 g of mannitol

Must be reconstituted with 60 mL of preservative-free H2O NOT saline

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92
Q

What drug class is dantrolene

A

muscle relaxant

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93
Q

What are common side effects of dantrolene

A

Muscle weakness

Venous irritation

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94
Q

What are 11 steps in treating MH

A
  1. DC triggering agent
  2. Call for help
  3. Hyperventilate with 100% O2 at FGF 10 L/min
  4. Apply charcoal filter and new circuit
  5. Administer dantrolene or Ryanodex
  6. Cool patient
  7. Correct lactic acidosis
  8. Treat hyperkalemia
  9. Protect against dysrhythmias
  10. Maintain UO >2 mL/hr
  11. Check coagulation status
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95
Q

How is anesthesia maintained once MH is identified

A

Start TIVA and stop volatile anesthetic

96
Q

What are 3 benefits of hyperventilation with 100% O2 at 10 L/min once MH is identified

A
  1. Facilitates CO2 elimination
  2. Enhances O2 delivery
  3. Drives K+ into cells
97
Q

When is dantrolene d/c’d

A

Once symptoms of hypermetabolism subside

98
Q

What is the continued dose of dantrolene in the ICU

A

1 mg/kg q6 hrs
OR
0.1-0.3 mg/kg/hr for 48 - 72 hrs

99
Q

When should the diagnosis of MH be reconsidered?

A

If >20 mg/kg of dantrolene has been used

100
Q

What are 3 methods to aid in cooling the MH pt

A
  1. Cold IVF
  2. Cold fluid lavage of stomach and bladder
  3. Ice packs
101
Q

How can lactic acidosis be addressed in the MH pt

A

Sodium bicarb 1 - 2 mEq/kg

titrate to ABG base deficit

102
Q

What are 3 methods of treating hyperkalemia in the MH pt

A
  1. CaCl 5 - 10 mg/kg IV
  2. Insulin 0.15 units/kg + D50 1 mL/kg
  3. Hyperventilation
103
Q

How do you protect against dysrhythmias in a pt with MH

A

Give class 1 antiarrhythmics

  1. Procainamide 15 mg/kg
  2. Lidocaine 2 mg/kg
104
Q

What medication should be avoided when administering dantrolene and why

A

CCBs

They can precipitate life-threatening hyperkalemia

105
Q

Why should UO be maintained >2 mL/kg/hr

A

Protect against renal injury from free myoglobin

106
Q

In a pt with MH, what are 3 methods to maintain UO >2 mL/kg/hr

A
  1. IV hydration
  2. Mannitol 0.25 g/kg IV
  3. Furosemide 1 mg/kg IV
107
Q

What is Duchenne muscular dystrophy

A

An x-linked, recessive dz that results from the absence of dystrophin protein

108
Q

What is dystrophin

A

Critical structural component of the cytoskeleton of skeletal and cardiac muscle cells
It helps anchor actin and myosin to the cell membrane

109
Q

What happens in the absence of dystrophin

A

The sarcolemma is destabilized during muscle contraction and increases membrane permeability

110
Q

What is released from the myocyte when dystrophin is not present

A
  1. creatine kinase

2. myoglobin

111
Q

How is Ca++ affected by the absence of dystrophin

A

Ca++ can freely enter the cell and activate proteases that destroy the contractile elements, causing inflammation, fibrosis, and cell death

112
Q

Should pts with DMD be given succinylcholine?

Why or why not

A

NO
Because the absence of dystrophin allows extrajunctional nicotinic receptor to populate the sarcolemma, predisposing the pts to severe hyperkalemia

113
Q

Why does succinylcholine have a black box warning for children

A

It can cause cardiac arrest and sudden death d/t hyperkalemia in undiagnosed children with skeletal muscle myopathy

114
Q

What are 5 pulmonary considerations for patients with Duchenne muscular dystrophy

A
  1. Kyphosis causing restrictive lung dz
  2. Decreased pulmonary reserve
  3. Increased secretions
  4. Increased risk of PNA
  5. Respiratory muscle weakness
115
Q

What are 3 cardiac considerations for patients with Duchenne muscular dystrophy

A
  1. Degeneration of cardiac muscle
  2. S/Sx of cardiomyopathy
  3. Thorough preop cardiac workup
116
Q

How does degeneration of the cardiac muscle affect patients with Duchenne muscular distrophy

A
  1. Reduces contractility
  2. Leads to papillary muscle dyfxn
  3. Mitral regurg
  4. Cardiomyopathy
  5. CHF
117
Q

What s/sx of cardiomyopathy may be present in patients with Duchenne muscular dystrophy

A
  1. Resting tachycardia
  2. JVD
  3. S3/S4 gallop
  4. Displaced PMI
118
Q

What should be included in a preop work-up in pts with DMD

A
  1. EKG
  2. Echo
  3. cardiac MRI
119
Q

What EKG changes may be present in pts with DMD

A
  1. Sinus tachycardia
  2. Short PR interval
  3. Posterobasal cardiac scarring
    - -Increased R wave in lead I
    - -Deep Q wave in limb leads
120
Q

What gastric abnormalities should be considered in pts with DMD

A

Increased risk of aspiration d/t:

  1. Impaired airway reflexes
  2. GI hypomotility
121
Q

What medications should be avoided in pts with MD

A
  1. Succinylcholine

2. Volatile anesthetics

122
Q

Define scoliosis

A

It is a lateral and rotational curvature of the spine and ribcage

123
Q

What is kyphoscoliosis

A

A posterior curvature of the spinal column

124
Q

What are 5 etiologies of scoliosis

A
  1. Idiopathic (80%)
  2. Congenital
  3. Myopathic (MD)
  4. Neuropathic (CP)
  5. Traumatic
125
Q

What is the Cobb angle in scoliosis

A

It describes the magnitude of the spinal curvature

126
Q

How is the Cobb angle measured

A
  1. The 2 most displaced vertebrae are identified on top and bottom
  2. A parallel line is drawn to each
  3. A perpendicular line is drawn to each
  4. The angle where they intersect is the Cobb angle
127
Q 
Describe the significance at for each Cobb angle
40-50
60
70
100
A 
40-50 = surgery indicated
60 = decreased pulm reserve
70 = pulm symptoms present
100 = Gas exchange significantly impaired with high risk of PPC
128
Q

What type of pulmonary defect occurs with scoliosis

A

Restrictive ventilatory defect compresses the lungs

129
Q

What are early signs of altered pulmonary mechanics in pts with scoliosis

A
  1. Decreased FEV1 and FRC
  2. Decreased chest wall compliance
  3. Normal FEV1/FVC ratio
130
Q

List the volumes and capacities that are decreased during early respiratory complications of scoliosis

A
  1. VC
  2. TLC
  3. FRC
  4. RV
131
Q

What are 7 late respiratory complications of scoliosis

A
  1. V/Q mismatching
  2. Hypoxemia
  3. Hypercarbia
  4. Pulm HTN
  5. Reduced response to hypercapnia
  6. Cor pulmonale
  7. Cardiorespiratory failure
132
Q

What 6 CV changes occur as a result of severe scoliosis

A
  1. RV hypertrophy d/t increased PVR
  2. RV strain
  3. RA enlargement
  4. MV prolapse
  5. MV regurg
  6. Coarc of aorta
133
Q

What are 2 airway complications r/t the prone position and scoliosis pts

A
  1. Upper airway edema

2. ETT kink or migration

134
Q

What is a possible neck complication r/t prone positioning in scoliosis pts

A

Neck rotation vertebral compression cerebral hypoperfusion

135
Q

What are 3 possible ocular complications r/t prone positioning in scoliosis pts

A
  1. Ischemic optic neuropathy
  2. Central retinal artery occlusion
  3. Corneal abrasion
136
Q

What are 2 possible upper extremity complications r/t prone positioning in scoliosis pts

A

Brachial plexus injury

Ulnar n. injury

137
Q

What are 3 possible lower extremity complications r/t prone positioning in scoliosis pts

A
  1. Pressure on iliac crest = lateral femoral cutaneous n. injury
  2. Pressure lateral to fibula = peroneal n. injury
  3. Hip flexion = femoral vein occlusion and DVT
138
Q

What are the complications from increased abdominal pressure r/t prone positioning in scoliosis pts

A
  1. Pressure transmitted to veins that drain the spine increase bleeding
  2. Reduced pulmonary compliance
139
Q

When can you assume a pt with scoliosis will need postop mechanical ventilation (respiratory value)

A

When VC<40% predicted

140
Q

What 3 pulmonary measure should be assessed preoperatively in the scoliosis pt

A
  1. Exercise tolerance
  2. ABG
  3. VC
141
Q

How is intubation complicated in scoliosis pts

A

If a pt has cervical scoliosis, intubation can be difficult

142
Q

Is the use of N2O recommended

A

N2O increased PVR which is usually already high in scoliosis pts
Avoid N2O

143
Q

What airway alteration may need to occur with scoliosis thoracic corrections higher than T8

A
  1. May require OLV

2. Possible DLT or bronchial-blocker

144
Q

Scoliosis surgery considerations r/t blood loss

A

Prepare for significant blood loss

  1. large bore IV access or CVC
  2. Type and x-match
  3. cell-saver
  4. autologous donation
145
Q

Hypotension to reduce blood loss during scoliosis surgery can carry what risk

A

MAP < 60 mmHg increases risk of cerebral hypoperfusion and ION

146
Q

How is end-organ perfusion monitored during scoliosis surgery

A
  1. ABG (d/t risk of metabolic acidosis)

2. UO

147
Q

What warming measures are taken during scoliosis surgery

A
  1. Active rewarming with forced air warmer

2. Fluid warmers

148
Q

What venous risks are possible in patients undergoing scoliosis surgery

How can it be identified

A

Venous air embolism

Dead space is increased and observed as a reduction in EtCO2 (with and increased PaCO2 - EtCO2 gradient)

149
Q

What are 6 risks of the wake-up test during scoliosis surgery

A
  1. Vascular access removal
  2. Tracheal extubation
  3. Awareness
  4. Pain
  5. Air embolism
  6. Damage to surgical instrumentation
150
Q

What pathway and vessels does SSEP monitor

A 
Pathway = Posterior spinal cord (dorsal column pathway)
Vessels = posterior spinal arteries
151
Q

Does NMB drugs interfere with SSEP or MEP

A 
SSEP = no
MEP = yes
152
Q

What pathway and vessel does MEP monitor

A 
Pathway = anterior spinal cord
Vessel = anterior spinal artery
153
Q

What 3 ways does rheumatoid arthritis impact the airway

A
  1. TMJ = limited mouth opening
  2. Cricoarytenoid joints = decreased glottic opening
  3. Cervical spine = AC sublux w/ flesion; ltd extension
154
Q

What symptoms may be present with cricoarytenoid arthritis

What can these symptoms result in

A
  1. Hoarseness
  2. Stridor
  3. Dyspnea

Result = airway obstruction

155
Q

What airway management adjustments should be made in the pt with rheumatoid arthritis

A

Smaller endotracheal tube

156
Q

What is the cause of AO subluxation in RA pts

A

D/t weakness of transverse axial ligament, which allows the odontoid process to directly compress the spinal cord at the level of the foramen magnum

157
Q

What are RA pts at risk for with AO subluxation

A

Quadriparesis or paralysis

158
Q

How is AO subluxation assessed and diagnoses

A

Assessed with lateral xray of c-spine

AO sublux = distance between anterior arch of atlas and odontoid process is >3 mm

159
Q

What are treatments for c-spine instability in RA pts

A
  1. Surgical correction with odontoid decompression and posterior cervical fusion
160
Q

What is the most common airway complication of RA

A

AO subluxation and separation of the AO articulation

161
Q

What is rheumatoid arthritis

A

An autoimmune dz that targets the synovial joints

162
Q

How does RA affect the entire body

A

There’s widespread systemic involvement d/t infiltration of immune complexes into the small and medium arteries leading to vasculitis

163
Q

What mediator plays a central role in the pathogenesis of RA

A

Cytokines – TNF and interleukin-1

164
Q

What are hallmark signs of RA

A

Morning stiffness that generally improves with activity

Painful, swollen, and warm joints

165
Q

How are lymph nodes affect in RA

A

Node enlargement in the cervical, axillary, and epitrochlear regions

166
Q

What joints are typically affected by RA

A

The proximal interphalangeal and metacarpophalangeal joints in the hands and feet

167
Q

What are possible eye complications r/t RA

A

Sjorgen’s syndrome = dry eyes prone to corneal abrasions

168
Q

What are possible nervous system complications of RA

A

Peripheral neuropathy d/t nerve entrapment

169
Q

What are possible endocrine complications of RA

A

Adrenal insufficiency and infection d/t chronic steroid use

170
Q

What are possible renal complications of RA

A

Renal insufficiency d/t vasculitis and NSAIDs

171
Q

What are 2 possible pulmonary complications of RA

A
  1. Pleural effusion

2. Restrictive pulmonary issues

172
Q

Why are pts with RA prone to restrictive pulmonary issues

A
  1. Diffuse interstitial fibrosis

2. Costochondral involvement limiting chest wall expansion

173
Q

What are 5 possible cardiac complications of RA

A
  1. Pericardial effusion or tamponade
  2. Restrictive pericarditis
  3. Aortic regurg
  4. Valvular fibrosis
  5. Coronary artery arteritis
174
Q

What are possible GI complications of RA

A

Chronic NSAID and steroid use effect on GI tract

175
Q

What are 2 hematologic complications of RA

A
  1. Anemia

2. Plt dysfxn d/t NSAID use

176
Q

What 3 laboratory tests are altered in pts with RA

Are they increased or decreased

A 
Rheumatoid factor (anti-Ig antibody) = INCREASED
C-reactive protein = INCREASED
Erythrocyte sedimentation rate = INCREASED
177
Q

What is the medication management of RA

A
  1. Antirheumatics
  2. Glucocorticoids
  3. NSAIDs
178
Q

How do antirheumatic drugs improve RA symptoms

A

They inhibit TNF interleukin-1 and -6. They also inhibit T cells and B lymphocytes

179
Q

What risks are carried with taking antirheumatic drugs

A

Increased risk for infection and cancer d/t suppression of the immune system

180
Q

What are 3 examples of antirheumatic drugs used for RA

A

Methotrexate, cyclosporine, etanercept

181
Q

If a pt is taking cyclosporine for RA, how does this affect depolarizing NMB

A

Succinylcholine duration is prolonged

182
Q

What methotrexate effects should be considered in RA pts

A

Liver dysfunction

Bone marrow suppression

183
Q

What is systemic lupus erthematosus

A

An autoimmune dz characterized by the proliferation of antinuclear antibodies

184
Q

What are the consequences of SLE

A

consequences occur in nearly every organ d/t antibody-induced vasculitis and tissue destruction

185
Q

What are the 2 most common problem associated with SLE

A
  1. Polyarthritis

2. Dermatitis

186
Q

What are 3 possible airway complications r/t SLE

A

Cricoarytenoiditis causing

  • Hoarseness
  • Stridor
  • Airway obstruction
187
Q

What are 3 possible nervous system complications associated with SLE

A
  1. Stroke
  2. Psychosis/dementia
  3. Peripheral neuropathy
188
Q

What is a renal complication associated with SLE

A

Nephritis with proteinuria

189
Q

What are 5 pulmonary complications associated with SLE

A
  1. Restrictive ventilatory defect
  2. Pulmonary HTN
  3. Interstitial lung dz w/ impaired diffusion capacity
  4. Pleural effusion
  5. Recurrent pulmonary emboli
190
Q

What are 5 cardiovascular complications associated with SLE

A
  1. Pericarditis
  2. Raynaud’s phenomenon
  3. HTN
  4. Conduction defects
  5. Endocarditis
191
Q

What are 5 hematologic complications associated with SLE

A
  1. Antiphospholipid antibodies
  2. Hypercoagulability
  3. Anemia
  4. Thrombocytopenia
  5. Leukopenia
192
Q

What 2 events can exacerbate SLE symptoms

A
  1. Stress

2. Drug exposure

193
Q

What are symptoms of drug-induced SLE

A
  1. arthralgia
  2. Anemia
  3. Leukopenia
  4. Fever
194
Q

What are the 11 most common factors and drugs that illicit SLE

A 
P = pregnancy
I = infection
S = surgery
S = stress
E = Enalapril
D = D-PCN
C = Captopril
H = Hydralazine
I = Isoniazid
M = Methyldopa
P = Procainamide
195
Q

What is the medical treatment for SLE

A
  1. Corticosteroids
  2. NSAIDs
  3. Immunosuppressants
  4. Antimalarials
196
Q

What immunosuppressants are commonly used in SLE

A
  1. Cyclophosphamide
  2. Azathioprine
  3. Methotrexate
  4. Mycophenolate mofetil
197
Q

What 2 antimalarials are used in SLE

A
  1. Hydroxychloroquine

2. Quinacrine

198
Q

What anesthetic considerations should be made with SLE pts that have cricoarytenoid arthritis

A
  1. Use smaller ETT
  2. Prepare for post-extubation laryngeal swelling and airway obstruction
  3. Give steroids for airway edema
199
Q

What anesthetic precautions should be considered in SLE pts taking cyclophosphamide

A

It inhibits plasma cholinesterase and increases succinylcholine duration

200
Q

What cardiac problems are associated with Marfan’s syndrome and why

A

Aortic dissection and aortic insufficiency

This is d/t aortic root dilation

201
Q

What spontaneous pulmonary complication are pts with Marfan’s at risk for
How can this be minimized

A

Increased risk for PTX

Careful monitoring of PIP

202
Q

4 Classic physical alterations of Marfan’s syndrome

A
  1. Extremely tall stature
  2. Pectus excavatum
  3. Kyphoscoliosis
  4. Hyperflexible joints
203
Q

What is Ehlers-Danlos syndrome

A

An inherited disorder of procollagen and collagen

204
Q

What complications are associated with Ehlers-Danlos syndrome

A

Spontaneous bleeding into joints

AAA

205
Q

What type of anesthesia should be avoided in pts with Ehlers-Danlos syndrome

A

Avoid regional anesthesia and IM injections d/t increased bleeding risk

206
Q

Why is increased bleeding a problem in Ehlers-Danlos syndrome

A

Not because of coagulopathy but d/t poor vessel quality

207
Q

What is osteogenesis imperfecta

A

A connective tissue disorder with autosomal dominant inheritance
“Brittle bone”

208
Q

What anesthetic considerations should be made with positioning and OI pts

A

Careful positioning because fractures can occur even with BP cuff inflation or fasciculations from meds

209
Q

What airway precautions should be taken in pts with OI

A

Very careful manipulation d/t risk of c-spine fracture and reduced cervical ROM

210
Q

What 4 pulmonary changes occur with OI and why

A
  1. Reduced chest wall compliance
  2. Reduced VC
  3. V/Q mismatch
  4. Arterial hypoxemia

d/t kyphoscoliosis and pectus excavatum

211
Q

How does increased serum thyroxine affect pts with OI

A

It increases BMR and VO2 and lead to hyperthermia

212
Q

Why can OI pts have blue sclera

A

Because the sclera is susceptible to fracture

213
Q

What is multiple sclerosis

A

A demyelinating disease of the CNS

214
Q

What symptoms do MS pts experience

A

Sensory and motor deficiencies

Autonomic instability

215
Q

Why are MS pts at risk for aspiration

A

Cranial nerve involvement causes bulbar muscle dyfxn

216
Q

What are 3 treatments for MS

A
  1. Corticosteroids
  2. Interferon
  3. Azathioprine
217
Q

What 2 events can exacerbate MS symptoms

A
  1. Stress

2. Increased body temp

218
Q

Which muscle relaxant should be avoided in MS pts and why

A

Succinylcholine

It can cause life-threatening hyperkalemia

219
Q

What is myotonic dystrophy

A

Prolonged contracture after a voluntary contraction

220
Q

What causes myotonic dystrophy

A

Dysfunctional Ca++ sequestration by the SR

221
Q

What are 3 things that can increase the risk of contractures in pts with myotonic dystrophy

A
  1. Succinylcholine
  2. NMB reversal w/ anticholinesterase
  3. Hypothermia (shivering)
222
Q

What 4 concerns should the anesthetist have when treating a pt with myotonic dystrophy

A
  1. Aspiration
  2. Respiratory muscle weakness
  3. Cardiomyopathy and dysrhythmias
  4. Sensitivity to anesthetic agents
223
Q

What is scleroderma

A

A condition causing excessive fibrosis in the skin and organs, especially microvasculature

224
Q

What airway complications are associated with scleroderma

A

Limited mouth opening d/t skin fibrosis

225
Q

What lung complications are associated with scleroderma

A
  1. Pulmonary fibrosis

2. Pulmonary HTN

226
Q

What cardiac complications are associated with scleroderma

A
  1. Dysrhythmias

2. CHF

227
Q

What renal complications are associated with scleroderma

A
  1. Renal failure

2. Renal artery stenosis leading to HTN

228
Q

What vascular complications are associated with scleroderma

A

Decreased vessel compliance leading to HTN

229
Q

What peripheral and cranial nerve complications are associated with scleroderma

A

Nerve entrapment by tight connective tissue leading to neuropathy

230
Q

What ocular complications are associated with scleroderma

A

Dryness predisposes to corneal abrasions

231
Q

What is CREST syndrome in reference to scleroderma

A

Calcinosis, Raynaud’s phenomenon, Esophageal hypomobility, Sclerodactyly, Telangiectasia

232
Q

How does telangiectasias in pts with scleroderma affect airway management

A

Spider veins of the mucosa increase the risk of bleeding during airway manipulation, especially with nasal intubation

233
Q

What is Paget’s disease

A

A condition associated with excess osteoblastic and osteoclastic activity that causes abnormally thick, but weak, bone deposits

234
Q

What causes Paget’s disease

A
  1. Excess parathyroid hormone

2. Calcitonin deficiency

235
Q

What are the most common problems associated with Paget’s disease

A

Pain and fractures

APEX-Neuro (3 decks)

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