analgesia and procedural sedation shawn dowling preceptor dr. ian wishart
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Analgesia and Procedural Sedation
Shawn Dowling
Preceptor
Dr. Ian Wishart
Analgesia Objectives
Basic Pain Pathophysiology Assessing Pain Management
Rx Not going to cover chronic pain, regional
anesthesia
Why do we need to talk pain…1. Pain is the most common complaint of ED patients.
2. One of the most essential missions of all health care providers should be the relief or prevention of pain and suffering.
3. Patients judge physicians by how they treat pain.
4. We cause pain.
5. Unrelieved pain is associated with a long list of potential negative physiologic and psychological outcomes.
Pain Pathophysiology
Black Box
Recognizing/Assessment of Pain Patient report is primary method of pain assessment
Numeric scales can be used as a guide and as a reference for evaluating analgesic effect, physician impression is junk
HR, BP, facial grimacing are poor indicators of pain Factors such as Ethnicity, Sex, Age, Cognitive functioning
affect our assessment of pain In the initial assessment – Ask what pain meds have
worked in the past
How good are we at recognizing and managing Pain?
Study
Convenience cohort of 71 patients, tertiary ED >18 yrs of age Pts were asked to rate their pain w/VAS and NRS
@ arrival and at discharge These ratings were then compared to those given
by EP’s/Nurses
Results
# of pts who received Rx based on initial NRS
Results
Conclusions Physicians and nurses consistently rated the pain
as less than the patient Pain:
49% stated pain was not relieved38% stated pain was somewhat relieved13% stated pain was relieved or completely relieved
ONLY 30% WERE SATISFIED WITH THEIR PAIN CONTROL
Pts in mild-moderate pain were unlikely to receive any analgesia
Only 2/3 of those w/severe pain received any analgesia & only 25% received opioids
This study supports what many prior studies had foundWe underestimate painWe undertreat pain both in the ED and at D/CAnd, as a result, pt are dissatisfied
But, we are improvingFrom 1997-2001, use of analgesics in the ED increased
by 18%2
2McCaig. National Hospital Ambulatory Medical Care Survey: 2001 ED Summary. National Center for Health Statistics, 2003
Approach to Pain Control Local/Regional
Will not cover today - see Bilal’s roundsSee this months CJEM for a review of hip # and femoral nerve block
Systemic Anti-inflammatories (NSAID’s, APAP, COX-2) – see Dr.
Ukraintz’s Grand Rounds Opioids – This we will talk about Adjuvants
Rx: TCA’s, muscle relaxants, anti-convulsants Others: Music, distraction, etc.
The principles of pain control3
•In general, we chose if people are going to continue to have pain, not because pain is unavoidable
•There is no reliable objective measure of pain
•Avoid the “squeaky-wheel-gets-the-oil” phenomenon of pain control
•Pain control must be individualized
•Anticipate rather than react to pain
•When possible, let patient control his or her pain
3Ducharme J. Acute pain and pain control:state of the art. Ann Emerg Med. June 2000;35:592-603
Opioids should be prescribed at fixed intervals to control pain, with additional as-needed doses as required. As-needed dosing by itself allows for gaps in pain control.
Intramuscular or subcutaneous routes of opioids are generally not indicated Erratic absorption and do not allow titration No evidence supporting the idea that these routes are safer Onset of action is approximately the same as with oral
preparations
Opioids
MOABind to specific receptors
Mu – Analgesia, RD, euphoria, physical dependenceKappa – Analgesia, sedation, RD, miosisSigma – Dysphoria, hallucinations, tachypnea, tachycardia
• Metabolized in the liver and excreted in the kidney• In renal failure metabolites accumulate and result in prolonged
duration of action
Meperidine (Demerol)• Onset of Action 5-10 minutes• Duration of Action 2-3 hours
• CNS Toxicity secondary to metabolite normeperidine, a cerebral irritant (anxiety, disorientation, tremors, seizures, hallucinations,psychosis). These effects not antagonized by naloxone.
• Care with Renal/Liver Disease (decreased excretion/metabolism – leads to increased normeperidine), in the Elderly,
• Avoid in pts on MAOI’s – hypertensive emergency• 1/8 the potency of IV Morphine with less benefits!• More Nausea/dysphoria than morphine• Poor ED analgesic choice!
Common Opioids Morphine
• Onset of Action 5-10 min• Duration 2.5 to 4hrs
• Routes: IV, IM, PO
• Mediates histamine release, therefore can cause hypotension
• Prices between the two are relatively similar
Fentanyl
• Onset of Action 1-2min• Duration 30-75min• Routes: IV, IM, TM• Chest wall rigidity: never any cases
in ED (occurs at high doses range of 10-15mcg/kg)
• Not supposed to cause histamine release
• 100 x more potent than morphine
Percocet
• Onset of Action: 30 minutes, Peak 1 hr• Duration: 2-3 hrs• One Percocet contains 325mg Tylenol, 5 mg oxycodone
• Maximum dose is 12/day b/c of Tylenol component (should not exceed 4gm/7)
• SE – same as codeine• Abuse potential – HIGH, significant euphoria
Name Dose MorphineIV Equiv
Peak Effect
Duration
Morphine 5 mg IV
10 mg IM
60 mg PO
5 mg IV 15-30 min
1 h
2 h
2-4hr
4-5hr
4-5hr
Fentanyl 50 ug IV 4 mg 2.5-10 min 30-75min
Demerol 50 mg IV
75 mg IM
5 mg 5-15 min
30 –60 min
3-4hr
Hydro -morphone
1 mg IV
1.5 mg IM
5 mg 15 min
30-60 min
2-3 hr
3-4 hr
Drug Dose Morphine IV Equiv
Peak Effect
Duration
Oxy-codone
5 mg po 3 mg IV 1 h 2-3 h
Codeine 200 mg po
130 mg im
5 mg IV 1 – 1.5 hr
30-60 min
4h
Ibuprofen
APAP
400 mg po
650 mg po
2 mg IV
1 mg IV
30–60 min 4 –6 h
Ketolorac 30 mg IV 5-6 mg IV 60-75 min 6-8 hr
T#3’s What are the three components of T#3’s
Why are these combined/amount?Tylenol (300mg) – we don’t really know (many
theories including CNS COX- inhibitor) Codeine (8, 15, 30 or 60mg)– we’ll review Caffeine (15 mg, except T#4 – no caffeine)
two fx – 1) oppose the sedative features of codeine, 2) added analgesia – not well established, but amount of added analgesia varies from 0-40%
Tylenol and Codeine
Codeine needs to be metabolized (specific CP450 enzyme in the liver) to morphine, which then acts as an analgesic at the CNS opioid receptors10% of caucasians lack this enzyme!!!May be one of the factors as to why some people find
they “don’t” respond to T#3’s
APAP vs T#3’s-Systematic Review4
OBJ: To assess whether adding codeine to tylenol has an additive analgesic effect; to assess their safety.
Design: Systematic review with meta-analysis. Trials: 24 of 29 trials met the inclusion criteria. Models studied in
the trials were postsurgical pain (21), postpartum pain (one), osteoarthritic pain (one), and experimentally induced pain (one). Dosages ranged from 400 to 1000 mg tylenol and 10 to 60 mg codeine
Main outcome measures: The sum pain intensity difference (efficacy analysis) and the proportion of patients reporting a side effect (safety analysis).
4Craen. Et al. Analgesic efficacy and safety of paracetamol-codeine combinations versus paracetamol alone: a systematic review BMJ 1996;313:321-325 (10 August)
Results Single dose pooled efficacy indicated that codeine + tylenol
provided a 5% increase in analgesia Incidence of side effects with each treatment was comparable in
the single dose trials. In the multidose studies a significantly higher proportion of side effects occurred with tylenol-codeine preparations.
Conclusion: The difference in analgesic effect between tylenol -codeine
combinations and tylenol alone was small but s.s. For occasional pain relief a tylenol -codeine combination might
be appropriate but repeated use increases the occurrence of side effects.
LimitationsDon’t mention baseline pain scoresMany argued that a 5% increase is not statistically
significant (5% of 15mm on a VAS is <1mm)Another group looked at RR and NNT. The RR was
1.25 (1.09-1.43). Number Needed to Treat: 9.1 people to get 50% pain
reduction with paracetamol plus 60 mg codeine
To Use or not to Use? Clinically significant benefit over tylenol alone, with
increasing s/e if used for >1 doseMod-severe pain – likely not adequate and will likely
need more than one doseMany argue that a NNT of 9 for Tx of pain is sub-
optimal?Consider in pts who state they respond well to T#3’s
Anti-emetic or not? Opioid-induced emesis is multi-factorial: histamine release, direct
gastroparetic effect and stimulates central chemoreceptor Occurs in approximately 20% of patients, somewhat dose-dpndt Effective agents are antihistamines(gravol) or ondansetron If pt has Hx of significant emesis/nausea, give anti-emetic 15
minutes before opioid In general, do not need to pre-treat with anti-emetic
Other analgesia options Music: variable success,
Distraction is a well-known aid for decreasing pain. Immobilization of injured extremities often decreases pain
considerably Use of regional anaesthesia instead of systemic analgesia
should be considered.
Pediatric pain control Children, including neonates, do feel pain and may suffer
adverse events if that pain is not properly controlled Pain management in children is as important as in adults
In one study no child with an extremity fracture was discharged with an analgesic prescription5
Only 37% of peds w/ LE # received analgesia while in the ED Only 24% of peds w/2 or 3 degree burns received analgesia
while in the ED6
5Ngai B, Ducharme J. Documented use of analgesics in the emergency department and upon release of patients with extremity fractures [letter]. Acad Emerg Med. 1997;4:1176-1178
6Petrack, E. Pain Management in the ED: Patterns of analgesic utilization. Pediatrics 1997;99(5):711-4.
Analgesia for Musculoskeletal Injuries in Children. A Blinded RCT Comparing Acetaminophen, Ibuprofen and Codeine by Clark, Plint, et al. - unpublished7
298 patients aged 7-18, who suffered acute MSK injuries VAS scales were measured at scheduled intervals RESULTS: The study groups were similar
At 1 hour, pain scores were lowered by 24.9mm in the ibuprofen group. This was statistically better than improvement from codeine and acetaminophen
At 4 hours, ibuprofen (30.9mm) and Codeine (23.3) both reached s.s. Tylenol did not s.s. decrease pain (13.3) By 4 hours 72.5% vs 60.4% vs 52.9% of the codeine, ibuprofen and
acetaminophen groups respectively has achieved adequate analgesia. CONCLUSIONS:
@ 1 Hr only ibuprofen had reached clinically significant decrease in pain @ 4 Hrs both ibuprofen and codeine had achieved clinically significant pain cont
In the pediatric ED, ibuprofen is the initial drug of choice for acute analgesia.
Opioids and Competence8, 9
Some have argued that the use of opioids affects ones competence and alters ones ability to give consent
There have been at least two studies that have challenged this dogma Both show that patients retain their ability to give informed consent
despite receiving analgesics One MD makes the arguments that “If pain meds are withheld,
patients may feel pressured to consent in order to obtain medication to relieve their suffering”
8Smithline HA, Mader TJ, Crenshaw BJ. Do patients with acute medical conditions have the capacity to give informed consent for emergency medicine research? Acad Emerg Med. 1999;6:776-80
9Vessey W, Siriwardena A. Informed consent in patients with acute abdominal pain. Br J Surg. 1998;85:1278-80
Procedural Sedation and Analgesia
In Skating over thin ice, our safety is in our speed,
-Ralph Waldo Emerson
PS is w/i our Scope of Practice
EP’s are well trained to Monitor patients during procedural sedationRecognize potential problems early and Intervene when necessary
Procedural Sedation
ObjectivesGoals of PSDefinitions Indications/Contra-indicationsApproachRxAddress a few of the many controversies
I apologize in advance
This is an area of EM with lots of ongoing controversy, debate and research
Unfortunately, much of the research is conflicting and less than optimal (not done in the ED setting, very heterogeneous, “doctored”)…
There are some guidelines to help us though
CONSENSUS Guidelines Innes, Murphy, Nijseen-Jordan. Procedural Sedation and
Anaglesia in the ED. Canadian Consensus Guidelines. J of EM vol 17: 145-5610.
Clinical Policy for Procedural Sedation and Analgesia in the ED. Annals of EM; May 1998: 31, 663-67711
PSA The practice formerly known
as “conscious sedation” - Goals of PS
1. Sedation, Analgesia,+/-Anxiolysis, +/- Amnesia
2. Facilitation of procedure
3. While ensuring pt safety (and not making ourselves cushinoid from all the stress)
Definition
Procedural SedationRefers to a technique of administering sedatives or
dissociative agents +/- analgesia to induce a state that allows the patient to tolerate unpleasant procedures while maintaining cardio-respiratory function/reflexes.
Ideal Rx?
Would provide analgesia, sedation, amnesia, motor control with a rapid onset and short duration
While being safe, effective, simple to administer and reversible
Obviously does not exist and therefore these are 2-hr rounds rather than 5 minutes.
General ApproachPre-Sedation1. 1st question should I do PS?-emergent or-ASA I/II and -no concerns w/a.w.
Hx-PMHx, Previous GA/sedation, Meds/all (egg/soya)-NPOP/E-VS-ASSESS a.w.-Establish baseline LOC-Cardio-respiratory exam
2. Consent-verbal or written
3.Preparation-Equipment, Personel, monitors, IV, Rx/reversal agents, resucitative equipment
4.Documentation
Sedation
1. Pre-oxygenate?
2. MonitoringBP, HR, pulse oximetry, LOC- AVPU, +/- capnography,
3. ?O2 during PS
4. Rx-Procedural Sedation Drugs
Post-Sedation
1. Monitor
2. D/c criteria
3. D/C instructions
Case #1
38 yr guy has a Dislocated shoulder. Before you reduce it, you plan on giving him some drugs.
What do you need to consider before procedural sedation?
Need to Consider Is this person a good candidate for PS?
How does one do this? No ED evidence for this, mostly extrapolated from
anesthesia recommendations
All upcoming recommendations are based on CAEP/ACEP PS consensus guidelines unless otherwise stated
CAEP guidelines A Quick Word…
March 1996 EM committee convened (peds and adults) Initially Canadian Anesthesia Society was involved – in
the end they did not support the final product…. Extensive review of literature Recommendations are a combination of clinical
trials (few), case series (many) and expert opinion (majority)
Pre-Sedation
Hx:Recent respiratory illnesses, PMHx, Prior GA/PS, Meds, Allergies (Rx, foods-why),Last Oral Intake
P/E VS Establish baseline LOC Cardiac exam Respiratory exam Airway
Look, Listen, Feel Evaluate with 1-2-3 (TMJ-mouth-thyro-omental distance) Mallampati Obstruction- Is there any indication of airway obstruction Neck Mobility
These pre-operative guidelines have very little evidence – the statement from the ASA is “there is insufficient published evidence to address the safety of any preoperative fasting period.”
Therefore their guidelines are “best guesses”
Fasting Times11
Why the ASA guidelines may not Apply to ED PS? Majority of our procedures are not elective Our goal is not to routinely achieve GA Logistically unrealistic ?Benefit (doing procedure) outweighs risk of
waiting (emotional, physical sequelae)
Fasting and Aspiration
In 27 years, no cases of aspiration in all-comers peds sedation12
Lots of controversy….
12Cote, Notterman, et al. Adverse Sedation Effects in Pediatrics. Pediatrics, 2004.
Prospective Case Series of 1014 consecutive PS pts from a PED
905 had fasting data on chart396 (44%) were appropriately fasted509 (56%) were did not meet ASA fasting criteria
Of the 396 that were fasted32 had an adverse event
Of the 509 that were not fasted35 had an adverse event
No statistical difference between the rates of a/e between the two groups
Conclusions
No significant difference in a/e between fasted -v- non-fastedDeeper sedation and increasing age increased
likelihood of a/e Rates of a/e were relatively low
Strengths of study
Prospective, ED based All PS was done by EP’s I think it’s generalizable to other PED’s
Limitations of study Sample size/power calculations were based on rates of a/e,
not aspiration risk – therefore real potential for type II error Not a blinded study Aspiration was not defined Pediatric Population - ? Applicable to adults Almost 50% of the drugs used were ketamine -? Applicable
to adults (no use of propofol or etomidate in this study) Fasting times were 9.6 hrs –v- 5.7 hrs (that’s pretty friggin
close to fasting, both groups were appropriately fasted for liquids
So, you decide to proceed w/PSA
What do you need to get from pt? What stuff/people do you need/want to mobilize?
Consent Verbal or written – document!!! Need to discuss
1. Objectives of Sedation
2. Benefits/Risks: • risk of dying from GA 1/160,000 (all comers), no #’s for PS
3. Limitations of the therapy
4. Alternatives
5. Duration of Post-sedation monitoring
6. What they can’t do post-sedation
Contra-Indications to PS
Absolute Lack of personnel experienced with airway
management or ALS/Unfamiliar with drugsLack of appropriate monitoring or resuscitative
equipmentAllergy or sensitivity to relevant Medications
Contra-Indications to PS
RelativeAirway abnormalities: facial/dental/anatomical
abnormalities that would make BVM/intubation difficult
Hemodynamically or neurologically unstable patientsHigh aspiration/Vomiting riskASA III/IV
Preparation
PersonnelPhysician and additional “qualified patient observer”
i.e. Nurse, Physician, RTAnother Physician?Their role is to observe pts airway patency, ventilation,
vital signs and monitoring devicesNo clear evidence to support this
Patient Monitoring Pre-sedation VS Frequent LOC assessment – AVPU good tool Observe ventilation and respiratory status Intermittent BP monitoring
If possibility or plan of sedating to the level of eyes closing Should have a pulse oximeter
+/- ECG for pts with CVD
These recommendations are based on consensus, not evidence
Although there is no evidence that cardiopulmonary monitoring is of evidence – lack of evidence shouldn’t preclude it’s use
Pre-oxygenate/supplemental 02? Two camps
1. Believe that pre-oxygenating the pt may mask hypoventilation and cause retention of CO2
2. Others say, yeah, but if I pre-oxygenate well (5 minutes or 5-7 FVC breaths), I’m afforded a 5-8 minute apnea buffer if need be
In one study, 43% of men desated to <90% during sleep, 13% to <75%
Raises question of whether desats are significant? Evidence: nothing conclusive EMRAP – give them O2, especially with drugs like
propofol where short periods of apnea are expected
Capnography? Rationale is that capnography can identify inadequate
ventilation before desats occur Excellent correlation between ETCO2 and PaCO2, Correlation not as good when measured by nasal cannula No evidence to suggest that it will reduce complications
but may alert to subclinical respiratory depression (defined as ETCO2 >50, increase >10 from baseline, absent waveform)
Recommendations
CAEPNot mentioned in their guidelines
ACEPListed as an Option to be considered if patients
ventilatory effort cannot be visualized Not available in CHRA
Procedural Sedation ChecklistWhat would people have by the bedside?What would people want nearby?
Equipment This stuff needs to be at the bedside
PS Rx Reversal Agents Pulse Ox, BP cuff O2 source, NC/BVM +/- IV
This equipment needs to be readily available Cardiac monitoring Laryngoscope/tubes Crash cart
Equipment
Definitions
Sedation Response Airway Vent CVS
Light/
Moderate
Purposeful/Respond to verbal
normal normal normal
Deep Repeated
Painful
Possible
intervene
Possible
abnormal
Usually
normal
GA No
response
Often
intervene
Frequent
abnormal
Maybe
abnormal
Unfortunately… Although it’s broken up into convenient
categories, monitoring levels of sedation is inherently poor and…
The reality is that sedation is more of a continuum with infinite possible endpoints rather than two possible endpoints
Before starting the procedure, you should have pretty good idea of what your general endpoint is
Tips for smooth PSRisk Assessment/Airway AssessmentPlan aheadTITRATION: Rapid IV boluses are more likely to
cause unexpected deteriorationThere is a point during the PS that a patient is at highest
risk – depends on drug – be prepared !!GA should be viewed as an a/e and should be avoided
when possible
In moderate sedation, Goal is 3-4, avoid 5-6 Does not stay in level 4 for
greater than 15 minutes
In deep sedation Pt are not to remain in 6 for
>15 minutes
Case #2
9 yr boy presents with complex facial laceration. He’s very anxious and distressed. You decide to sedate him for the procedure. Anything particular with Pediatrics?What drugs do you want to use?
Any specific questions you need to ask?Any drugs to pre-treat with?
What is the rationale for these?
Pediatrics
ChildrenHigher mg/kg dosingNarrower safety margin<6 mo – slower drug clearance, increased BBB
penetration, decreased Lean Body Mass
Good article for peds inclined Attempted to prospectively look at the AAP/ASA
guidelines in PS and see outcomes (a/e, sedation depth, sedation failure)
Attempted to tease out some of the factors that influenced complication rates
Not just ED (includes all PS done in this hospital)
Hoffman. Risk Reduction in Pediatric Sedation in Application of an AAP/ASA Process Model. Pediatrics, Feb 2002; 109:236-43
Six Skills of Highly Effective Pediatric PSA (Adults as well)1. Keep Your End Point and Goal in Mind
Risk assessment and patient selection
2. Know How To Get To Where You Are Going Determine ideal depth of sedation/analgesia
3. Control the Environment
4. Choose the Right Rx, Dose and Route
5. Anticipate Complications
6. Recovery and Documentation
Ketamine Class
Dissociative agent – does not fall w/in the sedation classification
MOADisconnects the thalamus from the limbic system via
simultaneously depressing cortical function while stimulating limbic system
Creates trancelike state characterized by potent analgesia, sedation, amnesia
Ketamine
PharmacologyRoutes: IV/IM/PO/PR/INDose: IV - 1-2mg/kg IM - 4-5mg/kgOnset (min): IV – 1, IM – 5Duration: IV – 15 min, IM – 15-30 min
IV: Given as a bolus over 60 seconds, with titration doses given (not frequently needed)
Ketamine Indications:
Any brief painful or emotionally disturbing procedure in children
Generally not recommended for imaging since only require anxiolysis/ involuntary movements may interfere with imaging
Only Absolute CI’s are < 3 mths, >45 yrs, CAD and prior psychiatric illness
Ketamine Advantages
Rapid onset/Short Duration Maintain CVS and Resp reflexes Minimal Resp depression
Minimal apnea and when it occurs is usually at around 1 minute after dose and resolves rapidly
Bronchodilation – what’s the mechanism of this
Ketamine A/E
LaryngospasmResult of “hypersensitive” laryngeal reflex IR approx 0.4%1 (from a review of nearly 12,000
cases)And only a small fraction (2 in 12,000) required
intubationIn one study of endoscopy – 9.4% IR with upper
endoscopy and 0% with colonoscopy13
13Green. Ketamine Sedation for pediatric gastroenterology Procedures. J Peds Gastro. 2001
KetamineHypersalivation
Thought to maybe increase risk of laryngospasm secondary to laryngeal irritation
Brown et al (unpublished data) looked at 297 children and found similar salivation scores between those receiving ketamine + atropine and those receiving only ketamine
Don’t know much about study, validity, etc ?Significance
Increase muscular tone/purposeful movements
Ketamine ?Increase in ICP
1974-2003 small prospective randomized studies done with intravenous ketamine for sedation on ventilated head injured patients
No change or significant improvement in ICP No change in cerebral perfusion pressure Maintains cerebral autoregulation
Vomiting HTN/Tachycardia
Usually not clinically significant
Emergence Phenomena - Thought to be due to re-connection of thalamus and cortex Wathen. Does Midazolam alter the clinical
effects of IV ketamine sedation in children? Annals of EM, December 200014
RCT/double blinded: ketamine IV (1mg/kg) + glycopyrrolate (5micrograms/kg) +/-midazolam (0.1mg/kg)
266 pts Median age 6.2 yrs (4.5 mths to 16 yrs) Looked specifically at emergence phenomena, but also looked at
all a/e
A/EResp events (apnea, laryngospasm, desats
<90%) – 4.5%Vomiting – 18.7%Emergence Phenomena* in the ED – 26.7%
-13.3% were considered significantEmergence Phenomena* at home – 22.4%*Defined a priori as agitation, dysphoria,
euphoria, active dreaming, nightmares, hallucinations
Significant if severe agitation, nightmares or hallucinations occurred
Significant Emergence PhenomenaKetamine – 7.1%Ketamine + Midaz group – 6.2%
Not statistically significant (sample and power calculations were done)
PLUS, Midaz group had (statistically signific)More agitation (prior studies have also shown this)More oxygen desats
ConclusionBoth groups had equally effective sedationMidaz did not decrease emergence, but
increased agitation and incidence of desats
Ketamine Post-Recovery Agitation
Sherwin. Does Adjunctive Midazolam reduce recovery agitation after ketamine for pediatric procedures? Annals of EM, March 200015.
RCT/double blinded: atropine + ketamine 1.5mg/kg +/- midazolam (0.5mg/kg, max 2g)
104 childrenMedian age 6 years (12mth – 15 yrs)Used VAS to determine whether “not agitated” to
“worst possible agitation” – not a validated tool
Pre-sedation – VAS 7 midaz group, 6 in placebo
Recovery agitation – 5 in midaz group, 6.5 in placebo
Not statistically significant, (power and sample sizes were calculated)
ConclusionsMidazolam does not decrease recovery agitationStudy noticed that presedation agitation increased
your risk of recovery sedation – subgroup analysis showed that they did not benefit either
Ketamine
Future QuestionsHow safe is it in adults? Is there a specific subset of people that would benefit
from pre-treatment with a BZD?i.e. those that are agitated pre-sedation?
Is there a benefit to adding atropine? Is ketamine S(+) enantiomer better?
Current studies on-going in Europe
Case #3
Your working at the PLC and a 15 yr guy presents with a dislocated patella. PMHx – nil.You decide to give him some PSA.
Senior guys: What are your options?What combination are you going to use?
Case #4 51 yr male w/ stable, new onset a-fib.
No Contra-Indications to PSBP 160/80
What Drug do you want to use?Any specific history questions based on drug?Why? How are you going to give it?
Propofol
ClassSedative-hypnotic, alkyl phenol
Composed ofPurified eggSoyabean oil
PharmacologyHighly lipid soluble therefore it crosses BBB quickly
and has a large volume of distributionOnset of action: 1 min (one “arm-brain”)Duration of action: 8-10 min, but this can increase with
higher dosesClearance of the drug is not affected by renal or hepatic
dysfunction and levels do not accumulate
Route/DosingOnly available IV, 10 mg/mLDose
As a bolus: start low and go slow, but go 20 mg bolus, then 10-20 mg/45-60 seconds until desired effect Ducharme (EP in New Brunswick) suggests titrating until pt has a
verbal response to being shaken State no cases of apnea or serious 02 desats with this technique
(unpublished data) and propofol doses range from 40-160 mg
Propofol Indications
Not clear guidelines but…Short, intensely painful procedures
i.e. cardioversion, hip/shoulder reduction
CI’s Absolute
Egg/Soya Allergy Relative
Hemodynamically unstableElderly
Advantages Quick onset, short duration/recovery Anti-emetic properties Minimal anesthetic hangover Increases seizure threshold Good amnestic properties High patient satisfaction
Disadvantages and A/E Respiratory depression/Apnea
Mechanism is via increase sensitivity to CO2 (same mechanism as opioids and BZD, so be careful if using together)
10-60% depending on study (typically dose dependent) CVS: myocardial depressant
Anesthesia literature states 25-40% decrease in MAP with 2-2.5mg/kg Multiple studies have shown that it drops BP more than thiopental or
etomidate No analgesic properties Pain at injection site – from protein component
Can decrease by combining with 1-2 mL lido
Propofol for PS - Adults Numerous studies
Many of the studies are done in stable, elective, pre/peri-operative pts – may not be able to generalize to ED patients
Many decent studies in the procedural specialties (cardiology, GI) that have shown
Better patient satisfaction, Shorter recovery time, less vomiting
Few good ED studies for PS Most are for RSI
Many studies done for Cardioversion Not ED setting, Use much higher doses of propofol – most use
2.5/kg,
Propofol studies in the ED 12 studies done in the ED
6 were in Peds (n=878)6 were in Adults (n=114)
Incidence of RD: 0-50% Dosing variable
Most studies did not have a max dose Some used adjuvant opioids (morphine or
fentanyl), others did not
Endpoint variable – Poorly defined“desired level of sedation”, Loss of lid reflexTolerating noxious stimuli w/o complaint
Pre-oxygenationVariable, study dependent
Study Type #’s Start Dose A/E
1. Swanson
2. Swanson
3. Havel
4. Guenther-Skokan
5. Miner
6. Godambe
(Adults)
Descr
Rand
Blind
Pros
Cases
Pros
Rand
4
20
43
40
21
59
0.14 mg/kg
0.21 mg/kg
1 mg/kg
1 mg/kg
Not stated
1 mg/kg
None
2 apnea, 1 assisted vent
5 hypoxia (12%)
14 oversedated
12 hypoxia (30%)
22 RD (41%)
5 hypoxia, 5 ass V
18 hypoxia (31%)
No apnea
Study Type #’s Start Dose A/E7. Miner
8. Miner
9. Coll-Vincent
10. Bassett
11. Guenther
12. Pershad
Pros
Pros
Pros
Rand
Case
Series
Pros
Cons
Retro
Case
54
103
9
393
291
52
Not stated
1mg/kg
1.5mg/kg
1mg/kg
1mg/kg
1mg/kg
22 RD(41%)
5 hypoxia, 5 ass V
25 RD(49%)
5 hypoxia, 2 ass V
4 hypoxia,2 apnea
19 hypoxia (5%)
3 apnea w/ass V
15 hypoxia (5%)
12 partial obstr
3 apnea w/ass V
3 RD (6%)
One of the Propofol studies Miner, et al. Randomized Clinical Trial of Propofol versus
Methohexital for PS during Fracture and Dislocation Reduction in the ED. Acad EM, Sept 2003;10:931-716.
103 patients randomized: 52 received methohexital (brevatil) 1mg/kg followed by 0.5mg/kg Q3-5m, 51 received propofol - 1mg/kg followed by 0.5mg/kg Q3-5m
All Pts received adjuvant morphine Cont Monitoring: VS, ETCO2, Pulse oximetry, BIS scores Incl: >18 yrs, reduction of # or dislocation Excl: unable to give consent, allergy to either drug, intoxicated
Baseline patient characteristics were the same Outcomes
Depth of SedationOccurrences of RD/HypotensionProcedural SuccessPatient outcomes
Perceived PainRecall of the ProcedureSatisfaction with the Procedure
Supplemental O2 was given at discretion of EP RD: defined as
Loss of ETCO2 waveform, >10 increase in ETCO2 from baseline, desat<90%
Hypotension:Drop >20% from baseline
Outcomes No significant difference in depth of sedation RD
48% w/methohexital 49% w/propofol More pts in the propofol group received suppl O2 Those who received only 1 dose of propofol had significantly less RD –
subgroup analysis Six pts required BVM (2 propofol, 4 methohexital), none required
BVM for >1 minute, none had sats <90% for greater than 1 minute No significant declines in BP were detected
Procedural Success94% for methohexital, 98% for propofol
Patient Satisfaction/Recall/PainNo statistically significant differences
WeaknessesDon’t mention the procedural sedation endpointState BIS score <70 increases RD, avg score was 65Not BLINDEDNo significant decline in BP conflicts with most other
propofol studiesNegative study???others
Unpublished Data Be skeptical but…
EMRAP guy (Al Sacchetti) suggests: Pre-oxygenate w/100% NRB: gives you a buffer in case pt has apneic
period Pre-Treat with Lido (1-2mL) Bolus (0.75-1.0 mg/kg), given slowly Perform procedure Followed by small bolus PRN With 10 yrs experience at their hospital – no complications, no BVM -
conveniently never described was they consider complications
PS registry from 6 hospitals200 Cases
Propofol: # 1 Rx, 100% success rate for procedures. No reports of patients needing to be BVM.
What this data means???
Propofol- The arguments for and against PROpofol
Don’t need ED evidence RD is real, but very transient Pts go deep, but transiently Short recovery High pt satisfaction Low Aspiration IR Great anti-emetic/less V
Against Propofol Not enough ED evidence RD is underestimated Low BP is underestimated Pts go too deep-?monitoring ?doctored studies Potency makes it difficult to
titrate ?Aspiration risk-?fasted, type II
errors
Case # 5 87 yr old man, with Distal
radius # from a FOOSH injury.
Ortho asks you to give him a little sedation so they can push on his wrist.
PMHx: COPD (on home O2), Aortic Stenosis
MEDS: A bunch All – none P/E – BP 100/50, Obese, bearded guy
What do you do?
Do you want to give him PSA? Is this an urgent/emergent procedure?
If not, do you have options? NEED TO CONSIDER HOW IT WOULD LOOK
IF SOMETHING WENT WRONG!!!
Elderly and PSA
ElderlyMore prone to cardiopulmonary decompensationProlonged duration
Less fat/muscleCrappy kidneysRx-Rx Interactions
More Co-morbidities
Controversies
Should we use opioids with it?Recognize that adding another drug increases incidence
of a/e.Morphine or fentanyl?
Will it make it’s way into the peds ED’s? Patient-controlled sedation? Is the RD clinically significant?
Etomidate
ClassNon-barbituate sedative-hypnotic
MOAWorks thru the GABA receptorSedationNo analgesia
PharmacologyDose IV: 0.1-0.2mg/kgOnset of Action: 1 minDuration of Action: 10-15 min
Contra-Indications3P’sPregnantPoor adrenal fxPrior Seizure
AdvantagesLess CVS effects b/c no histamine releaseFavorable reduction in ICP?Less RD than other agents (propofol, thiopental)
A/E & DisadvantagesRDVomitingMyoclonus Inhibits corticosteroid sxn, probably not an issue with
single dose/PS
Etomidate – studies
Falk, Zed. Etomidate for PS in the ED. Annals of Pharmacotherapy. July-Aug 2004.
Schenarts, Burton. Adrenocortical Dysfunction. Academic Emergency Medicine. Jan 2001, vol 8.
Ruth, Burton. IV Etomidate for PS in ED patients. Academic Emergency Medicine. Jan 2001, vol 8.
Midazolam
ClassShort acting BZD
MOAProvides anxiolysis, amnesia, sedationFacilitates action of GABA (inhibitory NT) via
inhibiting glycine
PharmacologyRoutes: IV/IM/PO/TM/PROnset: IV/IN 1-5 m, IM 5-15 m, PO >30mPeak: IV 1-2m, IM 15-60 m, IN 10m, Duration: Up to 2 hoursDose: 0.05-0.1mg/kg
Usually start w/1-2 mg titrating up to effect
Hepatic metabolism, renal clearance
AdvantagesShort half-lifeGood sedation/Amnesia/AnxiolysisReversibleMultiple administration routes
CI: Allergy to midazolam (?other BZD’s) Disadvantages/Cautions
Resp: Potent Respiratory depression b/c of increased sensitivity to CO2 (amplified by use of opioid)
CVS: Hypotension and bradycardiaCNS: Agitation, involuntary mvmt, paradoxical
hyperactivity, nystagmus, slurred speechBe very careful with elderly!!
Use smaller doses (start with 0.5, titrate by 0.25-0.50mg)
Reversal Agents
FlumazenilBZD receptor antagonistPharmacology
Onset: IV 1-2mPeak: 5-10mDuration: 45-90mDose: 0.1mg (0.01mg/kg) titrating up to a max of 2mg
CIAllergyUse of BZD for seizuresChronic BZD use – risk of ppt withdrawal seizureNot recommended in serious TCA overdose
Case reports of seizures
After administration, should monitor x 120 to monitor for rebound RD
Narcan
MOAOpioid receptor antagonistPharmacology
Onset: IV 1-2mPeak: 5-10mDuration: 1-4 hrsDose: 2.0 mg or 0.1mg to 0.2 mg (10-100mics/kg) titrated to
response up to a max of 10 mg
CI - AllergyCautious use in those w/physical dependence on
opioids or Agitated abusive pts(?prophylactic restraints)
After administration, should monitor x 120 to monitor for rebound RD
What constitutes an a/e?
Studies have used many different outcomesResp: desats<90%, ETCOs >50, Increase >10 from
baseline, absent waveform, aspirationGI: vomiting, CVS: sBP <20%, Admission to higher level of care than was expected
D/C criteria CAEP• Satisfactory a.w. patency, V,
CVS fx and hydration• LOC back to baseline• Pt can sit unassisted (if age
appropriate)• Tolerates PO intake• Pt or responsible adult
understands d/c instructions• Monitor x 2 hrs if given
reversal agent
ACEP
• Pain and d/c are addressed• No new S/Sx• Minimal nausea• VS are w/i N range• Pt is conscious and
responds appropriately• Resp Status is @ baseline
Prospective, data collection 1341 pts included, standardized data collection by
nurse, telephone f/u at 24 hrs Classified a/e as 1. Serious (life-threatening or
requiring medical intervention) and 2. Other Referred to a/e as Primary (1st a/e) or Secondary (if
they occurred any pt after Primary)
Results Timing of a/e
92% during the procedure Serious a/e: Median time 2 m (range –104 to +40 m??)
Three a/e occurred relatively late (all hypoxia) All were secondary a/e At 26m, 30m, 40m No pts required hospitalization based a/e from PS
No Primary a/e > 25 minutes after final medication
Weaknesses Poor f/u – only 64%
15% of these reported an a/e Vomiting (76%) Unspecified (4%) Ataxia (3%) Facial swelling, rash, AP, fatigue, nightmares, hives, confusion, HA (each
had 1 patient)
Rx of choice was versed +/- fentanyl One pt desated to 87% w/stridor 60 minutes after final drug,
BUT excluded b/c insufficient documentation No power/sample size calculations
Looked specifically at a/e from PS, but not necessarily from abnormal neuromuscular dysfx – i.e. did the kid fall walking out the ED and need his head suturedLikely an issue if we want to try to generalize this to
older kids and adults
D/C Criteria CAEP Baseline physical status/mental status Sit and talk appropriately Responsible caregiver present Verbal instructions – return if… Written d/c instructions Minimal 2 hr observation if reversal agents used Document discharge condition
D/C instructions (CAEP)
Avoid dangerous activities (biking, swimming, driving, etc…) until the effects of the medications have passed
You may feel dizzy, nauseated – start with fluids and progress as tolerated
Avoid EtOH, sleeping pills or any meds that can cause drowsiness x 24 hrs
Pre-Sedation1. 1st question should I do PS?-emergent or-ASA I/II (include table)and -no concerns w/a.w.
Hx-PMHx, Previous GA/sedation, Meds/all (egg/soya)-NPOP/E-VS-ASSESS a.w.-Establish baseline LOC-Cardio-respiratory exam
2. Consent-verbal or written
3.Preparation-Equipment, Personel, monitors, IV, Rx/reversal agents, resucitative equipment
4.Documentation
Sedation
1. Pre-oxygenate? 2MonitoringBP, HR, pulse oximetry, LOC- AVPU, +/- capnography,
3. ?O2 during PS
4. Rx-Procedural Sedation Drugs
Post-Sedation
1. Monitor
2. D/c criteria
3. D/C instructions
General Approach: Pre-Sedation, Sedation, Post-sedation
The END
References - General Pain Management in the ED. Emergency Medicine Reports. Feb 2002. Pediatric Pain Control. Pediatric Emergency Medicine Reports. Aug 1999. Acute Pain Management in the ED. EMR. July 26, 2004. Procedural Sedation: Part 1. EMR. Oct 7, 2002. Procedural Sedation: Part 1. EMR. Oct 21, 2002. Pediatric Procedural Sedation: Keeping it Safe and Simple. PEMR. Feb 1, 2001. The Six Skills of Highly Effective Pediatric Sedation. PEMR. Aug 1997. Procedural Sedation: EMRAP, July 2004.
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