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SEE/BOARD STUDY > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Which autoimmune disease has IgG antibodies that destroy post-junctional, nicotinic, Ach receptors at the neuromuscular junction?

A

Myasthenia gravis

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2
Q

How does skeletal muscle weakness occur in myasthenia gravis?

A

There aren’t enough receptors to translate the extracellular signal into an intracellular response.

This manifests as skeletal muscle weakness.

Ach is present in sufficient quantity

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3
Q

What gland plays a key role in Myasthenia Gravis?

A

Thymus gland plays a key role.

A thymectomy brings symptom relief to many patients.

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4
Q

What is a key feature of myasthenia gravis in terms of the skeletal muscle function.

A

The skeletal muscle weakness becomes worse later in the day or develops with exercise.

Periods of rest allow for recovery of skeletal muscle function.

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5
Q

What are the symptoms of myasthenia gravis?

A

Diplopia, ptosis (earliest signs)

Bulbar muscle weakness (muscles of mouth and throat) which leads to dysphagia, dysarthria, and difficulty handling saliva

Dyspnea with exertion

Proximal muscle weakness

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6
Q

What are some situations that exacerbate symptoms of myasthenia gravis?

A

Pregnancy

Infection

Electrolyte abnormalities

Surgical and psychological stress

Aminoglycoside antibiotics

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7
Q

What do you have to worry about with pregnancy and the placenta with myasthenia gravis?

A

Pregnancy intensifies the symptoms of myasthenia gravis.

Anti-AchR IgG antibodies cross the placenta and cause weakness in 15-20 percent of neonates.

This can persist up to 2-4 weeks, which is consistent with the half-life of the Anti-AchR IgG antibodies in the neonate’s circulation.

These neonates may require airway management.

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8
Q

What are four ways to treat myasthenia gravis?

A

Anticholinesterases

Immunosuppression

Surgery

Plasmapheresis

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9
Q

What is the first line oral medical treatment for myasthenia gravis?

A

Oral Pyridostigmine is the first line medical treatment.

Overdoes in anticholinesterases causes cholinergic crisis and muscle weakness.

Cholinergic crises may be difficult to differentiate from myasthenic crisis.

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10
Q

What is the Tensilon Test?

A

It will determine if the patient is in cholinergic crisis or myasthenic crisis.

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11
Q

How do you administer the Tensilon Test?

A

Administering 1-2 mg IV edrophonium

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12
Q

Based on the Tensilon test, how can you tell if the patient is in cholinergic crisis or myasthenic crisis?

A

Administering 1-2 mg IV edrophonium.

If muscle weakness is made worse, then the patient has cholinergic crisis. An anticholinergic is the appropriate treatment for this patient.

If there is an improvement in muscle strength, then the patient had an exacerbation of myasthenic symptoms.

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13
Q

What four immunosppressions can you use for myasthenia gravis?

A

Corticosteroids

Cyclosporine

Azathioprine

Mycophenolate

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14
Q

What surgery can you perform for myasthenia gravis?

A

Thymectomy reduces circulating Anti-AchR IgG in most patients

Surgical approach may be via median sternotomy or by the transcervical approach.

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15
Q

What treatment for myasthenia gravis can provide a temporary relief during myasthenic crisis or prior to thymectomy?

A

Plasmapheresis

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16
Q

A patient with myasthenia gravis, they will have an increased sensitivity to which drugs as well as an increased resistance to which drug?

A

Because there is a reduction in the number of nicotinic receptors (type-M) at the neuromuscular junction, patients with myasthenia gravis have an increased sensitivity to NON-DEPLARIZING NMBs and a resistance to SUCCINYLCHOLINE.

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17
Q

How should you dose nondepolarizers in a patient with myasthenia gravis?

A

Patients will have an increased sensitivity with nondepolarizers.

This causes an increased potency.

Reduce dose by 1/2 to 2/3 and monitor the response with nerve stimulator.

Remember that volatile anesthetics cause skeletal muscle relaxation by acting in the ventral horn of the spinal cord. In many cases, this eliminates the need for neuromuscular blockers.

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18
Q

What would be the RSI dose for succinylcholine for a patient with myasthenia gravis?

A

1.5-2.0 mg/kg

Pyridostigmine is the mainstay of medical management.

It impairs the efficacy of pseudocholinesterase. This prolongs the duration of succinylcholine.

Remember that volatile anesthetics cause skeletal muscle relaxation by acting in the ventral horn of the spinal cord. In many cases, this eliminates the need for neuromuscular blockers.

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19
Q

What are some post operative concerns for a patient with myasthenia gravis?

A

Patient are very sensitive to the effects of residual neuromuscular blockade.

Bulbar muscle weakness (mouth and throat) manifests as difficulty oral secretions. This increases the risk of pulmonary aspiration.

Patients should be counseled on the need for post operative ventilation..

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20
Q

What would increase the risk for a patient for post operative ventilation, if they have myasthenia gravis?

A

Disease duration > 6 years

Daily pyridostigmine > 750mg/day

Vital capacity < 2.9L

COPD

Surgical approach: Median sternotomy > transcervical thymectomy

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21
Q

What are other names for Myasthenic Syndrome?

A

Eaton-Lambert Syndrome

Lambert-Eaton Myasthenic syndrome (LEMS)

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22
Q

What is Eaton-Lambert Syndrome?

A

A disorder of the neuromuscular junction that results in skeletal muscle weakness.

AKA Lambert-Eaton Myasthenic syndrome (LEMS) or Myasthenic Syndrome

NOT the same as myasthenia gravis.

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23
Q

What is the pathophysiology of Eaton-Lambert syndrome?

A

IgG mediated destruction of the PRESYNAPTIC voltage-gated calcium channel at the presynaptic nerve terminal.

When the action potential depolarizes the nerve terminal, Ca+2 entry into the presynaptic neuron is limited, thereby reducing the amount of Ach that is released into the synaptic cleft.

The postsynaptic nicotinic receptor is present in normal quantity and functions normally.

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24
Q

What are the clinical presentation of Eaton-Lambert syndrome?

A

The proximal muscles are most affected, and weakness is generally worse in the morning and gets better throughout the day.

The respiratory musculature and diaphragm become weak.

Autonomic nervous system dysfunction causes orthostatic hypotension, slowed gastric motility, and urinary retention.

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25
Q

What is the treatment of Eaton-Lambert syndrome?

A

3,4-diaminopyridine (DAP) increase Ach release from the presynaptic nerve terminal and improves the strength of contraction.

Anticholinesterases are not helpful and the Tensilon test does not aid in diagnosis.

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26
Q

Which disease will cause a patient to be sensitive to succinylcholine AND nondepolarizers?

A

Eaton-Lambert syndrome

doses should be reduced.

Volatile anesthetics provide enough muscle relaxation for most surgical procedures.

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27
Q

What is a common co-morbidity with patients with Eaton-Lambert syndrome?

A

Upwards of 60 percent of patients have small-cell carcinoma of the lung (oat-cell carcinoma).

Consider the possibility of this disorder in all patients with suspected lung CA undergoing mediastinoscopy, bronchoscopy, or thoracoscopy.

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28
Q

Will anticholinesterasese be effective for a patient with Eaton-Lambert syndrome?

A

Reversal with anticholinesterases may be inadequate despite proper dosing.

Patients are at high risk for post-operative ventilatory failure.

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29
Q

What is the pathophysiology of Guillain-Barre?

A

AKA acute idiopathic polyneuritis

Is an immunologic assault on the myelin in the peripheral nerves.

Action potential can’t be conducted, so the motor endplate never receives the incoming signal.

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30
Q

How long does Guillain-Barre last?

A

Usually persists for ~ 2 weeks and ends with full recovery in ~ 4 weeks

About two percent of those affected with GBS will develop chronic inflammatory demyelinating polyneuropathy.

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31
Q

What is the clinical presentation of Guillain-Barre?

A

A flu-like illness usually precedes paralysis by 1-3 weeks.

The most common culprits are Campylobacter jejuni bacteria, Epstein-Barr virus, and cytomegalovris. Other causes include vaccinations, surgery, and lymphomatous disease.

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32
Q

What are some signs and symptoms of Guillain-Barre?

A

Flaccid paralysis begins in the distal extremities and ascends bilaterally towards the proximal extremities, trunk, and face.

Intercostal muscle weakness impairs ventilation.

Facial and pharyngeal weakness causes difficulty swallowing

Sensory deficits include: paresthesias, numbness, and/or pain.

Autonomic dysfunction is common: tachycardia or bradycardia, hypertension or hypotension, diaphoresis or anhidrosis, and orthostatic hypotension

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33
Q

What is the treatment for Gullain-Barre?

A

Medical treatment includes plasmapheresis and/or IV IgG

In contrast to multiple sclerosis, steroids and interferon do not improve this condition.

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34
Q

What are the major anesthetic concerns with a patient with Gullain-Barre?

A

Skeletal muscle denervation

Impaired ventilation

Autonomic dysfunction

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35
Q

How does Succinylcholine and nondepolarizers affect a patient with gullain-barre?

A

Avoid succinylcholine. There is a risk of hyperkalemia from proliferation of extrajunctional Ach receptors.

There is an increased sensitivity of nondepolarizers

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36
Q

What is the response to indirect acting sympathomimetics and a patient with gullain-barre?

A

There is an exaggerated response to indirect acting sympathomimetics due to up-regulation of postjunctional adrenergic receptors.

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37
Q

Patients with autonomic dysfunction and gullain-barre are at risk for?

A

Hemodynamic instability from anesthesia, position changes, positive pressure ventilation, and blood loss.

They require intra-arterial pressure monitoring

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38
Q

What drugs are not useful in a patient with gullain-barre?

A

Steroids

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39
Q

What type of anesthesia is controvesial with a patient that has gullain-barre?

A

Regional anesthesia

There is inconclusive data for this.

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40
Q

What is Familial periodic paralysis?

A

It is characterized by acute episodes of skeletal muscle weakness accompanied by changes in the serum potassium concentration.

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41
Q

What are the two variants of familial periodic paralysis?

A

Hypokalemic

Hyperkalemic

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42
Q

Even though the cause of familial periodic paralysis is unknown, what are a few things that are understood about it?

A

It is disorder of the skeletal muscle membrane (reduced excitatbility)

It is not a disease of the neruomuscular junction

Hypokalemic periodic paralysis is associated with calcium channelopathy.

Hyperkalemic periodic paralysis is associated with sodium channelopathy.

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43
Q

Which type of Familial periodic paralysis is associated with sodium channelopathy?

A

Hyperkalemic periodic paralysis

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44
Q

Which type of Familial periodic paralysis is associated with calcium channelopathy?

A

Hypokalemic periodic paralysis

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45
Q

What is the diagnosis for hypokalemic periodic paralysis ?

A

It is present if skeletal muscle weakness follows a glucose-insulin infusion.

The patient became weak after the serum K+ was reduced.

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46
Q

What is the diagnosis for hyperkalemic periodic paralysis ?

A

It is present if skeletal muscle weakness follows oral potassium administration.

The patient became weak after the serum K+ was increased.

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47
Q

What is the treatment for Familial periodic paralysis?

A

Acetazolamide is the treatment for both forms of this disease.

It creates a non-anion gap acidosis, which protects against hypokalemia, and it also facilitates renal potassium excretion, which guards against hyperkalemia.

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48
Q

How does acetazolamide treat hypokalemic periodic paralysis?

A

It creates a non-anion gap acidosis

This protects against hypokalemia

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49
Q

How does acetazolemide treat hyperkalemic periodic paralysis?

A

It facilitates renal potassium excretion

This guards against hyperkalemia

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50
Q

What are some anesthetic considerations for a patient familial periodic paralysis?

A

Hypothermia must be avoided at all costs. It is recommended that these patients remain normothermic even when they are placed on cardiopulmonary bypass!

Serial serum potassium monitoring is indicated.

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51
Q

What should you not administer with a patient that has hypokalemic periodic paralysis?

A

Glucose containing solutions

Potassium wasting diuretics

Beta-2 agonists

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52
Q

What should you not administer with a patient that has hyperkalemic periodic paralysis?

A

Succinylcholine

Potassium containing solutions (LR)

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53
Q

What is safe to administer with a patient that has hypokalemic periodic paralysis?

A

Succinylcholine

Nondeoplarizers

Acetazolamide

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54
Q

What is safe to administer with a patient that has hyperkalemic periodic paralysis?

A

Glucose containing solutions

Potassium wasting diuretics

Beta-2 agonists

Nondepolarizers

Acetazolamide

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55
Q

What is Malignant Hyperthermia?

A

It is an inherited disease of skeletal muscle that is characterized by disordered calcium homeostasis.

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56
Q

What are the two classes of drugs that is know to trigger malignant hyperthermia?

A

Halogenated agents

succinylcholine

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57
Q

What is the pathophysiology of malignant hyperthermia?

A

When the T-tubule is depolarized, extracellular Ca+2 enters the myocyte via the dihydropyridine receptor.

This activates the defective ryandoine receptor (RyR1), which instructs the sarcoplasmic reticulum to release way too much calcium into the cell.

(RyR1 is like a Ca+2 faucet that can not be turned off)

Not only is there more Ca+2 to engage with the contractile elements, but the cell attempts to return the excess Ca+2 to the SR via the SERCA2 pump.

Both processes consume a substantial amount of ATP, increase O2 consumption, and increase CO2 production.

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58
Q

What are the consequences of Increased intracellular calcium in the myocyte?

A

sustained muscle contraction

accelerated metabolic rate and rapid depletion of ATP

increased O2 consumption

Increased CO2 and heat production

Mixed respiratory and lactic acidosis

Sarcolemma breaks down

Potassium and myoglobin leak into the systemic circulation

Rigidity from sustained contraction

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59
Q

What are the three co-existing diseases that MH is linked to?

A

King-Denborough syndrome

Central core disease

Multiminicore disease

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60
Q

What is Duchenne Muscular Dystrophy?

A

The patient does not code for dystrophin.

The absence of dystrophin destabilizes the sarcolemma during muscle contraction and increases membrane permeability.

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61
Q

What happens to extracellular Ca+ in Duchenne Muscular Dystrophy?

A

Extracellular Ca+2 is free to enter the cell, which can increase the rate of metabolism

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62
Q

What happens to intracellular potassium in Duchenne Muscular Dystrophy?

A

Intracellular potassium is free to exit the cell, which can result in hyperkalemic cardiac arrest.

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63
Q

What happens to myoglobin in Duchenne Muscular Dystrophy?

A

Myoglobin is free to exit the cell, which can cause renal failure.

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64
Q

An MH-like syndrome is associated with Duchenne muscular dystrophy, this is due to what?

A

It is due to rhabdomyolysis.

It is not true MH.

Dantrolene will not treat this.

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65
Q

What agents can initiate a MH-like syndrome in the patient with Duchenne Muscular Dystrophy?

A

Halogenated agents

Succinylcholine

avoid these agents

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66
Q

ANY pt with Duchenne muscular dystrophy or other muscular dystrophy who sustains a cardiac arrest on induction should be assumed to have what electrolyte abnormalitiy?

A

Hyperkalemia

Should be immediately treated with calcium chloride

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67
Q

The risk of MH is NOT increased in which disorders?

A

Becker muscular dystrophy

Neuroleptic malignant syndrome

Myotonia congentia

Myotonic dystrophy

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68
Q

What factors will increase the risk of MH?

A

Male sex

Youth

Geography - families from Wisconsin, Nebraska, West Virginia, and Michigan

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69
Q

What is the most sensitive indicator for malignant hyperthermia?

A

EtCO2 that rises out of proportion to minute ventilation

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70
Q

MH can occur how much later after exposure to a triggering agent?

A

Can occur as late as six hours after exposure to a triggering agent.

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71
Q

What are the early symptoms of MH?

A

Tachycardia

Tachypnea

Masseter spasm

Warm soda lime

Irregular heart rhythm

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72
Q

What are the intermediate symptoms of MH?

A

Cyanosis

Patient warm to touch

Irregular heart rhythm

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73
Q

What are the late symptoms of MH?

A

Muscle rigidity

Cola-colored urine

Coagulopathy

Irregular heart rhythm

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74
Q

What is trismus?

A

It is a tight jaw that can still me opened

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75
Q

What is Masseter Muscle rigidity?

A

It is a jaw that cannot be opened

If a patient has this, assume MH until proven otherwise.

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76
Q

What medications causes trismus?

A

Succinylcholine

This is a normal response, it’s okay to proceed with surgery if trismus occurs in isolation.

It’s probably wise to convert to a non-triggering agent for MH.

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77
Q

What are some conditions that should be considered in the differential diagnosis of MH?

A

Thyroid storm

Malignant neuroleptic syndrome

Sepsis

Pheochromocytoma

Serotonergic syndrome

Heat stroke

Metastatic carcinoid

Cocaine intoxication

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78
Q

Who should have a halothane contracture test?

A

Anyone who has experienced MH or masseter spasm should have the halothane contracture test for diagnosis.

Although this is the definitive test for diagnosis, it only has an 80 percent specificity, so there is a risk of a false-negative result

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79
Q

What are the two mechanisms of action for Dantrolene?

A
  1. It halts Ca+2 release from the RyR1 receptor

2. It prevents Ca+2 entry into the myocyte, which reduced the stimulus for calcium-induced calcium release

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80
Q

What is the most common side effect of Dantrolene?

A

Dantrolene is classified as a muscle relaxant.

Most common side effects are muscle weakness and venous irritation

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81
Q

Dantrolene comes in what amount per each vial?

A

Each vial contains 20mg of dantrolene + 3g of mannitol

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82
Q

How do you reconstitute dantrolene?

A

Each vial must be reconstituted with 60 mL of preservative free water.

NaCl introduces additional solute, which prolongs the time required for dantrolene to dissolve into the diluent.

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83
Q

What is the treatment for MH after stabilization?

A

After the patient is stabilized, he should be observed in the ICU. MH may reoccur up to 36 hours.

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84
Q

How do you prepare for a patient at risk for MH?

A

Prophylaxis dantrolene is unwarranted.

Flush anesthesia machine with high flow O2. About 20 to over 100 minutes depending on the model.

All external parks should be removed and replaced (Co2 absorbent, circuit, breathing bag)

Vaporizers must be physically removed from the machine.

If patient doesn’t present with s/sx of MH within the first hour of the procedure, it us unlikely that it will occur later.

Patients should be monitored for 1-4 hours in the PACU. Discharge home is ok.

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85
Q

What are the first two steps of treating MH according to Nagelhout?

A
  1. Discontinue the triggering agent (volatile agent and/or succinylcholine)
  2. Call for help, and inform the surgeon to end the procedure.
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86
Q

What is the third step in treating MH according to Nagelhout?

A

Hyperventilate with 100 percent O2 at a minimum FGF of 10L/min

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87
Q

What is the fourth step in treating MH according to Nagelhout?

A

Administer dantrolene

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88
Q

What will hyperventilating with 100 percent of O2 at a minimum FGF of 10L/min do when treating a patient with MH?

A

This facilitates CO2 elimination
It enhances O2 delivery
It drives K+ into cells

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89
Q

When should you stop dantrolene?

A

Stop dantrolene with symptoms of hypermetabolism subsides

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90
Q

What is the dose for dantrolene?

A

2.5 mg/kg IV and repeat q 5-10 min

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91
Q

How much does each vial of Ryanodex contain?

A

Each vial contains dantrolene 250mg and only requires 5mL of sterile water diluent

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92
Q

What is the fifth step in treating MH according to Nagelhout?

A

Cool the patient until temp drops below 38 degrees C

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93
Q

How can you cool the patient that is experiencing MH?

A

Cold IVF

Cold fluid lavage of stomach and bladder

Ice Packs

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94
Q

What is the sixth step for treating MH according to Nagelhout?

A

Correct Lactic acidosis

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95
Q

How do you treat lactic acidosis in a patient with active MH?

A

Sodium bicarbonate 1-2 mEq/kg IV titrated to ABG and base deficit

96
Q

What is the 7th step in treating MH according to Nagelhout?

A

Treat Hyperkalemia

97
Q

How do you treat hyperkalemia in a pt with active MH?

A

CaCl 5-10 mg/kg IV

Insulin 0.15 units/kg + D50 1mL/kg

Hyperventilation

98
Q

What is the 8th step in treating MH according to Nagelhout?

A

Protect against dysrhythmias (class I antiarrhytmics)

99
Q

What drugs can you use to protect against dyshythmias in a pt that has active MH?

A

Procainamide 15mg/kg IV

Lidocaine 2mg/kg IV

Co-administartion of a CCB with dantrolene can precipitate life-threatening hyperkalemia

100
Q

What is the 9th step in treating MH according to Nagelhout?

A

Maintain urine output >2 mL/kg/hr

101
Q

How can you maintain urine output in a patient with active MH?

A

IV hydration

Mannitol 0.25 g/kg IV

Furosemide 1 mg/kg IV

Protects against renal injury from myoglobin

102
Q

What is the last step in treating MH according to Nagelhout?

A

Disseminated intravascular coagulation is a late complication and signals impending demise

-Check coagulation panels

103
Q

What are some forms of Muscular Dystrophy?

A

Duchenne Muscular Dystrophy

Becker

Emery-Dreifuss

Facioscapulohumeral

Limb-girdle muscular dystrophy

104
Q

Duchenne muscular dystrophy is what type of genetic disorder?

A

X-linked recessive disease

Results from the absence of the dystrophin protein

105
Q

What happens in the absence of dystrophin?

A

The absence of dystophin allows extrajunctional receptors to populate the sarcolemma. It also destabilizes the sarcolemma during muscle contraction and increases membrane permeability.

This predisposes these patients to hyperkalemia following succinylcholine administration.

106
Q

What is Dysthrophin?

A

It is a critical structural component of the cytoskeleton of skeletal and cardiac muscle cells.

It helps anchor actin and myosin to the cell membrane.

107
Q

What happens when the breakdown of sarcolemma occurs in Duchenne Muscular Dystrophy?

A

This allows creatine phosphokinase and myoglobin to enter the systemic circulation.

108
Q

What happens to calcium in the pt with Duchenne Muscular Dystrophy?

A

Calcium freely ensures the cell, which activates proteases that destroy the contractile elements and causes inflammation, fibrosis, and cell death.

109
Q

Which population is Duchenne muscular dystrophy common in?

A

Males

Presents with atrophy and painless muscle degeneration.

In the first decade of life, there is a progressive deterioration of skeletal strength culminating in profound weakness.

These patients often require surgical correction of scoliosis and contractures and rarely live past 30 years.

110
Q

What are four key pathophysiologic features for Duchenne?

A

Respiratory Considerations

Cardiac Considerations

EKG Changes

Gastrointestinal Considerations

111
Q

What is the respiratory considerations for a pt with Duchenne?

A

Kyphoscoliosis (restrictive lung disease)

  • Leads to decreased pulmonary reserve
  • Leads to increased secretions and risk of penumonia

Respiratory muscle weakness

112
Q

What is the cardiac considerations for a pt with Duchenne?

A

Degeneration of cardiac muscle

-Leads to reduced contractility, papillary muscle dysfunction, mitral regurgitation, cardiomyopathy, and CHF

113
Q

What are signs of cardiomyopathy in a patient with Duchenne?

A

Tachycardia

Jugular venous distention

S3/S4 gallop

Displacement of the point of maximal impulse

114
Q

What is the gold standard to evaluate cardiac function in a pt with Duchenne?

A

Echocardiogram

115
Q

What are expected EKG changes in a patient with Duchenne?

A

Impaired cardiac conduction leads to sinus tachycardia and short PR interval

Scarring of the posterobasal aspect (back/front) of the L ventricle manifests as increased R wave amplitude in lead one, and Deep Q waves in the limb leads

116
Q

What are the expected gastrointestinal considerations for a pt with Duchenne?

A

Impaired airway reflexes and gastrointestinal hypomotility

leads to increased risk of pulmonary aspiration

117
Q

What is scoliosis?

A

Lateral and rotational curvature of the spine

118
Q

What is Kyphoscoliosis?

A

Posterior curvature of the spinal column

119
Q

What is the etiology of scoliosis?

A

Idiopathic (80 percent)

Congenital

Myopathic (muscular dystrophy and amyotonia congenita)

Neuropathic (cerebral palsy, syringomyelia, Friedreich’s ataxia)

Traumatic

120
Q

What is Cobb Angle?

A

Describes the magnitude of spinal curvature.

  • The two most displace vertebrae are identified (top and bottom)
  • A line is drawn parallel to each
  • A perpendicular line is drawn from each of these lines
  • The angle where they intersect is the Cobb Angle.
121
Q

What is the significance of a cobb angle of 40-50?

A

Indication for surgery

122
Q

What is the significance of a cobb angle of 60?

A

Decreased pulmonary reserve

123
Q

What is the significance of a cobb angle of 70?

A

Pulmonary symptoms present

124
Q

What is the significance of a cobb angle of 100?

A

Gas exchange significantly impaired

Higher risk post-op pulmonary complications

125
Q

What is the goal of spinal fusion in a pt with scoliosis

A

The goal of spinal fusion with instrumentation is to stop the progression of the curvature and prevent further deterioration of cardiopulmonary function

126
Q

What are early respiratory complications of scoliosis?

A

Restrictive ventilatory defect

  • FEV1 and FRC are decreased
  • FEV1/FVC ratio is normal

Decreased lung volumes

  • VC
  • TLC
  • RV
  • FRC

Decreased chest wall compliance

127
Q

What are late respiratory complications of scoliosis?

A

V/Q mismatching

Hypoxemia

Hypercarbia (sign of impending failure)

Pulm HTN

Reduced response to hypercarpnia

Cor pulmonale

Cardiorespiratory failure

128
Q

What are some cardiac complications in a pt with scoliosis?

A

RV hypertrophy

Mitral valve prolapse (most common)

Mitral regurgitation

coarctation of the aorta

129
Q

How does RV hypertrophy develop in a pt with scoliosis?

A

As a result of increased pulmonary vascular resistance.

EKG may reveal RV strain and right arterial enlargement

130
Q

What are the airway complications of a pt in the prone position that has scoliosis?

A

Upper airway edema - consider leak test

Ett kick or inadvertent extubation

131
Q

What are the neck complications of a pt in the prone position that has scoliosis?

A

Neck rotation

Leads to vertebral compression

Leads to cerebral hypoperfusion

132
Q

What are eye complications of a pt in the prone position that has scoliosis?

A

Ischemic optic neuropathy d/t hypoperfusion and/or increased venous pressure

Corneal abrasion

133
Q

What are the upper extremities complications of a pt in the prone position that has scoliosis?

A

Brachial plexus injury

Ulnar n. injury

134
Q

What are the lower extremities complications of a pt in the prone position that has scoliosis?

A

Pressure on iliac crest
-Leads to lateral femoral cutaneous n. injury

Pressure lateral to fibula
-Leads to peroneal n. injury

Hip flexion
-Leads to femoral vein occlusion, DVT

135
Q

What are the abdomen complications of a pt in the prone position that has scoliosis?

A

Increased abdominal pressure

  • Transmitted to veins that drain the spine which leads to back bleeding (no valves)
  • Reduced pulmonary compliance (Jackson frame is better than Wilson frame)
136
Q

How can you assess the respiratory respiratory reserve in a pt with scoliosis?

A

Exercise tolerance

ABG

Vital capacity

VC < 40% predicted correlates w/ requirement for post-op ventilation.

137
Q

Thoracic correction higher than what level might need one lung ventilation for a pt with scoliosis?

A

T8

Use a double lumen tube or bronchial blocker

138
Q

How will you observe a venous air embolism in a pt with scoliosis?

A

VAE is observed as a reduction in EtCO2 (increased PaCO2 - EtCO2 gradient).

A central line aids in aspiration of entrained air.

VAE increases dead space.

139
Q

What would nitrous oxide increase if you use it for a pt with scoliosis?

A

Increases PVR.

May already have cor pulmonale

140
Q

How can you prepare for significant blood loss in a pt undergoing corrective scoliosis?

A

IV access

Type and Crossmatch

Autologous donation

Cell saver

141
Q

What risks are associated with deliberate hypotension in a pt undergoing corrective scoliosis?

A

Deliberate hypotension to maintain MAP 60 mmHg carries the risk of cerebral hypoperfusion and ischemic optic neuropathy.

Monitor end organ perfusion with serial ABG (metabolic acidosis) and urine output.

142
Q

What is the wake-up test?

A

It is a method of assessing neurologic integrity during complex spine surgery.

Neurologic injury (paraplegia) is a feared complication of spine surgery.

143
Q

How is the wake-up test performed?

A

The anesthetic agents are turned off, and the patient is allowed to awaken.

Next, the pt is asked to move both hands and feet.

Once neurologic integrity is assured, the patient is re-anesthetized until the conclusion of surgery.

144
Q

What happens if the pt is unresponsive during a wake-up test?

A

You can wait longer or reverse reversible agents (NMB, opioids, benzos)

145
Q

What would happen if the pt can move his hands but but their feet during a wake-up test?

A

The surgeon should reduce distraction on the spinal rods.

146
Q

What are the risks of the wake-up test?

A

Tracheal extubation

Removal of intravenous or arterial lines

Air embolism

Awareness

Pain

Damage to surgical instrumentation

147
Q

What part of the spinal cord does SSEP monitor?

A

Posterior cord (dorsal column pathway)

148
Q

What arteries is SSEP associated with?

A

Posterior spinal arteries

149
Q

Does NMB interfere with SSEP?

A

No

SSEP monitors sensory, NOT motor function

150
Q

What does SSEP stand for?

A

Somatosensory Evoked Potentials

151
Q

What part of the cord does MEP monitor?

A

Anterior cord

152
Q

What arteries is MEP associated with?

A

Anterior spinal artery

153
Q

Can you use NMB with MEP?

A

DO NOT use NMB with MEP, it monitors motor function.

154
Q

What three places does Rheumatoid arthritis affect?

A

Temporomandibular joint — Limited mouth opening

Crioarytenoid joints — Decreased diameter of glottic opening

Cervical spine — Atlanto-occipital subluxation with flexion — Limited exrension

155
Q

What part of the TMJ limits the mouth opening in a pt with Rheumatoid arthritis?

A

Synovitis of the TMJ can limit mouth opening.

Temporomandibular Joint

156
Q

How does crioarytenoid arthritis present clinically?

A

Hoarseness

Stridor

Dyspnea

May result in airway obstruction

Edema or erythema of the vocal cords can suggest this as well.

157
Q

What do you have to be considered with in a pt with rheumatoid arthritis and the cricoarytenoid joint?

A

It reduces the diameter of the glottic opening.

May increase difficulty of passing the ET tube past the vocal cords.

Use a smaller ET tube to minimize laryngeal trauma.

Pt at risk for postextubation airway obstruction.

158
Q

What is the most common airway complication of RA?

A

Altlantoaxial subluxaition and separation of the atlanto-odontoid articultion.

159
Q

What causes atlantoaxial subluxation and separation of the athlanto-odontoid articulation?

A

Cause by the weakening of the transverse axial ligament, which allows the odontoid to directly compress the spinal cord at the level of the foramen magnum.

The patient is at risk for quadriparesis or paralysis

160
Q

How is altantoaxial subluxation diagnosed?

A

A lateral x-ray of the cervical spine.

Confirming the distance between the anterior arch of the atlas and the onontoid process is greater than 3 mm.

161
Q

Where else can subaxial subluxation occur besides C1-C2 in a pt with RA?

A

Most commonly in C5-6.

Neck motion can cause spinal cord injury.

162
Q

What does surgical correction entail for a patient with altantoaxial subluxation?

A

Odontoid decompression and posterior cervical fusion

163
Q

Is thoracolumbar spine affected by RA?

A

It is not generally affected

164
Q

What is the pathophysiology of RA?

A

Autoimmune disease that targets the synovial joints.

There is also widespread systemic involvement due to infiltration of immune complexes into the small and medium arteries leading to vasculitis.

Cytokines (TNF and interleukin-1) also play a central role in the pathogenesis of RA.

165
Q

What is the hallmark sign of RA?

A

Morning stiffness that generally improves with activity.

Joints are painful, swollen, and warm.

Other symptoms include weakness, fatigue, and anorexia.

166
Q

What areas can you see enlarge lymph nodes for a pt with RA?

A

Cervical

Axillary

Epitrochlear regions

167
Q

How much more common is RA seen in women?

A

2-3 x more in women

168
Q

What are the pulmonary complications in a pt with RA?

A

Pleural effusion

Restrictive ventilatory pattern

  • Diffuse interstitial fibrosis
  • Costochondral involvement limits chest wall expansion
169
Q

What are the cardiac complications in a pt with RA?

A

Pericardial effusion or tamponade

Restrictive pericarditis

Aortic regurgitation

Valvular fibrosis

Coronary artery arteritis

170
Q

What are the hematologic complications in a pt with RA?

A

Anemia

Platelet dysfunction secondary to NSAIDs

171
Q

What are the Renal complications in a pt with RA?

A

Renal insufficiency due to

  • Vasculitis
  • NSAIDs
172
Q

What are the endocrine complications in a pt with RA?

A

Adrenal insufficiency and infections due to:

-Steroids

173
Q

What are the GI complications in a pt with RA?

A

Gastric ulceration due to

  • NSAIDs
  • Steroids
174
Q

What are the eye complications in a pt with RA?

A

Sjogren’s syndrome

-risk of corneal abrasion

175
Q

What are the nervous system complications in a pt with RA?

A

Peripheral neuropathy due to

-Nerve entrapment

176
Q

What Labs will be increased for a pt that has RA?

A

Rheumatoid factor is an anti-immunoglobin antibody that is increased in 90 precent of patients with RA

C-reactive protein is increased

Erythrocyte sedimentation rate is increased

177
Q

What is the medical management for a pt with RA?

A

Aims at reducing inflammation w/

Antirheumatics
glucocorticoids
NSAIDs

178
Q

What is the relationship between cylcosprine and succinylcholine?

A

Cyclosporine prolongs the duration of succinylcholine

179
Q

What are some complications of methotrexate?

A

Causes liver dysfunction

Suppresses the bone marrow

180
Q

What are some examples of Disease-Modifying Antrirheumatic Drugs?

A

Methotrexate

Cyclosporine

Etanercept

181
Q

How does Disease-Modifying Antirheumatic drugs improve symptoms?

A

They inhibit tumor necrosis factor (TNF), interleukin-1 and -6, and inhibit T cells and B lymphocytes.

All these drugs suppress the immune system and increase risk of infection and cancer.

182
Q

What is Lupus?

A

It is an autoimmune disease characterized by the proliferation of antinuclear antibodies.

It affects nearly every organ system.

Most of the consequences are the direct result of antibody induced vasculitis and tissue destruction.

183
Q

Which sex does SLE target?

A

SLE is a disease that targets young women (~ 1:1000)

184
Q

What are the most common problems with SLE?

A

Polarthritis

Dermatitis

Arthritis can affect any joint, but it generally does not involve the spine.

185
Q

What percent of pts develop a malar butterfly rash?

A

33-50 percent

186
Q

What are the airway complications of SLE?

A

Crioarytenoiditis Leads to hoarseness, stridor, and airway obstruction

Recurrent laryngeal nerve palsy

187
Q

What are the pulmonary complications of SLE?

A

Restrictive ventilatory defect

Pulm HTN

Interstitial lung disease w/ impaired diffusing capacity

Pleural effusion

Recurrent PE

188
Q

What are the cardiovascular complications of SLE?

A

Pericarditis (tamponade is uncommon)

Raynaud’s phenomenon

Hypertension

Conduction defects

Endocarditis

189
Q

What are the hematologic complications of SLE?

A

Antiphospholipid antibodies

Hypercoagulability

Anemia

Thrombocytopenia

Leukopenia

190
Q

What are the renal complications of SLE?

A

Nephritis with proteinuria

191
Q

What are the nervous system complications of SLE?

A

Stroke

Psychosis/dementia

Peripheral neuropathy

192
Q

Drug induced Lupus generally persists for several weeks to months and presents with?

A

Mild symptoms of arthralgia

Anemia

Leukopenia

Fever

193
Q

Most common stress or drugs exposure that cause exacerbation of SLE?

A

Pregnancy

Infection

Surgery

Stress

Enalapril

D-penicillamine

Captopril

Hydralazine

Isoniazid

Methyldopa

Procainamide

194
Q

What it is the medical treatment for Lupus?

A

Aims to support the immune system and reduce the inflammatory response.

Corticosteroids
NSAIDs
Immunosppressants
Antimalarials

195
Q

What are some examples of immunosuppressants for treating Lupus?

A

Cylcophosphamide

Azathioprine

Methorexate

Mycophenolate mofetil

196
Q

What are some examples of antimalarials?

A

Hyrdroxychlororquine

Quinacrine

197
Q

What can cricoarytenoid arthritis may present clinically as?

A

Hoarseness

stridor

airway obstruction

198
Q

Lupus pts will have a prolonged aPTT, this makes them prone to?

A

State of hypercoagulability and thrombosis.

Risk for stroke, DVT, and PE.

Antiphospholipid antibodies may delvelop.

199
Q

What does cylophosphamide do to plasma cholinesterase and succinylcholine?

A

Inhibit plasma cholinesterase

Increase duration of succinycholine

200
Q

What is Marfan Syndrome?

A

It is a connective tissue disorder with autosomal dominant inheritance (think aortic insufficiency and AAA)

201
Q

What is the classic problem with Marfan syndrome?

A

A dilated aortic root that sets the stage for aortic insufficiency and aortic dissection (minimize wall stress with beta blockers)

202
Q

What are some clinical presentations of Marfan Sydrome?

A

Often tall with pectus excavatum (sunken chest)

Kyphoscoliosis

Hyperflexiable joints (careful with position)

203
Q

What are some risks with Marfan syndrome?

A

Abdominal aortic aneurysm

Cardiac tamponade (if aortic dissection)

Mitral prolapse

Spontaneous pneumothorax (careful with PIP)

204
Q

What is Ehlers-Danlos Syndrome?

A

It is an inherited disorder of procollagen and collagen (think spontaneous bleeding into joints and AAA)

205
Q

What is the classic problem with Ehlers-Danlos?

A

Arterial aneurysm and increased bleeding tendency.

Bleeding is the result of poor vessel integrity (not coagulopathy).

206
Q

What type of anesthesia should you avoid in Ehlers-Danlos?

A

Regional anesthesia and IM injections due to bleeding risk.

Excessive bleeding can also occur during invasive line placement or trauma during airway management.

207
Q

What is a common complication of Ehlers-Danlos syndrome?

A

Pneumothroax

208
Q

What is Osteogensis Imperfecta?

A

A connective tissue disorder with autosomal dominant inheritance (think weak bones)

209
Q

What is the classic problem with Osteogensis Imperfecta?

A

Brittle bones (careful w/ position)

Fractures can occur during NIBP inflation of following fasciculations caused by succinylcholine.

Careful with airway manamegent (risk for c-spine and reduced cervical ROM)

210
Q

Which disease can you find blue sclera?

A

Osteogenesis imperfecta.

The sclera is susceptible to fracture.

211
Q

Is the risk for MH increased in a pt with Osteogensis Imperfecta?

A

The risk for MH is NOT increased.

212
Q

What will you see in thyroxine levels in a patient with osteogensis imperfecta?

A

Serum thyroxine is increased in > 50 percent of patients

Increased BMR and VO2
Leads to hyperthermia

213
Q

What leads to reduced chest wall compliance and vital capacity in a pt with osteogensis imperfecta?

A

Kyphoscholiosis and pectus excavatum reduce chest wall compliance and vital capacity

Leads to V/Q mismatch

Leads to Arterial hypoxemia

214
Q

What is multiple Sclerosis?

A

It is a demyelinating disease of CNS

215
Q

Which medication can cause life-threatening hyperkalemia in a patient with MS?

A

Succinylcholine

216
Q

What two things can exacerbate s/sx of Multiple Sclerosis?

A

Stress

Increased body temperature (as small as 1 degree C)

217
Q

What drugs do you use to treat a pt with multiple Sclerosis?

A

Corticosteroids

Interferon

Azathioprine

218
Q

What dysfunction causes an aspiration risk for for pts with multiple sclerosis?

A

Cranial nerve involvement causes bulbar muscle dysfunction

219
Q

What is Myotonic Dystrophy?

A

It is characterized by prolonged contracture after a voluntary contraction.

This is the result of dysfunctional calcium sequestration by the sarcoplasmic reticulum.

Contractions can be so severe that they interfere with ventilation and intubation.

220
Q

What are three things that increase the risk of contractures in a pt with Myotonic Dystrophy?

A

Succinylcholine (use a nondepolarizer instead)

NMB reversal with anticholinesterases (theoretical concern - consider sugammadex)

Hypothermia (shivering leads to sustained contractions)

221
Q

Patients with myotonic dystrophy are also at risk for?

A

Aspiration

Respiratory muscle weakness

Cardiomyopathy and dysrhythmias

Sensitivity to anesthetic agents

222
Q

Are pts with myotonic dystrophy at risk for MH with halogenated anesthetic?

A

They may safely receive halogenated anesthetic, it does not put them at risk for MH.

223
Q

What Scleroderma cause?

A

Sclerodema causes fibrosis in the skin and organs, particularly in the microvasculature

224
Q

What is CREST syndrome?

A

A type of scleroderma.

Clacinosis
Raynaud's phenomenon
Esophageal hypomotility
Slerodactyly
Telangiectasia
225
Q

What is troublesome with Telangiectasias and a pt w/ scleroderma?

A

Telangiectasias (spider veins) increase the risk of mucosal bleeding, and this can become problematic during airway manipulation (particularly during nasal intubation).

Patients with scleroderma often has limited mouth opening, which may necessitate nasal fiberoptic intubation.

226
Q

What happens with the airway in a pt with Scleroderma?

A

Skin fibrosis

Leads to limited mouth opening and mandibular mobility

227
Q

What happens with the lungs in a pt with Scleroderma?

A

Pulmonary fibrosis

Pulm HTN

228
Q

What happens with the heart in a pt with Scleroderma?

A

Dysrhythmias

CHF

229
Q

What happens with the blood vessels in a pt with Scleroderma?

A

Decreased compliance

Leads to HTN

230
Q

What happens with the kidneys in a pt with Scleroderma?

A

Renal failure and renal artery stenosis

Leads to HTN

231
Q

What happens with the peripheral and cranial nerves in a pt with Scleroderma?

A

Nerve entrapment by tight connective tissue

Leads to neuropathy

232
Q

What happens with the eyes in a pt with Scleroderma?

A

Dryness predisposes to corneal abrasion

233
Q

What is Paget’s Disease associated with?

A

Excessive osteobalstic and osteolastic activity that causes abnormally thick, but weak, bone deposits.

234
Q

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

A

Pain

Fractures

Peripheral nerve entrapment can occur.

235
Q

What causes Paget’s disease?

A

Excessive parathroid hormone

or

Calcitonin deficiency

236
Q

Is there any vascular involvement with paget’s disease?

A

No vascular involvement

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