Musculoskeletal Anesthesia Considerations
Nerve to Muscle Interaction (sequence of actions)
Spinal Cord
Motor Nerve Axon
Synaptic Cleft
NMJ
Muscle Unit
Muscle Fibers
Muscle Cell
Mechanism of muscle contraction:
As the action potential approaches the motor nerve ending, calcium ions (Ca2+) influx into the nerve terminal, resulting in Ach being released into the synaptic cleft.
The release of Ach prompts the release of Ca2+ in the muscle fibers, leading to muscle fiber shortening and thus contraction.
Following this, Ach undergoes hydrolysis, Ca2+ is pumped back into the muscle fiber, allowing the muscle to relax.
Muscle Cell Physiology
Typical ion distribution:
Potassium ions (K+) predominantly inside the cell, Sodium ions (Na+) predominantly outside.
During contraction (CTX):
Outflow of K+ and inflow of Na+.
Myasthenia Gravis
Myasthenia Gravis (MG) is a heterogenous autoimmune disorder characterized by chronic dysfunction at the neuromuscular junction (NMJ) and altered function of the thymus gland.
Risk Factors
Predominantly affects individuals under 50 years old, with a higher incidence in women
Older adults affected equally
Abrupt onset
Characterized by periods of exacerbation and remission
Symptoms (Sx)
Muscle weakness that worsens with activity and does not fully resolve with rest
Fatigue
Ptosis (drooping of eyelids) and Diplopia (double vision)
Dysphagia (difficulty swallowing)
Treatment (Tx)
Cholinesterase Inhibitors (e.g., Pyridostigmine)
Mechanism: Inhibits hydrolysis of Ach, increasing its availability at the NMJ.
Corticosteroids to reduce inflammation and immune response.
IVIg for immune modulation.
Thymectomy (surgical removal of the thymus gland)
Emergent Situations
Myasthenic Crisis: A condition resulting from inadequate Ach leading to exacerbation of MG and resultant profound muscle weakness.
Cholinergic Crisis: A condition caused by overdose of medications leading to excess Ach which causes a depolarizing block and profound muscle weakness.
Anesthesia Considerations for MG
Mild Disease
Elective procedures should be performed when patients are stable and on minimal medications.
Cholinesterase Inhibitors should be withheld as they can cause a vagal response during intubation.
Severe Disease
Only proceed with urgent or emergent cases
Cholinesterase Inhibitors taken up to the morning of surgery
General Guidelines:
Increased risk of aspiration
Preferential use of Regional or Local Anesthesia due to:
Improvement of post-operative analgesia and respiratory function
Elimination of the need for peri-operative neuromuscular blockade
Amide local anesthetics preferred over esters
Earlier neuraxial anesthesia is recommended for laboring patients to mitigate risks associated with fatigue/weakness/stress
Avoid pre-operative sedation and opioid usage to minimize risks.
Use of Laryngeal Mask Airway (LMA) is advisable to reduce the requirement for muscle relaxants.
Reversal of neuromuscular blockade may precipitate a cholinergic crisis.
Extubation Criteria:
Complete and sustained return of muscle strength
Intact upper airway reflexes
Resumption of spontaneous ventilation
Tracheal intubation with ventilatory support may be necessary in the post-procedural phase.
Predictor Factors for Difficulties:
Body Mass Index (BMI) > 28
Duration of surgery > 2-6 hours (or years of age?)
Pyridostigmine dose > 750 mg/day
Malignant Hyperthermia
Definition
A hypermetabolic disorder of skeletal muscle, primarily inherited in an autosomal dominant pattern.
Commonly triggered by inhaled volatile anesthetics and succinylcholine used during anesthesia. Other rarer triggers include:
Stress
Vigorous exercise
Heat
Risk Factors
Individuals <15 years old
Male population
Symptoms (Sx)
Sustained muscle contractions (e.g., jaw clenching)
fever
Tachycardia
Tachypnea
Skin mottling
Hyperkalemia
Dysrhythmias
Treatment (Tx)
Discontinue inhaled anesthesia and succinylcholine immediately
Administer Dantrolene Sodium intravenously for a minimum of 24 hours
Use cooling blankets to manage body temperature
Provide hyperventilation with 100% O2 at a rate of 10L/min
Emergent Situations: The condition can rapidly progress to muscle cell destruction and lead to excessive hyperkalemia, resulting in life-threatening cardiac arrest.
Prophylaxis
Inquire about family history of malignant hyperthermia.
Avoid the use of volatile inhaled anesthetics and succinylcholine.
Utilize cooling blankets to prevent hyperthermia.
Monitor core body temperature vigilantly.
Ensure Dantrolene Sodium is readily available in the clinical setting.