- Email: [email protected]
Propofol in emergency medicine
PAIN MANAGEMENT/EDITORIAL
Propofol in Emergency Medicine: Pushing the Sedation Frontier Steven M. Green, MD Baruch Krauss, MD, EdM From the Department of Emergency Medicine, Loma Linda University Medical Center and Children’s Hospital, Loma Linda, CA (Green); and the Division of Emergency Medicine, Children’s Hospital and Harvard Medical School, Boston, MA (Krauss).
See related articles, p. 767, p. 773, and p. 783. [Ann Emerg Med. 2003;42:792-797.]
Is propofol an appropriate agent for use as part of emergency department (ED) procedural sedation and analgesia? Few questions in emergency medicine are currently as controversial. No one disputes that propofol exhibits numerous exceptionally desirable characteristics as a procedural sedation and analgesia agent. First, its clinical effect is essentially immediate after intravenous administration (“one arm–brain circulatory time”). Second, its marked potency reliably produces effective procedural sedation and analgesia conditions, even for very painful procedures. Third, recovery after sedation is extremely short, typically between 5 and 15 minutes. Finally, patient satisfaction is high because propofol has anti-emetic and apparent euphoric properties. It is no wonder that this agent has revolutionized anesthesiology practice. Many emergency physicians have already extrapolated this proven operating room success to our setting, using propofol as a single agent or in combination with an opioid, to successfully induce brief but potent sedation for short, painful procedures such as orthopedic manipulations, cardioversion, and abscess drainage. However, this application is based on limited experience because, thus far, only 8 small series of ED propofol use have been formally reported (Table).1-8 Despite this, proponents believe that there are sufficient stud-
Copyright © 2003 by the American College of Emergency Physicians. 0196-0644/2003/$30.00 + 0 doi:10.1016/mem.2003.409
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ies in the anesthesia literature demonstrating the safety and efficacy of propofol to justify its use in the ED.9 Although hypotension, apnea, pain on injection, and bacterial contamination of the lipid emulsion have been reported, the primary criticism of propofol for procedural sedation and analgesia has focused on the greater sedation depth that typically results from propofol. Using the traditional propofol for procedural sedation and analgesia combination of midazolam and fentanyl, emergency physicians can reliably (albeit laboriously) titrate patients to either a state of “moderate sedation” (ie, purposeful responsive to verbal or tactile stimulation)10 or “deep sedation” (ie, purposeful responsive to repeated or painful stimulation).10 It is widely accepted that such moderate sedation is unlikely to be associated with impairment of protective airway reflexes, and thus aspiration risk in this setting is minimized.11 In contrast, however, the ultrarapid onset and high potency of propofol make it more difficult to titrate and prone to potentially substantial overshoot. Within 30 seconds of a single intravenous dose of propofol, a patient’s sedation depth could, without always a high level of predictability, be compatible with moderate sedation, deep sedation, or perhaps general anesthesia.12 Although all nondissociative sedatives can induce depth at all levels of the sedation continuum, in practice, propofol is primarily used for deep sedation.3-8,13 Anesthesiologists have been especially concerned about propofol use by nonanesthesiologists14 and have not differentiated such practitioners by skill set, lumping together emergency physicians with dentists, radiologists, and gastroenterologists.15,16 Pharmacy and therapeutics committees in many hospitals have blocked use of propofol for ED procedural sedation and analgesia because of objection by anesthesiologists on the committee. The paucity of data on the safety of propofol for ED procedural sedation and analgesia has made it difficult at times to overcome these objections. Four years ago, one of us characterized propofol as “not yet ready for prime time” in emergency medicine.12 This cautionary commentary raised concerns regarding the risk of inadvertent oversedation with propofol, personnel requirements, Joint Commission on Accreditation of Healthcare Organizations (JCAHO) standards, and fasting in the setting of deep sedation. Large case
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series were recommended to better characterize the safety of this agent in the unique hands of emergency physicians. Three articles in the current issue of Annals substantially advance our understanding of propofol in emergency medicine and address many of these important issues. Coll-Vinent et al17 report a small but elegant randomized controlled trial of 4 different sedative regimens for ED cardioversion of adults with atrial fibrillation. A major strength of this study is that the 4 sedative regimens were compared using this identical brief but highly painful procedure. In contrast, most ED procedural sedation and analgesia research has been complicated by the inclusion of a wide variety of procedures requiring a wide range of sedation depth. Although Coll-Vinent et al found all regimens to be effective, propofol demonstrated exceptionally short recovery times (median 10 minutes) and a favorable adverseeffect profile. Etomidate was judged less desirable as a result of associated myoclonus, which was generalized and intense in one case. Midazolam demonstrated substantially longer recoveries, and attempts in a fourth trial arm to shorten recovery time with flumazenil were unsuccessful because of resedation. Bassett et al18 report the largest series to date of propofol use for ED procedural sedation and analgesia.
They prospectively developed and implemented a protocol at their children’s hospital and then performed 393 consecutive sedation events over a 2-year period. Efficacy for these primarily orthopedic manipulations was uniformly high, and adverse events were less than reported in prior series. They noted hypoxia in 5%, partial airway obstruction requiring airway repositioning in 3%, and apnea with assisted ventilation in 0.8%. This is not substantially higher than adverse effect rates established for midazolam and fentanyl (1.3% desaturation, 0.3% assisted ventilation)19 and provides the first large-denominator safety profile for ED propofol. At this same children’s hospital ED, Guenther et al20 report their experience administering propofol procedural sedation and analgesia for elective procedures in a short-stay unit immediately adjacent to the ED. Emergency physicians performed 291 consecutive prescheduled sedation events primarily for oncologic procedures, with uniform efficacy and a similar profile of adverse airway events (hypoxia in 5%, partial airway obstruction requiring airway repositioning in 4%, apnea with assisted ventilation in 1%). Although these were not ED patients, this series further reinforces the capability of emergency physicians to administer propofol. Additionally, it provides a stimulus for other EDs to develop similar “sedation units” so that our procedural
Table.
Published research on propofol administration in emergency medicine.* Study
Patients
Dose
Existing publications Swanson et al1 Swanson et al2 Havel et al3
4 adults 20 adults 43 children
0.14 mg/kg/min titrated 0.21 mg/kg/min titrated 1 mg/kg load, then infusion
Guenther-Skokan et al4 Miner et al5 Godambe et al6
40 children 21 adults 59 children
Miner et al7 Miner et al8 New in this issue Coll-Vinent et al17 Bassett et al18
54 adults 51 adults
1 mg/kg load, then 0.5 mg/kg prn Not stated 1 mg/kg load, then “smaller aliquots” prn Not stated 1 mg/kg load, then 0.5 mg/kg prn
9 adults 393 children
1.5 mg/kg bolus 1 mg/kg load, then 0.5 mg/kg prn
Guenther et al20
291 children
1 mg/kg load, then 0.5 mg/kg prn
Adverse Effects
None 2 apnea (1 with assisted ventilation) 5 hypoxia (12%) 14 “oversedation” (32%) 12 hypoxia (30%) 4 respiratory depression (19%), 1 with hypoxia. No assisted ventilation 18 hypoxia (31%) No apnea events 22 respiratory depression (41%), 5 with hypoxia and 5 with assisted ventilation 25 respiratory depression (49%), 5 with hypoxia and 2 with assisted ventilation 4 hypoxia, 2 apnea 19 hypoxia (5%) 11 partial airway obstruction requiring airway repositioning (3%) 3 apnea with assisted ventilation (0.8%) 15 hypoxia (5%) 12 partial airway obstruction requiring airway repositioning (4%) 3 apnea with assisted ventilation (1%) 1 bradycardia (0.3%)
prn, As needed. * Excluding abstracts.
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sedation and analgesia skills can benefit other lessskilled practitioners. Perhaps the most remarkable feature of the study by Guenther et al,20 however, is that essentially all of the sedated children had advanced underlying illness. Ninety percent were American Society of Anesthesiologists (ASA) physical status classification 3 (“a patient with severe systemic disease”), and patients in such higher ASA classes have traditionally been considered at greater risk for procedural sedation and analgesia complications. Despite this, the adverse event profile was essentially identical to the healthy ED patients (97% ASA class 1 and 3% ASA class 2) reported by Bassett et al.18 The adults in the study by Coll-Vinent et al17 all had substantial underlying cardiac disease, although the sample size of this study was too small to reliably profile safety. The studies by Bassett et al18 and Guenther et al20 are also significant in confirming the safety of simple bolus dosing (ie, a 1 mg/kg load followed by 0.5 mg/kg as required). Prior studies by Swanson et al1,2 and Havel et al3 have recommended more complicated syringe infusion pumps. Taken in aggregate, these 3 studies lend further evidence for the efficacy of propofol and show that emergency physicians can, in accordance with a clearly defined protocol, administer propofol with a low rate of adverse events, all of which were minor and successfully managed without adverse outcomes. Many emergency physicians will regard these reports as a longawaited validation of the safety of propofol in the ED and a green light toward widespread implementation of this agent for procedural sedation and analgesia. Although these studies have advanced our knowledge of ED propofol use, some important questions remain. What is the incidence and extent of respiratory depression with propofol?
The Bassett et al18 and Guenther et al20 studies report rates of hypoxia and assisted ventilation (Table) only slightly higher than those typical of midazolam and fentanyl. A higher incidence would reasonably be expected because of propofol’s greater potency, and indeed prior studies (including from this same institution) report hypoxia in up to 30%.3,4,6 Was this dramatic decrease in adverse effects the result of improved operator experience? It is certainly possible; however, the more likely explanation is that most cases of respiratory depression were instead masked in the new studies by the addition of high-flow (5 to 10 L/min) supplemental oxygen. Such
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preoxygenated patients can tolerate respiratory depression and even frank apnea for 1 to 3 minutes, depending on age and underlying physical status, without an apparent oxygen desaturation or need for assisted ventilation.21 The authors did not use capnography, and so the incidence and extent of actual respiratory depression was not quantified. The only capnography data with ED propofol thus far come from Miner et al,5,7,8 who found hypercapnia in 19% to 49%. These data provide compelling evidence that transient, subclinical respiratory depression is likely to be typical with this agent. Such knowledge, combined with the positive experience noted in the studies by Bassett et al18 and Guenther et al,20 suggests that supplemental oxygen should perhaps be routine during all propofol sedation. The most serious procedural sedation and analgesia complication in emergency medicine is aspiration, not respiratory depression, and accordingly we would prefer to avoid assisting ventilations (and thereby insufflating the stomach) whenever possible. Given the ultrashort duration of action of propofol, it would appear probable that, in many circumstances, one could simply “wait out” an occurrence of propofol-associated respiratory depression, assuming substantial preoxygenation. In contrast, such an expectation would not be reasonable for midazolam or other longer-acting sedatives. The primary argument against the use of supplemental oxygen during procedural sedation and analgesia is that pulse oximetry constitutes a fail-safe, that is, it is a mechanical marker of respiratory depression should it for some reason be overlooked clinically. Administration of high-flow oxygen throughout deep sedation largely negates this capability,22-25 creating a compelling case for the addition of capnography to routine deep sedation monitoring. Capnography is equally accurate with and without supplemental oxygen. Capnography has been shown to be the earliest indicator of acute airway obstruction, respiratory depression, apnea, and laryngospasm5,22,23,26-28; a direct and accurate measure of respiratory rate28; and a more sensitive monitor than health professionals in detecting respiratory compromise.27-30 Early detection of respiratory compromise is especially important in infants and toddlers who have smaller functional residual capacity and greater oxygen consumption relative to older children or adults.21,31 Continuous oxygenation and ventilation monitoring during procedural sedation and analgesia would permit ready mechanical detection of hypoxia and respiratory
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depression and apnea regardless of supplemental oxygen. The use of these combined technologies for ED propofol sedation is strongly recommended. Is ED administration of propofol deep sedation or general anesthesia? Does this distinction matter clinically?
Whether propofol procedural sedation and analgesia induces general anesthesia or deep sedation has been, and continues to be, an emotional flash point.14 According to JCAHO definitions, the characteristic that distinguishes the 2 states is the presence or absence of a “purposeful response following repeated or painful stimulation.”10 Unfortunately, none of the 3 new propofol studies report their sedation depth in a manner directly comparable with JCAHO definitions. Bassett et al18 and Guenther et al20 describe a target endpoint—“tolerance of noxious stimuli without patient complaint”—which is technically compatible with either state. Coll-Vinent et al17 used Ramsay scale scoring and noted that the maximal sedation for all of their patients was 6 (ie, “no response” to pain; a score of 5 would have been “sluggish response to pain,” similar to deep sedation). Thus, it seems reasonable to assume that all of Coll-Vinent et al’s patients experienced transient general anesthesia, and that at least some of Bassett et al and Guenther et al’s patients met this technical standard as well. Assuming that some or most of these patients crossed the amorphous boundary between deep sedation and general anesthesia, is this distinction clinically relevant, or does it instead represent a political squabble of semantics? Indeed, procedural sedation and analgesia guidelines from the American Academy of Pediatrics do not differentiate the states and consider them equivalent in terms of patient monitoring and risk of adverse events (“the state and risks of deep sedation may be indistinguishable from those of general anesthesia” and “deep sedation and general anesthesia are virtually inseparable for purposes of monitoring”).32,33 Despite these perceptions of nuance, the distinction between these 2 entities will remain important because of differential aspiration risk (detailed in the next section), hospital credentialing, and JCAHO standards. In most hospitals in the United States, emergency physicians are credentialed for moderate and deep sedation, with general anesthesia privileges limited to rapid sequence intubation. Thus, any propofol technique achieving consistent general anesthesia might quickly lead to hospital-initiated restrictions based on scope of practice. Emergency physicians must be cog-
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nizant of their specific hospital privileges and any restrictions or credentialing requirements imposed by their local JCAHO-mandated hospital-wide sedation policies. The JCAHO does not prohibit propofol use by emergency physicians. Instead, it permits individual hospitals to set their own policies on the basis of their resources and perspectives. The caveat is that the standards of sedation care must be “comparable” throughout the institution. “Comparable” does not necessarily mean “identical,” and thus practices in the ED and other hospital areas, such as the operating room, may differ to the degree that the global standard of care is not compromised and the variance is reasonable. Recent changes in the ASA standards for basic anesthetic monitoring mandate that anesthesiologists use capnography for all general anesthesia care (intubated and nonintubated patients, in and out of the operating room).34 Thus, it would behoove emergency physicians to add capnography to their propofol protocols to better mirror the propofol practices of anesthesiologists. What is the risk of aspiration with propofol?
Aspiration is the most feared complication of ED procedural sedation and analgesia and, fortunately, has not been reported in our setting.35 The JCAHO monikers of moderate and deep sedation are in and of themselves not clinically important. Instead, these arbitrary categories of patient responsiveness are intended as surrogate markers for important items such as loss of protective airway reflexes and cardiopulmonary depression. There is no dispute that mild to moderate sedation is associated with consistent retention of protective airway reflexes and that, on the other end of the sedation continuum, inhalational general anesthesia is associated with consistent loss of these airway reflexes. In the continuum between these extremes is deep sedation, which “may be accompanied by a partial or complete loss of protective reflexes.”32,33 The exact point at which such reflex loss becomes clinically important is unknown, because there are no research data to answer this critical question and there is no safe and practical way to assess the status of protective airway reflexes. Critics of ED propofol use will maintain that pushing the deep sedation frontier represents an inordinate risk of aspiration. Furthermore, they will argue that in the ED this particular risk is enhanced because patients will not always be fasted to the extent typical for elective preoperative guidelines.35,36 In the current propofol stud-
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ies, the elective short-stay unit patients of Guenther et al20 were fasted according to ASA guidelines for elective anesthesia,37 and those of Coll-Vinent et al17 were fasted 4 hours. The ED protocol of Bassett et al18 stipulated no oral intake within 3 hours; however, these authors acknowledge subsequent protocol violations in 13%. Despite these criticisms, there is currently no evidence to document that propofol (as used in the current studies) impairs airway reflexes to any clinically important degree. Secondly, ED procedures are short and most of these journeys to the deep sedation frontier are brief—lasting from seconds to several minutes. This is distinctly different from the prolonged anesthesia cases typical of the operating room where adverse events have been shown to increase with the length of general anesthesia.27 Thirdly, propofol is an anti-emetic, and vomiting with this agent is rare. Finally, the ASA elective fasting guidelines are consensus based rather than evidence based,37 and cannot be specifically extrapolated to the nonelective ED setting.11,35 Thus, despite a full realization that pushing beyond the deep sedation frontier will result in general anesthesia and loss of protective airway reflexes, there is no evidence that propofol as administered in the current studies creates undue aspiration risk. Certainly, practitioners must carefully adhere to widely accepted recommendations for minimizing aspiration risk,11,35 including the aggressive avoidance of oversedation and the need for assisted ventilation. Although the necessity of routine presedation fasting before moderate and dissociative sedation is open to debate,35 the aspiration risk with deep sedation (and especially its frontier) is undoubtedly higher. A substantially more conservative stance is therefore indicated when individualizing decisions regarding propofol procedural sedation and analgesia in the setting of recent oral intake. What are the indications for use of propofol for ED procedural sedation and analgesia?
The optimal role for propofol would appear to be for procedures such as those performed in these 3 new reports: either brief, intensely painful procedures (eg, cardioversion, orthopedic manipulation, bone marrow aspiration) or brief interventions that require marked anxiolysis and immobilization to be accomplished (eg, ocular burn examination, intrathecal medication administration). The key word here is “brief.” Use of propofol for longer procedures (eg, complex laceration repair) would require repeated dosing of this extremely short-acting agent or the initiation and titration of an
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infusion. The safety profile of extended propofol administration in the ED setting cannot be verified by the current reports and cannot be recommended pending further research. So, which is preferable for pediatric ED procedural sedation and analgesia—propofol or ketamine? Both create superb procedural conditions for these highly painful procedures. The primary advantage of propofol over ketamine lies in its brief recoveries; discharge times after completion of procedures occurred in a median of 18 minutes in the Bassett et al18 study and a median of 25 minutes in the Guenther et al20 study. Indeed, Godambe et al6 compared propofol/fentanyl and ketamine/midazolam for pediatric orthopedic procedures and found that the former agents exhibited a shorter mean recovery time (by 23 minutes) and total sedation time (by 33 minutes) than the latter. Although no apnea occurred in either group, the rate of desaturations was significantly greater in the propofol/fentanyl group (31% versus 7%). Ketamine proponents will argue that the longer recoveries typical of this agent are perhaps counterbalanced by the simpler personnel requirements (ie, no emergency physician dedicated to monitoring throughout) and diminished concern regarding aspiration risk and fasting because of the unique retention of protective airway reflexes with ketamine. Thus, the selection between ketamine and propofol for procedural sedation and analgesia in children will likely depend on unique institutional experience, resources, and the extent of concern regarding aspiration risk. Perhaps the greatest ED potential for propofol will be for brief, intensely painful procedures (eg, cardioversion, hip relocation) in adults. Ketamine is not suitable for many adults,38 particularly the elderly, and there are not yet large enough prospective series using methohexital or etomidate to reliably profile their safety for ED procedural sedation and analgesia. Hopefully, the successes noted in the current studies will spur investigators to compile large safety series of propofol in adults. So is propofol now “ready for prime time” in emergency medicine? Apparently it is—within the framework of a rigorous protocol and appropriate patient monitoring. Some anesthesiologists will maintain that studies the size of those existing for general anesthesia, literally hundreds of thousands of cases, are necessary to validate the profile of newer procedural sedation and analgesia agents. However, essentially nothing in the rest of medicine can possibly measure up to this standard of scrutiny. Most established therapies are based
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on hundreds rather than thousands of patients, and ED practice patterns and standard of care must of necessity be based on smaller samples. We do not have absolute proof of safety (as we similarly do not have with ketamine or fentanyl/midazolam), but we now have enough evidence for propofol to be an acceptable standard of care (like ketamine and fentanyl/midazolam) in emergency medicine. The positive experience noted in the current studies should ideally be replicated in both academic and community ED settings, and the addition of capnography and objective scoring of sedation depth is highly desirable. If serious adverse outcomes such as aspiration should occur with propofol, or any other procedural sedation and analgesia agents for that matter, they should be promptly reported in the literature. Practitioners must be vigilant in their monitoring and in their avoidance of oversedation and extremely careful in their sedation of patients with recent oral intake. They must be prepared to justify the safety of this agent in their hands, as was similarly done with ketamine in the previous decade. Regardless of the remaining questions and ongoing controversy, however, it appears that propofol has now rightfully earned its place in emergency medicine. The authors report this study did not receive any outside funding or support. Dr. Krauss is a paid consultant of Oridion, Inc., a capnography manufacturer. Reprints not available from the authors. Address for correspondence: Steven M. Green, MD, Loma Linda University Medical Center, A-108, 11234 Anderson Street, Loma Linda, CA 92354; E-mail [email protected].
REFERENCES 1. Swanson ER, Seaberg DC, Stypula RW, et al. Propofol for conscious sedation: a case series [letter]. Acad Emerg Med. 1995;2:661-663. 2. Swanson ER, Seaberg DC, Mathias S. The use of propofol for sedation in the emergency department. Acad Emerg Med. 1996;3:234-238. 3. Havel CJ, Strait RT, Hennes H. A clinical trial of propofol vs midazolam for procedural sedation in a pediatric emergency department. Acad Emerg Med. 1999;6:989-997. 4. Guenther-Skokan E, Pribble C, Bassett KE, et al. Use of propofol sedation in a pediatric emergency department: a prospective study. Clin Pediatr (Phila). 2001;40:663-671. 5. Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med. 2002;9:275-280. 6. Godambe SA, Elliot V, Matheny D, et al. Comparison of propofol/fentanyl versus ketamine/midazolam for brief orthopedic procedural sedation in a pediatric emergency department. Pediatrics. 2003;112:116-123. 7. Miner JR, Biros MH, Heegaard W, et al. Bispectral electroencephalographic analysis of patients undergoing procedural sedation in the emergency department. Acad Emerg Med. 2003;10:638-643. 8. Miner JR, Krieg S, Johnson C, et al. Randomized clinical trial of propofol versus methohexital for procedural sedation during fracture and dislocation reduction in the emergency department. Acad Emerg Med. 2003;10:931-937.
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9. Ducharme J. Propofol in the emergency department: another interpretation of the evidence. Can J Emerg Med. 2001;3:311-312. 10. Joint Commission on Accreditation of Healthcare Organizations. Sedation and Anesthesia Care standards. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations; 2003. 11. Green SM, Krauss B. Pulmonary aspiration risk during ED procedural sedation: an examination of the role of fasting and sedation depth. Acad Emerg Med. 2002;9:35-42. 12. Green SM. Propofol for emergency department procedural sedation: not yet ready for prime time. Acad Emerg Med. 1999;6:975-978. 13. Lowrie L, Weiss AH, Lacombe C. The pediatric sedation unit: a mechanism for pediatric sedation. Pediatrics. 1998;102:e30. 14. Means LJ, Ferrari L, Mancuso TJ, et al. The pediatric sedation unit: a mechanism for safe pediatric sedation [letter]. Pediatrics. 1999;103:199-201. 15. American Society of Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 1996;84:459-471. 16. American Society of Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 2002;96:1004-1017. 17. Coll-Vinent B, Sala X, Fernández C, et al. Sedation for cardioversion in the emergency department: analysis of effectiveness in four protocols. Ann Emerg Med. 2003;42:767-772. 18. Bassett KE, Anderson JL, Pribble CG, et al. Propofol for procedural sedation in children in the emergency department. Ann Emerg Med. 2003;42:773-782. 19. Pena BMG, Krauss B. Adverse events of procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med. 1999;34:483-490. 20. Guenther E, Pribble CG, Junkins EP Jr, et al. Propofol sedation by emergency physicians for elective pediatric outpatient procedures. Ann Emerg Med. 2003;42:783-791. 21. Patel R, Lenczyk M, Hannallah RS, et al. Age and the onset of desaturation in apnoeic children. Can J Anaesth. 1994;41:771-774 22. Poirier MP, Gonzalez Del-Rey JA, McAneney CM, et al. Utility of monitoring capnography, pulse oximetry, and vital signs in the detection of airway mishaps: a hyperoxemic animal model. Am J Emerg Med. 1998;16:350-352. 23. Kaneko Y. Clinical perspectives on capnography during sedation and general anesthesia in dentistry. Anesthesia Progress. 1995;42:126-130. 24. Hart LS, Berns SD, Houck CS, et al. The value of end-tidal CO2 monitoring when comparing three methods of procedural sedation for children undergoing painful procedures in the emergency department. Pediatr Emerg Care. 1997;13:189-193. 25. Anderson JA, Vann WF. Respiratory monitoring during pediatric sedation: pulse oximetry and capnography. Pediatr Dent. 1988;10:94-101. 26. Weingarten M. Respiratory monitoring of carbon dioxide and oxygen: a ten-year retrospective. J Clin Monit. 1990;6:217-225. 27. Cote CJ, Liu LM, Szyfelbein SK, et al. Intraoperative events diagnosed by expired carbon dioxide monitoring in children. Can Anaesth Soc J. 1986;33:315-320. 28. Vargo JJ, Zuccaro G, Dumot JA, et al. Automated graphic assessment of respiratory activity is superior to pulse oximetry and visual assessment for the detection of early respiratory depression during therapeutic upper endoscopy. Gastrointest Endosc. 2002;55:826-831. 29. Croswell RJ, Dilley DC, Lucas WJ, et al. A comparison of conventional versus electronic monitoring of sedated pediatric dental patients. Pediatr Dentistry. 1995;17:332-329. 30. Muttitt SC, Finer NN, Tierney AJ, et al. Neonatal apnea: diagnosis by nurse versus computer. Pediatrics. 1988;82:713-720. 31. Farmery AD, Roe PG. A model to describe the rate of oxyhaemoglobin desaturation during apnoea. Br J Anaesth. 1996;76:284-291. 32. American Academy of Pediatrics Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics. 1992;89:1110-1115. 33. American Academy of Pediatrics Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: addendum. Pediatrics. 2002;110:836-838. 34. American Society of Anesthesiologists. Standards for basic anesthetic monitoring. Available at: http://www.asahq.org/publicationsAndServices/standards/02.html. Accessed July 22, 2003. 35. Green SM. Fasting is a consideration—not a necessity—for emergency department procedural sedation and analgesia. Ann Emerg Med. 2003;42:647-650. 36. Agrawal D, Manzi SF, Gupta R, et al. Preprocedural fasting state and adverse events in children undergoing procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med. 2003;42:636-646. 37. American Society of Anesthesiologists. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. Anesthesiology. 1999;90:896-905. 38. Green SM, Li J. Ketamine in adults: what emergency physicians need to know about patient selection and emergence reactions. Acad Emerg Med. 2000;7:278-281.
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Propofol in Emergency Medicine: Pushing the Sedation Frontier Steven M. Green, MD Baruch Krauss, MD, EdM From the Department of Emergency Medicine, Loma Linda University Medical Center and Children’s Hospital, Loma Linda, CA (Green); and the Division of Emergency Medicine, Children’s Hospital and Harvard Medical School, Boston, MA (Krauss).
See related articles, p. 767, p. 773, and p. 783. [Ann Emerg Med. 2003;42:792-797.]
Is propofol an appropriate agent for use as part of emergency department (ED) procedural sedation and analgesia? Few questions in emergency medicine are currently as controversial. No one disputes that propofol exhibits numerous exceptionally desirable characteristics as a procedural sedation and analgesia agent. First, its clinical effect is essentially immediate after intravenous administration (“one arm–brain circulatory time”). Second, its marked potency reliably produces effective procedural sedation and analgesia conditions, even for very painful procedures. Third, recovery after sedation is extremely short, typically between 5 and 15 minutes. Finally, patient satisfaction is high because propofol has anti-emetic and apparent euphoric properties. It is no wonder that this agent has revolutionized anesthesiology practice. Many emergency physicians have already extrapolated this proven operating room success to our setting, using propofol as a single agent or in combination with an opioid, to successfully induce brief but potent sedation for short, painful procedures such as orthopedic manipulations, cardioversion, and abscess drainage. However, this application is based on limited experience because, thus far, only 8 small series of ED propofol use have been formally reported (Table).1-8 Despite this, proponents believe that there are sufficient stud-
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ies in the anesthesia literature demonstrating the safety and efficacy of propofol to justify its use in the ED.9 Although hypotension, apnea, pain on injection, and bacterial contamination of the lipid emulsion have been reported, the primary criticism of propofol for procedural sedation and analgesia has focused on the greater sedation depth that typically results from propofol. Using the traditional propofol for procedural sedation and analgesia combination of midazolam and fentanyl, emergency physicians can reliably (albeit laboriously) titrate patients to either a state of “moderate sedation” (ie, purposeful responsive to verbal or tactile stimulation)10 or “deep sedation” (ie, purposeful responsive to repeated or painful stimulation).10 It is widely accepted that such moderate sedation is unlikely to be associated with impairment of protective airway reflexes, and thus aspiration risk in this setting is minimized.11 In contrast, however, the ultrarapid onset and high potency of propofol make it more difficult to titrate and prone to potentially substantial overshoot. Within 30 seconds of a single intravenous dose of propofol, a patient’s sedation depth could, without always a high level of predictability, be compatible with moderate sedation, deep sedation, or perhaps general anesthesia.12 Although all nondissociative sedatives can induce depth at all levels of the sedation continuum, in practice, propofol is primarily used for deep sedation.3-8,13 Anesthesiologists have been especially concerned about propofol use by nonanesthesiologists14 and have not differentiated such practitioners by skill set, lumping together emergency physicians with dentists, radiologists, and gastroenterologists.15,16 Pharmacy and therapeutics committees in many hospitals have blocked use of propofol for ED procedural sedation and analgesia because of objection by anesthesiologists on the committee. The paucity of data on the safety of propofol for ED procedural sedation and analgesia has made it difficult at times to overcome these objections. Four years ago, one of us characterized propofol as “not yet ready for prime time” in emergency medicine.12 This cautionary commentary raised concerns regarding the risk of inadvertent oversedation with propofol, personnel requirements, Joint Commission on Accreditation of Healthcare Organizations (JCAHO) standards, and fasting in the setting of deep sedation. Large case
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series were recommended to better characterize the safety of this agent in the unique hands of emergency physicians. Three articles in the current issue of Annals substantially advance our understanding of propofol in emergency medicine and address many of these important issues. Coll-Vinent et al17 report a small but elegant randomized controlled trial of 4 different sedative regimens for ED cardioversion of adults with atrial fibrillation. A major strength of this study is that the 4 sedative regimens were compared using this identical brief but highly painful procedure. In contrast, most ED procedural sedation and analgesia research has been complicated by the inclusion of a wide variety of procedures requiring a wide range of sedation depth. Although Coll-Vinent et al found all regimens to be effective, propofol demonstrated exceptionally short recovery times (median 10 minutes) and a favorable adverseeffect profile. Etomidate was judged less desirable as a result of associated myoclonus, which was generalized and intense in one case. Midazolam demonstrated substantially longer recoveries, and attempts in a fourth trial arm to shorten recovery time with flumazenil were unsuccessful because of resedation. Bassett et al18 report the largest series to date of propofol use for ED procedural sedation and analgesia.
They prospectively developed and implemented a protocol at their children’s hospital and then performed 393 consecutive sedation events over a 2-year period. Efficacy for these primarily orthopedic manipulations was uniformly high, and adverse events were less than reported in prior series. They noted hypoxia in 5%, partial airway obstruction requiring airway repositioning in 3%, and apnea with assisted ventilation in 0.8%. This is not substantially higher than adverse effect rates established for midazolam and fentanyl (1.3% desaturation, 0.3% assisted ventilation)19 and provides the first large-denominator safety profile for ED propofol. At this same children’s hospital ED, Guenther et al20 report their experience administering propofol procedural sedation and analgesia for elective procedures in a short-stay unit immediately adjacent to the ED. Emergency physicians performed 291 consecutive prescheduled sedation events primarily for oncologic procedures, with uniform efficacy and a similar profile of adverse airway events (hypoxia in 5%, partial airway obstruction requiring airway repositioning in 4%, apnea with assisted ventilation in 1%). Although these were not ED patients, this series further reinforces the capability of emergency physicians to administer propofol. Additionally, it provides a stimulus for other EDs to develop similar “sedation units” so that our procedural
Table.
Published research on propofol administration in emergency medicine.* Study
Patients
Dose
Existing publications Swanson et al1 Swanson et al2 Havel et al3
4 adults 20 adults 43 children
0.14 mg/kg/min titrated 0.21 mg/kg/min titrated 1 mg/kg load, then infusion
Guenther-Skokan et al4 Miner et al5 Godambe et al6
40 children 21 adults 59 children
Miner et al7 Miner et al8 New in this issue Coll-Vinent et al17 Bassett et al18
54 adults 51 adults
1 mg/kg load, then 0.5 mg/kg prn Not stated 1 mg/kg load, then “smaller aliquots” prn Not stated 1 mg/kg load, then 0.5 mg/kg prn
9 adults 393 children
1.5 mg/kg bolus 1 mg/kg load, then 0.5 mg/kg prn
Guenther et al20
291 children
1 mg/kg load, then 0.5 mg/kg prn
Adverse Effects
None 2 apnea (1 with assisted ventilation) 5 hypoxia (12%) 14 “oversedation” (32%) 12 hypoxia (30%) 4 respiratory depression (19%), 1 with hypoxia. No assisted ventilation 18 hypoxia (31%) No apnea events 22 respiratory depression (41%), 5 with hypoxia and 5 with assisted ventilation 25 respiratory depression (49%), 5 with hypoxia and 2 with assisted ventilation 4 hypoxia, 2 apnea 19 hypoxia (5%) 11 partial airway obstruction requiring airway repositioning (3%) 3 apnea with assisted ventilation (0.8%) 15 hypoxia (5%) 12 partial airway obstruction requiring airway repositioning (4%) 3 apnea with assisted ventilation (1%) 1 bradycardia (0.3%)
prn, As needed. * Excluding abstracts.
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sedation and analgesia skills can benefit other lessskilled practitioners. Perhaps the most remarkable feature of the study by Guenther et al,20 however, is that essentially all of the sedated children had advanced underlying illness. Ninety percent were American Society of Anesthesiologists (ASA) physical status classification 3 (“a patient with severe systemic disease”), and patients in such higher ASA classes have traditionally been considered at greater risk for procedural sedation and analgesia complications. Despite this, the adverse event profile was essentially identical to the healthy ED patients (97% ASA class 1 and 3% ASA class 2) reported by Bassett et al.18 The adults in the study by Coll-Vinent et al17 all had substantial underlying cardiac disease, although the sample size of this study was too small to reliably profile safety. The studies by Bassett et al18 and Guenther et al20 are also significant in confirming the safety of simple bolus dosing (ie, a 1 mg/kg load followed by 0.5 mg/kg as required). Prior studies by Swanson et al1,2 and Havel et al3 have recommended more complicated syringe infusion pumps. Taken in aggregate, these 3 studies lend further evidence for the efficacy of propofol and show that emergency physicians can, in accordance with a clearly defined protocol, administer propofol with a low rate of adverse events, all of which were minor and successfully managed without adverse outcomes. Many emergency physicians will regard these reports as a longawaited validation of the safety of propofol in the ED and a green light toward widespread implementation of this agent for procedural sedation and analgesia. Although these studies have advanced our knowledge of ED propofol use, some important questions remain. What is the incidence and extent of respiratory depression with propofol?
The Bassett et al18 and Guenther et al20 studies report rates of hypoxia and assisted ventilation (Table) only slightly higher than those typical of midazolam and fentanyl. A higher incidence would reasonably be expected because of propofol’s greater potency, and indeed prior studies (including from this same institution) report hypoxia in up to 30%.3,4,6 Was this dramatic decrease in adverse effects the result of improved operator experience? It is certainly possible; however, the more likely explanation is that most cases of respiratory depression were instead masked in the new studies by the addition of high-flow (5 to 10 L/min) supplemental oxygen. Such
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preoxygenated patients can tolerate respiratory depression and even frank apnea for 1 to 3 minutes, depending on age and underlying physical status, without an apparent oxygen desaturation or need for assisted ventilation.21 The authors did not use capnography, and so the incidence and extent of actual respiratory depression was not quantified. The only capnography data with ED propofol thus far come from Miner et al,5,7,8 who found hypercapnia in 19% to 49%. These data provide compelling evidence that transient, subclinical respiratory depression is likely to be typical with this agent. Such knowledge, combined with the positive experience noted in the studies by Bassett et al18 and Guenther et al,20 suggests that supplemental oxygen should perhaps be routine during all propofol sedation. The most serious procedural sedation and analgesia complication in emergency medicine is aspiration, not respiratory depression, and accordingly we would prefer to avoid assisting ventilations (and thereby insufflating the stomach) whenever possible. Given the ultrashort duration of action of propofol, it would appear probable that, in many circumstances, one could simply “wait out” an occurrence of propofol-associated respiratory depression, assuming substantial preoxygenation. In contrast, such an expectation would not be reasonable for midazolam or other longer-acting sedatives. The primary argument against the use of supplemental oxygen during procedural sedation and analgesia is that pulse oximetry constitutes a fail-safe, that is, it is a mechanical marker of respiratory depression should it for some reason be overlooked clinically. Administration of high-flow oxygen throughout deep sedation largely negates this capability,22-25 creating a compelling case for the addition of capnography to routine deep sedation monitoring. Capnography is equally accurate with and without supplemental oxygen. Capnography has been shown to be the earliest indicator of acute airway obstruction, respiratory depression, apnea, and laryngospasm5,22,23,26-28; a direct and accurate measure of respiratory rate28; and a more sensitive monitor than health professionals in detecting respiratory compromise.27-30 Early detection of respiratory compromise is especially important in infants and toddlers who have smaller functional residual capacity and greater oxygen consumption relative to older children or adults.21,31 Continuous oxygenation and ventilation monitoring during procedural sedation and analgesia would permit ready mechanical detection of hypoxia and respiratory
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depression and apnea regardless of supplemental oxygen. The use of these combined technologies for ED propofol sedation is strongly recommended. Is ED administration of propofol deep sedation or general anesthesia? Does this distinction matter clinically?
Whether propofol procedural sedation and analgesia induces general anesthesia or deep sedation has been, and continues to be, an emotional flash point.14 According to JCAHO definitions, the characteristic that distinguishes the 2 states is the presence or absence of a “purposeful response following repeated or painful stimulation.”10 Unfortunately, none of the 3 new propofol studies report their sedation depth in a manner directly comparable with JCAHO definitions. Bassett et al18 and Guenther et al20 describe a target endpoint—“tolerance of noxious stimuli without patient complaint”—which is technically compatible with either state. Coll-Vinent et al17 used Ramsay scale scoring and noted that the maximal sedation for all of their patients was 6 (ie, “no response” to pain; a score of 5 would have been “sluggish response to pain,” similar to deep sedation). Thus, it seems reasonable to assume that all of Coll-Vinent et al’s patients experienced transient general anesthesia, and that at least some of Bassett et al and Guenther et al’s patients met this technical standard as well. Assuming that some or most of these patients crossed the amorphous boundary between deep sedation and general anesthesia, is this distinction clinically relevant, or does it instead represent a political squabble of semantics? Indeed, procedural sedation and analgesia guidelines from the American Academy of Pediatrics do not differentiate the states and consider them equivalent in terms of patient monitoring and risk of adverse events (“the state and risks of deep sedation may be indistinguishable from those of general anesthesia” and “deep sedation and general anesthesia are virtually inseparable for purposes of monitoring”).32,33 Despite these perceptions of nuance, the distinction between these 2 entities will remain important because of differential aspiration risk (detailed in the next section), hospital credentialing, and JCAHO standards. In most hospitals in the United States, emergency physicians are credentialed for moderate and deep sedation, with general anesthesia privileges limited to rapid sequence intubation. Thus, any propofol technique achieving consistent general anesthesia might quickly lead to hospital-initiated restrictions based on scope of practice. Emergency physicians must be cog-
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nizant of their specific hospital privileges and any restrictions or credentialing requirements imposed by their local JCAHO-mandated hospital-wide sedation policies. The JCAHO does not prohibit propofol use by emergency physicians. Instead, it permits individual hospitals to set their own policies on the basis of their resources and perspectives. The caveat is that the standards of sedation care must be “comparable” throughout the institution. “Comparable” does not necessarily mean “identical,” and thus practices in the ED and other hospital areas, such as the operating room, may differ to the degree that the global standard of care is not compromised and the variance is reasonable. Recent changes in the ASA standards for basic anesthetic monitoring mandate that anesthesiologists use capnography for all general anesthesia care (intubated and nonintubated patients, in and out of the operating room).34 Thus, it would behoove emergency physicians to add capnography to their propofol protocols to better mirror the propofol practices of anesthesiologists. What is the risk of aspiration with propofol?
Aspiration is the most feared complication of ED procedural sedation and analgesia and, fortunately, has not been reported in our setting.35 The JCAHO monikers of moderate and deep sedation are in and of themselves not clinically important. Instead, these arbitrary categories of patient responsiveness are intended as surrogate markers for important items such as loss of protective airway reflexes and cardiopulmonary depression. There is no dispute that mild to moderate sedation is associated with consistent retention of protective airway reflexes and that, on the other end of the sedation continuum, inhalational general anesthesia is associated with consistent loss of these airway reflexes. In the continuum between these extremes is deep sedation, which “may be accompanied by a partial or complete loss of protective reflexes.”32,33 The exact point at which such reflex loss becomes clinically important is unknown, because there are no research data to answer this critical question and there is no safe and practical way to assess the status of protective airway reflexes. Critics of ED propofol use will maintain that pushing the deep sedation frontier represents an inordinate risk of aspiration. Furthermore, they will argue that in the ED this particular risk is enhanced because patients will not always be fasted to the extent typical for elective preoperative guidelines.35,36 In the current propofol stud-
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ies, the elective short-stay unit patients of Guenther et al20 were fasted according to ASA guidelines for elective anesthesia,37 and those of Coll-Vinent et al17 were fasted 4 hours. The ED protocol of Bassett et al18 stipulated no oral intake within 3 hours; however, these authors acknowledge subsequent protocol violations in 13%. Despite these criticisms, there is currently no evidence to document that propofol (as used in the current studies) impairs airway reflexes to any clinically important degree. Secondly, ED procedures are short and most of these journeys to the deep sedation frontier are brief—lasting from seconds to several minutes. This is distinctly different from the prolonged anesthesia cases typical of the operating room where adverse events have been shown to increase with the length of general anesthesia.27 Thirdly, propofol is an anti-emetic, and vomiting with this agent is rare. Finally, the ASA elective fasting guidelines are consensus based rather than evidence based,37 and cannot be specifically extrapolated to the nonelective ED setting.11,35 Thus, despite a full realization that pushing beyond the deep sedation frontier will result in general anesthesia and loss of protective airway reflexes, there is no evidence that propofol as administered in the current studies creates undue aspiration risk. Certainly, practitioners must carefully adhere to widely accepted recommendations for minimizing aspiration risk,11,35 including the aggressive avoidance of oversedation and the need for assisted ventilation. Although the necessity of routine presedation fasting before moderate and dissociative sedation is open to debate,35 the aspiration risk with deep sedation (and especially its frontier) is undoubtedly higher. A substantially more conservative stance is therefore indicated when individualizing decisions regarding propofol procedural sedation and analgesia in the setting of recent oral intake. What are the indications for use of propofol for ED procedural sedation and analgesia?
The optimal role for propofol would appear to be for procedures such as those performed in these 3 new reports: either brief, intensely painful procedures (eg, cardioversion, orthopedic manipulation, bone marrow aspiration) or brief interventions that require marked anxiolysis and immobilization to be accomplished (eg, ocular burn examination, intrathecal medication administration). The key word here is “brief.” Use of propofol for longer procedures (eg, complex laceration repair) would require repeated dosing of this extremely short-acting agent or the initiation and titration of an
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infusion. The safety profile of extended propofol administration in the ED setting cannot be verified by the current reports and cannot be recommended pending further research. So, which is preferable for pediatric ED procedural sedation and analgesia—propofol or ketamine? Both create superb procedural conditions for these highly painful procedures. The primary advantage of propofol over ketamine lies in its brief recoveries; discharge times after completion of procedures occurred in a median of 18 minutes in the Bassett et al18 study and a median of 25 minutes in the Guenther et al20 study. Indeed, Godambe et al6 compared propofol/fentanyl and ketamine/midazolam for pediatric orthopedic procedures and found that the former agents exhibited a shorter mean recovery time (by 23 minutes) and total sedation time (by 33 minutes) than the latter. Although no apnea occurred in either group, the rate of desaturations was significantly greater in the propofol/fentanyl group (31% versus 7%). Ketamine proponents will argue that the longer recoveries typical of this agent are perhaps counterbalanced by the simpler personnel requirements (ie, no emergency physician dedicated to monitoring throughout) and diminished concern regarding aspiration risk and fasting because of the unique retention of protective airway reflexes with ketamine. Thus, the selection between ketamine and propofol for procedural sedation and analgesia in children will likely depend on unique institutional experience, resources, and the extent of concern regarding aspiration risk. Perhaps the greatest ED potential for propofol will be for brief, intensely painful procedures (eg, cardioversion, hip relocation) in adults. Ketamine is not suitable for many adults,38 particularly the elderly, and there are not yet large enough prospective series using methohexital or etomidate to reliably profile their safety for ED procedural sedation and analgesia. Hopefully, the successes noted in the current studies will spur investigators to compile large safety series of propofol in adults. So is propofol now “ready for prime time” in emergency medicine? Apparently it is—within the framework of a rigorous protocol and appropriate patient monitoring. Some anesthesiologists will maintain that studies the size of those existing for general anesthesia, literally hundreds of thousands of cases, are necessary to validate the profile of newer procedural sedation and analgesia agents. However, essentially nothing in the rest of medicine can possibly measure up to this standard of scrutiny. Most established therapies are based
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on hundreds rather than thousands of patients, and ED practice patterns and standard of care must of necessity be based on smaller samples. We do not have absolute proof of safety (as we similarly do not have with ketamine or fentanyl/midazolam), but we now have enough evidence for propofol to be an acceptable standard of care (like ketamine and fentanyl/midazolam) in emergency medicine. The positive experience noted in the current studies should ideally be replicated in both academic and community ED settings, and the addition of capnography and objective scoring of sedation depth is highly desirable. If serious adverse outcomes such as aspiration should occur with propofol, or any other procedural sedation and analgesia agents for that matter, they should be promptly reported in the literature. Practitioners must be vigilant in their monitoring and in their avoidance of oversedation and extremely careful in their sedation of patients with recent oral intake. They must be prepared to justify the safety of this agent in their hands, as was similarly done with ketamine in the previous decade. Regardless of the remaining questions and ongoing controversy, however, it appears that propofol has now rightfully earned its place in emergency medicine. The authors report this study did not receive any outside funding or support. Dr. Krauss is a paid consultant of Oridion, Inc., a capnography manufacturer. Reprints not available from the authors. Address for correspondence: Steven M. Green, MD, Loma Linda University Medical Center, A-108, 11234 Anderson Street, Loma Linda, CA 92354; E-mail [email protected].
REFERENCES 1. Swanson ER, Seaberg DC, Stypula RW, et al. Propofol for conscious sedation: a case series [letter]. Acad Emerg Med. 1995;2:661-663. 2. Swanson ER, Seaberg DC, Mathias S. The use of propofol for sedation in the emergency department. Acad Emerg Med. 1996;3:234-238. 3. Havel CJ, Strait RT, Hennes H. A clinical trial of propofol vs midazolam for procedural sedation in a pediatric emergency department. Acad Emerg Med. 1999;6:989-997. 4. Guenther-Skokan E, Pribble C, Bassett KE, et al. Use of propofol sedation in a pediatric emergency department: a prospective study. Clin Pediatr (Phila). 2001;40:663-671. 5. Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med. 2002;9:275-280. 6. Godambe SA, Elliot V, Matheny D, et al. Comparison of propofol/fentanyl versus ketamine/midazolam for brief orthopedic procedural sedation in a pediatric emergency department. Pediatrics. 2003;112:116-123. 7. Miner JR, Biros MH, Heegaard W, et al. Bispectral electroencephalographic analysis of patients undergoing procedural sedation in the emergency department. Acad Emerg Med. 2003;10:638-643. 8. Miner JR, Krieg S, Johnson C, et al. Randomized clinical trial of propofol versus methohexital for procedural sedation during fracture and dislocation reduction in the emergency department. Acad Emerg Med. 2003;10:931-937.
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9. Ducharme J. Propofol in the emergency department: another interpretation of the evidence. Can J Emerg Med. 2001;3:311-312. 10. Joint Commission on Accreditation of Healthcare Organizations. Sedation and Anesthesia Care standards. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations; 2003. 11. Green SM, Krauss B. Pulmonary aspiration risk during ED procedural sedation: an examination of the role of fasting and sedation depth. Acad Emerg Med. 2002;9:35-42. 12. Green SM. Propofol for emergency department procedural sedation: not yet ready for prime time. Acad Emerg Med. 1999;6:975-978. 13. Lowrie L, Weiss AH, Lacombe C. The pediatric sedation unit: a mechanism for pediatric sedation. Pediatrics. 1998;102:e30. 14. Means LJ, Ferrari L, Mancuso TJ, et al. The pediatric sedation unit: a mechanism for safe pediatric sedation [letter]. Pediatrics. 1999;103:199-201. 15. American Society of Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 1996;84:459-471. 16. American Society of Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 2002;96:1004-1017. 17. Coll-Vinent B, Sala X, Fernández C, et al. Sedation for cardioversion in the emergency department: analysis of effectiveness in four protocols. Ann Emerg Med. 2003;42:767-772. 18. Bassett KE, Anderson JL, Pribble CG, et al. Propofol for procedural sedation in children in the emergency department. Ann Emerg Med. 2003;42:773-782. 19. Pena BMG, Krauss B. Adverse events of procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med. 1999;34:483-490. 20. Guenther E, Pribble CG, Junkins EP Jr, et al. Propofol sedation by emergency physicians for elective pediatric outpatient procedures. Ann Emerg Med. 2003;42:783-791. 21. Patel R, Lenczyk M, Hannallah RS, et al. Age and the onset of desaturation in apnoeic children. Can J Anaesth. 1994;41:771-774 22. Poirier MP, Gonzalez Del-Rey JA, McAneney CM, et al. Utility of monitoring capnography, pulse oximetry, and vital signs in the detection of airway mishaps: a hyperoxemic animal model. Am J Emerg Med. 1998;16:350-352. 23. Kaneko Y. Clinical perspectives on capnography during sedation and general anesthesia in dentistry. Anesthesia Progress. 1995;42:126-130. 24. Hart LS, Berns SD, Houck CS, et al. The value of end-tidal CO2 monitoring when comparing three methods of procedural sedation for children undergoing painful procedures in the emergency department. Pediatr Emerg Care. 1997;13:189-193. 25. Anderson JA, Vann WF. Respiratory monitoring during pediatric sedation: pulse oximetry and capnography. Pediatr Dent. 1988;10:94-101. 26. Weingarten M. Respiratory monitoring of carbon dioxide and oxygen: a ten-year retrospective. J Clin Monit. 1990;6:217-225. 27. Cote CJ, Liu LM, Szyfelbein SK, et al. Intraoperative events diagnosed by expired carbon dioxide monitoring in children. Can Anaesth Soc J. 1986;33:315-320. 28. Vargo JJ, Zuccaro G, Dumot JA, et al. Automated graphic assessment of respiratory activity is superior to pulse oximetry and visual assessment for the detection of early respiratory depression during therapeutic upper endoscopy. Gastrointest Endosc. 2002;55:826-831. 29. Croswell RJ, Dilley DC, Lucas WJ, et al. A comparison of conventional versus electronic monitoring of sedated pediatric dental patients. Pediatr Dentistry. 1995;17:332-329. 30. Muttitt SC, Finer NN, Tierney AJ, et al. Neonatal apnea: diagnosis by nurse versus computer. Pediatrics. 1988;82:713-720. 31. Farmery AD, Roe PG. A model to describe the rate of oxyhaemoglobin desaturation during apnoea. Br J Anaesth. 1996;76:284-291. 32. American Academy of Pediatrics Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics. 1992;89:1110-1115. 33. American Academy of Pediatrics Committee on Drugs. Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: addendum. Pediatrics. 2002;110:836-838. 34. American Society of Anesthesiologists. Standards for basic anesthetic monitoring. Available at: http://www.asahq.org/publicationsAndServices/standards/02.html. Accessed July 22, 2003. 35. Green SM. Fasting is a consideration—not a necessity—for emergency department procedural sedation and analgesia. Ann Emerg Med. 2003;42:647-650. 36. Agrawal D, Manzi SF, Gupta R, et al. Preprocedural fasting state and adverse events in children undergoing procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med. 2003;42:636-646. 37. American Society of Anesthesiologists. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. Anesthesiology. 1999;90:896-905. 38. Green SM, Li J. Ketamine in adults: what emergency physicians need to know about patient selection and emergence reactions. Acad Emerg Med. 2000;7:278-281.
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