Procedural Sedation

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Procedural Sedation Devin Herbert Jan 24/13
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Thank yous Drs. Simon Bartley Rob
Lafreniere Rick Morris Matt Erskine Jamie McLellan
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Objectives Definition of procedural sedation Why
sedate in the ED? Guidelines Comparison with
Calgary Medications Tips and tricks
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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.
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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.
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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.
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Pre-sedation preparation and fasting. Physician
skill set, personnel and equipment. Clinical and
technological monitoring. Documentation and
post-sedation care.
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General principles Consider regional anesthesia
or the OR. Sedation and analgesia are distinct
processes. Determine a goal depth of
sedation. Titrate, dont calculate. Avoid
general anesthesia.
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Pre-sedation history Consent Past medical
history Medications - including in the
ED Allergies Prior anesthetic/sedation
history Last oral intake
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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.
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Pre-sedation history Consent Past medical
history Medications - including in the
ED Allergies Prior anesthetic/sedation
history Last oral intake
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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.
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Pre-sedation physical exam Vital signs Airway
assessment - ie. BOOTS, MMAP Cardiorespiratory
exam Level of consciousness
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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.
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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.
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Capnography predicted all hypoxemic events, with
an average difference of 60sec. NNT6 False
positive rate of 27
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Capnography provides an early warning of
respiratory depression, which could lead to
hypoxia.
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Pro Provides earliest possible evidence of
respiratory depression, decreases hypoxemia and
therefore increases safety.
Con Adverse events are largely transient
hypoxemia, not clinical outcomes. High false
positive rate.
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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.
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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.
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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.
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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.
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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.
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Ketofol Classically, a 11 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.
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RCT comparing single-syringe Ketofol to Propofol
alone. Primary outcome was respiratory
depression. No difference between groups. Ketofol
may be smoother.
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RCT comparing a Ketamine bolus, followed by
Propofol thereafter, to Propofol alone. No
difference in major outcomes. Trend towards
smoother sedation with combo.
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Midazolam Binds postsynaptic GABA receptors,
hyperpolarizing neurons, reducing
excitability. Dose 0.02-0.04mg/kg IV
q5min Onset 3-5min Duration lt2hrs Risk of
delayed and prolonged sedation.
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Nitrous oxide NMDA antagonist, with various other
ion channel and receptor effects. Dose typically
11 mix with oxygen (Entonox) Onset
immediate Duration lt3min Provides mild
anxiolysis and analgesia.
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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.
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Dexmedetomidine Short acting alpha-2
agonist. Dose 1ug/kg IV over 10min, then
infusion Potential role in patients with high
sympathetic tone.
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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.
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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.
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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, CVCs, LPs.
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Summary PSA vs. regional anesthesia vs.
OR Pre-medications given? Titrate, dont
calculate Build a toolbox of key drugs If
hypoventilation, give stimulation Should we
adopt a new monitoring standard of practice in
Calgary?