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 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 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.

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: mg/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: mg/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: mg/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: mg IV q2-3min Onset: ~2min Duration: min 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?