Transcript Dose - Calgary Emergency Medicine

Procedural
Sedation
Devin Herbert
Jan 24/13
Thank you’s
Drs. Simon Bartley
Rob Lafreniere
Rick Morris
Matt Erskine
Jamie McLellan
Objectives
Definition of procedural sedation
Why sedate in the ED?
Guidelines
Comparison with Calgary
Medications
Tips and tricks
Procedural sedation definition
Procedural sedation (PSA) is the
administration of sedatives or dissociative
anesthetics to induce a depressed level of
consciousness while maintaining
cardiorespiratory function so that a medical
procedure can be performed with little or no
patient reaction or memory.
Levels of sedation
Minimal sedation - Normal response to verbal stimuli.
Moderate sedation - Purposeful response to verbal or tactile
stimulation. Airway, ventilation and cardiovascular function
adequate.
Dissociative sedation - Ketamine induced analgesia, sedation
and amnesia with relatively preserved airway reflexes and
ventilatory drive.
Deep sedation - Purposeful response after painful stimuli. May
require airway intervention and have inadequate ventilation.
General anesthesia - Unarousable to pain. Often require
airway intervention. Ventilation is frequently inadequate and
cardiovascular function may be impaired.
Why do PSA in the ED?
1. Many patients undergo painful, non-elective procedures in the ED.
2. These procedures are generally brief, with the painful component
lasting seconds to minutes, making them ill-suited to the operating
room.
3. Most ED procedures can be abandoned immediately if patient
deterioration occurs.
4. The following skills, intrinsic to safe outpatient analgesia and
sedation, are core skills for emergency medicine practitioners:
a. the ability to monitor respiratory and cardiovascular status,
b. resuscitation skills, and the ability to deal with airway compromise,
hypoventilation, and circulatory impairment.
c. intimate knowledge of, and experience with major tranquilizers,
sedative-hypnotics, opioids, and reversal agents.
d. varying degrees of experience in providing procedural sedation for
their patients.
Pre-sedation preparation and fasting.
Physician skill set, personnel and equipment.
Clinical and technological monitoring.
Documentation and post-sedation care.
General principles
Consider regional anesthesia or the OR.
Sedation and analgesia are distinct processes.
Determine a goal depth of sedation.
“Titrate, don’t calculate”.
Avoid general anesthesia.
Pre-sedation history
Consent
Past medical history
Medications - including in the ED
Allergies
Prior anesthetic/sedation history
Last oral intake
Showed no harm in patients with simple egg allergy.
Rare case reports of immediate allergic reactions, although
only in patients with complicated allergy histories.
Continue to recommend avoidance in true egg anaphylaxis.
Pre-sedation history
Consent
Past medical history
Medications - including in the ED
Allergies
Prior anesthetic/sedation history
Last oral intake
One reported case of aspiration in 4657 adult and
17672 pediatric patients.
Overall, no evidence to recommend routine fasting.
Some patients may require individualized risk vs.
benefit assessment.
Pre-sedation physical exam
Vital signs
Airway assessment - ie. BOOTS, MMAP
Cardiorespiratory exam
Level of consciousness
Personnel and equipment
Physician with airway management, life support
skills and pharmacology knowledge.
Additional patient observer, such as an additional
physician, nurse or RT.
Monitored bed, with pulse oximeter and blood
pressure machine.
Bedside oxygen, suction, OPA and BVM.
Readily available cardiac monitor, airway cart and
crash cart.
Monitoring
Proportional to the level of sedation.
Routine vital signs and clinical observation.
Sedation to depth of eye closure requires
pulse oximeter with audible beeps.
Consider supplemental oxygen.
Procedural sedation record is recommended,
including vital signs, drug doses and timing
and complications.
Capnography predicted all hypoxemic events, with an
average difference of 60sec.
NNT=6
False positive rate of 27%
Capnography provides an early warning of respiratory
depression, which could lead to hypoxia.
Pro
Con
Provides earliest possible
evidence of respiratory
depression, decreases
hypoxemia and therefore
increases safety.
Adverse “events” are
largely transient
hypoxemia, not clinical
outcomes.
High false positive rate.
Post-sedation care
Observe patients until cardiorespiratory
function and level of consciousness are
normal.
Patients should be able to sit, drink and
understand the discharge instructions.
If reversal agents are used, patients should be
observed for two hours.
Fentanyl
Super potent synthetic opioid agonist,
increases pain threshold and inhibits
ascending pain pathways.
Dose: 0.5-2mcg/kg IV
Onset: immediate
Duration: 30-60min
Less histamine release = less hypotension.
Propofol
GABA receptor agonist, with some NMDA
receptor antagonism, resulting in sedation and
amnesia.
Dose: 0.5mg/kg IV bolus, then 0.25mg/kg
q45sec
Onset: 30sec
Duration: 3-10min (dose dependent)
Risk of respiratory depression and hypotension.
Ketamine
NMDA receptor antagonist, resulting in
dissociative analgesia, sedation and amnesia.
Dose: 0.25-1mg/kg IV or 2-4mg/kg IM
Onset: 30sec IV or 3-4min IM
Duration: 5-10min IV or 12-25min IM
Risk of hypersalivation, emergence reactions
and laryngospasm.
8282 Ketamine sedations with 22 cases of
laryngospasm.
No association with age or any clinical factors.
Likely an idiosyncratic reaction.
No role for co-administration of anticholinergic drugs.
Ketofol
Classically, a 1:1 mixture of Ketamine and
Propofol (both 10mg/ml) in a single syringe.
Dose: 0.5mg/kg IV bolus, then 0.25mg/kg IV
q1min
Onset: 30sec
Duration: 5-10min
Purported benefit is hemodynamic stability
and reduced respiratory depression.
RCT comparing single-syringe Ketofol to Propofol alone.
Primary outcome was respiratory depression.
No difference between groups.
Ketofol may be “smoother”.
RCT comparing a Ketamine bolus, followed by Propofol
thereafter, to Propofol alone.
No difference in major outcomes.
Trend towards “smoother” sedation with combo.
Midazolam
Binds postsynaptic GABA receptors,
hyperpolarizing neurons, reducing excitability.
Dose: 0.02-0.04mg/kg IV q5min
Onset: 3-5min
Duration: <2hrs
Risk of delayed and prolonged sedation.
Nitrous oxide
NMDA antagonist, with various other ion
channel and receptor effects.
Dose: typically 1:1 mix with oxygen (Entonox)
Onset: immediate
Duration: <3min
Provides mild anxiolysis and analgesia.
Etomidate
Ultrashort-acting non-barbituate hypnotic.
Dose: 0.1-0.2mg/kg IV, then 0.05mg/kg IV
q3-5min
Onset: 30-60sec
Duration: 3-5min
Myoclonus seen in ~20% of patients and risk
of adrenal suppression.
Dexmedetomidine
Short acting alpha-2 agonist.
Dose: 1ug/kg IV over 10min, then infusion
Potential role in patients with high
sympathetic tone.
Naloxone
Pure opioid antagonist, displaces opioid from
receptors.
Dose: 0.04-0.4mg IV q2-3min
Onset: ~2min
Duration: 30-120min
Beware in chronic opiate users.
Flumazenil
Competitive antagonist at GABA receptors.
Dose: 0.2mg IV q1min, to max of 1mg
Onset: 1-3min
Duration: ~1hr
Really beware in chronic EtOH or BDZ users.
Sedate like a wizard
Take note of the drugs given by EMS and in
the ED.
Consider 1ml of 1% Lidocaine IV prior to
Propofol.
If hypoventilation, give stimulation.
“When did you join the secret service”?
Consider low dose Ketamine +/- Midazolam
for non-emergent chest tubes, CVC’s, LP’s.
Summary
PSA vs. regional anesthesia vs. OR
Pre-medications given?
“Titrate, don’t calculate”
Build a toolbox of key drugs
“If hypoventilation, give stimulation”
Should we adopt a new monitoring standard
of practice in Calgary?