While it is very hard job to choose trustworthy certification questions / answers resources with respect to review, reputation and validity because people find ripoff due to choosing wrong service. Killexams.com fabricate it sure to serve its clients best to its resources with respect to exam dumps update and validity. Most of other's ripoff report complaint clients near to us for the brain dumps and pass their exams happily and easily. They never compromise on their review, reputation and character because killexams review, killexams reputation and killexams client self-confidence is valuable to us. Specially they win supervision of killexams.com review, killexams.com reputation, killexams.com ripoff report complaint, killexams.com trust, killexams.com validity, killexams.com report and killexams.com scam. If you view any erroneous report posted by their competitors with the appellation killexams ripoff report complaint internet, killexams.com ripoff report, killexams.com scam, killexams.com complaint or something enjoy this, just sustain in intellect that there are always obnoxious people damaging reputation of obliging services due to their benefits. There are thousands of satisfied customers that pass their exams using killexams.com brain dumps, killexams PDF questions, killexams rehearse questions, killexams exam simulator. Visit Killexams.com, their sample questions and sample brain dumps, their exam simulator and you will definitely know that killexams.com is the best brain dumps site.
Back to Braindumps Menu
000-399 test prep | 000-M50 existent questions | AHIMA-CCS rehearse test | 70-543-CSharp pdf download | 000-235 cram | M2150-768 questions answers | C2170-051 brain dumps | 000-875 braindumps | 920-132 free pdf download | 156-915-65 existent questions | M2065-659 dumps questions | ST0-066 study guide | M2010-720 rehearse test | 000-349 cheat sheets | 2VB-602 mock exam | M2040-671 questions and answers | 00M-227 dump | COG-605 rehearse questions | 920-259 dumps | A4040-124 rehearse questions |
Murder your 920-324 exam at first attempt!
killexams.com Nortel Certification commemorate publications are setup by means of IT experts. Lots of students had been complaining that there are too many questions in such a lot of rehearse assessments and exam guides, and they are just worn-out to maintain enough money any more. Seeing killexams.com professionals drudgery out this comprehensive version at the very time as nonetheless assure that every one the understanding is blanketed after deep studies and analysis.
Inside seeing the existent braindumps of the brain dumps at killexams.com you will gladden to know that every actual test is available here. For the IT professionals, they maintain provided almost All exam question with explanations and reference where applicable. they maintain an approach to build it straightforward for their shoppers to hold certification test with the assist of killexams.com confirmed and hearty to goodness braindumps. For an excellent destiny in its space, their brain dumps are the satisfactory choice.
killexams.com Discount Coupons and Promo Codes are as under;
WC2017 : 60% Discount Coupon for All exams on web site
PROF17 : 10% Discount Coupon for Orders over $69
DEAL17 : 15% Discount Coupon for Orders over $99
SEPSPECIAL : 10% Special Discount Coupon for All Orders
A high-quality dumps making will subsist a basic section that creates it honest for you to require Nortel certifications. In any case, 920-324 braindumps PDF offers agreement for candidates. The IT declaration will subsist a very valuable robust enterprise if one does not determine actual route as obvious rehearse test. Thus, they maintain got actual and updated dumps for the composition of certification test.
At killexams.com, they provide completely verified Nortel 920-324 actual Questions and Answers that are simply needed for Passing 920-324 exam, and to induce certified with the assistance of 920-324 braindumps. they maintain an approach to nearly assist people improve their understanding to memorize the and certify. It is a wonderful preference to spice up your profession as an expert within the business.
High character 920-324 products: they maintain their experts Team to ensure their Nortel 920-324 exam questions are always the latest. They are All very chummy with the exams and testing center.
How they sustain Nortel 920-324 exams updated?: they maintain their special ways to know the latest exams information on Nortel 920-324. Sometimes they contact their partners who are very chummy with the testing heart or sometimes their customers will email us the most recent feedback, or they got the latest feedback from their dumps market. Once they find the Nortel 920-324 exams changed then they update them ASAP.
Money back guarantee?: if you really fail this 920-324 Communication Server (CS) Rls. 4.0 Database Administrator and don’t want to wait for the update then they can give you full refund. But you should forward your score report to us so that they can maintain a check. They will give you full refund immediately during their working time after they find the Nortel 920-324 score report from you.
Nortel 920-324 Communication Server (CS) Rls. 4.0 Database Administrator Product Demo?: they maintain both PDF version and Software version. You can check their software page to view how it looks like.
killexams.com Huge Discount Coupons and Promo Codes are as under;
WC2017 : 60% Discount Coupon for All exams on website
PROF17 : 10% Discount Coupon for Orders greater than $69
DEAL17 : 15% Discount Coupon for Orders greater than $99
DECSPECIAL : 10% Special Discount Coupon for All Orders
When will I find my 920-324 material after I pay?: Generally, After successful payment your username/password are sent at your email address within 5 min. But if there is any detain in bank side for payment authorization, then it takes itsy-bitsy longer.
920-324 Practice Test | 920-324 examcollection | 920-324 VCE | 920-324 study guide | 920-324 practice exam | 920-324 cram
Killexams 9L0-625 existent questions | Killexams HP2-B85 existent questions | Killexams HP3-045 questions and answers | Killexams MB2-184 exam questions | Killexams JN0-311 braindumps | Killexams 000-382 rehearse questions | Killexams EX0-100 bootcamp | Killexams A2040-410 rehearse test | Killexams 000-834 cheat sheets | Killexams 000-019 free pdf download | Killexams 922-072 free pdf | Killexams LOT-928 study guide | Killexams VCS-352 existent questions | Killexams CRCM examcollection | Killexams 300-101 rehearse exam | Killexams 7693X rehearse test | Killexams 70-569-VB exam prep | Killexams 000-085 questions and answers | Killexams HP5-B05D brain dumps | Killexams 9L0-508 pdf download |
killexams.com huge List of Exam Study Guides
Killexams 000-317 braindumps | Killexams 000-101 VCE | Killexams 922-095 mock exam | Killexams 156-315-76 existent questions | Killexams C2180-181 bootcamp | Killexams UM0-200 questions and answers | Killexams 132-S-916.2 cheat sheets | Killexams 156-115.77 existent questions | Killexams HPE2-T22 rehearse test | Killexams HP0-A113 examcollection | Killexams 00M-645 test prep | Killexams HPE0-S48 braindumps | Killexams 250-255 rehearse Test | Killexams 70-354 free pdf | Killexams 1Z0-932 exam prep | Killexams 1Z0-102 study guide | Killexams E20-005 rehearse test | Killexams HP2-E21 brain dumps | Killexams 4A0-106 study guide | Killexams 300-135 brain dumps |
Communication Server (CS) Rls. 4.0 Database Administrator
Pass 4 sure 920-324 dumps | Killexams.com 920-324 existent questions | https://www.textbookw.com/
The purpose of the Society of Anesthesia and Sleep Medicine (SASM) Guideline on Intraoperative Management of Adult Patients With Obstructive Sleep Apnea (OSA) is to present recommendations based on the available scientific evidence. In light of a paucity of well-designed, high-quality studies in this perioperative field, a great section of the present recommendations was developed by experts in the bailiwick taking into account published evidence in the literature and utilizing consensus processes, including the grading of the level of evidence. At times, when specific information on patients with OSA was not available in the literature, evidence in highly correlated patient populations, specifically those with obesity, was considered if appropriate. When this was the case, it is explicitly stated in various parts of this document.
The guideline presented may not subsist suitable for All clinical settings and patients. Thus, its consideration requires an assessment of appropriateness by clinicians on an individualized basis. Among many factors, the actuality of institutional protocols, individual patient-related conditions, the invasiveness of an intervention, and the availability of resources exigency to subsist considered. The present rehearse guideline is not intended to define standards or represent absolute requirements for patient care. Adherence to this guideline cannot guarantee successful outcomes but rather should aid health supervision professionals and institutions to formulate plans for improved management of patients with OSA. The present recommendations reflect the current situation of learning and its interpretation by a group of experts in the bailiwick at the time of publication. periodic reevaluations of the literature will subsist needed, and novel scientific evidence should subsist considered between updates. Deviations from this guideline in the practical setting may subsist justifiable, and such deviations should not subsist interpreted as a basis for negligence claims.
OSA is a common and frequently undiagnosed disorder defined by the repeated collapse of the upper airway with resultant blood oxygen desaturation events during sleep.1,2 OSA has been associated with adverse long-term health outcomes and has been linked to increased perioperative complication risk.3–5 Indeed, a comprehensive review of the literature performed by a job coerce appointed by SASM revealed substantial risk for adverse events, especially pulmonary complications, to subsist associated with OSA in the perioperative period.6 Based on the elevated risk for perioperative complications, the recently published SASM Guideline on Preoperative Screening and Assessment of Adults With Obstructive Sleep Apnea recommends that attempts should subsist made to appropriately identify patients with OSA, with the goal to raise awareness among providers, mitigate risk, and improve outcomes.7 While recommendations for preoperative screening and assessment of patients with OSA and their optimal preparation for surgery are now available, there is a paucity of evidence-based guidance for the intraoperative management of this patient population. Thus, there remains a lack of evidence-based rehearse recommendations regarding techniques for airway management, selection of anesthetic agents, and drugs, as well as altenative of anesthetic technique.
This document is derived from results of an extensive consensus process based on a systematic literature search, review, and analysis performed by experts in the field. It is a follow-up to the previously published SASM Guideline on Preoperative Screening and Assessment of Adult Patients With Obstructive Sleep Apnea.7 Given the great amount of related literature in this arena, this study focuses only on intraoperative patient care. Postoperative supervision issues are not considered and may subsist the topic of future projects.
What Other Guidelines and Reviews Are Available?
Previous OSA-related rehearse guidelines8–12 maintain been published by the American Society of Anesthesiologists,8,9 the Society for Ambulatory Anesthesia,10 the American Academy of Sleep Medicine,11 the SASM,7 the International Bariatric Consensus Guideline Group,13 and the job coerce on best rehearse recommendations for the anesthetic perioperative supervision and pain management in weight loss surgery.14
Why Was This Guideline Developed and How Does It differ From Existing Guidelines?
This guideline was developed to provide evidence-based recommendations for the intraoperative management of patients with OSA. Therefore, a observant examination of the current literature using a systematic review approach with a focus on airway management, commonly used anesthesia-related drugs and agents, and anesthetic techniques in this patient population was conducted. The job coerce recognizes that there has been recent progress in attempts to subcategorize patients with OSA according to anatomic predisposition, arousal thresholds, muscle responsiveness, and ventilatory control characteristics.15 However, given the lack of evidence in this context, statements were made referring to patients with OSA as a generic group. Nevertheless, phenotypic subcategorization may allow the progress of individual risk profiling in the future.
The level of this guideline was to present recommendations based on the best current evidence. Clinical research as it relates to best perioperative practices in OSA is burdened by numerous difficulties. The intraoperative setting involves a host of concurrent interventions and expend of anesthetic medications, making it difficult to single out specific factors that potentially drive the adverse outcome. lack of preoperative polysomnography data within publications represents a further challenge, making it difficult to involve information of the impact of disease severity. Ethical considerations in study designs regarding the randomization of patients with known OSA were additional obstacles in this context. Furthermore, the job coerce recognizes that there is a tendency to underreport medical complications, rendering it difficult to establish the legal perioperative risk.16 Presenting the current available evidence and its limitations should raise awareness regarding the exigency for high-quality studies in the future.
Specific aims were to: (1) evaluate considerations of difficult airway management in patients with OSA, (2) assess the impact of individual anesthesia-related drugs and agents in the supervision of patients with OSA, and (3) evaluate best anesthetic techniques in this patient population. To achieve these aims, a question-driven approach was sought.
In areas lacking adequate published evidence, the job coerce sought to establish expert consensus while considering related literature. Patients affected by sleep-disordered breathing unrelated to OSA, including hypoventilation syndromes, periodic breathing, and central apnea unrelated to OSA, were not considered in this project. This decision was made a priori to reduce the influence of heterogeneity in their assessment given the lack of evidence on which to base recommendations for these specific populations.
GUIDELINE job FORCE
The job coerce was comprised of 14 members of SASM, an international society devoted to advancing the supervision for clinical problems shared by anesthesiology and sleep medicine clinicians. Given that this project included only intraoperative aspects, the job coerce included 12 anesthesiologists and 2 anesthesiology research fellows. Members of the job coerce participate expertise on the topic of sleep-disordered breathing in the perioperative setting and included practitioners from both academic and nonacademic settings from various parts of the United States, Canada, and Europe.
A systematic review of the literature addressing the intraoperative management of patients with OSA was conducted after search terms were developed by the job force. Three groups were established, each focusing on one of the focus areas (Table 1). Group 1 investigated whether patients with OSA are at increased risk for difficult airway management. Group 2 investigated the impact of various anesthesia-related drugs and agents used in the intraoperative supervision of patients with OSA. Group 3 evaluated the result of anesthesia technique in patients with OSA. Leaders and group members are listed in the acknowledgments section of the article.
Literature Search Strategy
With the champion of a research librarian, a literature search was performed for each group, including publications from 1946 to September 2016. Databases searched included (1) Medline, (2) ePub Ahead of Print/Medline In-process, (3) Embase, (4) Cochrane Central Register of Controlled Trials, (5) Cochrane Database of Systematic Reviews, (6) PubMed-NOT-Medline, and (7) ClinicalTrials.Gov. The search focused on studies of adult individuals (≥18 years of age) and published in English. Continued literature surveillance was done through January 2018.
Excerpt of the Controlled Vocabulary Terms and Key Words Included in the Systematic Search.
Group 1: “sleep apnea, obstructive,” “obstructive sleep apnea,” “obstructive sleep apnea syndrome,” “sleep disordered breathing,” “obesity hypoventilation syndrome,” “apnoea or apnea,” “hypopnoea or hypopnea,” “airway,” “intubation,” “extubation,” “airway management,” “airway obstruction,” “airway extubation,” “intubation, intratracheal,” “intubation.mp,” “laryngeal masks,” “respiration, artificial,” “positive pressure respiration,” “respiratory mechanics,” “continuous positive airway pressure,” “supine position,” “apap.mp,” “bipap.mp,” “cpap.mp,” “facemask,” “ventilat.mp,” “patient positioning,” “difficult mask ventilation,” “supraglottic airway devices,” and “surgical airway.”
Group 2: “sleep apnea, obstructive,” “obstructive sleep apnea,” “obstructive sleep apnea syndrome,” “sleep disordered breathing,” “obesity hypoventilation syndrome,” “apnoea or apnea,” “hypopnoea or hypopnea,” “postoperative period,” “complications or outcome,” “perioperative care,” “perioperative complications,” “intraoperative complications,” “postoperative complications,” “outcome,” “risk,” “morbidity,” “mortality and death,” “anesthesia,” “anesthetics,” “anesthetics, intravenous,” “inhalational anesthesia,” “volatile anesthesia,” “anesthetics local,” “analgesia, opioid,” “hypnotics and sedatives,” “adverse effects,” “intravenous regional anesthesia,” “sedation,” “sedatives,” “short acting,” “nonsteroid of nonsteroid or nasaids,” “opioid,” “complication,” “muscle relaxant,” “rocuronium, atracurium,” “cis-atracurium,” “vecuronium,” “mivacurium,” “suxamethonium or succinylcholine,” “rapacuronium,” “pancuronium,” “skeletal muscle relaxant,” “neuromuscular reversal agents,” “sugammadex,” “residual neuromuscular block,” “drug effects,” “adverse effects,” “adverse drug reactions,” “abnormalities drug induced,” “adverse drug events,” “adverse drug reactions reporting systems,” “morbidity,” and “mortality.”
Group 3: “sleep apnea, obstructive,” “obstructive sleep apnea,” “obstructive sleep apnea syndrome,” “sleep disordered breathing,” “obesity hypoventilation syndrome,” “apnoea or apnea,” “hypopnoea or hypopnea,” “postoperative period,” “complications or outcome,” “perioperative care,” “perioperative complications,” “intraoperative complications,” “postoperative complications,” “outcome,” “risk,” “morbidity,” “mortality and death,” “anesthesia, epidural,” “anesthesia, spinal,” “anesthesia, general,” “major conduction anesthesia,” “treatment outcome,” “treatment failure,” “mortality,” “outcome,” “peripheral nerve blocks,” “nerve blocks,” “anesthesia regional,” “anesthesia technique,” “sedation,” “sedative medication,” “deep sedation,” “secure airway,” “airway,” “multimodal analgesia,” “balanced anesthesia,” “opioid sparing,” and “opioids.”
Full search strategies in Medline for All groups are reported in the Supplemental Digital Content 1, SASM Guideline Intraoperative OSA Appendix, http://links.lww.com/AA/C373; Supplemental Digital Content 2, Search Anesthesia Technique, http://links.lww.com/AA/C374; Supplemental Digital Content 3, Search Difficult Airway and OSA, http://links.lww.com/AA/C375; Supplemental Digital Content 4, Search Intraoperative Medication expend in Patients With OSA, http://links.lww.com/AA/C376; Supplemental Digital Content 5, Search Strategy NMBA, http://links.lww.com/AA/C377.
Furthermore, minute reviews addressing difficult airway, anesthesia-related drugs and agents, specifically those involving neuromuscular blocking agents (NMBAs) and opioids, were conducted and summarized in sunder systematic reviews by the respective SASM focus groups (members listed in the acknowledgments) to participate the evidence gathered and expand the scope of the present guideline.
In the respective groups, ≥2 reviewers assessed titles and abstracts for eligibility by using the standardized format of the Covidence platform.17 This step was followed by a full-text review and data extraction. Furthermore, a citation search by a manual review of references from primary or review articles was performed to compile additional pertinent results. Any disagreements were resolved by consensus among reviewers or by consulting with the respective SASM groups via face-to-face meetings, teleconferences, or email communications. Study designs considered included randomized controlled trials (RCTs), prospective and retrospective observational studies, case series, systematic reviews, and meta-analyses. Within this literature, the presence or risk for OSA was based on polysomnography, screening questionnaires, clinical assessment, chart diagnosis, medical history, or International Classification of Diseases (ICD)-9 codes from administrative or billing records, while studies reported on at least 1 outcome of interest. Existing guidelines were cross-checked for completeness of references.
Data extracted from these studies included nature of study, demographic data, comorbidities, procedure type, anesthesia-related interventions and medications, adverse events, as well as other clinically valuable outcomes and effects.
Exclusion criteria were: nonhuman studies, non-English language, review articles, single case reports, studies reporting on the confirmed expend of medications commonly used intraoperatively such as confirmed opioid medication, and studies without outcome reporting. For group 3, studies not directly comparing anesthesia modalities were moreover excluded.
Level of Evidence and Recommendations
The Oxford level of Evidence (Oxford LOE) tool was utilized to evaluate the character of evidence of individual studies.18 Grading the power of recommendations and character of the underlying evidence enhances the usefulness of clinical rehearse guidelines.19 Therefore, the approach according to the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system20,21 was utilized with esteem to the body of evidence and the progress of guideline recommendations.22 As specified by GRADE, the character of evidence is classified into high, moderate, low, and very low levels, according to factors that involve study methodology, consistency and precision of results, and directness of evidence.19 These levels were assigned to the body of evidence of each respective recommendation within their focus zone and reflect the self-confidence in estimates of the legal effect.21 When affecting from evidence to recommendations, the GRADE approach focuses on 4 factors: poise between profit and harm, conviction of evidence, values and preferences, and resource considerations.22 The power of recommendation is separated into tenacious and fragile and defines the extent to which one can subsist confident that the desirable consequences outweigh its undesirable consequences (Table 2).23
In-person SASM Intraoperative Guideline job coerce meetings took dwelling at special sessions during the SASM annual meetings in Chicago, IL (2016), and Boston, MA (2017), as well as the International Anesthesia Research Society annual meeting in Washington, DC (2017). Furthermore, multiple teleconferences and electronic communications took dwelling throughout this time period. prefatory results and implications of findings were presented and discussed at the 2017 SASM annual meeting in Boston, MA.
1. DIFFICULT AIRWAY AND OSA
1.1. Question: Are patients with OSA at increased risk for difficult airway management and finish special precautions exigency to subsist taken?
1.1. Recommendation: Known or suspected OSA should subsist considered an independent risk factor for difficult intubation, difficult mask ventilation, or a combination of both. Adequate difficult airway management precautions should subsist taken.
Level of evidence: Moderate; Grade of recommendation: Strong
The perception of OSA as an valuable risk factor for difficult airway management is widely held among anesthesiologists and intensive supervision physicians. In the absence of RCTs, several prospective and retrospective controlled studies maintain supported this assumption.24–39
Association Between OSA and Difficult Airway Management
After applying the designated search strategy and removing duplicates, 4806 references were screened for title and/or abstract. After reviewing 25 full-text articles, 16 studies were identified as reporting on the association between difficult airway management and OSA, while 9 studies were excluded.40–47 A minute summary of associations between OSA and various difficult airway management components is provided in Supplemental Digital Content, Table A1, http://links.lww.com/AA/C373.
Among the included studies, 5 were retrospective24,25,27,35,36 and 11 were prospective controlled studies.26,28–34,37–39 Ten studies confirmed OSA by overnight polysomnography24,25,27,29,35 or electronic database entries,28,30,31,34,37 3 used the STOP-Bang screening questionnaire,33,38,39 2 identified patients by clinical diagnosis,26,36 and 1 used both polysomnography and the STOP-Bang questionnaire.32
In total, 266,603 patients were included in 16 studies. Of those patients, 32,052 had OSA (identified by polysomnography, electronic database, chart or clinical diagnoses, and STOP-Bang questionnaires) and 234,551 did not. In summary, 12 studies reported on difficult intubation,24–29,31–33,35,38,39 6 on difficult mask ventilation,28,30,31,36,38,39 2 on both difficult intubation and mask ventilation,28,37 and 2 on failed supraglottic airway.27,34 Several studies reported >1 difficult airway outcome. No study was available on the exigency for a surgical airway (Supplemental Digital Content, Table A1, http://links.lww.com/AA/C373).
Concerning difficult intubation and OSA, 7 of 12 studies showed positive associations.24,25,28,33,35,38,39 Of 6 studies, 5 demonstrated a significant impact of OSA on difficult mask ventilation.28,30,36,38,39 In the 2 studies that reported on combined difficult intubation and mask ventilation, both demonstrated a significant impact of OSA.28,37 Although 5 studies assessing difficult intubation26,27,29,31,32 and 1 study evaluating difficult mask ventilation31 did not find a significant association with OSA, the overall estimates showed a positive association between OSA and difficult airway. This finding suggests that patients with OSA are at increased risk of difficult airway management compared to patients without OSA. minute data, analysis, and results on the association between OSA and difficult airway will subsist reported in a sunder systematic review with meta-analysis by the SASM airway focus group (members listed in acknowledgments).
One prospective controlled study34 reported on the expend of the LMA Unique® (Teleflex Incorporated, Morrisville, NC), and an additional retrospective investigation27 reported on a sunder unspecified supraglottic airway device. No significant association was organize between OSA and failed supraglottic devices.
Prevalence of OSA in Patients With Difficult Intubation
Two studies elucidated the association between OSA and difficult intubation in a transpose manner by investigating the rate of OSA among patients with difficult intubation. In a retrospective study, Hiremath et al,24 using an apnea-hypopnea index (AHI) ≥10 as a cutoff, organize that 53% of patients with difficult airway had OSA. This finding was confirmed by a prospective controlled study by Chung et al.29 using an AHI ≥5 as a cutoff for OSA diagnosis. Patients who were determined to maintain a difficult airway were referred for polysomnography after surgery, and 66% were shown to maintain OSA.
Kim and Lee35 showed that patients with an AHI ≥40 had a significantly higher prevalence of difficult intubation. For patients with OSA with AHIs ≤40, 40–70, and ≥70, the incidence of difficult intubation was 3.3%, 19.3%, and 27.6%, respectively.35 Anatomical skeletal and soft tissue changes may contribute to a difficult airway in OSA. However, these observations are “hypothesis-generating” rather than “hypothesis-proving” findings. The shared anatomical abnormalities explain the positive association between difficult airway and OSA.
A number of studies evaluated the association of difficult airway management with OSA using the STOP-Bang questionnaire to identify patients at towering risk of OSA.32,33,38,39 The sensitivity and specificity of the STOP-Bang questionnaire can vary according to the prevalence and severity of OSA.48 This variation can create false-positive and false-negative cases in both OSA and non-OSA groups, leading to potential misclassification bias.
One of the contributing factors for adverse respiratory events in patients with OSA is the increased risk of difficult airway management, such as difficult intubation, difficult mask ventilation, or both. In a recent report, there were 7 litigation cases where OSA was associated with either death or anoxic brain injury due to difficult airway management in the configuration of failure to reintubate in the postoperative period.49 learning about the association between OSA and difficult airway may improve perioperative airway management and dwindle airway-related complications.
In view of ethical considerations, it is difficult to execute RCTs in patients with OSA to determine its associations with difficult airway management. As a result, only observational prospective and retrospective studies are available in the literature. The linger estimates of these studies indicate that there is an increased risk of difficult airway management in patients with OSA. Due to the great number of trials and great patient numbers, the overall character of the body of evidence was considered to subsist moderate using the GRADE approach20,21 and the Oxford LOE.18
2. INTRAOPERATIVE MEDICATION expend IN PATIENTS WITH OSA
A great body of literature supports the notion that the effects of surgery and anesthesia pose unique hazards to patients with OSA.5,50,51 Anesthetic agents and analgesic drugs interact with consciousness, sleep, and ventilatory drive,52,53 and thus they deserve consideration when caring for patients with OSA. In addition, upper airway and pulmonary physiology, including upper airway dilator muscle activity, are impacted by pharmacological and mechanical elements (airway manipulation) of anesthesia with practicable increased detriment in OSA.54–56 The following section discusses questions related to the effects of various agents and drugs commonly utilized intraoperatively in patients with OSA.
2.1 Neuromuscular Blocking Agents
2.1.1 Question: Are patients with OSA at increased risk for postoperative respiratory complications from the expend of NMBAs?
2.1.1 Recommendation: Patients with OSA who received NMBAs may subsist at increased risk of effects of postoperative residual neuromuscular blockade, hypoxemia, or respiratory failure.
Level of evidence: Low; Grade of recommendation: Weak
2.1.2 Question: Does the altenative of neuromuscular blocking reversal agent impact the risk of postoperative respiratory complications in patients with OSA?
2.1.2 Recommendation: Currently, there is insufficient evidence to hint the preference of any neuromuscular blocking reversal agent to reduce the risks of postoperative respiratory complications in patients with OSA.
Level of evidence: Low; Grade of recommendation: No recommendation
NMBAs are commonly used to optimize intubation conditions and provide surgical relaxation for various procedures. However, residual neuromuscular blockade has been reported to occur in ≤64% of patients in postanesthesia supervision units.57 The expend of NMBAs and residual neuromuscular blockade has been associated with significant postoperative respiratory complications such as hypoxemia,58 upper airway obstruction,58 and pneumonia.59 towering doses of NMBA given during abdominal surgery were associated with an increased risk of 30-day readmission, increased length of hospital stay, and increased hospital cost.60 A retrospective review of a single-center database showed that patients who required tracheal intubation within the first 3 days after surgery had a significantly higher frequency of NMBA administration and reversal with neostigmine.61 Residual neuromuscular blockade may persist despite the administration of neostigmine reversal, especially when neuromuscular monitoring is not utilized.62
It is unclear whether patients with OSA may subsist at higher risk for postoperative respiratory complications due to the adverse effects of postoperative residual neuromuscular blockade compared to patients without OSA. Moreover, it is uncertain whether the nature of reversal agent impacts the risk of postoperative complications in patients with OSA. Patients with suspected61 or confirmed50,63,64 OSA maintain been shown to subsist at increased risk for early postoperative respiratory complications, including emergent intubation,63,64 mechanical ventilation,63,64 noninvasive ventilation,63,64 respiratory failure,50 desaturation,6,50 and pneumonia.64 The expend of NMBA was not described in these studies.6,50,63,64 Many patients with OSA are obese and maintain anatomical risk factors that may increase vulnerability to the effects of residual neuromuscular blockade on the upper airway and pharyngeal function.
Our literature search yielded 5 studies that were heterogeneous in terms of study design, types of surgery, and types of respiratory complications.65–69 Many studies were excluded because OSA diagnosis or expend of NMBA was not described.
One RCT11 and 2 observational studies66,67 were included to address the question of whether patients with OSA are at a higher risk for postoperative respiratory complications from the expend of NMBA compared to patients without OSA. Although the level of evidence was limited (Oxford LOE 2–3), the studies hint that patients with OSA who received NMBA may subsist at increased risk of effects of residual neuromuscular blockade, postoperative respiratory failure, and hypoxemia.65–67 The results of their review are consistent with previous studies showing that patients with OSA are at higher risk of postoperative respiratory failure and hypoxemia than patients without OSA.6,61,70,71 Even partial residual neuromuscular blockade that does not evoke respiratory symptoms can impair upper airway dilator muscle function.72 Minimizing the expend and dose of NMBA, monitoring the level of neuromuscular blockade, and complete reversal of NMBA before extubation may subsist particularly valuable for patients with OSA.9
While not considering OSA status, reversal of NMBA with sugammadex, a cyclodextrin used to transpose rocuronium,73 has been shown to dwindle the incidence of residual paralysis compared to the anticholinesterase inhibitor, neostigmine.74 A recent Cochrane review of 41 studies comparing sugammadex with neostigmine concluded that patients receiving sugammadex versus neostigmine had 40% fewer composite adverse events (bradycardia, postoperative nausea and vomiting, and residual neuromuscular blockade).75 Patients receiving sugammadex had less desaturation and exigency for transitory oxygen supplementation; however, the OSA status was not reported in these reviews, limiting its value to assess its differential result in this subpopulation.74,75
There are limited studies comparing the impact of different neuromuscular blocking reversal agents on postoperative respiratory complications in patients with OSA. They identified 1 RCT68 and 1 observational study69 that compared sugammadex to neostigmine. In the 2 studies, 209 patients with OSA and 185 patients without OSA were included.68,69 The RCT (n = 74) organize that patients receiving sugammadex versus neostigmine had less postoperative respiratory complications (desaturation, hypoxemia, apnea, airway manipulation, airway usage, reintubation, continuous positive airway pressure [CPAP] therapy, and invasive mechanical ventilation).68 There was no disagreement in airway obstruction. The observational study (n = 320) compared sugammadex to a historical cohort of patients who received neostigmine reversal for laparoscopic bariatric surgeries. Patients with OSA who received sugammadex versus neostigmine had less postoperative chest radiographic changes (atelectasis, pleural effusions), 6.9% vs 16.3% (odds ratio [OR], 0.36; 95% CI, 0.18–0.8),69 but there were no differences in postoperative mechanical ventilation or hospital length of stay. Although both studies showed a reduction in some postoperative respiratory complications, the evidence is limited because the number of patients included in the RCT (Oxford LOE: 2) was small,68 and the observational study (Oxford LOE: 3) reported no disagreement in clinical outcomes.69
Currently, there is insufficient evidence to recommend the expend of sugammadex over neostigmine to reduce the risk of postoperative respiratory complications in patients with OSA. More trials with larger sample sizes are needed in this patient population.
2.2.1 Question: Are patients with OSA at increased risk for opioid-related respiratory events?
2.2.1 Recommendation: Patients with OSA may subsist at increased risk for adverse respiratory events from the expend of opioid medications.
Level of evidence: Low; Grade of recommendation: Weak
2.2.2 Question: Is pain perception and opioid potency altered in patients with OSA?
2.2.2 Recommendation: The possibility of altered pain perception in patients with OSA should subsist considered.
Level of evidence: Low; Grade of recommendation: Weak
While opioids are highly effectual in treating moderate to ascetic pain, their intrinsic capacity to repress ventilatory drive demands caution in OSA. Despite consensus among perioperative physicians to restrict or avoid opioids in OSA,9 the presence of robust, high-quality scientific evidence to demonstrate the merit of heightened concern and steer safe opioid rehearse in this population is limited.76
Nevertheless, despite limitations with respect to the character of evidence suggesting an adverse impact of acute opioid administration in OSA, current literature indicates that a heightened concern regarding opioid expend in this population may subsist justified. A summary of evidence is provided in Supplemental Digital Content, Table A2, http://links.lww.com/AA/C373.
Specifically, 17 observational studies exploring the impact of systemic opioid expend in OSA were identified. While the majority demonstrated an association between opioid expend and adverse perioperative outcomes in OSA,61,77–89 this was not confirmed by all.66,90,91 It should subsist famed that, particularly among observational analyses, there is notable heterogeneity with esteem to the modality of OSA assessment, ranging from the gold touchstone of polysomnography to identification by screening questionnaires or patient history. Furthermore, potential selection color should subsist considered in these studies. In recent publications, a comparison of postoperative complications among patients with and without OSA within the very study cohort revealed that the incidence of postoperative pulmonary (2.49% vs 1.83%), cardiac (2.81% vs 0.23%), gastrointestinal (0.45% vs 0.33%), renal (3.47% vs 1.83%), and thromboembolic (0.41% vs 0.33%) complications was higher in patients with OSA at similar opioid dose levels.88,92 Additional analysis of the impact of opioid dose increase within patients with OSA demonstrated an associated increase in the odds for gastrointestinal complications, prolonged length of stay, and increased hospital cost, while no further increase in risk for pulmonary complications was observed, possibly due to increased levels of monitoring afforded to this population.88 A higher incidence of postoperative complications in OSA versus non-OSA in this context was moreover organize by Blake et al77 and Esclamado et al,80 while the latter conducted their study in upper airway surgery, a procedure with a potentially inherent influence on respiratory outcome.80
Chung et al79 demonstrated an opioid dose-dependent postoperative worsening of sleep-disordered breathing associated with the severity of OSA (expressed by AHI), although this result may maintain been fairly small. manful patients with OSA had a significantly higher central apnea index on postoperative night 1 versus female patients with OSA. In this context, numerous other observational studies took a different approach by investigating the event of critical, life-threatening respiratory events, such as respiratory failure and naloxone requirement and identifying drivers for these complications.61,81–84,86,87 Moreover, a recent systematic review reported that the majority of surgical patients with OSA experiencing perioperative death or near-death events received a morphine equivalent dose of <10 mg/d.89 Subramani et al89 suggested that a dose-response pattern with increased odds for complications at increasing opioid dose levels (ORs of 1.0, 1.5, and 3.0 at opioid doses of <10, 10–25, and >25 mg; P for trend <.005) exists.
In contrast, others66,85 who restricted their focus to patients with obesity, a population of towering OSA prevalence,2 demonstrated that, although postoperative respiratory complications in the context of opioid analgesia were common, surprisingly, OSA could not subsist established as an independent risk factor.66,85 However, a factor potentially causing an underestimation of a practicable deleterious result of OSA was the postoperative expend of positive airway pressure therapy among patients with OSA.85 Moreover, a proof of concept analysis by Wang et al91 suggested that the experimental oral administration of 30 mg controlled-release morphine in 10 volunteers outside the surgical setting paradoxically improved oxygenation through modulating chemoreflexes.91 In summary, evidence from observational analyses suggests that opioid expend in the presence of OSA presents a risk factor for postoperative critical respiratory events (Oxford LOE 3–4).61,79,81–84,86,87,89
With esteem to evidence from RCTs, 6 such studies were identified (Oxford LOE 2).93–98 In a volunteer study, Bernards et al94 directly demonstrated that opioid administration during sleep increased the number of central apneas, leading to decreased saturation levels in patients with OSA versus those without OSA.94 Abdelmageed et al93 demonstrated that opioid dose reduction significantly reduced the incidence of central apneas and respiratory events in patients with OSA.93 While interesting, it must subsist famed that opioid reduction may dwindle respiratory depression and related complications in the generic population as well.92 Using a nonvalidated OSA prediction instrument, Blake et al95 showed that central apneas and respiratory events were related to the dose of morphine administered postoperatively. However, differences in the event of respiratory complications between patients with touchstone morphine patient-controlled analgesia and an opioid-sparing regimen could not subsist established.95
Other studies explored the safety of neuraxial opioid administration in patients with OSA.99–102 In a systematic review, Orlov et al99 organize that the incidence of major cardiorespiratory complications after neuraxial opioid administrations was 4.1% among patients with OSA. However, the authors moreover emphasized that significant limitations in the character of evidence and persistent underreporting of adverse events prevented an accurate and robust assessment of legal perioperative risk.16,99 A prospective study in patients having a cesarean delivery with intrathecal morphine administration demonstrated that OSA and obesity were associated with approximately a 2-fold increase in risk for desaturation.100 However, another observational analysis of 990 patients undergoing orthopedic surgery with intrathecal morphine could not find an association between OSA and adverse pulmonary events.101
In summary, limited literature suggests that patients with OSA may subsist at increased risk for opioid-related respiratory adverse events. However, high-quality evidence to champion and prove this notion is largely lacking (Oxford LOE 2–4).
Pain and Opioid Analgesia in OSA.
A systematic evaluation of opioid-related respiratory effects in OSA requires focused attention on closely related issues such as pain perception and pharmacology of opioid analgesia. A summary of evidence is provided in Supplemental Digital Content, Table A3, http://links.lww.com/AA/C373 (Oxford LOE 3). Characterizing these relationships is valuable because the dose of opioids that is required to deal pain, as well as the sensitivity to these medications, directly influence the likelihood of opioid-induced respiratory depression.
Disturbed sleep continuity and intermittent hypoxia are 2 valuable features of OSA. Studies in humans maintain repeatedly demonstrated that fragmented103,104 or chronically curtailed sleep87,105 and insomnia,106 a condition highly comorbid with OSA,107 are associated with heightened sensitivity to pain.108
Among 3 identified studies examining the response to experimental pain in subjects suffering from OSA, 1 study organize that patients with OSA and comorbid temporomandibular joint disorder experienced hypoalgesia to pressure-related pain,109 while another reported a significant increase in pain threshold after restoring sleep continuity with the application of CPAP therapy.110 In contrast, the third investigation organize no association between wake-after-sleep-onset or nocturnal nadir blood oxygen saturation (SpO2) polysomnographic parameters and threshold/tolerance to thermal pain.111
In the context of confirmed pain, a retrospective analysis of prospectively collected data from the Cleveland Family Study showed that confirmed intermittent hypoxia was associated with more frequent confirmed pain complaints, even after adjusting for the potentially hyperalgesic result of sleep fragmentation and systemic inflammation.112
Despite the primary goal to focus on the adult patient population in this guideline, a significant amount of evidence originates from the pediatric population and deserves mention here particularly because they show contradictory findings to those organize among adults. In children undergoing adenotonsillectomy for treatment of OSA, 2 case–control studies, 1 retrospective113 and 1 prospective,114 showed that patients with a preoperative nocturnal nadir SpO2 <85% required half the dose of morphine to deal postoperative pain, versus those with a nadir SpO2 ≥85%. Two prospective case–control studies in the very population did not confirm these findings.115,116 In the first study, African American children versus Caucasian children with OSA presented with more pain requiring a higher dose of morphine for postoperative analgesia.115 The second study showed that children with OSA (respiratory disturbance index >5) required more morphine for postoperative analgesia, but they moreover demonstrated a higher incidence of opioid-related respiratory complications.116
In adults, 1 retrospective analysis organize that bariatric patients with nocturnal hypoxemia (expressed as percentage of total sleep time spent at oxygen saturation [SaO2] <90%) required less opioids for postoperative analgesia,117 whereas another prospective study did not detect any association between preoperative nocturnal hypoxemia and postoperative opioid expend in generic surgical patients with OSA.118 A more minute and comprehensive summary of evidence on the potential impact of acute opioid analgesia in OSA is provided in a sunder systematic review by the SASM opioids focus group (members listed in the acknowledgments).
2.3.1 Question: Are patients with OSA at increased risk for adverse events from the expend of propofol for procedural sedation?
2.3.1 Recommendation: Patients with OSA may subsist at increased risk for adverse respiratory events from the expend of propofol for procedural sedation.
Level of evidence: Moderate; Grade of recommendation: Strong
The literature discussed for the purpose of the recommendation reflects evidence of import for patients receiving propofol for sedation in a procedural setting, that is, drug-induced sleep endoscopy (DISE), gastroenterological endoscopy, or dentistry. The expend of propofol to induce generic anesthesia purposefully suppresses respiratory activity and was thus deferred in this section.
Propofol is the most commonly used agent for DISE.119,120 A summary of findings from 5 studies120–124 is shown in Supplemental Digital Content, Table A4, http://links.lww.com/AA/C373 (Oxford LOE: 2–4). Both body mass index (BMI) and severity of OSA correlated with a greater likelihood of a patient having multiple sites of airway collapse and a higher possibility of circumferential and total airway obstruction during DISE.119,125 The goal of propofol administration for DISE is to produce a sleep-like loss of consciousness and muscle relaxation to precipitate pharyngeal narrowing and collapse in vulnerable individuals. To avoid the problem of profound relaxation or central apnea, it has been suggested that initial dosing for DISE subsist judiciously titrated.120,126
Attempts maintain been made to formulate a mathematical equation to model the pharmacokinetics for propofol in patients with obesity (Supplemental Digital Content, Table A5, http://links.lww.com/AA/C373).127–130 dubiety regarding dosing scalar adjustments that may subsist required in patients with obesity, as well as the concomitant expend of depressant drugs with synergistic effects (midazolam,131 ketamine,132,133 dexmedetomidine,134 opioids135), further add to the exigency for heightened vigilance when using propofol for patients with OSA. Propofol has a relatively steep dose-response curve compared to other sedatives/hypnotics, thus underscoring the import of observant titration.131,136,137 Adverse effects are not uncommon in patients with OSA undergoing procedures with propofol sedation. A summary of findings from 5 studies138–143 is shown in Supplemental Digital Content, Table A6, http://links.lww.com/AA/C373. OSA, increased BMI, manful gender, American Society of Anesthesiologists physical status ≥III, initial dose of propofol, and increased age were organize to subsist independent risk factors for hypoxemic incidents. Airway interventions were common in patients receiving propofol, although indications for airway intervention were left to the discretion of the anesthesia provider. Whether precautionary or subsequent to an obstructed airway, apneic, or desaturation episode, such airway interventions were undoubtedly done to prevent or mitigate a sedation-related adverse event. The expend of capnography was associated with a decreased incidence of hypoxic events compared to touchstone monitoring solitary during sedation with propofol144 in patients with OSA.140
2.4 Inhalational Agents
2.4.1 Question: Are patients with OSA at increased risk for residual effects of inhalational anesthetic agents?
2.4.1 Recommendation: There is a lack of evidence to assess residual effects of inhalational anesthetic agents in the population with OSA.
Level of evidence: Moderate; Grade of recommendation: No recommendation
There is a lack of scientific literature to steer best intraoperative practices in OSA regarding the preferred technique among various inhalational agents and intravenous propofol for the maintenance of anesthesia. Nevertheless, a significant amount of evidence has been published on the generic population and patients with obesity.145 Evidence from the population with obesity may merit consideration in this context, given the proximate association to OSA,146 reflected in the substantial OSA prevalence of ≤90% in manful bariatric patients.147,148 Notably, there is significant overlap between obesity and OSA with esteem to challenges in generic anesthesia because of altered cardiorespiratory physiology, including decreased functional residual capacity, upper airway obstruction, and the propensity to hypoxemia in perioperative settings.149,150
This renders the era of emergence and recovery from anesthesia of towering concern regarding the risk for detrimental outcomes.56,146
In this context, 25 studies were identified that compared the efficacy and recovery profile among the most common inhalational agents and intravenous propofol.65,151–174 A summary of evidence is provided in Supplemental Digital Content, Tables A7 and A8, http://links.lww.com/AA/C373. Comparing propofol and isoflurane, propofol was suggested to subsist associated with a faster recovery from anesthesia and improved postoperative respiratory control in 2 RCTs.154,155 However, sevoflurane was organize to subsist superior to propofol in 2 RCTs due to faster anesthesia recovery and improved hemodynamic stability.152,153 In addition, recently Fassbender et al151 reported no disagreement with esteem to postoperative obstructive and hypoxemic events between the 2 anesthetic agents when combined with remifentanil. Furthermore, comparing propofol and desflurane, 1 study demonstrated that the expend of propofol impaired pulmonary duty and SpO2 to a greater degree than desflurane,157 while another could not confirm these differences.156 Thus, current evidence indicates that sevoflurane and desflurane might subsist superior to intravenous propofol in terms of anesthesia recovery in patients with obesity (Oxford LOE: 2).
Similarly, 4 RCTs conducted in the population with obesity supported the notion that sevoflurane was associated with auspicious features compared to isoflurane.65,158–160 In particular, Sudré et al65 demonstrated that sevoflurane embedded in a short-acting anesthetic regimen comprised of remifentanil, rocuronium, and ropivacaine improved emergence from anesthesia and reduced respiratory complications, postoperative anesthesia supervision unit stay, and hospital length of linger when compared to isoflurane within a long-acting regimen. This analysis emphasized the colorable profit of generally utilizing short-acting medications with esteem to All anesthetic drug classes, including opioids and NMBA, among patients at higher perioperative risk.65 The majority of studies, however, focused on the comparative effectiveness between sevoflurane and desflurane,161,163,165,167 demonstrating improved anesthesia recovery with desflurane (Oxford LOE: 2).162,164,166,168,169,174 Notably, limitations inherent to the nature of these comparisons can prevent the detection of differences. For instance, Eger and Shafer175 showed that differences in postoperative wake-up times among anesthetics were minimal at lower anesthetic concentrations,175 while the duration of anesthesia176 and BMI present valuable covariates.174
Summarizing the evidence, a well-designed systematic review by Liu et al171 provided a comprehensive comparison with quantitative analysis of immediate postoperative recovery after desflurane, isoflurane, sevoflurane, and intravenous propofol anesthesia in patients with obesity. In addition, a rather petite clinical affliction by Juvin et al170 moreover compared desflurane, isoflurane, and propofol together in 1 analysis. Both Liu et al171 and Juvin et al170 established desflurane as the most auspicious anesthetic agent because of its superior postoperative recovery profile. Specifically, it was observed that patients who received desflurane anesthesia required less time to respond to commands, eye opening, hand squeezing, tracheal extubation, and appellation stating. Moreover, desflurane reduced sedation levels171 and conferred higher postoperative SpO2.170,171
It appears, therefore, that postoperative recovery might occur faster and with improved hemodynamic stability after anesthesia with desflurane followed by sevoflurane (Supplemental Digital Content, Table A7, http://links.lww.com/AA/C373), and these findings maintain moreover been observed in the generic population.177–180
Consistently, desflurane and sevoflurane feature low blood-gas partition coefficients,171 conferring greater intraoperative control of anesthesia depth, as well as rapid and consistent postoperative emergence and recovery.161,181,182
These properties, in turn, imply earlier achievement of baseline respiratory duty with potentially better protection against aspiration and improved oxygenation.183 This has moreover been supported by the observation of decreases in hypoxemia in clinical trials.170,171 Both obesity and OSA predispose patients to higher risk of postoperative upper airway obstruction and sober hypoxemia,184 thus suggesting a profit associated with early and rapid recovery of active airway control and alertness.171
Another intervention, possibly promoting increased safety in OSA, is the intraoperative monitoring of anesthesia depth. This has been suggested by Ibraheim et al172 and Freo et al,173 who demonstrated that monitoring for titration of levels of inhalational agents reduced the required anesthetic dosage and improved the postanesthetic recovery in patients with obesity.
Furthermore, Katznelson et al185 suggested that recovery time after generic anesthesia in patients with and without obesity can subsist accelerated using either isocapnic or hypercapnic hyperpnea.185
In summary, the available evidence supports the expend of desflurane and sevoflurane in patients with obesity (Oxford LOE: 2). Given the tenacious association between obesity and OSA, and the benefits of accelerating and improving postoperative anesthesia recovery, these outcomes are desirable and may apply to patients with OSA as well. However, except for 2 RCTs,151,154 no studies specifically in OSA are available, and thus no specific recommendations can subsist made.
2.5.1 Question: Are patients with OSA at increased risk for adverse events from the expend of ketamine?
2.5.1 Recommendation: There is a lack of evidence to assess residual effects of ketamine in the population with OSA.
Level of evidence: Very low; Grade of recommendation: No recommendation
The literature is scarce with esteem to complications associated with ketamine in patients with OSA.
Ketamine has mostly been studied with respect to its potent analgesic effects as a sedative and hypnotic and, more recently, to reduce opioid use.186–188 There are only a few studies involving ketamine expend in patients with OSA, but data are insufficient to draw any hard conclusions.189,190
Adverse effects of ketamine, such as neuropsychiatric effects, signs of increased sympathetic system activation (hypertension and tachycardia), and hypersalivation, are well documented in patients without OSA.191,192 Although patients with OSA are not specifically studied, these adverse events most likely translate to increased risk in this patient population as well. Adverse events are mostly seen in patients who received towering doses, signification >0.5 mg/kg boluses and 100 µg/kg/h infusions.193
Ketamine has been shown to maintain some advantageous effects. Studies demonstrated that ketamine, when combined with other sedative medications, mostly propofol, may dwindle respiratory-related adverse effects.194,195 One such prospective observational study looking at sedation-related risk factors (airway obstruction, hypoventilation, and desaturation) for procedural sedation organize ketamine to subsist a protective factor.195 De Oliveira et al194 reported that ketamine decreased duration and severity of hypercapnia in patients undergoing breast surgery under deep sedation.
Furthermore, Drummond196 studied the result of ketamine versus midazolam on upper airway function. Interestingly, they organize decreased upper airway muscle activity in the midazolam group, which resulted in airway obstruction, whereas no change in muscle activity was observed in the ketamine group. In another study, genioglossus muscle activity, tidal volume, and respiratory rate maintain been shown to subsist increased after administration of towering and low doses of ketamine in rats.197 Upper airway dilator muscle activity plays an valuable role in patients who are at risk of upper airway obstruction. Despite the lack of data on ketamine in the patient population with OSA, available information suggests that these patients could profit from potentially auspicious respiratory effects over other sedatives. hard conclusions, however, cannot subsist drawn at this time.
2.6.1 Question: Are patients with OSA at increased risk for adverse events from intravenous benzodiazepine sedation?
2.6.1 Recommendation: Patients with OSA may subsist at increased risk for adverse respiratory events from intravenous benzodiazepine sedation. Intravenous benzodiazepine sedation should subsist used with caution.
Level of evidence: Moderate; Grade of recommendation: Weak
Although the literature is immature on the topic of differential effects of intravenous benzodiazepine sedation in patients with OSA compared to those without OSA, studies hint that the expend of intravenous benzodiazepines is associated with airway compromise in patients with OSA. Intravenous benzodiazepine sedation is routinely used to induce airway collapse for diagnostic purposes in OSA.
Much of the literature revolves around the expend of intravenous benzodiazepines for DISE in a diagnostic context to examine locations and patterns of obstruction in patients with OSA.119,198–210 Midazolam is the most commonly used intravenous benzodiazepine for DISE. In 7 studies,199,200,202,205,207,208,210 the majority of patients had multilevel obstruction, especially those with higher AHI. Two studies evaluated sleep staging during midazolam-induced sleep. The first showed that patients spent the most time in nonrapid eye movement sleep stage N1 and N2 but not in stage N3 and rapid eye movement (REM) sleep.198 The second reported that patients reached N2 sleep without further deepening of sleep stage.201 Because most obstructive events occur in N1 and N2 sleep, DISE with intravenous midazolam is considered a obliging option to study obstructive events in patients with OSA.102,105
Interestingly, Sadaoka et al209 organize that patients with OSA had oxygen desaturation and apneas during DISE with intravenous diazepam more frequently than simple snorers.
Another category of studies described the expend of intravenous benzodiazepines for sleep imaging.211–214 Thus, a retrospective analysis by Lee et al213 compared 53 patients with OSA to 10 simple snorers. All patients with OSA had desaturation events after 2 mg of midazolam, but not anyone in the simple snorers group had such events.213
We identified 5 studies evaluating intravenous benzodiazepines in the context of other endoscopic or surgical procedures.215–219 Midazolam was used either solitary or in combination with fentanyl. One study did not specify which benzodiazepines were used.218 Three studies215,216,219 compared outcomes between patients with and without OSA. In a retrospective cohort study by Adler et al,215 215 patients undergoing routine endoscopy were randomized to 4 groups: patients with OSA undergoing endoscopy with propofol or midazolam + fentanyl and patients without OSA undergoing endoscopy with propofol or midazolam + fentanyl. A comparison of patients with and without OSA receiving midazolam and fentanyl showed that desaturation events and other complications were not significantly different.215 Notably, doses of midazolam and fentanyl needed for colonoscopy were slightly lower in patients with OSA, although the procedure time was moderately longer.
Cha et al216 published a prospective study that compared cardiopulmonary complications during routine esophagogastroduodenoscopy under sedation with midazolam between 31 patients with OSA and 65 wholesome controls. Patients with OSA received a higher dose of midazolam than patients without OSA, but cardiopulmonary complications were not increased in patients with OSA.
Mador et al219 conducted a prospective study in 904 patients undergoing endoscopy to investigate whether OSA, assessed by the Berlin questionnaire, increases the risk of complications during sedation with midazolam and fentanyl. Major complications were observed in 3.25% of patients with low risk for OSA and in 1.9% of patients with towering risk for OSA (OR, 0.6; 95% CI, 0.26–1.46; P = .21). Minor complications were observed in 10.56% of patients with low OSA risk and 10.63% of patients with towering OSA risk (OR, 1.01; 95% CI, 0.65–1.56; P = 1.0), suggesting that OSA was not associated with increased risk for cardiopulmonary complications during endoscopy under sedation with midazolam and fentanyl in this analysis.
In conclusion, 5 studies directly compared outcomes between patients with and without OSA after intravenous benzodiazepine sedation in the context of anesthesia.209,213,215,216,219 However, only 2 studies209,213 were able to establish a higher risk for respiratory complications in patients with OSA (Oxford LOE: 3). A summary of evidence is provided in Supplemental Digital Content, Table A9, http://links.lww.com/AA/C373.
2.7 α-2 Agonists
2.7.1 Question: Are patients with OSA at increased risk for adverse events from the expend of α-2 agonists?
2.7.1 Recommendation: There is a lack of evidence to assess adverse effects of α-2 agonists in the OSA population.
Level of evidence: Low; Grade of recommendation: No recommendation
Dexmedetomidine and clonidine are centrally acting α-2 agonists with sedative, analgesic, and sympatholytic properties. Dexmedetomidine, in particular, has been suggested to intuition minimal respiratory depression. Because OSA is associated with an increased risk of adverse postoperative pulmonary events,6 the potentially auspicious respiratory profile and analgesic-sparing effects theoretically fabricate α-2 agonists appealing for this population. When assessing the risk of adverse events with the expend of α-2 agonists, no eligible studies compared patients with OSA to patients without OSA. The majority of studies focused on OSA or bariatric populations, comparing the expend of α-2 agonists to either placebo or other medications. The body of literature is limited by a petite total number of subjects, incongruous results, lack of uniformity in outcomes, and low adverse event rates. Although many studies demonstrate statistical differences in hemodynamic parameters with α-2 agonists, the translation into clinically meaningful outcome differences is not supported at this time.
Four studies123,124,220,221 compared the expend of dexmedetomidine to propofol in DISE as summarized in Supplemental Digital Content, Table A10, http://links.lww.com/AA/C373 (propofol in DISE has moreover been discussed in Section 2.3). In a string by Capasso et al,123 patients receiving propofol had a significantly increased likelihood of complete tongue base obstruction versus partial or no obstruction compared to those receiving dexmedetomidine. The 2 other studies that examined aspects of airway obstruction did not demonstrate significant differences between the dexmedetomidine and comparison groups.220,221
Three DISE studies measured intraprocedural respiratory and hemodynamic parameters. Two studies demonstrated a dwindle in respiratory rate and lower SpO2 with propofol compared to dexmedetomidine.124,221 In the study by Cho et al,220 hint SpO2 of the dexmedetomidine-remifentanil and propofol groups did not differ; however, it was significantly lower in the propofol-remifentanil group.220 This study showed no hemodynamic differences, a finding shared by Kuyrukluyildiz et al.124 Conversely, Yoon et al221 observed similar hint arterial pressure (MAP) but lower hint heart rate (HR) with dexmedetomidine and no episodes of clinically significant bradycardia. Kuyrukluyildiz et al124 measured postprocedure outcomes, finding significantly lower MAP and HR with dexmedetomidine. hint SpO2 and respiratory rate were higher with dexmedetomidine, although only 1 patient receiving propofol required additional oxygen supplementation.124
These 4 studies were examined in a systematic review, which concluded that dexmedetomidine appeared to capitulate a more stable cardiopulmonary profile, while propofol offered a faster onset, a shorter half-life, and potentially a greater degree of airway obstruction.222 The authors emphasized that neither propofol nor dexmedetomidine has been validated in replicating the obstruction that occurs during sleep. The obstructive patterns could subsist due to drug result rather than reflective of the natural sleep state. Consequently, additional investigation is necessary to ascertain the optimal sedative in DISE.
For studies involving procedures other than DISE, adverse events were characterized according to respiratory effects, hemodynamic effects, and recovery profile (Supplemental Digital Content, Table A11, http://links.lww.com/AA/C373).
Two studies reported respiratory outcomes during sedation procedures. In a descriptive string of 20 patients at towering risk of OSA, 13 required interventions for airway obstruction and 2 for desaturation during endoscopy with combined dexmedetomidine–propofol sedation.134 An RCT in upper respiratory procedures demonstrated that, compared to propofol target-controlled infusion, dexmedetomidine expend resulted in lower desaturation incidence, higher SpO2 at most time points, and lower rates of airway obstruction.223
Data are limited regarding respiratory effects of dexmedetomidine in the postoperative recovery period. A descriptive string of bariatric patients reported adequate saturations with supplemental oxygen without the exigency for CPAP.224 Studies with quantitative data hint that intraoperative expend of dexmedetomidine may not strike the respiratory rate in bariatric patients225 and when compared to placebo may maintain a better recovery profile in individuals undergoing uvuloplasty.93 In another group of patients receiving postoperative sedation after uvulopalatopharyngoplasty, the dexmedetomidine group experienced less ascetic and less frequent cough during extubation and less respiratory depression compared to the propofol group.226 Finally, in a retrospective review comparing patients undergoing airway reconstruction surgery who received dexmedetomidine versus those who did not, neither group required interventions for airway compromise.227
Two studies examined the result of clonidine on respiratory parameters and sleep in patients with OSA.228,229 In an RCT of 8 patients, clonidine compared to placebo suppressed the amount of time in REM sleep and decreased apnea duration during REM while not affecting overall AHI.228 Minimum SpO2 levels were higher in the clonidine group (86% ± 1.5% vs 84% ± 1.0%), reaching statistical but arguably not clinical significance. Pawlik et al229 performed an RCT in patients with OSA undergoing ear, nose, and throat surgery, with patients receiving either oral clonidine or placebo the night before and 2 hours before surgery. AHI in the night of surgery did not differ from baseline or between the 2 treatment groups. In both groups, the desaturation index decreased on the preoperative night, the day of the operation, and the postoperative night compared to their respective baseline measurements but did not differ between groups.
The hemodynamic effects of α-2 agonists were assessed according to varied outcome measures, including vital sign measurements, categorical descriptors, and exigency for rescue medications. Intraoperatively, 3 studies demonstrated significantly lower MAPs with α-2 agonists,229–231 while 1 study showed no difference.232 Heart rate was significantly lower with dexmedetomidine in 3 studies,223,229,230 while no disagreement to controls was observed in 2 other studies.231,232 Chawla et al227 reported transitory loading dose hypertension followed by “titratable, controlled hypotension, and bradycardia.” Three studies223,227,231 demonstrated less frequent expend of rescue antihypertensives or β blockers among α-2 agonist groups intraoperatively; 1 study showed this postoperatively.229 Furthermore, 1 study demonstrated a greater incidence of exigency for phenylephrine champion in patients receiving dexmedetomidine.231 In studies reporting the exigency for atropine and/or ephedrine, the overall incidence was low, and no differences were reported between treatment groups.223,229 Among studies that measured postoperative hemodynamics, there was inconsistency as to whether MAP was decreased with α-2 agonists229–231 or similar to that of the control patients.93,225 Xu et al226 moreover characterized outcomes according to categorical variables and organize a decreased incidence of hypertension and tachycardia, as well as an increased incidence of bradycardia in the dexmedetomidine-treated group; the frequency of hypotension did not differ.
The potential role of α-2 agonists in modulating the sympathetic response is of clinical interest. Four studies226,229,231,233 examined the effects of α-2 agonists on hemodynamics at points of stimulation, such as intubation, incision, and extubation. Only 1 study compared the measurements of each group to their respective baseline values,226 while All compared the measurements between treatment groups. Blood pressure and HR in the α-2 agonist groups were either lower than or similar to their control groups. Another group observed less frequent spikes in MAP and HR in clonidine-treated patients, but this was not statistically significant.234
The effects of α-2 agonists on recovery profile varied. Three studies demonstrated shorter time to extubation with α-2 agonists,226,230,234 1 showed no disagreement compared to control patients,231 and another showed increased time to extubation.93 One string described prolonged drowsiness with dexmedetomidine,134 while another study showed no disagreement in sedation score compared to control patients.93 linger points related to postoperative nausea/vomiting were examined in 1 observational study225 and 3 RCTs.93,226,231
In summary, the literature on the differential result of α-2-agonists in patients with and without OSA is limited and results are nonuniform (Oxford LOE: 2–4). While a trend in statistical outcomes for some cardiorespiratory parameters may subsist observed, the clinical impact of these findings remains unknown.
3. ANESTHESIA TECHNIQUE
3.1 Question: Should regional anesthesia subsist preferred over generic anesthesia in patients with OSA?
3.1 Recommendation: When applicable, regional anesthesia is preferable over generic anesthesia in patients with OSA.
Level of evidence: Moderate; Grade of recommendation: Strong
A wide reach of literature and earlier guidelines maintain favored the expend of regional anesthesia techniques and multimodal analgesic approaches among patients with OSA despite itsy-bitsy scientific evidence to champion this practice.8,9 To address this matter, a systematic literature search was performed to summarize evidence on preferable anesthesia techniques in patients with OSA.
Anesthesia Technique as a Modifier of Postoperative Outcome.
With esteem to comparative effectiveness between generic and regional anesthesia specifically in patients with OSA, 6 observational studies were identified.61,235–239 A summary of evidence is provided in Supplemental Digital Content, Table A12, http://links.lww.com/AA/C373. Overall, studies indicated that the utilization of regional as opposed to generic anesthesia would improve postoperative outcome.79,235–239 The largest population-based analysis included >30,000 patients with OSA from >400 US hospitals undergoing joint arthroplasty procedures.235 Adjusted risk of numerous major complications was significantly lower in patients with OSA who received neuraxial anesthesia versus generic anesthesia. Furthermore, the addition of neuraxial to generic anesthesia versus the expend of generic anesthesia solitary was associated with improved outcome profiles. Additionally, the utilization of peripheral nerve blocks was associated with decreased odds for mechanical ventilation, critical supervision admissions, and prolonged hospital length of stay.235
Subsequent studies236,239 confirmed the previous findings, while 1 suggested benefits with esteem to mortality.239 Notably, in a prospective analysis investigating drivers of postoperative worsening of sleep-disordered breathing, Chung et al79 demonstrated that the utilization of generic anesthesia was associated with an increased central apnea index postoperatively, while 72-hour total opioid dose was a driver of increased AHI. This finding suggests that the residual effects of generic anesthesia may strike postoperative sleep architecture and sleep-disordered breathing in OSA.
Given the necessity of airway manipulation under generic anesthesia, other challenges inherent to OSA should subsist considered as well. The higher risk for a difficult airway in OSA has been discussed in Section 1. However, challenges with esteem to airway complications in patients with OSA issue to moreover extend to the time for emergence from anesthesia and the immediate postoperative period, potentially leading to the requirement of emergent airway interventions.240,241 Thus, consistent with the underlying pathogenesis of OSA, perioperative complications in these patients may subsist driven by upper airway obstruction.240,241 Recently, Ramachandran et al61 showed that OSA was an independent predictor of respiratory complications and unplanned intubation after generic anesthesia.
Another potential hazard associated with the expend of generic anesthesia is the frequent exigency for neuromuscular blockade. As described in Section 2.1, studies hint that patients with OSA who received NMDA may subsist at increased risk for effects of residual neuromuscular blockade and respiratory failure compared to the generic population.67,242 Therefore, the expend of regional anesthesia may offer advantages by virtue of avoiding upper airway effects, although the potential for the exigency to transfigure to generic anesthesia should always subsist considered.
Neural stimulation appears to subsist essential in initiating the surgical catabolic stress response,243,244 and regional anesthesia utilizing local anesthetics seems to reliably block this effect.245 Given the evidence suggesting potential OSA-related alterations in pain perception and opioid potency due to intermittent hypoxia and sleep fragmentation, as discussed in Section 2.2, regional anesthesia confers benefits by providing effectual pain relief while reducing opioid requirement,246,247 a key factor to consider in patients with OSA.112,248
In summary, despite the lack of high-quality RCTs, some evidence suggests a higher risk of complications with generic compared to regional anesthesia in patients with OSA (Oxford LOE 2–4). Thus, regional anesthesia should subsist considered by anesthesiologists whenever feasible.
RECOMMENDATIONS: EXECUTIVE SUMMARY
Patients with OSA should subsist considered at increased risk for difficult airway challenges compared to patients without OSA. This particularly applies to difficult intubation, difficult mask ventilation, or both. Data on the placement of supraglottic airway devices are scarce, but available evidence does not hint a disagreement between patients with and without OSA. Adequate difficult airway management precautions should subsist taken in patients with OSA.
Anesthetic and analgesic drugs can interact with or impact consciousness, sleep, upper airway anatomy and physiology, arousal responses, muscle activation, and ventilatory drive, potentially increasing perioperative risk in patients with OSA.
In patients with OSA, the utilization of NMBA may consult an increased risk for the effects of residual neuromuscular blockade, postoperative respiratory failure, or hypoxemia. Residual neuromuscular blockade could subsist a driver of the higher incidence of respiratory complications in OSA. While neuromuscular blocking reversal agents can dwindle postoperative residual paralysis and respiratory complications, current evidence does not favor any specific neuromuscular reversal agent with esteem to outcome.
Given the respiratory depressant effects of opioids, patients with OSA may subsist at increased risk for respiratory complications from the expend of these analgesic drugs. Furthermore, confirmed intermittent hypoxia and habitual sleep fragmentation may increase pain perception and augment opioid potency in OSA. These factors should subsist considered when administering opioids to patients with OSA.
Patients with OSA receiving propofol for procedural sedation may subsist at increased risk for respiratory compromise and hypoxemic events. In the absence of conviction regarding dosing and scalar adjustments to concomitant expend of other drugs and potential concurrent obesity, the utilization of propofol sedation in OSA requires a heightened level of vigilance as well as observant monitoring and titration to achieve desired effects.
There is a lack of evidence on residual effects and anesthesia recovery profiles of inhalational agents and intravenous propofol specifically for the population with OSA. However, evidence in patients with obesity, a population with a towering prevalence of OSA, indicates a potential superiority of sevoflurane and desflurane compared to intravenous propofol with esteem to emergence and recovery from anesthesia. Comparing sevoflurane and desflurane, the latter has been associated with improved anesthesia recovery in patients with obesity.
Evidence on the impact of ketamine specifically in OSA is largely lacking; however, adverse events such as psychiatric effects, sympathetic system activation, and hypersalivation, as usually observed in the generic population during utilization of towering doses, likely translate to OSA as well. Notably, however, emerging evidence indicates a potentially auspicious impact of ketamine over other sedatives with esteem to preservation of upper airway and ventilatory function.
Despite the scarcity of data on the comparative effectiveness of intravenous benzodiazepine sedation among patients with and without OSA, intravenous benzodiazepines are known to and are purposefully utilized to induce upper airway collapse for diagnostic purposes of OSA. Thus, the procedure of intravenous benzodiazepine sedation may subsist associated with airway compromise in OSA.
The potentially auspicious respiratory profile and analgesic-sparing effects of α-2 agonists may render these drugs advantageous to the population with OSA. However, current literature on the result of α-2 agonists in patients with OSA is limited and provides heterogeneous results. Thus, despite the detection of trends in statistical outcomes for some cardiorespiratory parameters, the clinical relevance of these findings remains unclear.
Evidence on the comparative effectiveness of generic versus regional anesthesia in the context of OSA is sparse. Nevertheless, the limited evidence in patients with OSA indicates a higher risk of complications with generic compared to regional anesthesia. When feasible, regional anesthesia may consult advantages such as avoidance of upper airway effects and neuromuscular blockade, effectual pain management, reduced opioid consumption, and efficient suppression of the systemic stress response. These features may subsist of profit to patients with OSA. Given these findings and in the absence of evidence suggesting a handicap of regional anesthesia, the utilization of these techniques should subsist considered preferable over generic anesthesia whenever feasible. A summary of evidence is provided in Supplemental Digital Content, Table A9, http://links.lww.com/AA/C373.
The SASM job coerce is divided into 9 groups addressing the questions surrounding (1) airway, (2) neuromuscular blocking agents, (3) opioids, (4) propofol, (5) inhalational agents, (6) benzodiazepines, (7) ketamine, (8) α-2 agonists, and (9) anesthesia technique. The leaders of the respective groups and its individual members were: (1) Difficult airway in OSA: Mahesh Nagappa (Leader), David T. Wong, Frances Chung, Satya Krishna Ramachandran; (2) NMBAs: Jean Wong (Leader), Frances Chung, Mandeep Singh; (3) Opioids: Crispiana Cozowicz (Leader), Anthony G. Doufas, Frances Chung, Stavros G. Memtsoudis; (4) Propofol: designate H. Stein (Leader), Frances Chung; (5) Inhalational agents: Girish P. Joshi (Leader), Crispiana Cozowicz, Stavros G. Memtsoudis; (6) Ketamine: Meltem Yilmaz (Leader); (7) Benzodiazepines: Stavros G. Memtsoudis (Leader), Lukas Pichler, Crispiana Cozowicz; (8) α 2-agonists: Megan L. Krajewski (Leader), Satya Krishna Ramachandran, Crispiana Cozowicz; and (9) Anesthesia technique: Stavros G. Memtsoudis (Leader), Crispiana Cozowicz. They would enjoy to express special thanks to the following participants in alphabetical order for their significant contribution in the systematic literature search and data analysis process: Marina Englesakis, Library and Information Services, University Health Network, University of Toronto, Toronto, Ontario, Canada; Rie Goto, Kim Barrett Memorial Library, Hospital for Special Surgery, modern York, NY; Bridget Jivanelli, Kim Barrett Memorial Library, Hospital for Special Surgery, modern York, NY; Eva E. Mörwald, MD, Department of Anesthesiology, Perioperative Medicine and Intensive supervision Medicine, Paracelsus Medical University, Salzburg, Austria; Khawaja Rashid Hafeez, MBBS, FCPS, Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada; Arvind Tuteja, MBBS, Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada; Vwaire Urhuru, MD, Department of Anesthesia, critical Care, and pain Management, Beth Israel Deaconess Medical Center, Boston, MA; Sarah M. Weinstein, BA, Department of Anesthesiology, Hospital for Special Surgery, modern York, NY.
Name: Stavros G. Memtsoudis, MD, PhD.
Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: S. G. Memtsoudis is a director on the boards of the American Society of Regional Anesthesia and pain Medicine (ASRA) and the Society of Anesthesia and Sleep Medicine (SASM). He is a 1-time consultant for Sandoz Inc and the holder of US Patent Multicatheter Infusion System US-2017-0361063. He is the owner of SGM Consulting, LLC, and co-owner of FC Monmouth, LLC. not anyone of these relations influenced the conduct of the present study.
Name: Crispiana Cozowicz, MD.
Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Mahesh Nagappa, MD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Jean Wong, MD, FRCPC.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: J. Wong has received research grants from Acacia Pharma.
Name: Girish P. Joshi, MBBS, MD, FFARCSI.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: G. P. Joshi received an honorarium from Baxter Pharmaceuticals, Mallinckrodt Pharmaceuticals, Merck Pharmaceuticals, and Pacira Pharmaceuticals.
Name: David T. Wong, MD, FRCPC.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Anthony G. Doufas, MD, PhD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Meltem Yilmaz, MD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: M. Yilmaz serves on the advisory board of VitaHEAT Medical.
Name: designate H. Stein, MD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Megan L. Krajewski, MD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Mandeep Singh, MBBS, MD, MSc, FRCPC.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: None.
Name: Lukas Pichler, MD.
Contribution: This author helped analyze the data and write the manuscript.
Conflicts of Interest: None.
Name: Satya Krishna Ramachandran, MD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: S. K. Ramachandran funded research from Merck, acute & Dohme, modern Jersey.
Name: Frances Chung, MBBS, FRCPC.
Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.
Conflicts of Interest: F. Chung received research grants from Ontario Ministry of Health and Long-Term supervision Innovation Fund, University Health Network Foundation, ResMed Foundation, Acacia Pharma, and Medtronics Inc STOP-Bang tool: proprietary to University Health Network, royalties from Up-To-Date.
This manuscript was handled by: David Hillman, MD.
1. Heinzer R, Vat S, Marques-Vidal P, et al. Prevalence of sleep-disordered breathing in the generic population: the HypnoLaus study. Lancet Respir Med. 2015;3:310–318.
2. Peppard PE, puerile T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177:1006–1014.
3. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365:1046–1053.
4. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;353:2034–2041.
5. Memtsoudis S, Liu SS, Ma Y, et al. Perioperative pulmonary outcomes in patients with sleep apnea after noncardiac surgery. Anesth Analg. 2011;112:113–121.
6. Opperer M, Cozowicz C, Bugada D, et al. does obstructive sleep apnea influence perioperative outcome? A qualitative systematic review for the Society of Anesthesia and Sleep Medicine job coerce on Preoperative Preparation of Patients With Sleep-Disordered Breathing. Anesth Analg. 2016;122:1321–1334.
7. Chung F, Memtsoudis SG, Ramachandran SK, et al. Society of anesthesia and sleep medicine guidelines on preoperative screening and assessment of adult patients with obstructive sleep apnea. Anesth Analg. 2016;123:452–473.
8. indelicate JB, Bachenberg KL, Benumof JL, et al; American Society of Anesthesiologists job coerce on Perioperative Management. rehearse guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists job coerce on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2006;104:1081–1093.
9. indelicate JB, Apfelbaum JL, Caplan RA, et al. rehearse guidelines for the perioperative management of patients with obstructive sleep apnea: an updated report by the American Society of Anesthesiologists job coerce on Perioperative Management of Patients With Obstructive Sleep Apnea. Anesthesiology. 2014;120:268–286.
10. Joshi GP, Ankichetty SP, Gan TJ, Chung F. Society for Ambulatory Anesthesia consensus statement on preoperative selection of adult patients with obstructive sleep apnea scheduled for ambulatory surgery. Anesth Analg. 2012;115:1060–1068.
11. Meoli AL, Rosen CL, Kristo D, et al; Clinical rehearse Review Committee; American Academy of Sleep Medicine. Upper airway management of the adult patient with obstructive sleep apnea in the perioperative period–avoiding complications. Sleep. 2003;26:1060–1065.
12. Seet E, Chung F. Management of sleep apnea in adults: functional algorithms for the perioperative period: continuing professional development. Can J Anaesth. 2010;57:849–864.
13. de Raaff CAL, Gorter-Stam MAW, de Vries N, et al. Perioperative management of obstructive sleep apnea in bariatric surgery: a consensus guideline. Surg Obes Relat Dis. 2017;13:1095–1109.
14. Schumann R, Jones SB, Cooper B, et al. Update on best rehearse recommendations for anesthetic perioperative supervision and pain management in weight loss surgery, 2004-2007. Obesity (Silver Spring). 2009;17:889–894.
15. Eckert DJ, White DP, Jordan AS, Malhotra A, Wellman A. Defining phenotypic causes of obstructive sleep apnea: identification of novel therapeutic targets. Am J Respir Crit supervision Med. 2013;188:996–1004.
16. Leape LL. Reporting of adverse events. N Engl J Med. 2002;347:1633–1638.
17. Innovation VH. Covidence systematic review software. Melbourne, Australia.
19. Schünemann HJ, Jaeschke R, Cook DJ, et al; ATS Documents progress and Implementation Committee. An official ATS statement: grading the character of evidence and power of recommendations in ATS guidelines and recommendations. Am J Respir Crit supervision Med. 2006;174:605–614.
20. Guyatt GH, Oxman AD, Vist GE, et al; GRADE Working Group. GRADE: an emerging consensus on rating character of evidence and power of recommendations. BMJ. 2008;336:924–926.
21. Balshem H, Helfand M, Schünemann HJ, et al. GRADE guidelines: 3. Rating the character of evidence. J Clin Epidemiol. 2011;64:401–406.
22. Neumann I, Santesso N, Akl EA, et al. A steer for health professionals to interpret and expend recommendations in guidelines developed with the GRADE approach. J Clin Epidemiol. 2016;72:45–55.
23. Andrews J, Guyatt G, Oxman AD, et al. GRADE guidelines: 14. Going from evidence to recommendations: the significance and presentation of recommendations. J Clin Epidemiol. 2013;66:719–725.
24. Hiremath AS, Hillman DR, James AL, Noffsinger WJ, Platt PR, Singer SL. Relationship between difficult tracheal intubation and obstructive sleep apnoea. Br J Anaesth. 1998;80:606–611.
25. Siyam MA, Benhamou D. Difficult endotracheal intubation in patients with sleep apnea syndrome. Anesth Analg. 2002;95:1098–1102.
26. Brodsky JB, Lemmens HJ, Brock-Utne JG, Vierra M, Saidman LJ. Morbid obesity and tracheal intubation. Anesth Analg. 2002;94:732–736.
27. Sabers C, Plevak DJ, Schroeder DR, Warner DO. The diagnosis of obstructive sleep apnea as a risk factor for unanticipated admissions in outpatient surgery. Anesth Analg. 2003;96:1328–1335.
28. Kheterpal S, Han R, Tremper KK, et al. Incidence and predictors of difficult and impossible mask ventilation. Anesthesiology. 2006;105:885–891.
29. Chung F, Yegneswaran B, Herrera F, Shenderey A, Shapiro CM. Patients with difficult intubation may exigency referral to sleep clinics. Anesth Analg. 2008;107:915–920.
30. Kheterpal S, Martin L, Shanks AM, Tremper KK. Prediction and outcomes of impossible mask ventilation: a review of 50,000 anesthetics. Anesthesiology. 2009;110:891–897.
31. Shah PN, Sundaram V. Incidence and predictors of difficult mask ventilation and intubation. J Anaesthesiol Clin Pharmacol. 2012;28:451–455.
32. Toshniwal G, McKelvey GM, Wang H. STOP-Bang and prediction of difficult airway in obese patients. J Clin Anesth. 2014;26:360–367.
33. Acar HV, Yarkan Uysal H, Kaya A, Ceyhan A, Dikmen B. Does the STOP-Bang, an obstructive sleep apnea screening tool, prognosticate difficult intubation? Eur Rev Med Pharmacol Sci. 2014;18:1869–1874.
34. Ramachandran SK, Mathis MR, Tremper KK, Shanks AM, Kheterpal S. Predictors and clinical outcomes from failed Laryngeal Mask Airway Unique™: a study of 15,795 patients. Anesthesiology. 2012;116:1217–1226.
35. Kim JA, Lee JJ. Preoperative predictors of difficult intubation in patients with obstructive sleep apnea syndrome. Can J Anaesth. 2006;53:393–397.
36. Cattano D, Killoran P, Cai C, Katsiampoura AD, Corso RM, Hagberg CA. Difficult mask ventilation in generic surgical population: observation of risk factors and predictors. F1000Res. 2014;3:1–9.
37. Kheterpal S, Healy D, Aziz MF, et al; Multicenter Perioperative Outcomes Group (MPOG) Perioperative Clinical Research Committee. Incidence, predictors, and outcome of difficult mask ventilation combined with difficult laryngoscopy: a report from the multicenter perioperative outcomes group. Anesthesiology. 2013;119:1360–1369.
38. Gokay P, Tastan S, Orhan ME. Is there a disagreement between the STOP-BANG and the Berlin Obstructive Sleep Apnoea Syndrome questionnaires for determining respiratory complications during the perioperative period? J Clin Nurs. 2016;25:1238–1252.
39. Corso RM, Petrini F, Buccioli M, et al. Clinical utility of preoperative screening with STOP-Bang questionnaire in elective surgery. Minerva Anestesiol. 2014;80:877–884.
40. Aceto P, Perilli V, Modesti C, Ciocchetti P, Vitale F, Sollazzi L. Airway management in obese patients. Surg Obes Relat Dis. 2013;9:809–815.
41. Benumof JL. Obstructive sleep apnea in the adult obese patient: implications for airway management. Anesthesiol Clin North America. 2002;20:789–811.
42. Biro P, Bloch KE. Case reports patient with obstructive sleep and difficult airway access. 1995;180:417–421.
43. Corso RM, Cattano D, Buccioli M, Carretta E, Maitan S. Post analysis simulated correlation of the El-Ganzouri airway rigor score with difficult airway. Braz J Anesthesiol. 2016;66:298–303.
44. Hukins C. Mallampati class is not useful in the clinical assessment of sleep clinic patients. J Clin Sleep Med. 2010;6:545–549.
45. Kim MK, Park SW, Lee JW. Randomized comparison of the Pentax AirWay Scope and Macintosh laryngoscope for tracheal intubation in patients with obstructive sleep apnoea. Br J Anaesth. 2013;111:662–666.
46. Neligan PJ, Porter S, Max B, Malhotra G, Greenblatt EP, Ochroch EA. Obstructive sleep apnea is not a risk factor for difficult intubation in morbidly obese patients. Anesth Analg. 2009;109:1182–1186.
47. Cattano D, Katsiampoura A, Corso RM, Killoran P, Cai C, Hagberg CA. Predictive factors for difficult mask ventilation in the obese surgical population. F1000Research. 2014:1–11.
48. Nagappa M, Liao P, Wong J, et al. Validation of the STOP-Bang Questionnaire as a screening tool for obstructive sleep apnea among different populations: a systematic review and meta-analysis. PLoS One. 2015;10:e0143697.
49. Fouladpour N, Jesudoss R, Bolden N, Shaman Z, Auckley D. Perioperative complications in obstructive sleep apnea patients undergoing surgery: a review of the legal literature. Anesth Analg. 2016;122:145–151.
50. Kaw R, Chung F, Pasupuleti V, Mehta J, Gay PC, Hernandez AV. Meta-analysis of the association between obstructive sleep apnoea and postoperative outcome. Br J Anaesth. 2012;109:897–906.
51. Hai F, Porhomayon J, Vermont L, Frydrych L, Jaoude P, El-Solh AA. Postoperative complications in patients with obstructive sleep apnea: a meta-analysis. J Clin Anesth. 2014;26:591–600.
52. Ankichetty S, Wong J, Chung F. A systematic review of the effects of sedatives and anesthetics in patients with obstructive sleep apnea. J Anaesthesiol Clin Pharmacol. 2011;27:447–458.
53. Hillman DR, Chung F. Anaesthetic management of sleep-disordered breathing in adults. Respirology. 2017;22:230–239.
54. McNicholas WT, Ryan S. Obstructive sleep apnoea syndrome: translating science to clinical practice. Respirology. 2006;11:136–144.
55. Ciscar MA, Juan G, Martínez V, et al. Magnetic resonance imaging of the pharynx in OSA patients and wholesome subjects. Eur Respir J. 2001;17:79–86.
56. Ehsan Z, Mahmoud M, Shott SR, Amin RS, Ishman SL. The effects of anesthesia and opioids on the upper airway: a systematic review. Laryngoscope. 2016;126:270–284.
57. Murphy GS, Brull SJ. Residual neuromuscular block: lessons unlearned. section I: definitions, incidence, and adverse physiologic effects of residual neuromuscular block. Anesth Analg. 2010;111:120–128.
58. Murphy GS, Szokol JW, Marymont JH, Greenberg SB, Avram MJ, Vender JS. Residual neuromuscular blockade and critical respiratory events in the postanesthesia supervision unit. Anesth Analg. 2008;107:130–137.
59. Bulka CM, Terekhov MA, Martin BJ, Dmochowski RR, Hayes RM, Ehrenfeld JM. Nondepolarizing neuromuscular blocking agents, reversal, and risk of postoperative pneumonia. Anesthesiology. 2016;125:647–655.
60. Thevathasan T, Shih SL, Safavi KC, et al. Association between intraoperative non-depolarising neuromuscular blocking agent dose and 30-day readmission after abdominal surgery. Br J Anaesth. 2017;119:595–605.
61. Ramachandran SK, Pandit J, Devine S, Thompson A, Shanks A. Postoperative respiratory complications in patients at risk for obstructive sleep apnea: a single-institution cohort study. Anesth Analg. 2017;125:272–279.
62. Fuchs-Buder T, Nemes R, Schmartz D. Residual neuromuscular blockade: management and impact on postoperative pulmonary outcome. Curr Opin Anaesthesiol. 2016;29:662–667.
63. Mokhlesi B, Hovda MD, Vekhter B, Arora VM, Chung F, Meltzer DO. Sleep-disordered breathing and postoperative outcomes after bariatric surgery: analysis of the nationwide inpatient sample. Obes Surg. 2013;23:1842–1851.
64. Memtsoudis SG, Stundner O, Rasul R, et al. The impact of sleep apnea on postoperative utilization of resources and adverse outcomes. Anesth Analg. 2014;118:407–418.
65. Sudré EC, de Batista PR, Castiglia YM. Longer immediate recovery time after anesthesia increases risk of respiratory complications after laparotomy for bariatric surgery: a randomized clinical affliction and a cohort study. Obes Surg. 2015;25:2205–2212.
66. Ahmad S, Nagle A, McCarthy RJ, Fitzgerald PC, Sullivan JT, Prystowsky J. Postoperative hypoxemia in morbidly obese patients with and without obstructive sleep apnea undergoing laparoscopic bariatric surgery. Anesth Analg. 2008;107:138–143.
67. Pereira H, Xará D, Mendonça J, Santos A, Abelha FJ. Patients with a towering risk for obstructive sleep apnea syndrome: postoperative respiratory complications. Rev Port Pneumol. 2013;19:144–151.
68. Ünal DY, Baran İ, Mutlu M, Ural G, Akkaya T, Özlü O. Comparison of sugammadex versus neostigmine costs and respiratory complications in patients with obstructive sleep apnoea. Turk J Anaesthesiol Reanim. 2015;43:387–395.
69. Llauradó S, Sabaté A, Ferreres E, Camprubí I, Cabrera A. Postoperative respiratory outcomes in laparoscopic bariatric surgery: comparison of a prospective group of patients whose neuromuscular blockade was reverted with sugammadex and a historical one reverted with neostigmine. Rev Esp Anestesiol Reanim. 2014;61:565–570.
70. Dowidar AE-RM, Basuni AS, EL-kalla RS, Eid GM. Influence of severity of obstructive sleep apnea on postoperative pulmonary complications in patients undergoing gastroplasty. Tanta Med J. 2016;44:58.
71. Liao P, Yegneswaran B, Vairavanathan S, Zilberman P, Chung F. Postoperative complications in patients with obstructive sleep apnea: a retrospective matched cohort study. Can J Anaesth. 2009;56:819–828.
72. Eikermann M, Vogt FM, Herbstreit F, et al. The predisposition to inspiratory upper airway collapse during partial neuromuscular blockade. Am J Respir Crit supervision Med. 2007;175:9–15.
73. Abrishami A, Ho J, Wong J, Yin L, Chung F. Sugammadex, a selective reversal medication for preventing postoperative residual neuromuscular blockade. Cochrane Database Syst Rev. 2009:Cd007362.
74. Abad-Gurumeta A, Ripollés-Melchor J, Casans-Francés R, et al; Evidence Anaesthesia Review Group. A systematic review of sugammadex vs neostigmine for reversal of neuromuscular blockade. Anaesthesia. 2015;70:1441–1452.
75. Hristovska AM, Duch P, Allingstrup M, Afshari A. Efficacy and safety of sugammadex versus neostigmine in reversing neuromuscular blockade in adults. Cochrane Database Syst Rev. 2017;8:CD012763.
76. Doufas A. Obstructive sleep apnea, pain, and opioid analgesia in the postoperative patient. Curr Anesthesiol Rep. 2014;4:1–9.
77. Blake DW, Chia PH, Donnan G, Williams DL. Preoperative assessment for obstructive sleep apnoea and the prediction of postoperative respiratory obstruction and hypoxaemia. Anaesth Intensive Care. 2008;36:379–384.
78. Bolden N, Smith CE, Auckley D, Makarski J, Avula R. Perioperative complications during expend of an obstructive sleep apnea protocol following surgery and anesthesia. Anesth Analg. 2007;105:1869–1870.
79. Chung F, Liao P, Elsaid H, Shapiro CM, Kang W. Factors associated with postoperative exacerbation of sleep-disordered breathing. Anesthesiology. 2014;120:299–311.
80. Esclamado RM, Glenn MG, McCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope. 1989;99:1125–1129.
81. Etches RC. Respiratory depression associated with patient-controlled analgesia: a review of eight cases. Can J Anaesth. 1994;41:125–132.
82. Lee LA, Caplan RA, Stephens LS, et al. Postoperative opioid-induced respiratory depression: a closed claims analysis. Anesthesiology. 2015;122:659–665.
83. Melamed R, Boland LL, Normington JP, et al. Postoperative respiratory failure necessitating transfer to the intensive supervision unit in orthopedic surgery patients: risk factors, costs, and outcomes. Perioper Med (Lond). 2016;5:19.
84. Ramachandran SK, Haider N, Saran KA, et al. Life-threatening critical respiratory events: a retrospective study of postoperative patients organize unresponsive during analgesic therapy. J Clin Anesth. 2011;23:207–213.
85. Weingarten TN, Hawkins NM, Beam WB, et al. Factors associated with prolonged anesthesia recovery following laparoscopic bariatric surgery: a retrospective analysis. Obes Surg. 2015;25:1024–1030.
86. Weingarten TN, Herasevich V, McGlinch MC, et al. Predictors of delayed postoperative respiratory depression assessed from naloxone administration. Anesth Analg. 2015;121:422–429.
87. Weingarten TN, Chong EY, Schroeder DR, Sprung J. Predictors and outcomes following naloxone administration during angle I anesthesia recovery. J Anesth. 2016;30:116–122.
88. Mörwald EE, Olson A, Cozowicz C, Poeran J, Mazumdar M, Memtsoudis SG. Association of opioid prescription and perioperative complications in obstructive sleep apnea patients undergoing total joint arthroplasties. Sleep Breath. 2018;22:115–121.
89. Subramani Y, Nagappa M, Wong J, Patra J, Chung F. Death or near-death in patients with obstructive sleep apnoea: a compendium of case reports of critical complications. Br J Anaesth. 2017;119:885–899.
90. Madani M. Effectiveness of Stadol NS (butorphanol tartrate) with ibuprofen in the treatment of pain after laser-assisted uvulopalatopharyngoplasty. J Oral Maxillofac Surg. 2000;58:27–31.
91. Wang D, Somogyi AA, Yee BJ, et al. The effects of a single mild dose of morphine on chemoreflexes and breathing in obstructive sleep apnea. Respir Physiol Neurobiol. 2013;185:526–532.
92. Cozowicz C, Olson A, Poeran J, et al. Opioid prescription levels and postoperative outcomes in orthopedic surgery. Pain. 2017;158:2422–2430.
93. Abdelmageed WM, Elquesny KM, Shabana RI, Abushama HM, Nassar AM. Analgesic properties of a dexmedetomidine infusion after uvulopalatopharyngoplasty in patients with obstructive sleep apnea. Saudi J Anaesth. 2011;5:150–156.
94. Bernards CM, Knowlton SL, Schmidt DF, et al. Respiratory and sleep effects of remifentanil in volunteers with moderate obstructive sleep apnea. Anesthesiology. 2009;110:41–49.
95. Blake DW, Yew CY, Donnan GB, Williams DL. Postoperative analgesia and respiratory events in patients with symptoms of obstructive sleep apnoea. Anaesth Intensive Care. 2009;37:720–725.
96. Huang HC, Lee LA, Fang TJ, Li HY, Lo CC, Wu JH. Transnasal butorphanol for pain relief after uvulopalatopharyngoplasty: a hospital-based, randomized study. Chang Gung Med J. 2009;32:390–399.
97. Lee LA, Wang PC, Chen NH, et al. Alleviation of wound pain after surgeries for obstructive sleep apnea. Laryngoscope. 2007;117:1689–1694.
98. Yang L, Sun DF, Wu Y, Han J, Liu RC, Wang LJ. Intranasal administration of butorphanol benefits ancient patients undergoing H-uvulopalatopharyngoplasty: a randomized trial. BMC Anesthesiol. 2015;15:20.
99. Orlov D, Ankichetty S, Chung F, Brull R. Cardiorespiratory complications of neuraxial opioids in patients with obstructive sleep apnea: a systematic review. J Clin Anesth. 2013;25:591–599.
100. Ladha KS, Kato R, Tsen LC, Bateman BT, Okutomi T. A prospective study of post-cesarean delivery hypoxia after spinal anesthesia with intrathecal morphine 150μg. Int J Obstet Anesth. 2017;32:48–53.
101. Thompson MJ, Clinger BN, Simonds RM, Hochheimer CJ, Lahaye LA, Golladay GJ. Probability of undiagnosed obstructive sleep apnea does not correlate with adverse pulmonary events nor length of linger in hip and knee arthroplasty using intrathecal opioid. J Arthroplasty. 2017;32:2676–2679.
102. Zotou A, Siampalioti A, Tagari P, Paridis L, Kalfarentzos F, Filos KS. Does epidural morphine loading in addition to thoracic epidural analgesia profit the postoperative management of morbidly obese patients undergoing open bariatric surgery? A pilot study. Obes Surg. 2014;24:2099–2108.
103. Roehrs T, Hyde M, Blaisdell B, Greenwald M, Roth T. Sleep loss and REM sleep loss are hyperalgesic. Sleep. 2006;29:145–151.
104. Smith MT, Edwards RR, McCann UD, Haythornthwaite JA. The effects of sleep deprivation on pain inhibition and impulsive pain in women. Sleep. 2007;30:494–505.
105. Roehrs TA, Harris E, Randall S, Roth T. pain sensitivity and recovery from mild confirmed sleep loss. Sleep. 2012;35:1667–1672.
106. Haack M, Scott-Sutherland J, Santangelo G, Simpson NS, Sethna N, Mullington JM. pain sensitivity and modulation in primary insomnia. Eur J Pain. 2012;16:522–533.
107. Luyster FS, Buysse DJ, Strollo PJ Jr.. Comorbid insomnia and obstructive sleep apnea: challenges for clinical rehearse and research. J Clin Sleep Med. 2010;6:196–204.
108. Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain. 2013;14:1539–1552.
109. Smith MT, Wickwire EM, Grace EG, et al. Sleep disorders and their association with laboratory pain sensitivity in temporomandibular joint disorder. Sleep. 2009;32:779–790.
110. Khalid I, Roehrs TA, Hudgel DW, Roth T. Continuous positive airway pressure in ascetic obstructive sleep apnea reduces pain sensitivity. Sleep. 2011;34:1687–1691.
111. Doufas AG, Tian L, Padrez KA, et al. Experimental pain and opioid analgesia in volunteers at towering risk for obstructive sleep apnea. PLoS One. 2013;8:e54807.
112. Doufas AG, Tian L, Davies MF, Warby SC. Nocturnal intermittent hypoxia is independently associated with pain in subjects suffering from sleep-disordered breathing. Anesthesiology. 2013;119:1149–1162.
113. Brown KA, Laferrière A, Moss IR. Recurrent hypoxemia in puerile children with obstructive sleep apnea is associated with reduced opioid requirement for analgesia. Anesthesiology. 2004;100:806–810.
114. Brown KA, Laferrière A, Lakheeram I, Moss IR. Recurrent hypoxemia in children is associated with increased analgesic sensitivity to opiates. Anesthesiology. 2006;105:665–669.
115. Sadhasivam S, Chidambaran V, Ngamprasertwong P, et al. Race and unequal affliction of perioperative pain and opioid related adverse effects in children. Pediatrics. 2012;129:832–838.
116. Sanders JC, King MA, Mitchell RB, Kelly JP. Perioperative complications of adenotonsillectomy in children with obstructive sleep apnea syndrome. Anesth Analg. 2006;103:1115–1121.
117. Turan A, You J, Egan C, et al. confirmed intermittent hypoxia is independently associated with reduced postoperative opioid consumption in bariatric patients suffering from sleep-disordered breathing. PLoS One. 2015;10:e0127809.
118. Chung F, Liao P, Yegneswaran B, Shapiro CM, Kang W. Postoperative changes in sleep-disordered breathing and sleep architecture in patients with obstructive sleep apnea. Anesthesiology. 2014;120:287–298.
119. Vanderveken OM, Maurer JT, Hohenhorst W, et al. Evaluation of drug-induced sleep endoscopy as a patient selection tool for implanted upper airway stimulation for obstructive sleep apnea. J Clin Sleep Med. 2013;9:433–438.
120. De Vito A, Agnoletti V, Berrettini S, et al. Drug-induced sleep endoscopy: conventional versus target controlled infusion techniques: a randomized controlled study. Eur Arch Otorhinolaryngol. 2011;268:457–462.
121. Rabelo FA, Küpper DS, Sander HH, Fernandes RM, Valera FC. Polysomnographic evaluation of propofol-induced sleep in patients with respiratory sleep disorders and controls. Laryngoscope. 2013;123:2300–2305.
122. Dotan Y, Pillar G, Tov N, et al. Dissociation of electromyogram and mechanical response in sleep apnoea during propofol anaesthesia. Eur Respir J. 2013;41:74–84.
123. Capasso R, Rosa T, Tsou DY, et al. Variable findings for drug-induced sleep endoscopy in obstructive sleep apnea with propofol versus dexmedetomidine. Otolaryngol Head Neck Surg. 2016;154:765–770.
124. Kuyrukluyildiz U, Binici O, Onk D, et al. Comparison of dexmedetomidine and propofol used for drug-induced sleep endoscopy in patients with obstructive sleep apnea syndrome. Int J Clin Exp Med. 2015;8:5691–5698.
125. Blumen M, Bequignon E, Chabolle F. Drug-induced sleep endoscopy: a modern gold touchstone for evaluating OSAS? section II: results. Eur Ann Otorhinolaryngol Head Neck Dis. 2017;134:109–115.
126. De Vito A, Carrasco Llatas M, Vanni A, et al. European position paper on drug-induced sedation endoscopy (DISE). Sleep Breath. 2014;18:453–465.
127. Cortínez LI, Anderson BJ, Penna A, et al. Influence of obesity on propofol pharmacokinetics: derivation of a pharmacokinetic model. Br J Anaesth. 2010;105:448–456.
128. Servin F, Farinotti R, Haberer JP, Desmonts JM. Propofol infusion for maintenance of anesthesia in morbidly obese patients receiving nitrous oxide: a clinical and pharmacokinetic study. Anesthesiology. 1993;78:657–665.
129. La Colla L, Albertin A, La Colla G, et al. No adjustment vs adjustment formula as input weight for propofol target-controlled infusion in morbidly obese patients. Eur J Anaesthesiol. 2009;26:362–369.
130. Dong D, Peng X, Liu J, Qian H, Li J, Wu B. Morbid obesity alters both pharmacokinetics and pharmacodynamics of propofol: dosing recommendation for anesthesia induction. Drug Metab Dispos. 2016;44:1579–1583.
131. Short TG, Chui PT. Propofol and midazolam act synergistically in combination. Br J Anaesth. 1991;67:539–545.
132. Thomas MC, Jennett-Reznek AM, Patanwala AE. Combination of ketamine and propofol versus either agent solitary for procedural sedation in the emergency department. Am J Health Syst Pharm. 2011;68:2248–2256.
133. Bojak I, Day HC, Liley DT. Ketamine, propofol, and the EEG: a neural bailiwick analysis of HCN1-mediated interactions. Front Comput Neurosci. 2013;7:22.
134. Hannallah M, Rasmussen M, Carroll J, Charabaty A, Palese C, Haddad N. Evaluation of dexmedetomidine/propofol anesthesia during upper gastrointestinal endoscopy in patients with towering probability of having obstructive sleep apnea. Anaesth pain Intensive Care. 2013;173.
135. Vuyk J. Pharmacokinetic and pharmacodynamic interactions between opioids and propofol. J Clin Anesth. 1997;9:23S–26S.
136. Sneyd JR, Rigby-Jones AE. modern drugs and technologies, intravenous anaesthesia is on the bound (again). Br J Anaesth. 2010;105:246–254.
137. Colao J, Rodriguez-Correa D. Rapidly metabolized anesthetics: novel alternative agents for procedural sedation. J Anesth Clin Res. 2016;7:11.
138. Mehta PP, Kochhar G, Kalra S, et al. Can a validated sleep apnea scoring system prognosticate cardiopulmonary events using propofol sedation for routine EGD or colonoscopy? A prospective cohort study. Gastrointest Endosc. 2014;79:436–444.
139. Coté GA, Hovis RM, Ansstas MA, et al. Incidence of sedation-related complications with propofol expend during advanced endoscopic procedures. Clin Gastroenterol Hepatol. 2010;8:137–142.
140. Friedrich-Rust M, Welte M, Welte C, et al. Capnographic monitoring of propofol-based sedation during colonoscopy. Endoscopy. 2014;46:236–244.
141. Nagels AJ, Bridgman JB, Bell SE, Chrisp DJ. Propofol-remifentanil TCI sedation for oral surgery. N Z Dent J. 2014;110:85–89.
142. Mador MJ, Abo Khamis M, Nag N, Mreyoud A, Jallu S, Mehboob S. Does sleep apnea increase the risk of cardiorespiratory complications during endoscopy procedures? Sleep Breath. 2011;15:393–401.
143. McVay T, Fang JC, Taylor L, et al. Safety analysis of bariatric patients undergoing outpatient upper endoscopy with non-anesthesia administered propofol sedation. Obes Surg. 2017;27:1501–1507.
144. Deitch K, Miner J, Chudnofsky CR, Dominici P, Latta D. Does linger tidal CO2 monitoring during emergency department procedural sedation and analgesia with propofol dwindle the incidence of hypoxic events? A randomized, controlled trial. Ann Emerg Med. 2010;55:258–264.
145. Gupta A, Stierer T, Zuckerman R, Sakima N, Parker SD, Fleisher LA. Comparison of recovery profile after ambulatory anesthesia with propofol, isoflurane, sevoflurane and desflurane: a systematic review. Anesth Analg. 2004;98:632–641.
146. Benumof JL. Obesity, sleep apnea, the airway and anesthesia. Curr Opin Anaesthesiol. 2004;17:21–30.
147. Peromaa-Haavisto P, Tuomilehto H, Kössi J, et al. Prevalence of obstructive sleep apnoea among patients admitted for bariatric surgery: a prospective multicentre trial. Obes Surg. 2016;26:1384–1390.
148. Duarte RL, Magalhães-da-Silveira FJ. Factors predictive of obstructive sleep apnea in patients undergoing pre-operative evaluation for bariatric surgery and referred to a sleep laboratory for polysomnography. J Bras Pneumol. 2015;41:440–448.
149. Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth. 2000;85:91–108.
150. Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP. critical respiratory events in the postanesthesia supervision unit: patient, surgical, and anesthetic factors. Anesthesiology. 1994;81:410–418.
151. Fassbender P, Bürgener S, Haddad A, Silvanus MT, Peters J. Perioperative incidence of airway obstructive and hypoxemic events in patients with confirmed or suspected sleep apnea: a prospective, randomized pilot study comparing propofol/remifentanil and sevoflurane/remifentanil anesthesia. BMC Anesthesiol. 2018;18:14.
152. Salihoglu Z, Karaca S, Kose Y, Zengin K, Taskin M. Total intravenous anesthesia versus single breath technique and anesthesia maintenance with sevoflurane for bariatric operations. Obes Surg. 2001;11:496–501.
153. Siampalioti A, Karavias D, Zotou A, Kalfarentzos F, Filos K. Anesthesia management for the super obese: is sevoflurane superior to propofol as a sole anesthetic agent? A double-blind randomized controlled trial. Eur Rev Med Pharmacol Sci. 2015;19:2493–2500.
154. Hendolin H, Kansanen M, Koski E, Nuutinen J. Propofol-nitrous oxide versus thiopentone-isoflurane-nitrous oxide anaesthesia for uvulopalatopharyngoplasty in patients with sleep apnea. Acta Anaesthesiol Scand. 1994;38:694–698.
155. Pizzirani E, Pigato P, Favretti F, et al. The post-anaesthetic recovery in obesity surgery: comparison between two anaesthetic techniques. Obes Surg. 1992;2:91–94.
156. Tanaka P, Goodman S, Sommer BR, Maloney W, Huddleston J, Lemmens HJ. The result of desflurane versus propofol anesthesia on postoperative delirium in superannuated obese patients undergoing total knee replacement: a randomized, controlled, double-blinded clinical trial. J Clin Anesth. 2017;39:17–22.
157. Zoremba M, Dette F, Hunecke T, Eberhart L, Braunecker S, Wulf H. A comparison of desflurane versus propofol: the effects on early postoperative lung duty in overweight patients. Anesth Analg. 2011;113:63–69.
158. Sollazzi L, Perilli V, Modesti C, et al. Volatile anesthesia in bariatric surgery. Obes Surg. 2001;11:623–626.
159. Torri G, Casati A, Albertin A, et al. Randomized comparison of isoflurane and sevoflurane for laparoscopic gastric banding in morbidly obese patients. J Clin Anesth. 2001;13:565–570.
160. Torri G, Casati A, Comotti L, Bignami E, Santorsola R, Scarioni M. Wash-in and wash-out curves of sevoflurane and isoflurane in morbidly obese patients. Minerva Anestesiol. 2002;68:523–527.
161. Arain SR, Barth CD, Shankar H, Ebert TJ. altenative of volatile anesthetic for the morbidly obese patient: sevoflurane or desflurane. J Clin Anesth. 2005;17:413–419.
162. De Baerdemaeker LE, Struys MM, Jacobs S, et al. Optimization of desflurane administration in morbidly obese patients: a comparison with sevoflurane using an “inhalation bolus” technique. Br J Anaesth. 2003;91:638–650.
163. De Baerdemaeker LE, Jacobs S, Den Blauwen NM, et al. Postoperative results after desflurane or sevoflurane combined with remifentanil in morbidly obese patients. Obes Surg. 2006;16:728–733.
164. Bilotta F, Doronzio A, Cuzzone V, Caramia R, Rosa G; PINOCCHIO Study Group. Early postoperative cognitive recovery and gas exchange patterns after balanced anesthesia with sevoflurane or desflurane in overweight and obese patients undergoing craniotomy: a prospective randomized trial. J Neurosurg Anesthesiol. 2009;21:207–213.
165. Ozdogan HK, Cetinkunar S, Karateke F, Cetinalp S, Celik M, Ozyazici S. The effects of sevoflurane and desflurane on the hemodynamics and respiratory functions in laparoscopic sleeve gastrectomy. J Clin Anesth. 2016;35:441–445.
166. Strum EM, Szenohradszki J, Kaufman WA, Anthone GJ, Manz IL, Lumb PD. Emergence and recovery characteristics of desflurane versus sevoflurane in morbidly obese adult surgical patients: a prospective, randomized study. Anesth Analg. 2004;99:1848–1853.
167. Vallejo MC, Sah N, Phelps AL, O’Donnell J, Romeo RC. Desflurane versus sevoflurane for laparoscopic gastroplasty in morbidly obese patients. J Clin Anesth. 2007;19:3–8.
168. La Colla L, Albertin A, La Colla G, Mangano A. Faster wash-out and recovery for desflurane vs sevoflurane in morbidly obese patients when no premedication is used. Br J Anaesth. 2007;99:353–358.
169. Kaur A, Jain AK, Sehgal R, Sood J. Hemodynamics and early recovery characteristics of desflurane versus sevoflurane in bariatric surgery. J Anaesthesiol Clin Pharmacol. 2013;29:36–40.
170. Juvin P, Vadam C, Malek L, Dupont H, Marmuse JP, Desmonts JM. Postoperative recovery after desflurane, propofol, or isoflurane anesthesia among morbidly obese patients: a prospective, randomized study. Anesth Analg. 2000;91:714–719.
171. Liu FL, Cherng YG, Chen SY, et al. Postoperative recovery after anesthesia in morbidly obese patients: a systematic review and meta-analysis of randomized controlled trials. Can J Anaesth. 2015;62:907–917.
172. Ibraheim O, Alshaer A, Mazen K, et al. result of bispectral index (BIS) monitoring on postoperative recovery and sevoflurane consumption among morbidly obese patients undergoing laparoscopic gastric banding. Middle East J Anaesthesiol. 2008;19:819–830.
173. Freo U, Carron M, Innocente F, Foletto M, Nitti D, Ori C. Effects of A-line Autoregression Index (AAI) monitoring on recovery after sevoflurane anesthesia for bariatric surgery. Obes Surg. 2011;21:850–857.
174. McKay RE, Malhotra A, Cakmakkaya OS, Hall KT, McKay WR, Apfel CC. result of increased body mass index and anaesthetic duration on recovery of protective airway reflexes after sevoflurane vs desflurane. Br J Anaesth. 2010;104:175–182.
175. Eger EI 2nd, Shafer S. The complexity of recovery from anesthesia. J Clin Anesth. 2005;17:411–412.
176. Ebert TJ, Robinson BJ, Uhrich TD, Mackenthun A, Pichotta PJ. Recovery from sevoflurane anesthesia: a comparison to isoflurane and propofol anesthesia. Anesthesiology. 1998;89:1524–1531.
177. Dexter F, Tinker JH. Comparisons between desflurane and isoflurane or propofol on time to following commands and time to discharge: a meta-analysis. Anesthesiology. 1995;83:77–82.
178. Macario A, Dexter F, Lubarsky D. Meta-analysis of trials comparing postoperative recovery after anesthesia with sevoflurane or desflurane. Am J Health Syst Pharm. 2005;62:63–68.
179. Dexter F, Bayman EO, Epstein RH. Statistical modeling of objective and variability of time to extubation for meta-analysis comparing desflurane to sevoflurane. Anesth Analg. 2010;110:570–580.
180. Agoliati A, Dexter F, Lok J, et al. Meta-analysis of objective and variability of time to extubation comparing isoflurane with desflurane or isoflurane with sevoflurane. Anesth Analg. 2010;110:1433–1439.
181. Yasuda N, Lockhart SH, Eger EI 2nd, et al. Comparison of kinetics of sevoflurane and isoflurane in humans. Anesth Analg. 1991;72:316–324.
182. Ogunnaike BO, Jones SB, Jones DB, Provost D, Whitten CW. Anesthetic considerations for bariatric surgery. Anesth Analg. 2002;95:1793–1805.
183. Eger EI 2nd.. Age, minimum alveolar anesthetic concentration, and minimum alveolar anesthetic concentration-awake. Anesth Analg. 2001;93:947–953.
184. Juvin P, Marmuse JP, Delerme S, et al. Post-operative course after conventional or laparoscopic gastroplasty in morbidly obese patients. Eur J Anaesthesiol. 1999;16:400–403.
185. Katznelson R, Naughton F, Friedman Z, et al. Increased lung clearance of isoflurane shortens emergence in obesity: a prospective randomized-controlled trial. Acta Anaesthesiol Scand. 2011;55:995–1001.
186. De Kock M, Lavand’homme P, Waterloos H. Balanced analgesia” in the perioperative period: is there a dwelling for ketamine? Pain. 2001;92:373–380.
187. Bell RF, Dahl JB, Moore RA, Kalso E. Perioperative ketamine for acute postoperative pain. Cochrane Database Syst Rev. 2006:CD004603.
188. Laskowski K, Stirling A, McKay WP, Lim HJ. A systematic review of intravenous ketamine for postoperative analgesia. Can J Anaesth. 2011;58:911–923.
189. Luscri N, Tobias JD. Monitored anesthesia supervision with a combination of ketamine and dexmedetomidine during magnetic resonance imaging in three children with trisomy 21 and obstructive sleep apnea. Paediatr Anaesth. 2006;16:782–786.
190. Cheng X, Huang Y, Zhao Q, Gu E. Comparison of the effects of dexmedetomidine-ketamine and sevoflurane-sufentanil anesthesia in children with obstructive sleep apnea after uvulopalatopharyngoplasty: an observational study. J Anaesthesiol Clin Pharmacol. 2014;30:31–35.
191. Strayer RJ, Nelson LS. Adverse events associated with ketamine for procedural sedation in adults. Am J Emerg Med. 2008;26:985–1028.
192. Melendez E, Bachur R. sober adverse events during procedural sedation with ketamine. Pediatr Emerg Care. 2009;25:325–328.
193. Gorlin AW, Rosenfeld DM, Ramakrishna H. Intravenous sub-anesthetic ketamine for perioperative analgesia. J Anaesthesiol Clin Pharmacol. 2016;32:160–167.
194. De Oliveira GS Jr, Fitzgerald PC, Hansen N, Ahmad S, McCarthy RJ. The result of ketamine on hypoventilation during deep sedation with midazolam and propofol: a randomised, double-blind, placebo-controlled trial. Eur J Anaesthesiol. 2014;31:654–662.
195. Taylor DM, Bell A, Holdgate A, et al. Risk factors for sedation-related events during procedural sedation in the emergency department. Emerg Med Australas. 2011;23:466–473.
196. Drummond GB. Comparison of sedation with midazolam and ketamine: effects on airway muscle activity. Br J Anaesth. 1996;76:663–667.
197. Eikermann M, Grosse-Sundrup M, Zaremba S, et al. Ketamine activates breathing and abolishes the coupling between loss of consciousness and upper airway dilator muscle dysfunction. Anesthesiology. 2012;116:35–46.
198. Abdullah VJ, Lee DL, Ha SC, van Hasselt CA. Sleep endoscopy with midazolam: sedation level evaluation with bispectral analysis. Otolaryngol Head Neck Surg. 2013;148:331–337.
199. Bachar G, Feinmesser R, Shpitzer T, Yaniv E, Nageris B, Eidelman L. Laryngeal and hypopharyngeal obstruction in sleep disordered breathing patients, evaluated by sleep endoscopy. Eur Arch Otorhinolaryngol. 2008;265:1397–1402.
200. Bachar G, Nageris B, Feinmesser R, et al. Novel grading system for quantifying upper-airway obstruction on sleep endoscopy. Lung. 2012;190:313–318.
201. Carrasco Llatas M, Agostini Porras G, Cuesta González MT, et al. Drug-induced sleep endoscopy: a two drug comparison and simultaneous polysomnography. Eur Arch Otorhinolaryngol. 2014;271:181–187.
202. De Corsa E, Fiorita A, Rizzotto G, et al. The role of drug-induced sleep endoscopy in the diagnosis and management of obstructive sleep apnoea syndrome: their personal experience. Acta Otorhinolaryngol Ital. 2013;33:405–413.
203. Gregório MG, Jacomelli M, Figueiredo AC, Cahali MB, Pedreira WL Jr, Lorenzi Filho G. Evaluation of airway obstruction by nasopharyngoscopy: comparison of the Müller maneuver versus induced sleep. Braz J Otorhinolaryngol. 2007;73:618–622.
204. Hamans E, Meeus O, Boudewyns A, Saldien V, Verbraecken J, Van de Heyning P. Outcome of sleep endoscopy in obstructive sleep apnoea: the Antwerp experience. B-ENT. 2010;6:97–103.
205. Hessel NS, de Vries N. Diagnostic work-up of socially unacceptable snoring: II. Sleep endoscopy. Eur Arch Otorhinolaryngol. 2002;259:158–161.
206. Iwanaga K, Hasegawa K, Shibata N, et al. Endoscopic examination of obstructive sleep apnea syndrome patients during drug-induced sleep. Acta Oto laryngol Suppl. 2003;550:36–40.
207. Koo SK, Choi JW, Myung NS, Lee HJ, Kim YJ, Kim YJ. Analysis of obstruction site in obstructive sleep apnea syndrome patients by drug induced sleep endoscopy. Am J Otolaryngol. 2013;34:626–630.
208. Ravesloot MJ, de Vries N. One hundred consecutive patients undergoing drug-induced sleep endoscopy: results and evaluation. Laryngoscope. 2011;121:2710–2716.
209. Sadaoka T, Kakitsuba N, Fujiwara Y, Kanai R, Takahashi H. The value of sleep nasendoscopy in the evaluation of patients with suspected sleep-related breathing disorders. Clin Otolaryngol Allied Sci. 1996;21:485–489.
210. Vroegop AV, Vanderveken OM, Boudewyns AN, et al. Drug-induced sleep endoscopy in sleep-disordered breathing: report on 1,249 cases. Laryngoscope. 2014;124:797–802.
211. Choi JK, Hur YK, Lee JM, Clark GT. Effects of mandibular advancement on upper airway dimension and collapsibility in patients with obstructive sleep apnea using dynamic upper airway imaging during sleep. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010;109:712–719.
212. Hillarp B, Nylander G, Rosén I, Wickström O. Videoradiography of patients with habitual snoring and/or sleep apnea: technical description and presentation of videoradiographic results during sleep concerning event of apnea, nature of apnea, and site of obstruction. Acta Radiol. 1996;37:307–314.
213. Lee CH, Mo JH, Kim BJ, et al. Evaluation of soft palate changes using sleep videofluoroscopy in patients with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. 2009;135:168–172.
214. Lee CH, Hong SL, Rhee CS, Kim SW, Kim JW. Analysis of upper airway obstruction by sleep videofluoroscopy in obstructive sleep apnea: a great population-based study. Laryngoscope. 2012;122:237–241.
215. Adler DG, Kawa C, Hilden K, Fang J. Nurse-administered propofol sedation is safe for patients with obstructive sleep apnea undergoing routine endoscopy: a pilot study. Dig Dis Sci. 2011;56:2666–2671.
216. Cha JM, Jeun JW, Pack KM, et al. Risk of sedation for diagnostic esophagogastroduodenoscopy in obstructive sleep apnea patients. World J Gastroenterol. 2013;19:4745–4751.
217. Cillo JE Jr, Finn R. Hemodynamics and oxygen saturation during intravenous sedation for office-based laser-assisted uvuloplasty. J Oral Maxillofac Surg. 2005;63:752–755.
218. Madan AK, Tichansky DS, Isom J, Minard G, Bee TK. Monitored anesthesia supervision with propofol versus surgeon-monitored sedation with benzodiazepines and narcotics for preoperative endoscopy in the morbidly obese. Obes Surg. 2008;18:545–548.
219. Mador MJ, Nadler J, Mreyoud A, et al. finish patients at risk of sleep apnea maintain an increased risk of cardio-respiratory complications during endoscopy procedures? Sleep Breath. 2012;16:609–615.
220. Cho JS, Soh S, Kim EJ, et al. Comparison of three sedation regimens for drug-induced sleep endoscopy. Sleep Breath. 2015;19:711–717.
221. Yoon BW, Hong JM, Hong SL, Koo SK, Roh HJ, Cho KS. A comparison of dexmedetomidine versus propofol during drug-induced sleep endoscopy in sleep apnea patients. Laryngoscope. 2016;126:763–767.
222. Chang ET, Certal V, Song SA, et al. Dexmedetomidine versus propofol during drug-induced sleep endoscopy and sedation: a systematic review. Sleep Breath. 2017;21:727–735.
223. Ma XX, Fang XM, Hou TN. Comparison of the effectiveness of dexmedetomidine versus propofol target-controlled infusion for sedation during coblation-assisted upper airway procedure. Chin Med J (Engl). 2012;125:869–873.
224. Bamgbade OA, Alfa JA. Dexmedetomidine anaesthesia for patients with obstructive sleep apnoea undergoing bariatric surgery. Eur J Anaesthesiol. 2009;26:176–177.
225. Dholakia C, Beverstein G, Garren M, Nemergut C, Boncyk J, Gould JC. The impact of perioperative dexmedetomidine infusion on postoperative narcotic expend and duration of linger after laparoscopic bariatric surgery. J Gastrointest Surg. 2007;11:1556–1559.
226. Xu J, Jin C, Cui X, Jin Z. Comparison of dexmedetomidine versus propofol for sedation after uvulopalatopharyngoplasty. Med Sci Monit. 2015;21:2125–2133.
227. Chawla S, Robinson S, Norton A, Esterman A, Taneerananon T. Peri-operative expend of dexmedetomidine in airway reconstruction surgery for obstructive sleep apnoea. J Laryngol Otol. 2010;124:67–72.
228. Issa FG. result of clonidine in obstructive sleep apnea. Am Rev Respir Dis. 1992;145:435–439.
229. Pawlik MT, Hansen E, Waldhauser D, Selig C, Kuehnel TS. Clonidine premedication in patients with sleep apnea syndrome: a randomized, double-blind, placebo-controlled study. Anesth Analg. 2005;101:1374–1380.
230. Feld JM, Hoffman WE, Stechert MM, Hoffman IW, Ananda RC. Fentanyl or dexmedetomidine combined with desflurane for bariatric surgery. J Clin Anesth. 2006;18:24–28.
231. Tufanogullari B, White PF, Peixoto MP, et al. Dexmedetomidine infusion during laparoscopic bariatric surgery: the result on recovery outcome variables. Anesth Analg. 2008;106:1741–1748.
232. Feld J, Hoffman WE, Paisansathan C, Park H, Ananda RC. Autonomic activity during dexmedetomidine or fentanyl infusion with desflurane anesthesia. J Clin Anesth. 2007;19:30–36.
233. Jayaraman L, Sinha A, Punhani D. A comparative study to evaluate the result of intranasal dexmedetomidine versus oral alprazolam as a premedication agent in morbidly obese patients undergoing bariatric surgery. J Anaesthesiol Clin Pharmacol. 2013;29:179–182.
234. Sollazzi L, Modesti C, Vitale F, et al. Preinductive expend of clonidine and ketamine improves recovery and reduces postoperative pain after bariatric surgery. Surg Obes Relat Dis. 2009;5:67–71.
235. Memtsoudis SG, Stundner O, Rasul R, et al. Sleep apnea and total joint arthroplasty under various types of anesthesia: a population-based study of perioperative outcomes. Reg Anesth pain Med. 2013;38:274–281.
236. Ambrosii T, Şandru S, Belîi A. The prevalence of perioperative complications in patients with and without obstructive sleep apnoea: a prospective cohort study. Rom J Anaesth Intensive Care. 2016;23:103–110.
237. Liu DY, Cai XL, Liu HY. [Obstructive sleep apnea hypopnea syndrome: surgical complications and strategy for avoidance]. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2009;44:555–560.
238. Liu SS, Chisholm MF, Ngeow J, et al. Postoperative hypoxemia in orthopedic patients with obstructive sleep apnea. HSS J. 2011;7:2–8.
239. Naqvi SY, Rabiei AH, Maltenfort MG, et al. Perioperative complications in patients with sleep apnea undergoing total joint arthroplasty. J Arthroplasty. 2017;32:2680–2683.
240. Biddle C. Comparative aspects of the airway during generic anesthesia in obese sufferers of sleep apnea and matched normals. Adv Pract Nurs Q. 1996;2:14–19.
241. Loube DI, Erman MK, Reed W. Perioperative complications in obstructive sleep apnea patients. Sleep Breath. 1997;2:3–10.
242. Xará D, Mendonça J, Pereira H, Santos A, Abelha FJ. Adverse respiratory events after generic anesthesia in patients at towering risk of obstructive sleep apnea syndrome. Braz J Anesthesiol. 2015;65:359–366.
243. Kehlet H. The stress response to surgery: release mechanisms and the modifying result of pain relief. Acta Chir Scand Suppl. 1989;550:22–28.
244. Kehlet H. Manipulation of the metabolic response in clinical practice. World J Surg. 2000;24:690–695.
245. O’Neill J, Helwig E. Postoperative management of the physiological effects of spinal anesthesia. J Perianesth Nurs. 2016;31:330–339.
246. Meng T, Zhong Z, Meng L. impact of spinal anaesthesia vs generic anaesthesia on peri-operative outcome in lumbar spine surgery: a systematic review and meta-analysis of randomised, controlled trials. Anaesthesia. 2017;72:391–401.
247. Macfarlane AJ, Prasad GA, Chan VW, Brull R. Does regional anesthesia improve outcome after total knee arthroplasty? Clin Orthop Relat Res. 2009;467:2379–2402.
248. Lam KK, Kunder S, Wong J, Doufas AG, Chung F. Obstructive sleep apnea, pain, and opioids: is the riddle solved? Curr Opin Anaesthesiol. 2016;29:134–140.
Last Spring, Microsoft unveiled their mode for Windows and the Internet of Things. It starts with the Raspberry Pi and Windows 10 IoT Core – a stripped down system with Windows API calls running on an ARM architecture. Yes, Microsoft is finally affecting away from the desktop, building a platform for a billion Internet of Things things, or filling the gap left by tens of thousands of POS terminals and ATMs running XP being taken offline. Either one is accurate.
Earlier this week, Microsoft announced the first public release of Windows 10 IoT Core. This is the review, but here’s the takeaway: run. race as fleet as you can away from Windows IoT. It’s not worth your time unless you maintain a burning covet to write apps for Windows, and even then you could finish a better job with less pains with any Linux distro.
When Windows 10 IoT was first announced, there was much hope for a Windows RT-like experience. Being able to race existent Windows applications on a Raspberry Pi would subsist a killer feature, and putting Skype on a Pi would hint real Jetsons-style video phones appearing in short order.
The majority of interaction with Windows 10 IoT Core is over the web. After booting and pointing a browser to the Pi, you’re presented with a rather complete web-based interface. Here, you can check out what devices are connected to the Pi, perceive at the running processes, and race modern apps. assume of this feature as a web-based Windows control panel.
While Windows 10 IoT uses the HDMI output on the Pi, this is merely informational, the video output capabilities of the Pi reserved for application-specific displays – digital signage, POS terminals and ATMs are where Windows 10 IoT Core excels. For general-purpose computing, you’re better off looking elsewhere.
Officially, the only way to install Windows 10 IoT Core is with a computer running Windows 10. There are a few ways around this is with the ffu2img project on GitHub. This Python script takes the special Microsoft .FFU image file format and turns it into an .IMG file that can subsist used with dd under *nix and Win32DiskImager on Windows.
Yes, Windows 10 is free for everyone with a relatively modern Windows box, but since the only requirement for running Windows 10 IoT core is putting an image on an SD card and monitoring a swarm of IoT Core devices, there is no intuition why this OS can’t subsist supplied in an .IMG file.
After putting the image on an SD card, installing Windows 10 IoT Core is as simple as any other Raspi distro: shove the card in the Pi, connect an Ethernet cable, and give it some power. No, you don’t exigency a keyboard or mouse; there’s very itsy-bitsy you can actually finish with the Pi. In fact, the only thing that is displayed through the Pi’s HDMI port is a screen giving you the IP address and what USB devices are attached.
The totality of the Windows 10 IoT Core experience
You finish find a few options for language and network settings, and there are a few tutorials and examples – connecting to Visual Studio and blinking an LED – but that’s it. The base user flavor of Windows 10 IoT Core is just network information, a device name, and a picture of a Raspberry Pi.
There are a few shortcomings of the Windows 10 IoT core for the Raspberry Pi. Officially, the only supported WiFi module is the official Raspberry Pi WiFi module with a BCM43143 chipset. By far, the most favorite WiFi module used for the Raspberry Pi (and something you should always carry around in your go-bag) is the Edimax EW-7811Un, a tiny WiFi module that uses a Realtek chipset. Odds are, if you maintain a Raspberry Pi 2, that WiFi module you picked up won’t work. Common sense would ordain that you could install the Windows driver for the Realtek chipset, but this is not the case; no Windows driver will ever drudgery with Windows 10 IoT core. Even devices from the Raspberry Pi foundation, enjoy the Raspberry Pi camera, are not supported by IoT core
If you’ve ever wanted clearer evidence the Windows 10 IoT core is not meant to subsist an extensible system enjoy every other Linux-based single board computer, you exigency only perceive a itsy-bitsy deeper. Digital audio is completely ignored, and pins 8 and 10 – normally reserved for a 3.3V UART on every other Raspberry Pi distribution – are reserved pins. Microsoft managed to fabricate a single board computer without a hardware UART.
Fortunately, some of these problems are temporary. A representative from the Windows On Devices team told us more WiFi dongles will subsist supported in the future; the only driver they were able to bring up in time is the official dongle from the Raspberry Pi foundation. A similar situation of engineering tradeoffs is the intuition for the lack of UART support.
Who is this for, exactly?
The feeling that Microsoft would reclaim out a non-operating system without champion for the de facto touchstone WiFi adapter, a hardware UART, or drivers for the majority of peripherals is one thing. Selling this to the ‘maker movement’ strains credulity. There is another explanation.
The Windows 10 IoT Core Watcher, the remote admin app for multitudes of Pis.
Let’s proceed over once again what Windows 10 IoT Core actually is. By design, you can write programs in Visual Studio and upload them to one or many devices running IoT core. These programs can maintain a familiar-looking GUI, and are actually pretty smooth to build given 20+ years of Windows framework development. This is not a device for makers, this is a device for point of sale terminals and ATMs. Windows XP – the operating system that is noiseless deployed on a frighting number of ATMs – is going away soon, and this is Microsoft’s attempt to reclaim their participate of that market. IoT Core isn’t for you, it isn’t for me, and it isn’t for the 9-year-old that wants to wink an LED. This is an OS for companies that exigency to supersede thousands of systems noiseless running XP Embedded and exigency Windows APIs in kiosks and terminals.
Save your SD card
For anyone with a Raspberry Pi 2 and an SD card, the only investment you’ll fabricate in trying out Windows 10 IoT Core is your time. It’s not worth it.
While Windows 10 IoT Core is much for any company that has a lot of Visual Basic and other engineering debt, it’s not meant for hackers, makers, or anyone building something new. For that, there are dozens of choices if you want an Internet-connected box that can subsist programmed and updated remotely. The Cloud9 IDE for the Pi and BeagleBone allow you to write code on single board computers without forcing you to install Visual Studio, and Linux is king for managing dozens or hundreds of boxes over the Internet.
This is not an OS that replaces everything out there. A Linux system will almost always maintain better hardware support, and this is especially legal on embedded devices. Windows 10 IoT Core is a beginning, and should subsist viewed as such. It’s there for those who want it, but for everyone else any one of a dozen Linux distributions will subsist better.
Professionalism may not subsist adequate to drive the profound and far-reaching changes needed in the health supervision system, but without it, the health supervision enterprise is lost.
— Lesser et al1
The concept of professionalism for health supervision providers and organizations can offer guidance for decision making in a fiscally difficult, rapidly changing, and ethically challenging environment. Professionalism is based on a specific set of principles and commitments that provide an orientation to the thoughts and actions of a given profession. These principles for physicians were enunciated in the Physician Charter on Medical Professionalism 13 years ago.2 That charter has been widely accepted by physicians, but its impact on the character of health supervision and patient flavor is increasingly recognized as intertwined with the professionalism of health supervision organizations.1,3
Indeed, structural factors in the health supervision system may impede physicians from alive up to the charter.4 Health supervision is now a three-trillion-dollar industry,5 with an estimated one-third of All spending being deemed “systematic waste,” including unnecessary and possibly harmful care.6 Hospitals and health supervision systems are focused necessarily on their own fiscal health during a time of major reform in supervision delivery and payment models; but at the very time, they can ensure the primacy of their missions, ethical and efficient operations, and patient and provider welfare. Professional ideology recognizes a towering priority for useful and needed drudgery and its sociable benefits. It does not avoid economic rewards. It simply requires that these rewards subsist acquired with confiscate attention to professional service and sociable responsibility.
Health supervision systems increasingly ordain the practices of health supervision professionals, for better or worse, as an increasing number of physicians are employed by hospitals and hospital systems.7 As such, health supervision organizations maintain an opportunity to positively and negatively influence the deportment of their employees and affiliated physicians. Most members of the health supervision team are motivated to finish the privilege thing. There are, however, many opportunities for health supervision providers and organizations to engage in activities that are not in concordance with the principles of medical professionalism.
This Perspective includes a Charter on Professionalism for Health supervision Organizations (referred to as the “Charter”; view Appendix 1) with the level of stimulating health supervision leaders, health professionals, policy stakeholders, and society to evaluate their current and preferred ways of operating, to ensure best practices in providing health supervision and improving health. They moreover portray the identification and resolution of a number of issues that arose during the creation of the Charter. These involve the rationale for a charter for organizational professionalism; the charter process, goals, domains, and obstacles; and finally, what they hope the Charter will accomplish. Their Perspective is offered by a subset of the Charter authors to provide its sociable context. It represents the ideas of the authors, not their institutions or the organizations that sponsored the Charter project.
Why a Charter on Organizational Professionalism?
A charter is a reflection of values and can subsist effectual in bringing about positive changes in a target audience. Evidence indicates that such a document can stimulate conversation and affirmation of the stated values. For example, since its publication in 2002, the Physician Charter on Medical Professionalism has been endorsed by over 130 organizations,8 and the number of related professionalism articles has quadrupled to over 600 annually.9 A charter or mission statement that incorporates social, ethical, or societal goals can moreover positively influence organizational success. Kanter’s10 research on financially successful companies revealed that an expressed commitment to sociable responsibility creates a buffer against uncertainty, evokes positive emotions, and stimulates motivation among employees. Along similar lines, Paine11 argues that companies gleam fiscal rewards when their programs feature such elements as community involvement and ethics. These views are supported by the growing list of companies seeking B company certification, which attests to a company’s commitment to society and the environment.12 Additionally, Nielsen’s 2014 survey of 30,000 consumers organize that 55% of respondents were willing to pay extra for products and services provided by companies committed to positive sociable and environmental issues.13
For these reasons and others discussed later in this article, members of the health supervision professions, patients, and representatives from hospitals and health supervision systems maintain collaborated to create a charter that outlines behaviors that champion an organizational culture of professionalism. The Charter on Professionalism for Health supervision Organizations is aspirational, supports a learning health system, and places the patient first. It seeks to ensure that the concept of fiduciary responsibility of health supervision organizations is broadened to involve not only the fiscal health of the organizations but moreover the health of the patients, the well-being of the organizations’ employees, and a responsibility to the community.
The Organizational Professionalism Charter Project was funded by grants from the Commonwealth Fund, the American Board of Internal Medicine Foundation, North Shore Long Island Jewish Health System, the Federation of American Hospitals, and the American Hospital Association. The authors of the original organizational professionalism publication3 and representatives of the grantors formed a Steering Committee to direct the project. The Steering Committee nominated individuals for the Writing Group who were approved by consensus and created the Charter. These writers represented a variety of disciplines, points of view, and stakeholders in health care. They included nurses, health system leaders, medical ethicists, and consumer advocates. Although some participants felt that they were to represent the organization that nominated them, the Charter was not topic to approval by any grantor or organization. Over a era of almost two years, the Writing Group met twice in person, first to settle what domains were valuable to address and that it would fabricate decisions by consensus, and then to mode the writing of the Charter. The Writing Group refined the document by conference calls and e-mail. As might subsist expected from such a diverse group, compromise was valuable for the final Charter to subsist approved by consensus. The issues that required the most vigorous discussions were whether health supervision is a “right,” whether to stipulate a specific percentage of margin that a health supervision organization ought to recur to the community, and the responsibility of health supervision organizations to address the sociable determinants of health.
The purpose of the Charter is to portray professionalism behaviors to which for-profit and not-for-profit hospitals and hospital systems may aspire. As the drudgery unfolded, the Writing Group recognized that the principles were pertinent to any health supervision organization. This article describes the evidence-based rationales for the behaviors of hospitals and hospital systems implied by these principles.
No organization can fully embody All of these behaviors. However, if they participate the values elaborated in the Charter’s preamble, they may identify activities described in the subsequent domain sections that align with their strategic initiatives. They offer evidence that implementing these behaviors would improve health supervision as well as the flavor of working or being cared for within health supervision organizations. Engaging outside partners—the community, government, and other organizations—creates the potential to strike population health, because partnerships among these are essential for addressing the sociable determinants of health.
At times, different sections of the Charter will hint competing actions. For example, touchstones of the Charter are to prioritize the health of individual patients and to improve the health of the community. However, being a steward of limited resources may affray with optimizing the health of each individual patient. Organizations may ethically win different actions based on their different missions and cultural values.14 Transparent discussions that involve patients and local communities will themselves maintain sociable benefit, because they may champion health supervision organizations choose paths that reflect both organizational and local values. However, when ethical dilemmas arise from conflicts between an organization’s self-interest and those of the community or patient, the community or patient interest takes precedence. While this premise of the Charter may look controversial, it is central to its content, consistent with the seminal Physician Charter on Medical Professionalism,2 and the source of its greatest potential sociable benefit.
The discussion in the following domain sections provides the rationale and evidence to champion the commitments requested in the Charter.
In 2001, the IOM report Crossing the character Chasm: A modern Health System for the 21st Century created a sense of urgency for reinventing a health supervision system built around six aims for improvement considered essential for better meeting patient-family needs.15 Among these six aims is patient-centered care, defined as “providing supervision that is respectful of and responsive to individual patient preferences, needs, and values, and ensuring that patient values steer All clinical decisions.”15 It requires collaboration among health supervision teams and effectual partnerships with patients, families, and other caregivers.16,17 Successful navigation from the traditional “doctor knows best” approach to one that engages patients and families to participate in their supervision and decision making is contingent on a culture of organizational leadership that values multidirectional collaboration and communication.17
The foundational characteristics of this vision for health supervision transformation are well aligned with the precepts of professionalism. Over time, organizations that integrate person-centric principles can flavor greater patient dependence and loyalty and teams that duty in a more coordinated manner.18 effectual rendezvous with patients and families can maintain a measurable impact on organizational improvement and has been cited as having the greatest potential for sustaining long-term system-wide transformation.19 Health systems and organizations that intentionally invite patients and families to participate in rounds, committees, and advisory panels and to participate their stories in the boardroom maintain accelerated improvements in the character of supervision they provide.20
In the terminal decade, many factors maintain influenced the expectation that patients and families win an active role in decisions that impact their health and health care,21 and studies demonstrate that this rehearse benefits All involved.22–24
Executive leadership is essential for achieving the cultural transformation needed to champion genuine partnerships with patients and families throughout their organizations.25 Leadership that is engaged and provides the resources needed to sustain strategies for patient-family input is critical for successful adoption of these practices. Organizations and systems that uphold patient partnerships as an integrated core value will exemplify professionalism and stand apart from others.20
This domain is aligned with Medicare’s adoption of measures of patient flavor measures as an valuable component of value, and thus payment. Although the exact measures of patient flavor and rendezvous remain controversial, the expectation of patient- and family-centeredness as a core value of health supervision organizations is here to stay.26
Successful transformation of health supervision systems will likely depend more on the sociable capital of organizations than their fiscal capital.27 While many professional entities provide guidelines for the deportment of individuals within their disciplines, it is the responsibility of leadership to portray a health supervision organization’s desired culture, articulate its rationale, and create the structures that champion it and ensure accountability. With this guidance, organizational culture is cocreated by patients, nonemployed workers, employees, and leadership. dependence in leadership requires that management deportment subsist consistent with the organizational mission, professional values, and expectations of employees.28 That dependence in revolve empowers individuals to propagate consonant behaviors into the various units where they work. Organizational culture is thus viewed as a complex adaptive system composed of interrelated microcultures.
There is increasing evidence of relationships between the culture of senior management,29 organizational culture,30 and the performance of health supervision organizations. Organizational leadership style influences both physician31 and nurse satisfaction and burnout.32 Although physician burnout has not been consistently tied to the character of care,33 nurse burnout has.34 Physician well-being is correlated with lower rates of turnover and can subsist improved through focused organizational interventions.35 A Rand study on physician well-being concluded that “the very considerations that apply outside medicine—for example, honest treatment; responsive leadership; attention to drudgery quantity, content, and pace—can serve as targets for policymakers and health delivery systems that search to improve physician professional satisfaction.”36 Achieving the “triple aim” may indeed require incorporating “care of the provider” into a “quadruple aim.”37 A healing environment can best subsist achieved when All those in the organization are afforded the very value and respect that clinicians aspire to give to patients. This requires soliciting, respecting, and incorporating the perspectives of employees.
High-value, cost-conscious rehearse moreover depends on interprofessional collaboration.38 Validated measures of team cohesion maintain been developed,39 and numerous studies demonstrate that better teamwork is correlated with better patient outcomes, patient satisfaction, organizational efficiency, patient engagement, and worker satisfaction.40 Studies are beginning to emerge that test whether interventions to improve teamwork moreover improve clinical outcomes, though more research is needed.41,42
Traditional clinical services account for only 10% to 20% of a population’s health, and genetics account for 20% to 30%.43,44 Spurred by well-articulated missions to create wholesome communities, model health supervision organizations maintain sought to address the remaining 50% to 70%—the so-called sociable determinants of health—in moneyed strategic partnerships with the communities they serve.45 The health of the U.S. population has improved significantly during the terminal century; however, many high-risk communities maintain not shared in the gains achieved by traditional health promotion strategies. There is growing recognition that promoting the health of populations requires a systems approach to understanding and addressing the sociable and environmental factors that can protect or undermine health.46
As awareness of the import of addressing “health” as a broader construct has grown, so too has awareness of the import of health supervision organizations joining together—in full partnership with each other and the communities they serve—to define barriers to health and health care, design interventions, maximize the value of investments, and implement modern strategies together to improve a community’s health.47 Partnerships of this nature require skill, collaboration, and a level of dependence that has not previously existed among most health supervision organizations and the communities they serve. Still, several notable examples maintain emerged.48 The Affordable supervision Act includes the requirement that nonprofit health supervision organizations demonstrate their “community benefit” beyond the customary charity supervision to involve community health assessments, planning, implementation, and evaluation.49 The expectation is that health supervision organizations will provide “a wide reach of services and activities that focus on improving health status and character of life in local communities.”50
In tandem with the mission to create wholesome communities, model health supervision organizations recognize that shifts in public policy toward population and outcomes-based reimbursement fabricate effectively addressing the sociable determinants of health mission critical to fiscal sustainability in a post-fee-for-service future.51,52 In this way, the long-term health of model health supervision organizations and the communities they serve are inextricably intertwined and must subsist addressed in existent partnerships where this reality is embraced by all.
Operations and commerce practices
In recent years, a vision for a health supervision system that continuously learns and improves has evolved.53,54 Efforts to enhance ethical deportment in health supervision organizations result in best operational and commerce practices and in existent benefits for patients.55 Furthermore, Tsai and colleagues56 organize that hospitals that rank towering on the expend of effectual management practices provide a higher character of supervision than lower-ranking hospitals, and hospital management’s expend of such practices is associated with a high-performing board of trustees.
Paine57 argues that increasingly, companies are launching ethics programs, values initiatives, and community involvement activities premised on management’s belief that “ethics pays.” In health care, this concept goes well beyond the economic value of branding and includes efforts at cost control, service character improvement, patient and staff safety, risk management, innovation, reputation, loyalty, and satisfaction for both patients and providers.
Bart and Tabone58 organize an valuable relationship between nonprofit hospital leadership satisfaction with mission statement and their organization’s performance. Their primary finding was that leaders finish in fact discriminate and differentiate in the wording of mission statements, which in revolve influences organizational deportment and performance. Of distinct import is a commitment to service quality, patient welfare, and satisfaction. Components typically not included in the mission are fiscal goals and competitive strategies. Ethical guidance in the configuration of mission statements are valuable tools for health systems to expend to improve organizational performance and increase employee motivation.59
Holy Cross Hospital System (HCHS) of South Bend, Indiana, provides an sample of a successful organizational program to ensure that HCHS’s organizational structure and performance were value based and mission driven.60 HCHS developed 11 mission standards, created opportunities for ownership, and fostered personal responsibility within the system to ensure the fulfillment of its mission. This process of mission discernment is expanded on by Gallagher and Goodstein54 and represents an ethically grounded and practical process to ensure the moral integrity of an organization. The key operational values of the HCHS mission statement were faith, service, excellence, empowerment, and stewardship. The core values that drove the discussion and progress of its mission were sociable justice and human dignity. fiscal and legal issues were considered, but this was proportionate to core service commitments to the destitute and vulnerable. As a result of sound moral grounding through its mission statement, HCHS was able to clarify choices among competing goals for the organization and find compromise for stakeholders both internal and external to the organization.
At the Harvard Vanguard Kenmore Medical Associates practice, where previous character improvement efforts had been associated with deteriorating morale, leadership implemented specific relationship-centered practices which defused pent-up excited and frustration in the staff, decreased isolation, built teamwork, and facilitated significant character improvement.61 They created an environment in which each clinician and staff person was treated with dignity, involved in identifying and solving quality-of-care issues, and incorporated into a systematic approach to continuous improvement. This facilitated the adoption of process improvement techniques pioneered by Toyota Production Systems, while at the very time improving morale.
Ethics guidance that is formalized in codes and organizational mission statements promotes ethical discourse and deliberation around institutional integrity and responsibility, and influences organizational deportment in meeting those goals.
The Charter is aspirational; it is meant to portray the deportment of a “model organization.” Many of its challenges are cultural, requiring both organizational leaders and employees to alter their historical views of their organizations and their roles within them. Traditionally, health supervision institutions maintain been hierarchical and physician focused. And despite recent financial, structural, and operational changes, health supervision institutions maintain not fundamentally altered the relationship between leadership and employees. Some individuals may subsist challenged by the more dynamic, open dialogue between leadership and the full spectrum of professions, employed nonprofessionals, and patients as described in the Charter. In addition, the Charter reminds All those individuals to focus on the ultimate goal of medicine, healing the patient. While the pace of drudgery can fabricate each job look an linger in itself, mindfulness of the larger institutional mission and each individual’s role within it can impart a sense of purpose to every job and signification to each activity.
Another challenge is altering the sociable determinants of health. The ecology of these determinants is complex and not fully understood. Nor is any sociable structure in a position to strike All the influences on these determinants. The Charter does not hint that health supervision organizations are solely answerable for improving the sociable determinants of health but, rather, suggests that they search strategic partnerships with other organizations, government, and local communities, consistent with their means and their unique missions, in order to improve the health of the community.
What They Want to Accomplish
This Charter complements existing treatises on professionalism, creating a document directed at health organizations and systems rather than a group of individuals. The Charter defines the professional competencies and behaviors that organizations can leverage to create an environment that promotes professional deportment throughout the organization. Developed by administrators, physicians, nurses, and patients, the Charter is a multidisciplinary pains that melds the aspirations of All involved to provide such an outcome.
We wish to ensure that this is a alive document similar to the Physician Charter on Medical Professionalism and will win lessons learned from the process employed with that charter. The job of accomplishing this will comfort with a representative multidisciplinary committee. The committee will search opportunities to publicize the document in professional and trade journals as well as opportunities to present the Charter at professional meetings. The Charter will reside on the Web site of the Foundation for Medical Excellence (www.tfme.org). A list of health supervision systems, professional organizations, and hospitals that endorse this Charter will subsist listed. A nonmonetary annual prize will subsist awarded to the most influential rehearse resulting from such commitments. They foresee a time when the Charter could subsist incorporated into criteria for acknowledging excellence in health supervision organizations by certifying organizations. Further, they will exact for feedback so that the document can subsist modified in the future as needed to appropriate to the dynamically changing world of health supervision delivery.
1. Lesser CS, Lucey CR, Egener B, Braddock CH 3rd, Linas SL, Levinson W. A behavioral and systems view of professionalism. JAMA. 2010;304:2732–2737.
2. American Board of Internal Medicine (ABIM) Foundation; American College of Physicians–American Society of Internal Medicine (ACP-ASIM) Foundation; European Federation of Internal Medicine. Medical professionalism in the modern millennium: A physician charter. Ann Intern Med. 2002;136:243–246.
3. Egener B, McDonald W, Rosof B, Gullen D. Perspective: Organizational professionalism: pertinent competencies and behaviors. Acad Med. 2012;87:668–674.
4. Campbell EG, Regan S, Gruen RL, et al. Professionalism in medicine: Results of a national survey of physicians. Ann Intern Med. 2007;147:795–802.
5. Martin AB, Hartman M, Benson J, Catlin A; National Health Expenditure Accounts Team. National health spending in 2014: Faster growth driven by coverage expansion and prescription drug spending. Health Aff (Millwood). 2016;35:150–160.
6. Fineberg HV. Shattuck lecture. A successful and sustainable health system—How to find there from here. N Engl J Med. 2012;366:1020–1027.
7. Singleton T, Miller P. The physician employment trend: What you exigency to know. Fam Pract Manag. 2015;22:11–15.
10. Kanter RM. How much companies assume differently. Harv Bus Rev. 2011;89:66–78.
11. Paine LS. Does ethics pay? Bus Ethics Q. 2000;10:319–330.
14. Tilburt JC. Addressing dual agency: Getting specific about the expectations of professionalism. Am J Bioeth. 2014;14:29–36.
15. Institute of Medicine. Crossing the character Chasm: A modern Health System for the 21st Century. 2001.Washington, DC: National Academy Press.
17. Mechanic D. Managed supervision and the imperative for a modern professional ethic. Health Aff (Millwood). 2000;19:100–111.
18. Anderson D. Competing on professionalism: Integrating patient supervision principles core values can boost performance. Trustee. 2014;67:1–4.
19. Reinertsen JL, Bisognano M, Pugh MD. Seven Leadership Leverage Points for Organization-Level Improvement in Health Care. 2008.2nd ed. Cambridge, MA: Institute for Healthcare Improvement.
20. Wynn JD. The transforming power of patient advisors. N C Med J. 2015;76:171–173.
21. Wolff JL, Boyd CM. A perceive at person- and family-centered supervision among older adults: Results from a national survey [corrected]. J Gen Intern Med. 2015;30:1497–1504.
22. Oshima Lee E, Emanuel EJ. Shared decision making to improve supervision and reduce costs. N Engl J Med. 2013;368:6–8.
23. Stacey D, Bennett CL, Barry MJ, et al. decision aids for people facing health treatment or screening decisions. Cochrane Database Syst Rev. 2011;10:CD001431.
24. Jha AK, Orav EJ, Zheng J, Epstein AM. Patients’ perception of hospital supervision in the United States. N Engl J Med. 2008;359:1921–1931.
25. Taylor J, Rutherford P. The pursuit of genuine partnerships with patients and family members: The challenge and opportunity for executive leaders. Front Health Serv Manage. 2010;26:3–14.
27. Lee TH, Campion EW, Morrissey S, Drazen JM. Leading the transformation of healthcare delivery—The launch of NEJM Catalyst. N Engl J Med. 2015;373:2468–2469.
29. Davies HT, Mannion R, Jacobs R, Powell AE, Marshall MN. Exploring the relationship between senior management team culture and hospital performance. Med supervision Res Rev. 2007;64:46–65.
30. Jacobs R, Mannion R, Davies HT, Harrison S, Konteh F, Walshe K. The relationship between organizational culture and performance in acute hospitals. Soc Sci Med. 2013;76:115–125.
31. Shanafelt TD, Gorringe G, Menaker R, et al. impact of organizational leadership on physician burnout and satisfaction. Mayo Clin Proc. 2015;90:432–440.
32. Poghosyan L, Clarke SP, Finlayson M, Aiken LH. Nurse burnout and character of care: Cross-national investigation in six countries. Res Nurs Health. 2010;33:288–298.
33. Linzer M, Manwell LB, Williams ES, et al; MEMO (Minimizing Error, Maximizing Outcome) Investigators. Working conditions in primary care: Physician reactions and supervision quality. Ann Intern Med. 2009;151:28–36, W6.
34. Spence Laschinger HK, Leiter MP. The impact of nursing drudgery environments on patient safety outcomes: The mediating role of burnout/engagement. J Nurs Adm. 2006;36:259–267.
35. Krasner MS, Epstein RM, Beckman H, et al. Association of an educational program in mindful communication with burnout, empathy, and attitudes among primary supervision physicians. JAMA. 2009;302:1284–1293.
36. Friedberg MW, Chen PG, Van Busum KR, et al. Factors Affecting Physician Professional Satisfaction and Their Implications for Patient Care, Health Systems, and Health Policy. 2013.Santa Monica, CA: RAND Corporation.
37. Bodenheimer T, Sinsky C. From triple to quadruple aim: supervision of the patient requires supervision of the provider. Ann Fam Med. 2014;12:573–576.
38. Stammen LA, Stalmeijer RE, Paternotte E, et al. Training physicians to provide high-value, cost-conscious care: A systematic review. JAMA. 2015;314:2384–2400.
39. Institute of Medicine. Measuring the impact of Interprofessional Education on Collaborative rehearse and Patient Outcomes. 2015.Washington, DC: National Academy Press.
40. Gittell JH. Kim C, Gretchen S. modern directions for relational coordination theory. In: Oxford Handbook of Positive Organizational Scholarship. 2011: London, UK: Oxford University Press; Chapter 30.
41. Cameron K, Mora C, Leutscher T, Calarco M. Effects of positive practices on organizational effectiveness. J Appl Behav Sci. 2011;47:266–284.
42. De Meester K, Verspuy M, Monsieurs KG, Van Bogaert P. SBAR improves nurse–physician communication and reduces unexpected death: A pre and post intervention study. Resuscitation. 2013;84:1192–1196.
45. Schlesinger M, Gray B, Carrino G, et al. A broader vision for managed care, section 2: A typology of community benefits. Health Aff (Millwood). 1998;17:26–49.
46. Lavizzo-Mourey R. Why they exigency to build a culture of health in the United States. Acad Med. 2015;90:846–848.
47. Westfall JM, Fagnan LJ, Handley M, et al. Practice-based research is community engagement. J Am Board Fam Med. 2009;22:423–427.
52. Jacobson RM, Isham GJ, Finney Rutten LJ. Population health as a means for health supervision organizations to deliver value. Mayo Clin Proc. 2015;90:1465–1470. http://dx.doi.org/10.1016/j.mayocp.2015.07.010. Accessed November 23, 2016.
53. Institute of Medicine (IOM). Best supervision at Lower Cost: The Path to Continuously Learning Health supervision in America. 2012.Washington, DC: National Academies Press.
54. Gallagher JA, Goodstein J. Fulfilling institutional responsibilities in health care: Organizational ethics and the role of mission discernment. Bus Ethics Q. 2002;12:433–450.
55. Carter K, Dorgan S, Layton D. Why Hospital Management Matters. 2012.Washington, DC: McKinsey & Company.
56. Tsai TC, Jha AK, Gawande AA, Huckman RS, bloom N, Sadun R. Hospital board and management practices are strongly related to hospital performance on clinical character metrics. Health Aff (Millwood). 2015;34:1304–1311.
57. Paine LS. Does ethics pay? Bus Ethics Q. 2000;10:319–330.
58. Bart CK, Tabone JC. Mission statement content and hospital performance in the Canadian not-for-profit health supervision sector. Health supervision Manage Rev. 1999;24:18–29.
59. Forehand A. Mission and organizational performance in the healthcare industry. J Healthc Manag. 2000;45:267–277.
60. Vandenberg P, vouchsafe MK. The necessity of mission integration. A system develops processes to weave values into the life of the organization. Health Prog. 1992;73:32–35.
61. Neuwirth A. Suchman A, Sluyter DJ. The Harvard Vanguard Kenmore rehearse experience: A focus on human progress and relationship building. In: Leading Change in Healthcare. 2011: London, UK: Radcliffe Publishing; Chapter 12.
Appendix 1 Charter on Professionalism for Health supervision Organizations
This document is intended to articulate a set of principles and behaviors for health supervision organizations that aspire to nurture professionalism, to cheer the pursuit of excellence by All employees, and to achieve outstanding health supervision with the broader community. The document is structured as a set of expectations as to how model health supervision organizations should subsist led and managed. It is aspirational and supports a health system that is dynamic and constantly trying to improve.
A key tenet of this document is that health supervision organizations maintain been gradually evolving so that the activities of model health supervision organizations should proceed beyond trying to deal disease and restore health. The drudgery of model health supervision organizations should involve health promotion, disease prevention, value-driven care, interdisciplinary collaboration, and community involvement, All within a fiscally answerable environment.
This evolution of the health supervision environment has and will continue to create challenges for All of the traditional professions that operate within health supervision organizations. As increasing numbers of the members of these professions are employed by and duty within these organizations, the organizations will maintain further opportunities to profoundly strike the professional behaviors of those individuals in both positive and negative ways. Organizational behaviors finish more than create an environment that influences the professionalism of those within it. They maintain a powerful influence on the environment beyond their walls: They interact with other organizations that strike health and can directly impact the sociable determinants of health in ways that individual professionals or health supervision professional membership organizations cannot.
This Charter was created to champion meet these challenges. There are four themes or concepts that apply to All health supervision organizations’ activities. First, model health supervision organizations exigency to emphasize the primacy of obligations to patients and ensure that All members of the organization reflect this priority in their day-to-day work. Second, model health supervision organizations promote the goal of broad access to health care. Third, model health supervision organizations are obliging stewards of resources invested in health care. Finally, model health supervision organizations are learning organizations. The organization continually transforms itself to execute its core mission better and to win on modern roles as the health system evolves.
The primary focus of health supervision organizations is the supervision and well-being of patients. Model organizations confederate with patients to ensure a patient-centered approach that supports the health of the all person, not just the treatment of disease.
Commitment to engagement
Model organizations invite active participation of patients and their formal and informal supervision partners in All pertinent aspects of care. These partnerships champion supervision that is respectful of and responsive to an individual’s priorities, goals, needs, and values. Utilizing communication strategies that engender trust, model organizations foster an outcomes-based approach to health that goes beyond delivery and receipt of health care.
Commitment to shared decision making
Together, patients and their supervision partners clarify and evaluate All supervision options and the best available evidence to choose a course of supervision consistent with the patient’s personal values and preferences. Organizational professionalism ensures that the culture, environment, and infrastructure champion the communication and literacy needs of All involved in the decision-making process.
Commitment to collaboration, continuity, and coordination
Model organizations foster effectual team-based supervision and champion the role of patients as members of teams. In collaboration with patients and their formal and informal supervision partners, model organizations ensure safe and effectual team transitions across settings and time to champion a “one patient, one team” model of care.
Commitment to measure what matters to patients
In partnership with patients, model organizations identify outcomes of interest to patients and expend patient-reported and -generated data to monitor progress and performance on those outcomes. Model organizations establish methods to champion their continuous learning from these data. They provide meaningful feedback to patients and their supervision partners related to these data and the learning from it.
Organizational culture is the set of beliefs and practices that creates the expectations, norms, and operational behaviors within an organization. Organizational culture is reflected in the well-being of patients and employees, employee retention, character of care, health outcomes, and elimination of medical error.
Commitment to the well-being of individuals
Model organizations promote the well-being of All those who are cared for or drudgery within them. Encouraging and modeling self-reflection and humility ensures that All interactions are respectful and that employees are valued and empowered.
Commitment to teamwork
Best supervision happens when All members of the team, including patients, participate information and decision-making responsibility. Ensuring teamwork requires organizational structures and processes that champion communication across staff and with patients.
Commitment to a wholesome workplace
Model organizations create drudgery environments that are physically and psychologically safe and provide tools and incentives for employees to achieve wholesome lifestyles.
Commitment to inclusion and diversity
Model organizations incorporate the voices of employees and patients in organizational initiatives, including clinical domains. They cheer respectful attention to alternative viewpoints. Communication training for All staff emphasizes teamwork, respect, inclusiveness, and cultural sensitivity. The workforce, including leadership, reflects the diversity of patients and the community.
Commitment to accountability
Model organizations create a culture of dependence and empowerment by articulating the mission and values of the organization, aligning policies, creating an infrastructure to promote those values, and eliminating activities that undermine professionalism. They align employee incentives with organizational values, reward success, provide supportive remediation for those who struggle to meet expectations, promote job satisfaction, and provide opportunities to learn. Model organizations cheer feedback to leadership regarding any flavor and observation of activities that compromise the organization’s values. Model organizations create an environment that encourages disclosure of events or suspect processes using learning gained to prevent harm and improve safety for patients and staff.
Model organizations collaborate with other health supervision organizations and the communities they serve to reduce health disparities related to factors such as education, income, and the environment. They focus particularly on preventable root causes of illness and access to appropriate, effective, culturally sensitive health care.
Commitment to address the sociable determinants of health
Clinicians frequently encounter root causes of preventable illnesses, such as environmental toxins, nutritional deficits, unhealthy behaviors, and other preventable sociable factors. Treating these in a clinical vacuum diminishes the organization’s full potential to improve health. Therefore, it is a model organization’s ethical responsibility to champion identify, understand, and address sociable determinants of health, and to incorporate this understanding into its work.
Commitment to confederate with communities
Model organizations engage in strategic partnerships with governmental entities, community organizations, and other organizations serving the community to identify and mitigate root causes of illness as well as to ensure effective, culturally confiscate care. Model health supervision organizations involve the community in organizational activities and governance, and their employees participate in community activities and governance.
Commitment to advocate for access and high-value care
Model organizations confederate with others to promote universal access and rational allocation of health supervision resources and to moderate incentive structures that finish not directly lead to high-value supervision and healthier communities. They advocate with communities for regulatory reforms to improve environmental conditions, mitigate barriers to health supervision access, and improve sociable services.
Commitment to community benefit
Model organizations and their leaders engage generously with community organizations and civic leaders to fabricate innovative, strategic investments that leverage improved community health.
Operations and commerce Practices
Model organizations ensure patient safety, clinical excellence, transparency, evidence-based practices, high-value care, and professional competence. They provide sensitive, respectful, compassionate, prompt, and courteous patient care.
Commitment to safeguard the privacy of patients and their health information
Model organizations must safeguard the privacy of patients and their health information. This is particularly valuable in the expend of electronic health records, which pose continually evolving challenges to the privacy and security of patient information.
Commitment to ethical operations
Ethics and compliance programs in model organizations articulate mission and values, guidelines for observing legal requirements, and standards for the highest ethical focus in addressing the health supervision needs of diverse populations. These programs require qualified senior-level executive leadership, mechanisms to set standards, evidence-based policies, comprehensive training and education, mechanisms to report violations without dread of retaliation, and approaches to monitor compliance and audit performance. Model organizations adhere to credentialing and regulatory standards in their operations, recruitment, training, education, and privileging.
Commitment to transparent management of conflicts of interest
Model organizations maintain systems to identify and address potential conflicts of interest. When patients may subsist affected, patient welfare is given priority.
Commitment to align incentives with values
Model organizations routinely review their incentive systems to ensure that they are in alignment with articulated organizational values.
Commitment to honest treatment, education, and development
Model organizations compensate employees fairly; provide confiscate profit packages; avoid staff shortages; and promote employee education, training, and growth.
Commitment to high-value care
The policies and practices of model organizations engender evidence-based supervision and treatment that are provided to every patient. Model organizations always strive for high-value, optimal clinical outcomes, aligned with the three aims of better care, wholesome populations, and reduced costs. They ensure that ordering practices for testing and treatment are evidence based and supported by standards of care.
Commitment to innovation
Model organizations strive to improve current models of care. Creating opportunities to assist other organizations to achieve similar success is a configuration of public service. The search for and implementation of innovative approaches to management, leadership, and patient supervision are valuable indicia of organizational professionalism.
Commitment to accounting and fiscal reporting standards
Model organizations ensure that their fiscal statements accurately reflect the performance of the organization. They create fiscal control systems and internal auditing mechanisms that ensure fiscal integrity.
Commitment to ensure honest and equitable access to health care
Model organizations pomp price transparency. They fabricate adjustments to bills for uninsured patients, so that they are not expected to pay substantially more than insured patients. They act fairly in granting “charity status” to patients who maintain no colorable means of paying the cost of treatment. They show flexibility in settling patient balances that exceed the patient’s fiscal capabilities.
Note: This Charter was created by the Organizational Professionalism Working Group:
May-Lynn Andresen, RN, BSN
Barry E. Egener, MD (Chair)
Ezekiel Emanuel, MD, PhD
David A. Fleming, MD, MA
Meg E. Gaines, JD, LLM
L. Keith Granger, BSRT
David Gullen, MD
Talmadge King, MD
Wendy Levinson, MD
Diana J. Mason, RN, PhD
Walter J. McDonald, MD
Sally Okun, RN, MMHS
Tim Rice, MPH, RPh
Bernie M. Rosof, MD
Rosemary Stevens, PhD, MPH
Alan Yuspeh, JD, MBA