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 sedationMinimal 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 equipmentPhysician 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

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.

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.

PropofolGABA 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?