Orthopaedic Analgesia
PHARMACOLOGY: CLASSES OF DRUGS
Local anesthetics
Vasoconstrictors
Opioids
Sedatives (benzodiazepines)
Others
LOCAL ANESTHETICS
Basic function
These drugs act by blocking voltage-gated sodium channels in axons, preventing action potential.
Local effect
Block is most effective in smaller, myelinated fibers that fire at high frequency.
Pain and temperature fibers are much more sensitive than pressure fibers, which are more sensitive than motor and proprioceptive fibers.
Toxicity
Central nervous system (CNS)
Results from intravenous absorption or injection and high plasma levels.
They block inhibitory pathways, leading to unopposed excitatory components.
Signs and symptoms include dizziness, tongue numbness, nystagmus, and seizures (tonic-clonic).
Cardiovascular-depressive effects
Weaker contraction and arteriolar dilatation occur.
High doses can result in ventricular fibrillation, which is difficult to treat. Twenty percent intralipid is now being used as an agent to reverse significant cardiac toxicity.
Neurotoxicity
In high concentrations, they can directly damage peripheral nerve fibers.
Lidocaine: rapid, potent, high penetration
Short acting
Most widely used local anesthetic: local anesthesia, regional, spinal, epidural
Bupivacaine: slower, potent
Longer lasting than lidocaine
Can separate motor and sensory block by altering concentration
Increased cardiac toxicity possibly
Ropivacaine
“Safer” version of bupivacaine with same analgesic characteristics considered to be associated with a lower incidence of significant cardiac toxicity
Maximal dose of commonly used local anesthetics
Lidocaine: 5 mg/kg (7 mg/kg if combined with epinephrine)
Calculation example:
Percent concentration × 10 = mg/mL of drug
1% lidocaine = 10 mg/mL of lidocaine
30-kg child, 1% lidocaine without epinephrine 10 mg/mL of lidocaine
5 mg/kg × 30 kg = 150 mg allowed
150 mg/10 mg/mL = 15 mL of 1% lidocaine
Bupivacaine: 1.5 mg/kg (3 mg/kg with epinephrine)
VASOCONSTRICTORS
Allow for longer lasting blockade (decreased blood flow, less drug leaves area).
They may also decrease local blood loss.
Epinephrine
Most widely used, diluted to 1/200,000
Should not be used for a digital block, Bier block, or ankle block
Mnemonic for areas not to use epinephrine: nose, hose (penis), fingers, toes
Phenylephrine is occasionally used in spinal anesthesia.
OPIOIDS
They are derived from the seed of the opium poppy, Papaver somniferum.
Morphine and codeine are directly from the plant; others are synthesized.
They act by binding to specific opioid receptors in the CNS (µ, σ, κ).
Th µ receptor is the one most responsible for the analgesic eff ect.
The action is both presynaptic and postsynaptic.
Central action/pain modulation
When activated, the µ receptor inhibits γ-aminobutyric acid (GABA)-ergic neurons that would otherwise inhibit pain inhibitory neurons.
They may also affect neurons in the thalamus and midbrain to modulate pain stimuli.
CNS effects
Analgesia, euphoria, sedation, respiratory depression, cough suppression, miosis, nausea
Peripheral effects
Cardiovascular: bradycardia
Gastrointestinal: decreased motility, constipation, constriction of biliary tree
Genitourinary: decreased renal function and increased sphincter tone
Morphine
Naturally occurring, oldest member of this drug class
Dosing for adults
Loading dose of 0.05 to 0.10 mg/kg intravenously (IV) followed by 0.8 to 10.0 mg/hour IV titrated to pain
Onset: 5 minutes
Relatively long lasting: 3 to 4 hours
Better for continuous dull pain rather than sharp/severe pain
Used for postoperative patient-controlled analgesia (PCA) 1-mg increments with a lockout of 6 to 10 minutes. Basal rates tend to increase episodes of hypoxia.
Meperidine (Demerol)
Most common emergency department narcotic
One-tenth as potent as morphine
Dosing for adults
Fifteen to 35 mg/hour slow IV infusion or 50 to 150 mg subcutaneously/intramuscularly every 3 to 4 hours as needed
Poorly titrated: 5- to 10-minute onset and 2- to 3-hour duration
Potential for CNS stimulation
Less commonly used for pain than in the past
Concern about bad interactions with monoamine oxidase inhibitors (MAOIs)
Fentanyl
100 × more potent and 7,000 × more lipophilic than morphine
Rapid uptake: 30 to 60 seconds with peak analgesia in 2 to 3 minutes
Duration: 20 to 30 minutes
Dose: 1 µg/kg slowly, with sedation often at 3 to 4 µg/kg
Risks: “tight chest syndrome,” bradycardia, respiratory depression
Naloxone, naltrexone (Narcan)
SEDATIVES
Benzodiazepines
In general, they produce anxiolysis and sedation and encourage sleep.
They are metabolized in the liver and excreted in the urine.
Mechanism
They act centrally, bind to, and activate the GABA-A receptor.
GABA is major inhibitory neurotransmitter in the CNS.
The GABA receptor is the chloride channel.
When activated, they hyperpolarize the membrane, making it less excitable.
Effects
Sedation, hypnosis, anesthesia, amnesia (anterograde), anticonvulsant effects, muscle relaxation, respiratory depression (especially in pulmonary patients)
Often increased when combined with opioids
Midazolam
Peak effect: 2 to 3 minutes
Water soluble, hepatic metabolization
Easily titrated with doses every 5 to 7 minutes
1 to 2 mg per dose (0.1 mg/kg/dose in children)
Flumazenil
Blocks the effect of benzodiazepines at the GABA receptor level.
It has a much shorter half-life than most benzodiazepines that are used clinically.
The dose is 0.1 to 0.2 mg IV (0.02 mg/kg in children).
Use with caution because it may precipitate seizures.
Ketamine
Dissociative anesthetic
Catatonic, amnestic, without loss of consciousness or loss of protective reflexes
Blockade of glutamic acid at the NRelated posts:
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