Society of Anesthesia & Sleep Medicine Newsletter

Society of Anesthesia & Sleep Medicine Newsletter Volume 3 u Issue 2 u 2014

Message from the President

tabase, Memtsoudis and colleagues extracted data on 530,089 patients who underwent total hip or total knee arthroplasty between 2006 and 2010 in nearly 400 hospitals in the United States. 12 OSA was present in Frances Chung, MBBS, FRCPC 8.4% of the cohort based on the In- President, SASM ternational Classification of Diseases 9th Revision-Clinical Modification Professor, Department of Anesthesiol- (ICD-9-CM) diagnostic codes. With ogy, Toronto Western Hospital, University continued on page 3 Health Network, University of Toronto President’s Message ��1, 3-4, 6 bstructive sleep apnea (OSA) bate upper airway collapsibility and is a prevalent disorder char- blunt the arousal response. Editor’s File ��2 acterized by recurrent epi- Several single-institution stud- Holding Your Breath…. Osodes of complete or partial collapse Too Long...... 5-6 ies have reported an association of the upper airway during sleep between OSA and a myriad of Apnea And Prematurity: A Need leading to intermittent hypoxemia adverse postoperative outcomes. For Better Understanding To and hypercapnia as well as sleep 8-11 In the absence of large-scale Improve Perioperative Neonatal fragmentation. A recent community- well-controlled prospective studies, Care...... 7-8, 13 based study reported an increasing analysis of administrative databases Strategies To Understand And prevalence of OSA in parallel with can shed some light on the associa- 1 Modify Postoperative Cognitive the obesity epidemic. Concur- tion between OSA and postoperative rently, the number of surgical cases Dysfunction: A Sleep outcomes and provide data that is Perspective...... 9-10, 13 performed globally is increasing. In more generalizable than single- fact, Weiser and colleagues estimated center smaller studies. This is of Sleep Apnea: An Update Of that 234 million major surgeries importance because implementation Pharmacologic Therapies... 11-13

were performed in 2004 worldwide. of systematic screening for OSA and STOP-BANG...... 14 2 Although the reported prevalence initiating treatment in the periop- SASM Department Membership of OSA in presurgical cohorts has erative period for those patients at Information ��15 varied, undoubtedly the vast major- risk would impose a significant cost SASM 2014 Annual Meeting ity of anesthesiologists are bound burden, particularly in the setting of Schedule of Events ��16-17 to encounter patients with OSA in large surgical volumes. their daily clinical practice. 3-7 This is SASM Officers & Board of In an observational study performed of clinical relevance since sedatives, Directors ��18 narcotics and anesthetics can exacer- using the Premier Perspective da- SASM Member Benefits ��18 Editor’s File

Satya Krishna Ramachandran, MD, FRCA Editor Assistant Professor in Anesthesiology and Director of Perioperative Quality Improvement University of Michigan, Ann Arbor, MI USA

The Trouble with Teams he trouble with teams is that considerations in determining the therapy are more likely to use it in the every team member has to available time between preoperative early postoperative period. Thus, key share the same mental model clinic visit and surgical date. Two, metrics of success of the preoperative Tnecessary to achieve a goal. The the need for pre-authorization of surgical home should include PAP advent of a few key team concepts key steps in polysomnography and rates in patients screened to be high in perioperative medicine, notably positive airway pressure (PAP) fitting risk for OSA, and PAP adherence the perioperative surgical home and introduces a minimum delay of days rates in patients with known OSA. We enhanced recovery protocols, are between steps, with additional steps look to expert bodies like the SASM to set to change the culture of patient needed postoperatively to maintain provide more detailed process guides care in the coming years. These therapy. At the risk of preaching to to help develop OSA protocols for processes have a direct impact on our the converted, the evidence that PAP local implementation. ability to efficiently screen and treat treatment of OSA has a large impact conditions such as sleep disorders on surgical outcomes is accumulating Introducing a perioperative OSA before elective surgery, employ robust rapidly. Dr. Babak Mokhlesi’s recent protocol in the framework of a busy risk reduction strategies and enable studies highlight better outcomes perioperative surgical home would effective postoperative care. I would in patients with sleep disordered address many of the challenges we like to talk about one such function breathing, largely driven by the face. But, for these fairly complex that has direct implications to our temporary and early presentation of processes to take root, it is imperative interest in sleep disorders. As several postoperative respiratory failure. The for us to participate in the planning of us have already experienced, a studies also describe a greater usage and implementation of these surgical tremendous amount of effort and of postoperative PAP in patients with homes. I’m sure we all will have investment is required to coordinate SDB. Squadrone previously showed a slightly different experiences of implementation of a preoperative several-fold reduction of respiratory the surgical home team, but our fast-track sleep study protocol. Our failure when PAP was used to treat common goal should remain the efforts are typically challenged by early postoperative hypoxia. This is allocation of appropriate resources two major constraints: one, surgical relevant to the perioperative surgical to this population of patients who scheduling preferences and urgency home because patients who are are at greater risk of postoperative of surgery are still the most important adherent with preoperative PAP complications. Go team! v

2 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Message from the President continued from page 1 robust statistical methodology fibrillation. 14,15 A recent meta- complications do not lead to an and after adjusting for important analysis of 13 single-center stud- increase in in-hospital mortality. confounders, they found that OSA ies also demonstrated a higher A few possibilities include obesity was independently associated incidence of respiratory failure, paradox or ischemia precondition- with increased odds ratio for cardiac events and ICU transfers ing playing a protective role.17-20 It the composite outcome of main patients with OSA. 8 is also possible that OSA patients jor postoperative adverse events In the study by Memt- with impending respiratory failure (OR 1.47; 95% CI 1.39-1.55). The soudis et al, despite the increased were recognized earlier and defini- association was stronger with pul- rates of complications, there was tive treatment (i.e. endotracheal monary complications (OR 1.86; no significant increase in the risk intubation or NIV) was imple- 95% CI 1.65-2.09) than cardiac of in-hospital mortality in patients mented in a more timely fashion. complications (OR 1.59; 95% CI with OSA. 12 In patients undergo- Indeed, Mokhlesi et al reported 1.48-1.71) with the risk of cardiac ing elective surgeries and bariatric that in the subgroup of postopera- complications mainly due to atrial surgeries OSA was also found not tive patients who were emergently fibrillation. The risk of emergent to be associated with increased in- reintubated, reintubation occurred reintubation was significantly in- hospital mortality. 14,15 D’Apuzzo et significantly earlier in OSA pa- 14,15 creased in patients with OSA (OR al examined a cohort of 258,488 patients. Another speculation 10.26; 95% CI 9.01-11.69). OSA tients undergoing revision total hip is that some of the patients with- patients without hypertension and arthroplasty or total knee arthro- out a diagnosis of OSA may have COPD were 14 times more likely plasty surgeries between 2006-2008. had unrecognized OSA leading to to receive mechanical ventilation Contrary to these studies, OSA was an under-estimation of mortality 5-7 and 46 times more likely to under- associated with increase in-hospital rates. Indeed, studies utilizing go non-invasive ventilation. OSA mortality (odds ratio 1.9; 95% CI cohorts from databases to identify was also independently associated 1.3-2.8) with a mortality of 0.2% in OSA patients are bound to include with escalation of care, increased patients without OSA and 0.4% in only those patients with diagnosed health care resource utilization patients with OSA.16 However, this OSA, leaving us to wonder, if 12 and length of stay. study only included patients under- outcomes in undiagnosed patients The types of complications associ- going revision arthroplasty which may be worse. Irrespective of the ated with OSA reported by Memt- may suggest a higher comorbidity reasons for these findings, however, soudis and colleagues are similar to burden. one should not lose sight of the fact the findings from a recent analysis that mortality is a rare outcome in So what do these results tell total hip and knee arthroplasties of the Nationwide Inpatient Sam- us? First and foremost, it appears 14,15 and that other more frequently en- ple. Mokhlesi et al examined a that OSA is consistently and inde- cohort of 1,058,710 hospitalized countered complications, although pendently associated with increased less severe, may be more relevant adult patients undergoing 4 catego- postoperative respiratory failure ries of elective procedures (ortho- drivers of medical decision making requiring invasive or noninvasive and resource utilization. pedic, prostate, abdominal and mechanical ventilation, pulmonary cardiovascular cases) and a cohort complications, and atrial fibrilla- Most large administrative databases of 91,028 adult patients undergoing tion.4,8,12,14-16 Second, despite lack longitudinal data therefore bariatric surgeries between 2004 an increase in adverse events and limiting inferences about outcomes and 2008. Similar to the Premier resource utilization, OSA does not after hospital discharge. A recent Perspective database, OSA was appear to be associated with in- observational cohort study of independently associated with sig- creased risk of in-hospital mortality 14,962 patients undergoing elective nificantly increased odds of emer- with the exception of revision total surgery at a single institution over gent intubation and mechanical hip or revision total knee arthro- a 4-year period also did not find an ventilation, noninvasive ventila- plasty.12,14-16 One can only speculate independent association between tion, respiratory failure, and atrial as to why increased postoperative continued on next page

Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 1 w 2014 3 President’s Message continued from previous page having high-risk for OSA and 30- This President’s message was written 12 Memtsoudis SG, Stundner O, Rasul R, Chiu 21 YL, Sun X, Ramachandran SK, Kaw R, Fleischut day or 1 year mortality. However, together with Babak Mokhlesi M.D. P. The impact of sleep apnea on perioperative there is overwhelming evidence M.Sc. and is adopted from “Post- utilization of resources and adverse outcomes. Anesth Analg 2014 in press. from longitudinal community and operative complications associated 13 Gami AS, Pressman G, Caples SM, Kanagala clinic-based studies that untreated with obstructive sleep apnea: Time R, Gard JJ, Davison DE, Malouf JF, Ammash severe OSA is an independent to wake up! Chung F, Mokhlesi B, NM, Friedman PA, Somers VK. Association of obstructive sleep apnea and atrial fibrillation. 22,23 predictor of mortality. Since Anesth Analg 2014; 118:251-3” Circulation 2004; 110: 364-367 the vast majority of patients with References 14 Mokhlesi B, Hovda MD, Vekhter B, Arora VM, clinically significant OSA remain Chung F, Meltzer DO: Sleep-disordered breath- 1 Peppard PE, Young T, Barnet JH, Palta M, Hagen ing and postoperative outcomes after elective undiagnosed, anesthesiologists EW, Hla KM. Increased prevalence of sleep- surgery: Analysis of the nationwide inpatient disordered breathing in adults. Am J Epidemiol sample. Chest 2013; 144: 903-14 can have a pivotal role in recog- 2013; 177: 1006-1014 nizing these patients and referring 15 Mokhlesi B, Hovda MD, Vekhter B, Arora VM, 2 Weiser TG, Regenbogen SE, Thompson KD, Chung F, Meltzer DO: Sleep-disordered breath- 5-7 them for clinical evaluation. Haynes AB, Lipsitz SR, Berry WR, Gawande AA. ing and postoperative outcomes after bariatric Recent studies have indeed shown An estimation of the global volume of surgery: surgery: Analysis of the Nationwide Inpatient A modelling strategy based on available data. Sample. Obes Surg 2013; 23: 1842-51 that continuous positive airway Lancet 2008; 372: 139-44 16 D’Apuzzo MR, Browne JA: Obstructive sleep pressure (CPAP) can effectively 3 Memtsoudis SG, Melanie C. Besculides MC, apnea as a risk factor for postoperative complica- treat OSA during the periopera- Mazumdar M. A Rude Awakening - The periop- tions after revision joint arthroplasty. J Arthro- erative sleep apnea epidemic. N Eng J Med 2013; plasty 2012; 27: 95-8 24 368:2352-3 tive period, decrease the risk 17 Bucholz EM, Rathore SS, Reid KJ, Jones PG, of postoperative emergent intu- 4 Memtsoudis S, Liu SS, Ma Y, Chiu YL, Walz JM, Chan PS, Rich MW, Spertus JA, Krumholz 25 Gaber-Baylis LK, Mazumdar M. Perioperative HM. Body mass index and mortality in acute bation, and have a beneficial pulmonary outcomes in patients with sleep apnea myocardial infarction patients. Am J Med. 2012; 26 long-term effect. However, it after noncardiac surgery. Anesth Analg 2011; 125: 796-803. 112: 113-21 is important to note that adher- 18 Martino JL, Stapleton RD, Wang M et al Extreme 5 Chung F, Yegneswaran B, Liao P, Chung SA, obesity and outcomes in critically ill patients. ence to CPAP therapy during the Vairavanathan S, Islam S, Khajehdehi A, Shapiro Chest 2011; 140: 1198-1206 perioperative period is suboptimal CM. STOP questionnaire: A tool to screen patients for obstructive sleep apnea. Anesthesiol- 19 Ozeke O, Ozer C, Gungor M, Celenk MK, Dincer and there is a need to explore ways ogy 2008; 108:812-21 H, Ilicin G. Chronic intermittent hypoxia caused by obstructive sleep apnea may play an important to improve compliance to CPAP 6 Singh M, Liao P, Kobah S, Wijeysundera DN, role in explaining the morbidity-mortality para- as well as explore alternative treat- Shapiro C, Chung F. Proportion of surgical dox of obesity. Med Hypothesis 2011; 76: 61-3 24,27,28 patients with undiagnosed obstructive sleep ment modalities. apnoea. Br J Anaesth 2013; 110: 629-36 20 Shah N, Redline S, Yaggi HK, et al. Obstruc- tive sleep apnea and acute myocardial infarction The results of these desperately 7 Finkle KJ, Searleman AC, Tymkew H, Tanaka CY, severity: Ischemic preconditioning? Sleep Breath Saager L, Safer–Zadeh E, Bottros M, Selvidge JA, 2013; 17:819-26 needed trials will also provide guid- Jacobsohn E, Pulley D, Duntley S, Becker C, Avi- ance for protocol developments that dan MS. Prevalence of undiagnosed obstructive 21 Lockhart EM, Willingham MD, Abdallah AB, sleep apnea among surgical patients in an aca- Helsten DL, Bedair BA, Thomas J, Duntley S, are supported by evidence and not demic medical centre. Sleep Med 2009; 10:753-8 Avidan MS. Obstructive sleep apnea screening 29-33 and postoperative mortality in a large surgical by opinions. Such significant 8 Kaw R, Chung F, Pasupuleti V, Mehta J, Gay PC, cohort. Sleep Med 2013; 14: 407-15 increases in adverse postoperative Hernandez AV. Meta-analysis of the association between obstructive sleep apnea and postopera- 22 Campos-Rodriguez F, Martinez-Garcia MA, de la outcomes in patients with diag- tive outcome. Br J Anaesth 2012; 109: 897-906 Cruz-Moron I, Almeida-Gonzalez C, Catalan-Se- rra P, Montserrat JM. Cardiovascular mortality nosed OSA is a wake up call for all 9 9. Kaw R, Pasupuleti V, Walker E, Ra- in women with obstructive sleep apnea with or stakeholders (i.e. patients, patient maswamy A, Foldvary-Schafer N. Postoperative without continuous positive airway pressure complications in patients with obstructive sleep treatment: a cohort study. Ann Intern Med. 2012; advocates, healthcare providers, apnea. Chest 2012; 141: 436-441 156: 115-22. hospital administrators, policy 10 Liao P, Yegneswaran B, Vairavanathan S, Zilber- 23 Marin JM, Marin JM, Carrizo SJ, Vicente E, makers and funding agencies). man P, Chung F. Postoperative adverse events Agusti AG. Long-term cardiovascular outcomes in patients with obstructive sleep apnea: A in men with obstructive sleep apnoea-hypopnoea Without their collective support retrospective matched cohort study. Can J Anesth with or without treatment with continuous we will continue to lack the high 2009; 56: 819-28 positive airway pressure: An observational study. Lancet. 2005; 365: 1046-53 level of evidence needed to guide 11 Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S, Islam S, Khajehdehi A, Shapiro 24 Liao P, Luo, Q, Elsaid H, Kang W, Shapiro CM, us in providing the best possible CM. Validation of the Berlin questionnaire and Chung F. Perioperative auto-titrated continuous perioperative care to our surgical American Society of Anesthesiologists checklist positive airway pressure treatment in surgical v as screening tools for obstructive sleep apnea patients with obstructive sleep apnea. A random- patients in surgical patients. Anesthesiology 2008; 108: ized controlled trial. Anesthesiology 2013; 119: 822-30 837-47 continued on page 6 4 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Massimo Ferrigno, MD, FCCM Chief, Anesthesiology Institute Cleveland Clinic Abu Dhabi Abu Dhabi, United Arab Emirates

Holding Your Breath….Too Long

pnea is a major concern in Hyperventilation effectively de- of the mouth and pharynx to move

both anesthesia and sleep creases CO2 stores at the beginning air into (glossopharyngeal insuf- medicine: inability to venti- of a breath-hold, greatly delaying flation, GI) and out of the lungs Alate a patient made unconscious by the diver’s hypercapnic respiratory (glossopharyngeal exsufflation, GE) 3 an anesthesiologist and OSA are drive. End-tidal PCO2 of around 20 . With GI before a dive, elite divers clinical examples of involuntary Torr are frequently observed prior are able to increase their lung vol- apnea. On the other hand, volun- to a dive and they appear to be well ume above their total lung capacity tary apnea is practiced by millions tolerated by elite divers, typically by almost 3 liters, resulting in a 4 of breath-hold divers around the without any neurological symptoms liter increase in the amount of gas world, with a few of them able to or signs of severe hypocapnia, such in the lungs due to the dangerously reach incredible depths and/or elevated intrapulmonary pressures

apnea durations on a single breath (exceeding 100 cmH2O) that they of air. In fact, the present depth re- produce4. This provides both ad- cord is a breath-hold dive to 700 ft ditional oxygen stores during the (214 m) by the Austrian Herbert apneic period and additional vol- Nitsch and the duration record of ume of intrapulmonary gas during breath-holding at the surface is descent to counteract dangerous 11 min 35 s by the French Sté- compression of their chest. By phane Mifsud1. using GE at great depths, divers Contributing to these elite perfor- can extract up to an additional 0.5 mances are the diving response, liters from the compressed lungs vigorous pre-dive hyperventila- (below residual volume at that tion and the use of glossopharyn- time) into their pharynx, to be geal breathing techniques. The used for pressure equalization in diving response consists mainly their middle ears, when conven- of a vagally-induced bradycardia, tional expiratory muscles are no reduced cardiac output and an longer effective. intense peripheral vasoconstric- An obvious danger of both deep tion which conserves the limited breath-hold diving and competi- oxygen available during a dive for as paresthesias and tetanic con- tive breath-holding at the surface the organs that are more sensi- tractions. Unfortunately, hyper- is hypoxia, with different time tive to hypoxia, such as the heart ventilation increases only slightly courses in the two sports: sudden and brain2. Interestingly, a more the oxygen stores; therefore the in the former and gradual in the pronounced diving response can diver may lose consciousness from latter [cf 2]. Actually, the worst result in a slower hemoglobin hypoxia before feeling the urge to hypoxia will be experienced by desaturation in the arterial blood breathe from hypercapnia. With the brain 10-15 s after breathing and a longer breath-holding time. regard to glossopharyngeal breathing, breath-hold divers use muscles continued on next page

Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 5 Holding Your Breath...Too Long continued from previous page

has resumed, reflecting the lungs- that lead to hypoxic loss of mo- tion of the diving response. Still, we to-brain circulation time. Dur- tor control (ironically referred as cannot conclude that this observa- ing diving, oxygen pressure in the “Samba” by elite divers) or even loss tion reflects a serious injury to the

arterial blood drops quickly and of consciousness. End-tidal PO2 breath-holder’s brain, but it raises dramatically in the very last part values as low as 19.6 Torr have been suspicion that repeated episodes of the ascent, due to the rapid fall measured at the end of maximal of hypoxia may have cumulative, in water pressure surrounding the breath-holds lasting between 256 deleterious effects. 6 diver’s chest, a phenomenon called and 306 s . Similar to what has been I hope that our clinical readers find “hypoxia of ascent”. For example, described in aviation medicine dur- the above information on voluntary according to Boyle’s law, lung pres- ing acute high-altitude exposures, forms of apnea both interesting sure (and, consequently, arterial the arterial PO2 values causing un- and, hopefully, relevant to their O2 pressure) will be halved during consciousness probably lie between practice. Thanks to these elite div- ascent from 20 m (66 ft, 2 ATA) to 20 and 35 Torr, depending on the ers, we have learned a great deal on the surface (1 ATA). Unfortunately, concomitant arterial PCO2 values, respiratory mechanics. Maybe, the this sometimes leads to hypoxic with hypocapnia having a deleteri- same will be possible with OSA, 7 loss of consciousness in divers who ous effect . where involuntary apnea plays a were otherwise not dangerously At this point, the natural question central role. v hypoxic at depth. Measurements is whether these repeated episodes References taken at the end of breath-hold of hypoxia can cause injury to the dives attest to this risk; for example, 1 http://www.aidainternational.org/ breath-holder’s brain. An increase 2 Ferrigno M. In: Bove and Davis’ Diving Medi- we recorded an alveolar PO2 of 30.6 in the concentration of the protein cine, Saunders 2004; 77-93. Torr at the end of a 70 m (230 ft) S100B in serum has been measured 3 Lindholm P et al. Respiratory, Physiology and 5 dive lasting about 150 s . During following maximal breath-holds Neurobiology 2009; 167: 189-194. competitive breath-holding at the 8 4 Loring SH et al. J Appl Physiol 2007; 102:841- ranging from 281 to 403 s . This 846. surface, divers typically float mo- protein is a nonspecific marker of 5 Ferretti G et al. J Appl Physiol 1991; 70: 794-802. tionless face down in a swimming brain damage and its increase could 6 Lindholm P et al. Undersea Hyperb Med 2006; pool, a practice called “static apnea”. be caused by asphyxia or other 33: 463-467. In this situation, hypoxia develops physiological responses to apnea, 7 Ernsting J et al. In: Aviation Medicine, Butter- worths 1988; 45-49. more slowly, gradually during the for example the increased arterial course of several minutes, fre- 8 Anderson JPA et al. J Appl Physiol 2009; 107: blood pressure that accompanies 809-815. quently reaching very low values the intense peripheral vasoconstric-

President’s Message conitnued from page 4

25 Squadrone V, Coha M, Cerutti E, Schellino MM, randomized controlled clinical trial. Chest. 2013; 30 Seet E, Han TL, Chung F. Perioperative clinical Biolino P, Occella P, Belloni G, Vilianis G, Fiore 144: 72–78. pathways to manage sleep-disordered breathing. G, Cavallo F, Ranieri VM, for the Piedmont Sleep Med Clin 2013; 8: 105-20 28 Guralnick AS, Pant M, Minhaj M, Sweitzer BJ, Intensive Care Units Network (PICUN). Con- Mokhlesi B. CPAP Adherence in patients with 31 Swart P, Chung F, Fleetham J. An order-based tinuous positive airway pressure for treatment newly diagnosed obstructive sleep apnea prior approach to facilitate postoperative decision- of postoperative hypoxemia: A randomized to elective surgery. J Clin Sleep Med. 2012; 8: making for patients with sleep apnea. Can controlled trial. JAMA 2005; 293: 589-595 501–6 Anesth J 2013; 60: 321-4 26 Mehta V, Subramanyam, Shapiro CM, Chung F. 29 Gross JB, Bachenberg KL, Benumof JL, Caplan 32 Adesanya AO, Lee W, Greilich NB, Joshi G. Health effects of identifying patients with undiag- RA, Connis RT, Cote CJ, Nickinovich DG, Pra- Perioperative management of obstructive sleep nosed obstructive sleep apnea in the preoperative chand, V, Ward DS, Weaver EM, Ydens L, Yu S. clinic: A follow-up study. Can J Anesth 2012; 59: apnea. Chest 2010; 138: 1489-98. Practice guidelines for the perioperative manage- 544-55 ment of patients with obstructive sleep apnea: A 33 Seet E, Chung F. Management of sleep apnea in 27 O’Gorman SM, Gay PC, Morgenthaler TI. Does report by the American Society of Anesthesiolo- adults - Functional algorithms for the periopera- auto-titrating positive airway pressure therapy gists Task Force on perioperative management of tive period. Can J Anesth 2010; 57: 849-64 improve postoperative outcome in patients at patients with obstructive sleep apnea. Anesthesi- risk for obstructive sleep apnea syndrome? A ology 2006; 104: 1081-93

6 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Viviane G. Nasr, MD Pediatric Cardiac Anesthesia Fellow Department of Anesthesiology and Critical Care Boston Children’s Hospital Boston, MA USA

Apnea and Prematurity: A Need for Better Understanding to Improve Periopera- tive Neonatal Care pnea and prematurity: a stantially different considerations in predicting the neonates at higher need for better understand- related to prematurity compared to risk for apnea and more important- ing to improve periopera- adults. The maturity of the central ly postoperative apnea. Ative neonatal care. nervous system (CNS) sleep cen- While apnea and short respiratory Every year, an estimated 15 million ter or malfunction in the respira- pauses may be of minimal con- babies are born preterm, defined as tory network, including the brain sequence if oxygenation is main- born alive before 37 weeks of preg- centers (frontal and insular cortex, tained, they can be challenging if nancy and this number continues hypothalamus, RAS, amygdala), the accompanied by hypoxemia. to rise, leading to an increase in the mechanoreceptors in the lungs and upper airways, the peripheral che- How is apnea defined in neonates? number of ‘preemies’ presenting Based on the definition by the 1 moreceptors on the carotid body, for surgical procedures . Most pre- American Academy of Pediatrics, mature infants born in the United and the central chemoreceptors on the ventral medullary surface affect it is the cessation of breathing for States each year are classified as 5,6 the output to the muscles of respi- more than 20 sec duration . If a either moderately or late preterm shorter pause of breathing associ- infants (32 to <37 weeks) account- ration. Immaturity in these areas of the CNS then can easily result in ated with bradycardia or oxygen ing for more than 70% of the desaturation occurs, it may be 2 apnea. preterm population . Prematurity labeled as apnea. However, there is increases the severity of conditions A prospective study currently in no current evidence-based research such as jaundice, anemia, infec- press showed that between the first defining a respiratory event as tions, and patent ductus arteriosus. two weeks and reaching term age, pathological based on the degree In addition, apnea of prematurity, sleep patterns in premature, very of change in heart rate and oxygen respiratory distress syndrome, low birth weight newborns undergo saturation rather than duration7. bronchopulmonary dysplasia, intra- major developmental changes, ventricular hemorrhages, necrotiz- expressed by more mature electro- The initial documentation of post- ing enterocolitis, gastroesophageal encephalography indexes and sleep operative apnea in former premature infants after general anesthesia reflux, and retinopathy of prematu- parameters. However, when reach- 8 rity occur frequently in the preterm ing term age, babies born prema- appeared in 1982 . The most com- infant and may have lasting conse- turely still show altered EEG pat- mon causes of apnea after surgery quences3,4,5. terns when compared to newborns besides prematurity are metabolic delivered at term, indicating a delay derangements (hypothermia, hypo- With the advances in intensive care glycemia, hypocalcemia, acidosis, medicines and increased survival of in the acquisition of normal matu- rational sleep patterns. Defining and hypoxemia) and pharmaco- neonates and especially preemies, logic effects. Pharmacologic effects understanding neonatal apnea be- this difference in sleep pattern and the timeline between premature cannot be avoided because most comes a must. Neonatal sleep medi- drugs used in anesthesia affect the cine in general is a domain under newborns and full term or even development and may have sub- adults may be helpful in the future continued on next page

Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 7 Apnea and Prematurity continued from previous page

respiratory system. Most inhala- respiratory centers in infants, trig- that a conservative approach for tional agents, opioids, and sedatives gering apneas in both instances. admission of patients born before depress the central response to This should be an area of active re- 37 weeks of gestation could be set carbon dioxide in adults in a dose- search for both of these populations for 50 weeks PCA19. Many hospitals related fashion. And this respira- and SASM can play a role. have written policies based on the tory depression is probably more The risk of perioperative apneic 60 weeks PCA data. Is it time to pronounced in neonates who have events in infants decreases with reevaluate? Open questions re- an immature respiratory center. increasing post conceptual age main regarding the maturation of Studies of adults have demonstrated (PCA). Some have suggested that sleep architecture in infancy, and both lack of the response to hypox- the likelihood of apnea was nearly the exact role of PCA, and what, if ia and potentiation of that response absent by 44 weeks PCA14, whereas anything, could be applied to adult- by hypercarbia in the presence of others reported that the risk of hood. halothane in concentrations as low apnea persisted until as late as 60 Neonatal perioperative apnea is as 0.1%; thus, residual anesthetic weeks PCA15,16. Although a debate of major importance, affecting the action may contribute to the devel- developed centered entirely around patient’s safety, length of hospi- 9 opment of apnea in infants . In ad- the post conceptual age at which tal stay and impacting the cost of dition, most pharmacologic agents infants remain at risk of apnea, no medical care. Review of the current used in anesthesia decrease muscle unified widely accepted guidelines data, but likely a prospective study tone of the upper airway, contrib- for perioperative monitoring have using a clear definition of neonatal uting to upper airway obstruction emerged. Preemies younger than apnea duration, and tracking of and decrease intercostal muscle 55 weeks PCA, especially if anemic associated bradycardia and hypoxia tone, reducing functional residual or with other cardiopulmonary and may lead to an updated guideline 10,11 capacity . Currently, it has been neurologic disorders, should be or validation of the current prac- shown that there is no significant admitted and monitored for twelve tice in anesthesiology. In addition, difference between general vs. hours prior to discharge. Caffeine, an in-depth understanding of the regional anesthetic techniques with although used to reduce the risk of neonatal sleep patterns and the respect to the occurrence of post- apnea, does alter the need for such relationship to apnea may help us 12 operative apneas in infants . In a monitoring. The landmark 1995 understand perioperative apnea, review of four studies that utilized meta-analysis by Coté et al used the its etiology and potentially guide regional (spinal, epidural, caudal) incidences reported in the included therapy accordingly. v versus general anesthesia in former studies to establish a prediction preterm infants undergoing ingui- References: curve, which pointed to a signifi- 1 http://www.who.int/mediacentre/factsheets/ nal herniorrhaphy in early infancy, cant reduction in the incidence of fs363/en/. Updated November 2013. there was no convincing evidence apnea at 52 to 54 weeks PCA, with 2 Martin J, et al. National Vital Statistics. Reports to support the use of spinal anes- an apnea incidence of less than 1% 2011;60(1):1–70. thesia, although it was observed at 54 weeks PCA17,18. The curve 3 Escobar GJ, et al. Semin Perinatol 2006; 30: that spinal anesthesia reduced the 28–33. created by this model had an upper 4 Hibbard JU et al. JAMA 2010;304:419–25. incidence of postoperative apnea confidence interval that extended 5 Fiore, JM, et al. Respiratory physiology and in those who were not given addi- to 60 weeks PCA, which represents neurobiology 2013; 189:213-222. 13 tional sedation . This is similar to the most conservative interpreta- 6 Nunes ML, et al. Clinical neurophysiology 2013. In press emerging data in adults with sleep tion for a safety margin based on disordered breathing. One explana- 17 7 American Academy of Pediatrics, Committee on these data . This conservative fetus and newborn. Pediatrics 2003; 111: 914-7. tion may be that deafferentation estimate is currently used in most 8 Elder DE, et al. Journal of paediatrics and child under conditions of regional anes- centers. However, a more recent health 2013; 49: E388-E396. thesia could exacerbate (centrally retrospective study conducted on 9 Kafer ER, et al. Int Anesthesiol Clin 1977; 15:1-38. mediated) sleep-disordered breath- former preterm infants admitted 10 Knill RL, et al. Anesthesiology 1978; 49:244-251. ing (SDB) symptoms in adults and for inguinal herniorrhaphy showed inhibit excitatory pathways in the continued on page 13 8 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Susana Vacas, MD, PhD

Strategies to Understand and Modify Postoperative Cognitive Dysfunction: A Sleep Perspective

mpairment of cognition after of postoperative cognitive decline, nism to peripheral trauma and surgery is a disturbing reality. activation of the innate immune resolves properly with no residual Postoperative delirium (POD), response following aseptic surgical cognitive consequences. Indeed, it Ilisted in the Diagnostic and Statis- trauma results in the elaboration is also possible that surgery for a tical Manual of Mental Disorder of hippocampal proinflammatory chronic inflammatory disease may (DSM-5)1, is characterized by inat- cytokines, which are capable of result in cognitive improvement tention, disorganized thinking and disrupting long-term potentia- by eliminating disease-inducing altered level of consciousness with tion, the neurobiologic correlate of cognitive impairment that may be acute onset and fluctuating course. memory6. Assuming that postop- associated with chronic inflamma- While some patients develop POD, erative neuroinflammatory changes tory disease. That said, some risk others develop a later onset form noted in rodent models also occur factors, such as obstructive sleep of postoperative cognitive decline in humans, the underlying mys- apnea (OSA), Metabolic Syndrome known as postoperative cognitive tery is that POCD is a relatively (MetaS), patients prone to neuro- dysfunction (POCD). It is esti- infrequent clinical event (± 10%)7 logical disease, and poor selection mated that POCD occurs in more whereas neuroinflammation always of sedative agents may each pro- than 10% of non-cardiac surgical occurs8,9. Is this because there are mote the intractable persistence patients2 over 60 years of age3 and several clinical conditions that can of neuroinflammatory response is independently associated with transform the self-limiting post- to surgery10-12. For an increasing poor short-term and long-term surgical neuroinflammatory re- number of patients with advanced outcomes including an increased sponse into one that is persistent? age, POCD is alarmingly common, 4,5 risk of mortality . Given the Studies have sought to identify fac- making postoperative central ner- number of major surgical inter- tors that may contribute to POCD, vous system dysfunction a looming ventions (requiring anaesthesia) which include surgery, as well as public health crisis given world’s and the increasing prevalence of in-patient care factors, and patient- rising elderly population. surgical interventions in patients related factors. If we divide the Clearly, the surgical effect of this with comorbidities, we can expect possible risk factors into categories neuroinflammatory trigger is just that many millions of patients will of modifiable/non-modifiable and one possible mechanism. Indeed, run the risk of developing POCD patient related/environmental, we environmental culprits can also of- every year. This possibility raises can both disentangle the causes of fer a window into the postoperative the stakes considerably: not only the neuroinflammatory cascade cognitive decline conundrum. One on an individual level, but also on a and also focus on possible clinical great suspect in this complex puzzle societal scale. adjustments and applications to is that of sleep disruption. Sleep is Despite this potential for disaster, stave it off. crucial for the repair of many types the exact pathophysiology that In the majority of patients, postop- of injury and disease, especially underlies POCD remains unde- erative neuroinflammation is part with regard to the central nervous fined. According to rodent models of the normal protective mecha- continued on next page

Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 9 Postoperative Cognitive Dysfunction continued from previous page

and immune systems; it also has procedures. Lack of sleep hygiene a perfect and unfortunate storm of anabolic, restorative properties results in cognitive dysfunction, factors with regard to POCD: to that improve both neurocogni- contributes to delirium, adversely put it another way, given the rise in tive and immune function. During affects immunity, and independent- surgeries and increasing number non rapid eye movement (NREM) ly increases both morbidity and of patients with chronic conditions sleep slow wave activity performs a mortality. Sleep disruption during worldwide, the stakes could not be homeostatic function to reduce the hospital care has the potential to higher. strength of synapses that has been adversely impact patients’ outcome Vulnerable patients need to be 13 acquired during wakeful activity . and also provides a direct finan- identified and risk/benefit should This synaptic homeostasis improves cial cost with respect to the length be considered before contemplating subsequent cognitive function by of hospital stay and depletion of the efficacy of surgical interven- allowing new changes in synaptic healthcare resources. A recent tion. Further studies are needed strength. For example, both NREM prospective study has also shown to understand which patients will and REM sleep are necessary for that patients with sleep disorders suffer from exacerbated inflamma- the consolidation of learning and have an increased likelihood of tion with an aim toward developing 10 memory while sleep deprivation exhibiting postoperative delirium . a biomarker that is quick to assay 14 results in cognitive dysfunction . Despite the common occurrence for clinicians and easy to compre- Sleep disturbance is commonly of both ICU delirium and sleep hend for patients and their families. observed in the hospital setting disruption in critically ill patients, a Concurrently, clinical interventions and include changes to sleep pat- causal relationship has not yet been need to be further developed to terns and quality (especially sleep well described. Still, the question promote the resolution of neuro- fragmentation), as well as sleep remains if we are doing all in our inflammation in the postoperative architecture. Polysomnographic power to avoid the development of patient population. Following both studies revealed extreme sleep POCD. tracks, we anticipate that postop- disruption in Intensive Care Unit While we realize that the etiology erative recovery for vulnerable pa- (ICU) patients with decreases in of cognitive dysfunction in surgi- tients will be greatly enhanced and total sleep-time, altered sleep ar- cal/ICU patients is multi-factorial, possible long-term consequences, chitecture (predominance of stage if the restorative and reparative such as postoperative neurodegen- 1 and 2 sleep, decreased or absent benefits of sleep mitigate the devel- eration, can be significantly re- stage 3 NREM and REM sleep), opment of inflammation and cogni- duced. Additional study is essential and sleep fragmentation15,16; also, tive dysfunction, this may result to elucidate on preventative strate- up to 50% of the total sleep-time in shorter ICU or postoperative gies, and underlying pathophysiol- occurred during daytime. Studies lengths of stay for critically ill pa- ogy of this disorder. If these studies have shown that fragmented sleep tients with a concomitant reduction can succeed in identifying patients is prevalent due to frequent arous- in healthcare costs. Furthermore, it prospectively, or early enough in als and awakenings, and that sleep is possible that the restorative prop- the advent of persistent inflamma- architecture is altered with an in- erties of sleep for cognition in the tion, interventions can be judi- crease in light sleep, and a decrease central nervous system can extend ciously and appropriately launched. in restorative slow wave sleep17. to the immune system with less v Environmental factors and health infection and/or greater likelihood References 18,19 care practices further contribute of survival from sepsis . 1 Association, A. P. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition: DSM- to sleep disruption in critically ill Non-resolution of inflammation 5. American Psychiatric Association, 2013. patients; these include disturbances is a factor that contributes to the 2 Abildstrom, H. et al. Acta Anaesthesiol Scand 44, like inappropriately high noise pathogenesis of POCD, which in 1246-1251 2000. levels, continuous ambient light, turn significantly increases mor- 3 Moller, J. T. et al. Lancet 351, 857-861, 1998. and the near constant performance bidity and mortality in surgical 4 Newman, M. F. et al. N. Engl. J. Med. 344, 395- of medical tests procedure and patients. We might be witnessing continued on page 13 10 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Shireen Ahmad, MD Professor, Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, IL USA

Sleep Apnea: An Update of Pharmacologic Therapies

urrent standard therapy ondansetron reduces the respira- undesirable side effects11. for obstructive sleep apnea tory disturbance index (RDI) in Serotonergic agents seem to have 3,4 (OSA) relies exclusively bulldogs but not in humans . positive effects in OSA and may Con mechanical devices whose ef- Based on successful use in nar- have increased efficacy in combina- fectiveness is hampered by poor colepsy, the tricyclic antidepres- tion with other agents. compliance due to lack of tolerabil- sant, protriptyline was studied in 1 Acetylcholinesterase Inhibitors ity, sometimes as high 50% . Oral patients with OSA. A reduction appliances may be better tolerated of REM sleep and improved noc- The cholinergic system plays an but are not as effective, and upper turnal oxygenation was observed, important role in the neural control airway surgery has limited long although the incidence of apneas of respiration and acetylcholine is term success. While there is a need and their duration was not altered5. one of the main neurotransmitters for systemic therapeutic agents, the involved in respiratory modula- Another small study in severe OSA 12 investigation into pharmacologic showed a decrease in nocturnal hy- tion during REM sleep . Applica- modalities has been hampered by poxemia and daytime somnolence6. tion of acetylcholine agonists to the absence of a suitable animal The improvement may have been the hypoglossal nerve in rats has model for drug screening and been shown to reduce genioglossus related to the reduction in REM 13 many drugs have been the result of sleep or the antidepressant effects. muscle tone . Pontine injection of serendipitous observations in other However, in a randomized con- the anticholinesterase drug carba- studies. This review will describe trolled trial (RCT) no significant chol in cats results in increased hy- several of the treatments that have difference was noted after 2 weeks poglossal nerve activity, while the been evaluated and their shortcom- of treatment7. injection of physostigmine into the ings. cholinergic neurons in the rostral Trials of the selective serotonin Serotonergic Agents ventrolateral medulla resulted in re-uptake inhibitors, fluoxetine prolonged firing of the hypoglossal Serotonin is known to alter sleep and paroxetine have been shown to and phrenic nerves and improve- and influence upper airway hypo- reduce the apnea-hypopnea index ment in respiration14. glossal motor neurons. The post (AHI) by 40 and 20% respectively8,9. synaptic receptors associated with Paroxetine has also been shown The cholinergic system affects dilator neurons centrally are pre- to increase genioglossus muscle regulation of breathing during dominantly 5-HT2A and 5-HT2C tone in awake healthy volunteers10. sleep. Cholinergic stimulation of subtypes, while the 5-HT1B and Mirtapazine is an antidepressant the respiratory center and carotid 5-HT2 receptors are inhibitory. with 5-HT1agonist and 5-HT2 and bodies increases the sensitivity to Stimulation of the peripheral 5-HT3antagonist properties and in hypoxia and hypercarbia and plays an important role in the regulation 5-HT2A, 5-HT2c, and 5-HT3 re- a placebo controlled study has been 12,15-17 ceptor subtypes has an inhibitory shown to decrease AHI by 46-52%. of ventilation in OSA . Cholin- effect on respiration (2). The func- Day time alertness, however, was ergic pathways are also involved in tions of these receptors are species not improved and in fact, seda- cerebral cortex activation related to specific. The 5-HT3 antagonist, tion and weight gain resulted, both continued on next page 11 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Sleep Apnea: An Update of Pharmacologic Therapies continued from previous page arousal and vigilance18. of the NMDA glutamate receptors the AHI by 50%37. Another RCT Acetylcholinesterase inhibitors and sabeluzole; a glutamate antago- comparing atenolol, amlodipine, increase central and peripheral nist reduced hypoxemic episodes enalapril, hydrochlorthiazide and acetylcholine levels and also ef- in patients with moderate to severe losartan demonstrated no effect 30 38 fect sleep. A double-blind placebo OSA . by any of the drugs . Clonidine is controlled RCT with intravenous Hormones an alpha-2 adrenergic agonist with REM suppressant activity and has physostigmine in patients with The effects of estrogen and proges- OSA, resulted in an increase in been shown to reduce REM-related terone on sleep-disordered breath- apnea in a small study of hyperten- REM sleep and a decrease in AHI ing are inconsistent. Estrogen has by 23%19. Similar results have been sive patients with OSA, but is un- been noted to reduce AHI by 25% safe in non-hypertensive patients39. reported with Donepezil, an oral and the combination of estradiol 20 cholinesterase inhibitor . Another and progestin reduced apneic epi- Wakefulness Promoting Agents recent double-blind, placebo con- sodes by 50%31,32. OSA is common OSA is associated with daytime trolled RCT of Donepezil in OSA in hypothyroid patients, however somnolence, which may not resolve patients demonstrated a significant the results of hormone therapy has with CPAP therapy. Modafinil is improvement in AHI, % time with only been shown to be beneficial in widely used in narcolepsy to pro- oxygen saturations <3% of baseline a couple of small studies33. This may mote wakefulness. In OSA patients, and desaturation index after one be related to the resolution of mac- modafinil and armodafinil reduced 21 month of therapy . Nicotine is a roglossia. In acromegaly treatment sleepiness and increased vigilance, respiratory stimulant and while nic- with octreotide reduced the AHI by but did not reduce AHI40,41. otine gum has been associated with 50%34. a reduction of AHI, transdermal Cytokine Inhibitor nicotine did not have this effect22-24. Weight Reduction Medication Pro-inflammatory cytokines such Methylxanthines Patients with OSA are frequently as TNF-alpha are elevated in OSA morbidly obese and there is data and etanercept, which is an in- In patients with central sleep apnea that suggests that every 1% re- hibitor of the agent that has been (CSA), theophylline has been duction in weight results in a 3% shown to reduce AHI by 15% and shown to significantly reduce AHI reduction in AHI35. The use of also reduce daytime sleepiness42. and improve oxygenation without sibutramine in a group of obese 25 It is clear from this review that reduction in sleep . In OSA on the men resulted in an 8.5% weight other hand, the reduction in AHI while several agents have been reduction that was accompanied by studied, there is no reliable and was small, but significant, however a 35% reduction in the respiratory 26 effective pharmacologic therapy for sleep quality was worsened . Ami- desaturation index (RDI)36. nophylline also has similar effects27. OSA. Development of these agents Antihypertensive Agents is limited by a lack of understand- Acetazolamide There is a strong association be- ing of the etiology and mechanism Acetazolamide is a carbonic an- tween hypertension and OSA and it of OSA and of an adequate animal hydrase inhibitor and stimulates has been suggested that antihyper- model. Drug therapy for OSA will ventilation by inducing a metabolic tensive agents may improve OSA be limited until there is a clearer v acidosis. Acetazolamide is more ef- by altering the afferent barorecep- understanding of the disease. fective in CSA than in OSA. In CSA tor activity and input to respira- References: apneic episodes were reduced by tory center in the brain. However, 1 Zozula R, et al. Curr Opin Pulm Med 2001; 7: as much as 80%, while in OSA the studies of antihypertensive agents 291-8. 28,29 reduction was only 20% . in this population have been incon- 2 Veasey SC. Am J Respir Med 2003; 2: 21-9. Glutamate Antagonists sistent. A large double-blind RCT 3 Veasey SC, et al. Sleep 2001; 24: 155-60. comparing metoprolol and cilaza- 4 Stradling J, et al. J Sleep Res 2003; 12: 169-70. The ventilatory responses to hy- 5 Brownell LG, et al. N Engl J Med 1982; 307: poxia are dependent on activation pril found that both drugs reduced 1037-42.

Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 12 Sleep Apnea: An Update of Pharmacologic Therapies continued from previous page

6 Smith PL, et al. Am Rev Respir Dis 1983; 127: 168: 1246-51. 34 Grunstein RR, et al. Ann Intern Med 1994; 121: 8-13. 478-83. 20 Hedner J, et al. Sleep Med 2005; 6: S54-5. 7 Whyte KF, et al. Sleep 1988; 11: 463-72. 35 Peppard PE, et al. J Am Med Assoc 2000; 284: 21 Sukys-Claudino L, et al. Sleep Med 2012; 13: 3015 – 21. 8 Hanzel DA, et al. Chest 1991; 100: 416-21. 290-296. 36 Yee BJ, et al. Int J Obes 2007; 31: 161-8. 9 Kraicza H, et al. Sleep 1999; 22: 61-7. 22 Gothe B, et al. Chest 1985; 87: 11-7. 37 Weichler U, et al. Cardiology 1991; 78: 124 - 130 10 Sunderram J, et al. Am J Respir Crit Care Med 23 Davila DG, et al. Am J Respir Crit Care Med 2000; 162: 925-9. 1994; 150: 469-74. 38 Kraiczi H, et al. Am J Respir Crit Care Med 2000; 161: 1423 – 8. 11 Carley DW, et al. Sleep 2007; 30: 35-41. 24 Zevin S, et al. Am J Ther 2003; 10: 170-5. 39 Issa FG. Am Rev Respir Dis 1992; 145 – 435 12 Bellingham MC, et al. Respir Physiol Neurobiol 25 Javaheri S, et al. N Engl J Med 1996; 335: 562-7. 2002; 131: 135-44. 40 Arnulf I, et al. Respiration 1997; 64: 159-61. 26 Hein H, et al. Eu J Med Res 2000; 5: 391-9. 13 Liu X, et al. J Physiol 2005; 565: 965-80 41 Roth T, et al. Clin Ther 2006, 28: 689-706. 27 Espinoza H, et al. Am Rev Respir Dis 1987; 136: 14 Haxhiu MA, et al. Respiration 1992; 101: 89-100. 80-4. 42 Vgontzas AN, et al. J Clin Endocrinol Metab 2004; 89: 4409-13. 15 Kubin I, et al. Resp Physiol Neurobiol 2004; 143: 28 White DP, et al. Arch Intern Med 1982; 142: 235-49. 1816-9. 16 Shirahata M, et al. Respir Physiol Neurobiol 2007; 29 Tojima H, et al. Thorax 1988; 43: 113-9. 157: 93-105. 30 HednerJ, et al. Sleep 1996; 19: 287-9. 17 Shao XM, et al. Acta Pharmacol Sin 2009; 30: 31 Pickett CK, et al. J Appl Physiol 1989: 66: 1656 761-70. – 61. 18 Jones BE. Philadelphia: Elsevier; 2005.p.136-53. 32 Keefe DL, et al. Menopause 1999; 6: 196-200. 19 Hedner J, et al. Am J Respir Crit Care Med 2003; 33 Grunstein RR, et al. Am J Med 1988; 85: 775 – 9.

Apnea and Prematurity continued from previous page 8

11 Tusiewicz K, et al. Anesthesiology 1977; 47:327- 15 Malviya S, et al. Anesthesiology 1993;78:1076-81. 2012; 47: 217-220. 337. 16 Kurth CD, et al. Anesthesiology 1991;75:22-6. 12 Krane EJ, et al. Anesth Analg 1995; 80:7-13 17 Coté CJ, et al. Anesthesiology 1995;82:809-22. 13 Steward DJ. Anesthesiology 1982; 56:304-6. 18 Fisher D. Anesthesiology 1995;82:807-8. 14 Craven PD, et al. Cochrane Database Syst Rev 19 Laituri CA, et al. Journal of pediatric surgery 2003.CD003669.

Postoperative Cognitive Dysfunction continued from page 10

402 2001. 9 Cibelli, M. et al. Ann Neurol 68, 360-368, 2010. 1032 1985. 5 Steinmetz, J. et al. Anesthesiology 110, 548-555 10 Flink, B. J. et al. Anesthesiology 116, 788-796 16 Hilton, B. A. J Adv Nurs 1, 453-468 1976. 2009. 2012. 17 Friese, R. S. et. al. J Trauma 63, 1210-1214, 2007. 6 Vacas, S. et al. Anesthesiology, doi:10.1097/ 11 Hudetz, J. A. et al. J Anesth 2011. 18 Riker, R. R. et al. J. Am. Med. Assoc. 301, 489- aln.0000000000000045 2013. 12 Degos, V. et al. Anesthesiology 118, 1362-1372, 499, 2009. 7 Monk, T. G. et al. Anesthesiology 108, 18-30 2013. 19 Pandharipande, P. P. et al. Crit Care 14, R38, 2008. 13 Tononi, G. et al. Sleep Med Rev 10, 49-62 2006. 2010. 8 Bromander, S. et al. Journal of Neuroinflamma- 14 Sanders, R. D. et al. CJA 58, 149-156 2011. tion 9, doi:10.1186/1742-2094-9-242 2012. 15 Aurell, J. et al. Br Med J (Clin Res Ed) 290, 1029-

Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 13 Jonathan P. Wanderer, MD, MPhil Department of Anesthesiology Vanderbilt University Medical Center Nashville, TN USA Using the STOP-BANG criteria for preoperative screening: A look at the frequency of Obstructive Sleep Apnea (OSA) from the preoperative clinic. STOP A VIEW FROM THE PREOP CLINIC

20 18 16 18% of patients arrive at 14 12 preoperative clinic with an 10 8 6 established diagnosis of OSA 4 2 0 Percent of Patients Arriving in of Patients Percent Preop Clinic with OSA Diagnosis Preop

11% of patients without an OSA diagnosis have a STOP BANG score greater than 5 based on these risk factors:

Snoring loudly (25%) Tired (21%) Observed apnea (6%)

Pressure high (52%) BMI above 35 (15%) Age above 50 (68%)

Neck size above 40 (24%) Gender male (41%) BAN G

We queried Vanderbilt University’s Perioperative Data Warehouse to identify diagnostic trends and risk factors associated with obstructive sleep apnea (OSA) after receiving approval from our institutional review board. Preoperative evaluations were identified for 173,583 patients evaluated between 1/1/2000 and 11/16/2013 in the Vanderbilt Preoperative Evaluation Center (VPEC) where the presence or absence of OSA was documented. These data were divided by year and are displayed as a percentage of patients seen each year with an established diagnosis of OSA at the tie of preoperative evaluation. VPEC implemented an electronic STOP-BANG screening tool1 in 3/2013. Preoperative evaluations were identified for 8,955 patients evaluated between 3/2013 and 11/16/2016 that took place in VPEC where the STOP-BANG screening tool was fully completed and patients did not have a diagnosis of OSA. The proportion of patients with a STOP-BANG score of 5 or greater was calculated. The prevalence of each risk factor in this population was determined, and is shown with patient icons that each represent 10% of that population.

References 1. Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y: High STOP-BANG score indicates a high probability of obstructive sleep apnoea. Br J Anaesth 2012; 108: 768-75.

Infographic created by Jonathan P. Wanderer, Medical Director, Vanderbilt Preoperative Evaluation Center, Associate Medical Director, Vanderbilt Anesthesiology & Perioperative Informatics Research Division, Instructor, Department of Anesthesiology, Vanderbilt Univer- sity School of Medicine, [email protected]. 14 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 Society of Anesthesia and Sleep Medicine Department

Using the STOP-BANG criteria for preoperative screening: Membership for $1000 A look at the frequency of Obstructive Sleep Apnea (OSA) from the preoperative clinic.

he Society of Anesthesia and Sleep Medicine (SASM) is a multidisciplinary group of clinicians and researchers who have an interest in TOP Ttopics concerning many aspects of perioperative care S that are at the heart of anesthesiology practice and A VIEW FROM THE PREOP CLINIC education, including the basic science and clinical aspects of sleep disordered breathing, airway manage- 20 ment, pulmonary medicine as well as patient safety. 18 16 18% of patients arrive at 14 12 preoperative clinic with an 10 Sleep medicine has recently been accredited by 8 6 established diagnosis of OSA 4 the American Board of Anesthesiology (ABA) as 2 0

Percent of Patients Arriving in of Patients Percent a board certifiable sub-specialty in anesthesiology, Preop Clinic with OSA Diagnosis Preop thus opening up tremendous opportunities to our 11% of patients without an OSA diagnosis have a specialty and its trainees in the practice of periop- STOP BANG score greater than 5 based on these risk factors: erative medicine.

Snoring loudly (25%) Tired (21%) Observed apnea (6%) A membership in SASM for all anesthesiology faculty/staff/residents would not only be of great educational and academic interest, but would offer valuable information in respect to career development. One of SASM’s goals is to promote scholarly Pressure high (52%) BMI above 35 (15%) Age above 50 (68%) activities for residents and junior faculty. Each year SASM recognizes best abstracts in clinical and basic science research by giving out six abstract awards. In addition, SASM is offering a $20,000 research grant in 2014. Neck size above 40 (24%) Gender male (41%) Realizing the large role that SASM can play in the education of anesthesiologists through its online and in print educational material, as well as information presented during its Annual Meeting immediately preceding the ASA Annual B Meeting. SASM has a departmental universal membership covering all staff (including anesthesiologists, CRNAs, AAs A G and other physician extenders) for a much reduced fee of $1,000, and all residents for an N additional fee of $600, to cover basic administrative costs.

Some of the membership benefits include: We queried Vanderbilt University’s Perioperative Data Warehouse to identify diagnostic trends and risk factors associated with obstructive sleep apnea (OSA) after receiving approval from our institutional review board. Preoperative evaluations were identified for 173,583 • Receive discounted registration fees for SASM Annual CME Meeting patients evaluated between 1/1/2000 and 11/16/2013 in the Vanderbilt Preoperative Evaluation Center (VPEC) where the presence or • Learn of collaborative research projects absence of OSA was documented. These data were divided by year and are displayed as a percentage of patients seen each year with an established diagnosis of OSA at the tie of preoperative evaluation. VPEC implemented an electronic STOP-BANG screening tool1 in • Access to educational material, featured articles, literature updates 3/2013. Preoperative evaluations were identified for 8,955 patients evaluated between 3/2013 and 11/16/2016 that took place in VPEC • A forum to evaluate and discuss the latest research where the STOP-BANG screening tool was fully completed and patients did not have a diagnosis of OSA. The proportion of patients with a STOP-BANG score of 5 or greater was calculated. The prevalence of each risk factor in this population was determined, and is shown • Education and clinical practices pertaining to sleep-disordered breathing Membership with patient icons that each represent 10% of that population. • Advice and counsel from members regarding various practice paradigms Info! References • Enhance your network of regional, national and international colleagues 1. Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y: High STOP-BANG score indicates a high probability of obstructive • Access to the SASM newsletter sleep apnoea. Br J Anaesth 2012; 108: 768-75. Membership can be applied for online, please visit the SASM website www.sasmhq.org Infographic created by Jonathan P. Wanderer, Medical Director, Vanderbilt Preoperative Evaluation Center, Associate Medical Director, Vanderbilt Anesthesiology & Perioperative Informatics Research Division, Instructor, Department of Anesthesiology, Vanderbilt Univer- sity School of Medicine, [email protected]. Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 15 4th Annual Meeting • Hotel Monteleone, New Orleans, LA October 9-10, 2014 • Schedule of Events

Thursday, October 9, 2014 Time Topic Moderator 1:00 - 1:05 pm Welcome Peter Gay, MD 1:05 - 3:00 pm Anesthesia Safety • Pain and Disrupted Sleep - A Bidirectional Relationship Bhargavi Gali, MD David Hillman, MD • Can Dexmedetomidine Replace Opioids? Mervyn Maze, MB, ChB • Carotid Body Chemoreceptor Function and Relationship to Anesthetic Agents Malin Fagerlund, MD, PhD • Is There An Ideal Anesthetic Regime for OSA? Matthias Eikermann, MD, PhD • The Mechanisms Underlying Long-term Memory Deficits After Anesthesia Beverley Orser, MD, PhD • Discussion/Q&A 3:00 - 3:25 pm Break 3:25 - 5:00 pm Workshop: Postoperative Monitoring & Non-Invasive Ventilation Respiratory Rate, Acoustic Monitor, Minute Ventilation, Expired CO2 Stavros Memtsoudis, • Respiratory Rate: Plethysmography vs. Acoustic Monitor MD, PhD Scott Kelley, MD vs. Michael Ramsay, MD • Minute Ventilation vs. Expired CO2 Monitoring Evan Pivalizza, MBChB, MD vs. Satya Krishna Ramachandran, MD • Discussion/Q&A 5:00 - 6:00 pm How to Do PAP Therapy: Michael Pilla, MD • AVAPS, Trilogy - Lisa Wolfe, MD • ASV, VPAP Adapt – Peter Gay, MD • Discussion/Q&A 6:00 - 6:30 pm Welcome Reception 6:30 - 8:30 pm Dinner 6:30 - 6:35 pm Welcome and Introductions Frances Chung, 6:35 - 6:45 pm IARS President Address – Denise Wedel, MD MB BS 6:45 - 7:30 pm Dinner Followed by Additional Speakers 7:30 - 8:00 pm Propofol: Murder, Mayhem and Mercy - Steven Shafer, MD 8:00 - 8:30 pm Zero by 2020: Time to Co-Operate - Joe Kiani, EEE Friday, October 10, 2014 7:00 - 7:55 am Registration and Continental Breakfast 7:15 - 7:55 am Annual General Meeting 7:55 - 8:00 am Welcome Frances Chung, MB BS Moderator: Peter Gay, MD 8:00 - 8:50 am Keynote: How New Technologies Will Impact Patient Safety Mark Warner, MD 8:50 - 9:30 am Keynote: Predicting Safety Hazards - MEWS, PEWS, SCHMEWS Tim Morgenthaler, MD 9:30 - 10:00 am Life Threatening Respiratory Events Lorri Lee, MD 10:00 - 10:15 am Q & A 10:15 – 10:45 am Refreshment Break and Poster Viewing

16 Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 4th Annual Meeting • Hotel Monteleone, New Orleans, LA October 9-10, 2014 • Schedule of Events

Friday, October 10, 2014 (continued) Moderator: Babak Mokhlesi, MD 10:45 - 11:10 am The Obstructive Sleep Apnea Phenotype Atul Malhotra, MD 11:10 - 11:35 am Preoperative Red Flags and Preparation of Patients with OSA Amy Guralnick, MD 11:35 am - Rational Pain Management in the Patient with Sleep Disordered Breathing Girish P. Joshi, MBBS 12:00 pm 12:00 - 12:15 pm Q & A 12:15 - 1:15 pm Lunch Break and Poster Viewing 1:15 - 1:45 pm Awards to Research Grant and Scientific Abstracts Winners Frances Chung, MB BS Presentations from Research Grant and Best of Abstract Winners Anthony Doufas, MD, PhD Moderator: Roop Kaw, MD 1:45 - 2:10 pm Should Upper Airway Surgery be Done as an Outpatient Surgery? Tucker Woodson, MD 2:10 - 2:35 pm Predicting Cardiac Arrest on the Wards: Past, Present and Future Matthew Churpek, MD, PhD 2:35 - 2:45 pm Q & A 2:45 - 3:15 pm Refreshment Break and Poster Viewing Moderator: Dennis Auckley, MD 3:15 - 3:40 pm Pregnancy and Obstructive Sleep Apnea Ellen Lockhart, MD 3:40 - 4:05 pm Adenotonsillectomy Outcomes in Treatment of Obstructive Sleep Apnea in Rakesh Bhattacha- Children rjee, MD 4:05 - 4:25 pm Guidelines for Perioperative Management of Patients with OSA Tracey Stierer, MD 4:25 - 4:45 pm Perioperative CPAP: Is It Efficacious? Frances Chung, MB BS 4:45 - 5:00 pm Q & A 5:00 pm i-Pad Giveaway and Closing Remarks Peter Gay, MD Invited Faculty

Dennis Auckley, MD Malin Fagerlund, MD, PhD Scott Kelley, MD Stavros Memtsoudis, MD, Michael Ramsay, MD MetroHealth Medical Center Karolinska Institutet and Covidien PhD Baylor University Medical Karolinska University Weill Cornell Medical College Center Rakesh Bhattacharjee, MD Joe Kiani, EEE University of Chicago Bhargavi Gali, MD Masimo Corporation Babak Mokhlesi, MD Steven Shafer, MD Mayo Clinic University of Chicago Stanford University Frances Chung, MB BS Lorri Lee, MD University of Toronto Peter Gay, MD Vanderbilt University Tim Morgenthaler, MD Tracey Stierer, MD Mayo Clinic Mayo Clinic John Hopkins University Matthew Churpek, MD, PhD Ellen Lockhart, MD University of Chicago Hospitals Amy Guralnick, MD Washington University School Beverley Orser, MD, PhD Mark Warner, MD University of Chicago of Medicine University of Toronto Mayo Clinic Anthony Doufas, MD, PhD Stanford University School of David Hillman, MD Atul Malhotra, MD Michael Pilla, MD Denise Wedel, MD Medicine Sir Charles Gairdner Hospital University of California, San Vanderbilt University Mayo Clinic Diego Matthias Eikermann, MD, Girish P. Joshi, MBBS Evan Pivalizza, MBChB, MD Lisa Wolfe, MD PhD University of Texas Mervyn Maze, MB, ChB University of Texas Health Northwestern University Massachusetts General Southwestern Medical Center University of California, San Science Center - Houston Feinberg School of Medicine Hospital Francisco Roop Kaw, MD Satya Krishna Tucker Woodson, MD Cleveland Clinic Ramachandran, MD Medical College of Wisconsin University of Michigan Medical Center Society of Anesthesia & Sleep Medicine w Volume 3 w Issue 2 w 2014 17 SASM Membership Benefits at a Glance…

hese are exciting times for SASM. While we are a new and growing organization, we feel our collaborative efforts will President give rise to unlimited opportunities. You have the ability to make an impact from the very start. Please consider join- Frances Chung, MBBS T University of Toronto ing SASM today! University Health Network Toronto, ON Canada The mission of SASM is to advance standards of care for clinical challenges shared by Anesthesiology and Sleep Medicine, President-Elect including perioperative management of sleep disordered breathing, as well as to promote interdisciplinary communication, Peter Gay, MD education and research in matters common to anesthesia and sleep. Mayo Clinic Rochester, MN USA Secretary Benefits of SASM Membership include: Babak Mokhlesi, MD • Significantly Reduced Registration Fees at SASM Sponsored Scientific Meetings University of Chicago Pritzker School of • SASM Newsletter Medicine • *Full Voting Rights in Electing SASM Board of Directors and SASM Officers Chicago, IL USA (*Dependent on membership category) Treasurer • Regular Receipt of “Literature Updates” and “Featured Articles,” Allowing All Members to Stay Current on New Girish P. Joshi, MBBS, MD, FFARCSI, Developments in theArea MBBS, MD, FFARCSI • Enhances Your Network of Regional, National and International Colleagues University of Texas Southwestern Medical School • Learn of Collaborative Research Projects Dallas, TX USA • Educational Material Posted on SASM Website for Members • Access to a “Discussion Forum” to Evaluate and Discuss the Latest Research, Education and Clinical Practices Per- Past President David Hillman, MBBS taining to OSA and Patients with Other Sleep-Disordered Breathing Sir Charles Gairdner Hospital • Get Advice and Counsel from Other Members Regarding Various Practice Paradigms Perth, Western Australia Directors The easiest and quickest route to join as a member of SASM is to visit our website, www.SASMhq.org, and pay by credit card by clicking on the Membership Information tab. You can also mail check payment to our office at the address provided Dennis Auckley, MD MetroHealth Medical Center below. Bay Village, OH USA Bhargavi Gali, MD SASM Classes of Membership: Mayo Clinic q Gold Patron Member - $250 Rochester, MN USA • Showing special support for SASM Roop Kaw, MD • This donation is inclusive of annual membership and avail- Cleveland Clinic Lerner College of able for all classes of membership. Medicine Cleveland, OH USA q Active Member - $100 Mervyn Maze, MB, ChB University of California, San Francisco • Physicians and Scientists. Active Members have voting San Francisco, CA USA rights, can hold office and serve on the Board of Directors. SASM Committees q Associate Member - $50 Clinical • Non-Physicians and Non-Scientists. Associate Members do Chair, Dennis Auckley, MD NOT have voting rights. Co-Chair, Bhargavi Gali, MD Conference & Education q Educational Member - $50 Chair, Peter Gay, MD • Fellows, Residents, Medical Students or other undergraduates. Co-Chair, Girish P. Joshi, MBBS, MD, Educational Members do NOT have voting rights. FFARCSI, MBBS, MD, FFARCSI Finance Please consider joining as a “Gold Patron” for 2014 Chair, Girish P. Joshi, MBBS, MD, FFARCSI, MBBS, MD, FFARCSI The additional donation beyond general membership will be used to promote scholarly activity in the area of anesthesia and sleep medicine and promote patient care programs in areas common to anesthesia and sleep medicine. Gold Patrons Membership will be recognized on our website for their extraordinary support of SASM efforts and will be invited to special events Chair, Stavros Memtsoudis Weill Cornell Medical College highlighting the programs made possible with their donations, including a keynote speaker dinner at the Annual Meeting. New York, NY USA Co-Chair, Babak Mokhlesi, MD SASM - NEW OFFICE LOCATION! 6737 W Washington Street, Suite 1300 Nominating Milwaukee, Wisconsin 53214 Chair, David Hillman, MBBS Research SASM is a 501(C)(3) non-profit organization. Membership dues may be deductible as a business expense. SASM Tax ID Chair, Roop Kaw, MD number is 27–4613034 SASM Subcommittees Abstract Chair, Anthony Doufas, MD Stanford University School of Medicine Stanford, CA USA Newsletter OSA Database Pediatric Scientific Update Communication Chair, Satya Krishna Chair, Norman Bolden, MD Chair, Kimmo Murto , MD, Chair, Susana Vacas, MD Chair, Michael Pilla, MD Ramachandran, MD MetroHealth Medical Center FRCPC University of California, San Vanderbilt University University of Michigan Medical Solon, OH USA Children’s Hospital of Eastern Francisco Nashville, TN USA Center Ontario/University of Ottawa San Francisco, CA USA Ann Arbor, MI USA Ottawa, ON Canada