Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Modern upper airway reconstructive surgery has a significant role in the treatment of adult obstructive sleep apnoea
- Sam Robinson (5 January 2008)
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Claim that modern upper airway surgery is as effective as CPAP to prevent death and cardiovascular morbidity in obstructive sleep apnoea
- Arthur Dawson (7 January 2008)
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Author reply to Sam Robinson
- Adam G Elshaug, John Moss (JEH and GJM are currently enjoying annual leave) (7 January 2008)
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Change?
- Edward M. Weaver (8 January 2008)
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Sam Robinson's reply to Adam Elshaug
- Sam Robinson (8 January 2008)
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No problem; no change
- Neville Shine (9 January 2008)
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In Agreement, BUT...
- Kent E. Moore, M.D., D.D.S. (11 January 2008)
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Sleep Surgery Survival Study - Clarifications
- Edward M. Weaver (11 January 2008)
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Sleep Surgery Cardiovascular Outcomes Study - Clarifications
- Edward M. Weaver (11 January 2008)
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Therapeutic nihilism
- Edward M. Weaver (11 January 2008)
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Elshaug et al. reply
- Adam G Elshaug, Assoc Prof John R Moss (22 January 2008)
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Sam Robinson, Senior Visiting ENT Surgeon Flinders Medical Centre & Memorial Hospital, Adelaide, South Australia, 5006
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While I agree with Elshaug et al that upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults, I do not agree that surgery should be restricted to controlled clinical trials. From a patient perspective, the principle issues are to control symptoms and minimize the risk of premature death. Substantial evidence in the literature supports value in surgery when these clinically relevant endpoints are used. Pecker et al showed equally large reductions in cardiovascular disease over a 7 year period in a surgically treated cohort, when compared to CPAP(Continuous airway pressure) or MAS (Mandibular advancement splint) treatments (1). Weaver compared 20,000 U.S. veterans treated with CPAP or surgery adjusting for multiple co-morbidities (2). Surgery produced a 3 year survival advantage over CPAP in a population with a high likelihood of inadequate nasal CPAP use. In a paper presented to the Australian Society of Otolaryngology, Head and Neck Surgery Annual Scientific Meeting 2007, my own series of 64 consecutive multilevel surgical patients was matched to 73 consecutive CPAP patients with a 3 year follow up. There was no difference between the groups when measuring global quality of life, daytime sleepiness or snoring control. Assessment utilized validated questionnaires. There is no clear evidence that achieving an RDI < 5 is necessary to effectively treat sleep apnoea. Significant variation in equipment and data interpretation between sleep laboratories exists, and there is ongoing debate about what constitutes a clinically significant level of disease. (3,4) Using the RDI as a sole outcome measure is misleading when comparing treatment with a device (CPAP or MAS) to surgical treatment. The devices offer good control when used, but may only be worn part of the sleep time, whereas surgery is applied to the total sleep time, but may have a lesser impact on the RDI. The “area under the curve” of efficacy x compliance is the critical issue, but has not been addressed by Elshaug et al. Obviously the devices offer no clinical benefit if not used, and use for only part of the sleep time is more common than full time use (5). Adult sleep apnoea is a prevalent condition with significant associated individual and public health risks. Whilst CPAP is the first line treatment, modern reconstructive airway surgery has a important role in clinical practice, and its use is supported in the literature. REFERENCES: 1.Pecker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7 year follow-up. Am J Respir Crit Care Med. 2002 Jul;166(2):159-65. 2.Weaver EM, Maynard C and Yueh B. Survival of veterans with sleep apnea: Continuous positive airway pressure versus surgery. Otolaryngol Head Neck Surg 2004;130:659-65. 3.Banks S, Barnes M, Tarquino N, Pierce RJ, Lack LC, McEvoy RD. Factors associated with maintenance of wakefulness test mean sleep latency in patients with mild to moderate obstructive sleep apnoea and normal subjects. J Sleep Res, 2004;13:71-782. 4.Aguirregomoscorta J I, Altube L, Menendez I, Romani A, Basualdo L V, Vallejo G. Comparison between the 1993 and 2002 Guidelines of the Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) for identifying respiratory events in polysomnography tests (Comparacion entre las normativas de la SEPAR de 1993 y 2002 en la lectura de los eventos respiratorios de las mismas polisomnografias).Archivos de bronconeumologia (Spain), Dec 2005;41(12):649-53 5.Powell N. Upper airway surgery does have a major role in the treatment of obstructive sleep apnea: “the tail of the dog.”J Clin Sleep Med 2005;1:236-40 Competing interests: None declared |
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Arthur Dawson, Senior Consultant, Scripps Clinic Sleep Center 10666 North Torrey Pines Road, La Jolla, CA 92037, USA
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Mr Robinson, in his response to Elshaug et al, concedes that upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults. However, he cites 2 references that suggest that upper airway surgery is as effective, or even more effective, than CPAP to prevent cardiovascular morbidity and death. Careful reading of the 2 articles shows that this conclusion is unjustified. The study of Peker et al included only 14 patients treated with CPAP, 22 with uvulopalatopharyngoplasty (UPPP) and 4 with an oral device. Of the CPAP patients, 64 percent did not adhere to treatment and only one subject with an oral appliance was considered “efficiently treated”. With such small numbers of subjects any statement about the relative efficacy of the therapies is meaningless. In the study by Weaver et al, CPAP was the therapy in 90 percent of the 20,000 US veterans while only 10 percent were treated with UPPP. While an attempt was made to adjust for confounding factors, they were not able to adjust for severity of sleep apnoea or for adherence to CPAP. It is highly likely that CPAP was the preferred treatment on those with more severe sleep apnoea and so the conclusion that UPPP confers a survival advantage over CPAP seems unwarranted. As Powell pointed out in the article cited, adherence to therapy is an “issue swept under the rug by sleep medicine”. In the patient who does not use CPAP a better outcome can be expected even with a partially effective surgical procedure where adherence is guaranteed. Competing interests: None declared |
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Adam G Elshaug, Hanson Institute Research Fellow and Lecturer School of Population Health and Clinical Practice, The University of Adelaide, SA, 5005, Australia, John Moss (JEH and GJM are currently enjoying annual leave)
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We thank Dr Robinson for his interest in our Change Page (1) and offer the following in reply to his rapid response dated 5 January, 2008. 1. The recommendation made in our Change Page that surgery should be restricted to controlled clinical trials echoes those made in the most recent Cochrane review in this area (2). We support this recommendation as we believe it will contribute to best evidence-informed practice. 2. For those interested in sourcing the original paper (3), please note the author spelling is ‘Peker’, not ‘Pecker’ as reported by Dr Robinson in his rapid response. This research by Peker et al. offers an important contribution to this area and we believe supports our Change Page entirely. Peker et al. did report equally large reductions in cardiovascular disease (CVD) over a 7 year period in a surgically treated cohort. However, there are some other important points from that study: 1) “When OSA was incompletely treated, the independent risk for CVD turned out to increase up to 11- fold, whereas efficient treatment of OSA significantly reduced this excess risk for CVD in OSA patients” (pg.163). So, CVD reductions were evident ONLY in those who received ‘efficient’ treatment (with surgery, CPAP or MAS) and, 2) in this study “approximately 50% of subjects undergoing UPPP still had OSA at the follow-up recording” (pg. 162) meaning they were inefficiently/ineffectively treated with UPPP alone. 3) There was cross- contamination of treatment where “during follow-up, treatment of OSA was initiated with CPAP (n=14) AND/or UPPP (n=22) AND/or oral device (n=4)” (pg 162) meaning surgery recipients may also have received CPAP treatment during follow-up. 4) Given the sample sizes one needs to be observant to statistical power and, 5) UPPP recipients had milder OSA to start with. In summary, therefore, like Peker et al. we support any efficient or effective surgical intervention and believe this is likely to improve health outcomes. However, the thrust of our Change Page is that, unfortunately, the proportion who receive an optimal outcome from a surgical approach is low and inconsistent and less than can be achieved by other means, as is elegantly presented by Peker et al. and many others. 3. Dr Robinson suggests “there is no clear evidence that achieving an RDI < 5 is necessary to effectively treat sleep apnoea”. In fact evidence in this area is building. In a recent publication (4) in the journal SLEEP, AGE, JRM, JEH and another co-author present evidence from over one dozen published articles that support this. Further, this is a classification endorsed by the American Academy of Sleep Medicine (AASM) and is the primary endpoint against which CPAP is judged. 4. Similarly, the research by Weaver et al. (5) holds a notable position in the literature but it should be interpreted in the light of the following observations. I note that some of these have been highlighted by the original authors. • In the study, OSA severity data were unavailable. This,
potentially, is a confounder as it effects treatment choice and outcome
i.e. those with mild OSA are more likely to receive UPPP. CPAP use data
were also unavailable so compliance was not assessed.
5. We take this opportunity to urge all surgeons, physicians and researchers involved in such trials to randomize them and to observe and address (in their data collection phase(s), not by controlling post hoc) the many potentially confounding factors that are so commonly over-looked and excluded in these trials. These potential confounding factors are discussed in detail in a paper published in the Journal of Evaluation in Clinical Practice (6). 6. We agree that ‘efficacy x compliance’ is an important consideration, and those interested to read the cited reports in our Change Page will gain an appreciation of this. We also direct interested readers to a policy discussion paper (7; free access online) where several of us include for discussion surgery for OSA as a case study. What remains unavoidable is that surgery is resource intensive; involving multiple visits to physicians, surgeons, overnight sleep clinics (if guidelines are met), theatre and ward recovery resources etc. This is particularly so given that modern reconstructive surgery most commonly involves multiple stages/operations over a period of time – which a substantial proportion of patients will not endure but drop out from (6). Our collective work in this area appreciates the potential for opportunity costs. This concept has been expressed thus by others, “Since resources are scarce relative to needs, the use of resources in one way prevents their use in other ways. The opportunity cost of investing in a healthcare intervention is best measured by the health benefits that could have been achieved had the money been spent on the next best alternative intervention or healthcare programme” (8) One brief example to illustrate this comes from a teaching hospital (Sydney, Australia): RCT; n=100; comparing CPAP initiation on ‘treatment as usual’ with ‘treatment X’. Results: 30% ‘failed’ CPAP with treatment as usual, while only 8% ‘failed’ CPAP with ‘treatment X’. What was treatment X? Answer: Two 1-hour Cognitive Behaviour Therapy (CBT) sessions (including a video of real CPAP users) plus treatment as usual (mask fitting and information) (9). Directing resources toward weight control initiatives is another option, particularly as it focuses on a primary risk factor for OSA and many other morbidities. Adam Elshaug and John Moss (Professors Hiller and Maddern are currently enjoying annual leave) References: (1) Elshaug AG, Moss JR, Hiller JE, Maddern GJ. Upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults. British Medical Journal, 2008; 336(7634): 44-45. doi:10.1136/bmj.39381.509213.AE (2) Sundaram S, Bridgman SA, Lim J, Lasserson TJ. Surgery for obstructive sleep apnoea. Cochrane Database Syst Rev 2005;(4):CD001004. (3) Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7 year follow-up. Am J Respir Crit Care Med. 2002; 166(2):159-65. (4) Elshaug AG, Moss JR, Southcott A, Hiller JE. Redefining success in airway surgery for Obstructive Sleep Apnea: A meta analysis and synthesis of the evidence. Sleep, 2007; 30(4): 461-467. (5) Weaver EM, Maynard C and Yueh B. Survival of veterans with sleep apnea: Continuous positive airway pressure versus surgery. Otolaryngol Head Neck Surg 2004;130:659-65. (6) Elshaug AG, Moss JR, Southcott A, Hiller JE. An analysis of the evidence-practice continuum: Is surgery for Obstructive Sleep Apnoea contraindicated? Journal of Evaluation in Clinical Practice, 2007; 13(1): 3-9. http://www.blackwell-synergy.com/toc/jep/13/1 (7) Elshaug AG, Hiller JE, Tunis SR, Moss JR. Challenges in Australian policy processes for disinvestment from existing, ineffective health care practices. Australia and New Zealand Health Policy, 2007; 4: 23 (31 October 2007). http://www.anzhealthpolicy.com/content/4/1/23 (8) Palmer S, Raftery J. Economic Notes: opportunity cost. British Medical Journal, 1999; 318(7197): 1551-1552. (9) Richards D, Bartlett D, Wong K, Malouff J, Grunstein R. Increased adherence to CPAP with a group cognitive behavioral treatment intervention: a randomized trial. Sleep 2007; 30(5): 635-640. Competing interests: None declared |
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Edward M. Weaver, Associate Professor of Otolaryngology University of Washington, 98108
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I applaud Dr. Elshaug and colleagues for critically evaluating a sample of existing evidence to strive for answers on treating the complex condition of sleep apnea. However, I have trouble understanding why Dr. Elshaug’s article appears in the BMJ Change Page (1). The Change Page aims to alert clinicians to the immediate need for a change in practice to make it consistent with current evidence. Dr. Elshaug’s thesis is “that upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults.” Currently, surgery is NOT considered first line therapy for sleep apnea in adults. Dr. Elshaug proposes the status quo, not change. Dr. Elshaug concludes that “Surgery for obstructive sleep apnoea should be done within controlled clinical trials. Patients should be informed about the trial, as well as of the inconsistent results of surgery, the associated pain, the potential side effects, and the potential for relapse.” As a sleep surgeon, I agree completely with Dr. Elshaug’s conclusions. We should try to increase the evidence base around surgical treatment (and CPAP therapy, weight loss, oral appliances, and novel new treatments). Good surgeons always advise patients that the polysomnography outcomes for surgery are difficult to predict, that surgery has potential side effects, and that there is a potential for relapse. An informed surgeon also explains to them that long-term studies support that surgery improves survival (2), appears to reduce the risk of cardiovascular disease in a significant proportion of patients (3), reduces motor vehicle crash risk (4), and tends to improve reaction times and quality of life (5). These discussions are critical in order for patients to have realistic expectations of salvage surgery as a means to improve, albeit rarely cure, their obstructive sleep apnea. None of these comments dictate a change to current practice. Edward M. Weaver, MD, MPH REFERENCES 1. Elshaug AG, Moss JR, Hiller JE, Maddern GJ. Upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults. Bmj 2008;336(7634):44-5. 2. Marti S, Sampol G, Munoz X, Torres F, Roca A, Lloberes P, et al. Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment. Eur Respir J 2002;20(6):1511-8. 3. Peker Y, Carlson J, Hedner J. Increased incidence of coronary artery disease in sleep apnoea: a long-term follow-up. Eur Respir J 2006;28(3):596-602. 4. Haraldsson PO, Carenfelt C, Lysdahl M, Tingvall C. Does uvulopalatopharyngoplasty inhibit automobile accidents? Laryngoscope 1995;105(6):657-61. 5. Woodson BT, Steward DL, Weaver EM, Javaheri S. A randomized trial of temperature-controlled radiofrequency, continuous positive airway pressure, and placebo for obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg 2003;128(6):848-61. Competing interests: None declared |
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Sam Robinson, ENT surgeon Memorial Hospital and Flinders Medical Centre, Adelaide, SA 5006 AUSTRALIA
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I welcome the opportunity to debate the issues raised with Dr Elshaug in his articles and subsequent rapid response dated 7th January. It should be noted that the views of Dr Elshaug and co- authors are at odds with current practice guidelines for the American Sleep Disorders Association, which support the use of upper airway surgery for adult obstructive sleep apnea when the devices (CPAP or MAS) are ineffective or rejected(1). I would like to address several issues covered in his reply: 1. Compliance with devices Until the rapid response of 7th January, Elshaug et al have not acknowledged in the text of any their articles the central issue of the area under the curve of efficacy x compliance, in comparing devices to surgical treatment of sleep apnoea. I commend them for now doing so. However, I am at a loss to explain why Dr Elshaug still interprets the Peker article (2) as supporting his view that “the proportion who receive an optimal outcome from a surgical approach is low and inconsistent and less than can be achieved by other means”. Peker found that efficient treatment from compliance of > 50% sleep time was achieved in only 36% of CPAP patients, and 25% of MAS patients. This compares to 50% of surgical patients (having only the simple intervention of UPP) achieving a > 50% reduction in RDI (i.e. the same area under the curve as CPAP or MAS, assuming full control of OSA when the device worn). I agree that efficient treatment of OSA with any modality is likely to lead to important health outcomes. In the Peker article, this was clearly more frequent in the surgical group than those treated with devices due to compliance issues. This does NOT mean that I am advocating treatment with surgery as first line. Elshaug et al have never produced any evidence to suggest that there is widespread surgery being performed as initial treatment instead of trialling CPAP or MAS first (which would be in breach of current practice guidelines (1)). Clearly, surgery has risks of post operative complications which don't apply to noninvasive treatments. However, the Peker article (and many others) show the dangers of leaving patients with significant sleep apnoea untreated when the devices are ineffective or not worn. In this situation, current guidelines dictate that stepwise surgery be offered to the patient, after advising the patient the likelihood of the success of each procedure and that possibility of multiple operations to achieve an acceptable outcome. 2. The perceived need to achieve an RDI < 5 with surgery Dr Elshaug claims that more than a dozen articles cited in his Sleep article (3) support his contention that achieving an RDI<5 is necessary with all treatment modalities. Let's look at the “landmark paper” (4) he quotes as the prime example in his paper in support of this. In this, Becker et al looked at the effect of therapeutic CPAP versus subtherapeutic CPAP on blood pressure control. If one looks at the true treatment effect for the whole night (i.e. area under the efficacy x compliance curve), the calculations are as follows: assuming the recommended 8 hours nightly sleep, then in the therapeutic CPAP group the RDI is 3.4 x 5.5 hours + 62.5 x 2.5 hours = 174.95 respiratory events/night = effective RDI of 21.9/hour. For the subtherapeutic group the RDI is 33.4 x 5.4 hours + 65 x 2.6 hours = 249.4 respiratory events/night = effective RDI of 43.7/hour. The current most widespread outcome measure using RDI applied to surgery is RDI < 20 (+/- > 50% total RDI reduction). As surgery is always applied 100% of sleep time, achieving an RDI < 20 with surgery is actually BETTER than the average therapeutic CPAP effect for the whole sleep time if applied 5.5 hours a night (as in this paper). I reiterate there is no clear evidence that mandates achieving an RDI < 5 as essential for surgery to be a useful intervention, and none of the papers he quotes establish his case. Furthermore the changing guidelines on measurement techniques and scoring criteria for polysomnography have made interpreting the literature even more difficult, and reliance on a single parameter such as the RDI more uncertain. Normative data of asymptomatic controls in one of our local sleep laboratories using pressure transducers to measure hypopnoeas yielded an RDI of 6.1 + 7.2 (mean + 2 SD), thus a pathological threshold of >15 (5). Other groups have demonstrated the need to adjust thresholds of disease upwards using the new measurement practices, although as Dr Elshaug correctly states, the Chicago criteria are still applied in the American Academy of Sleep Medicine guidelines. There is much active work happening to standardize polysomnography. Until the picture becomes clearer, it seems illogical to suggest that surgery must achieve an RDI below that of asymptomatic controls to be efficacious! Given that all of Dr Elshaug’s publications make the underlying assumption that an RDI < 5 be achieved to define surgical success, I find his conclusions unconvincing. 3. Surgery analyzed Elshaug et al correctly state that multilevel reconstructive upper airway surgery may involve multiple steps. Superior outcomes to [not "of", as originally posted] single level intervention (e.g. UPP alone) has been shown in a metanalysis(6). In subsequent reports, such as that of Nuruntarat the mean RDI for all patients fell from 47.9 + 8.4 pre-op to 18.6 + 4.1 at 3 years (N=46) equating to a response rate of 65% maintaining a RDI<20 long term (7). The article quoted to suggest a high dropout rate from a step wise protocol is poorly designed(8). The definitions of Phase 1 and Phase 2 are wrong and additional categories of operation are created for synonyms. As usual for Elshaug et al's publications, no ENT surgeon had input in the content of the paper. Personal communication (2007) with surgeons working at the institutions at which the surgery was performed reveals extended waiting times for sleep studies after surgery, and also long waiting lists for further steps in the stepwise protocol. The period of analysis therefore is likely to have missed many patients having further steps. Analyzing poorly performing institutions does not help to demonstrate the effectiveness or otherwise of contemporary upper airway surgery, so no conclusion can be drawn from this paper. I agree that surgery is resource intensive, but nevertheless appropriate in correctly selected patients. 4. What is the alternative to surgery? The compliance with CPAP has not changed substantially for many years. It is somewhat naive to pin the hopes of OSA sufferers on a single trial of cognitive behavioural therapy(9) as being the answer to those who cannot tolerate CPAP. Funding for upper airway surgery certainly does not need to be reduced to initiate this strategy in any case, as the cost is trivial compared to the investment of the patient and/or the health care provider in CPAP equipment costs over the lifetime of the patient. Mandibular advancement splints are variably effective, and compliance is again variable. In short, Elshaug and colleagues offer no alternative to the patient who cannot tolerate a device. The real motivation for articles by this group has been revealed in the last few paragraphs of his response. Justifying reduction in health care costs by reducing services using flawed analysis may be good politics. However let's not pretend that removing viable treatment options is to the patient's benefit! 1) Practice parameters for the treatment of obstructive sleep apnea in adults: the efficacy of surgical modifications of the upper airway. Report of the American Sleep Disorders Association. Sleep 1996 Feb;19(2):152-5 2) Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7 year follow-up. Am J Respir Crit Care Med. 2002 Jul;166(2):159-65. 3) Elshaug AG, Moss JR, Hiller JE, Maddern GJ. Upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults. BMJ 2008;336:44-45. 4) Becker H, Jerrentrup A, Ploch T, et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003;107:68-73. 5) Banks S, Barnes M, Tarquino N, Pierce RJ, Lack LC, McEvoy RD. Factors associated with maintenance of wakefulness test mean sleep latency in patients with mild to moderate obstructive sleep apnoea and normal subjects. J Sleep Res, 2004;13:71-782. 6) Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996;19(2):156-77 7) Neruntarat C. Genioglossus advancement and hyoid myotomy: short- term and long-term results. J Laryngol Otol. 2003;117(6):482-6 8) Elshaug AG, Moss JR, Southcott A, Hiller JE. An analysis of the evidence-practice continuum: is surgery for obstructive sleep apnoea contraindicated? J Eval Clin Pract 2007;13:3-9. 9) Richards D, Bartlett D, Wong K, Malouff J, Grunstein R. Increased adherence to CPAP with a group cognitive behavioral treatment intervention: a randomized trial. Sleep 2007; 30(5): 635-640 Competing interests: None declared |
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Neville Shine, ENT / Head & Neck Surgeon St James's Hospital, Dublin, Ireland
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The alleged clinical problem addressed by Elshaug on the Change page is one that simply does not exist. Where is the evidence that surgeons are performing surgery as first line treatment for obstructive sleep apnoea syndrome (OSAS)? Whilst surgery for OSAS may be increasing (though I am not convinced by his references that it universally is), one cannot infer from this that surgeons are ignoring CPAP as the primary treatment modality for OSAS. CPAP is widely accepted by the surgical community as well as the medical community as being the first line of treatment for OSAS. Any increase in surgeries performed for OSAS may be due to the recent increase in the numbers of patients diagnosed with OSAS due to improved availability and accessibility of diagnostic facilities and improved recognition of this entity by primary care physicians, amongst others. More patients with OSAS means more patients treated with CPAP, and inevitably more CPAP failures. It well acknowledged that CPAP, whilst the “gold standard”, is not universally acceptable to all patients and that up to 30% of patients (even those who experience a good sympotomatic response to treatment) will fail to tolerate CPAP in the medium to long term. A further non-reported cohort of patients refuse CPAP treatment from the off. These are the patients who should be considered possible surgical candidates. For the sake of completeness however, I do have a few specific comments: 1. The Cochrane Database is selectively quoted thus introducing a bias into the article. The Cochrane review of Surgery in OSAS is quite correctly alluded to and referenced. However the authors continue to recommend lifestyle modifications which have also been subject to a Cochrane review with no randomised trial data to support these recommendations. Consistency is necessary 2. The argument for surgery to be only performed within the context of a controlled clinical trial shows a significant lack of insight into the challenges facing the clinician who interacts on a daily basis with the individual patient. Randomized controlled trials are the accepted gold standard and the ideal to aspire to but such trials are extremely difficult to perform in surgery. Obviously the surgeons ability, equipoise and willingness to participate are important. The patients’ preference may be a significant stumbling block in recruitment and blinding patients would prove problematic. What would the surgery be compared to? These patients should all be CPAP failures. Is comparison to sham surgery ethical? Should it be compared to no surgery in order to control for regression to the mean? Or should surgical procedures be compared to each other? If so which ones? And finally, whilst the sweeping statement that surgery should only be performed in a controlled trial setting (a sentiment shared by the Scottish Intercollegiate Guidelines Network) sounds great, who will fund these studies? They require time and money. In the meantime, patients who may benefit from surgery (and yes I believe they do exist) may be denied potentially beneficial therapy. 3. The final sentence in the article suggests what we, as surgeons, should discuss with our patients preoperatively. The vast majority of surgeons (one can never say always in medicine) will discuss the risks, complications and sequelae of each and every operation they perform with each and every patient. The risks of not performing the operation and the possible benefits to the patient are also discussed. This is not only the typical surgeons routine but in most jurisdictions it represents informed consent which is both ethically and legally necessary to proceed! The role of the surgeon in adult OSAS remains to be fully elucidated. Interestingly, the “gold standard” for paediatric OSAS is adenotonsillectomy and has now become the most common indication for this procedure. And yet the Cochrane review regarding this treatment stated that “ this review did not find any evidence from randomised trials to support the use of adenotonsillectomy for sleep apnoea in children”. So we accept a lesser standard of evidence supporting surgery in our children than in adults for the same disease process. The reality is that the majority of surgical procedures do not have Level 1 evidence and to select out adult OSAS surgery to be only performed in a trial setting is probably not an achievable goal. Competing interests: None declared |
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Kent E. Moore, M.D., D.D.S., Oral & Maxillofacial Surgeon Charlotte, N.C. 28204
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At the risk of this turning into a personal clinical discussion, as an Oral & Maxillofacial Surgeon, several statements mentioned in the above discussions bear additional emphasis and/or consideration: 1) Of the three basic treatments for OSA: CPAP, oral appliances, and surgery- none of these modalities is perfect- each has problems. The trick is finding the therapy that the individual patient can tolerate, comply, and live with. 2) Not all surgical procedures for treatment of OSA are the same; it is not appropriate to group all surgical procedures for this disorder together. Discerning who to perform what procedure on is a challenge to any surgeon or team of surgeons. The goal should be to perform the most efficacious, therapeutic and beneficial procedure(s) for a given patient’s specific anatomic problem under as few anesthetic procedures as possible. 3) Published compliance data for oral appliances appears to be either equal to or superior to CPAP. 4) As Dr. Shine so eloquently points out above, surgeons are limited in their ability to produce Level I data (as is seen in the CPAP and oral appliance literature). Prospective, randomized, controlled surgical trials cannot ethically or easily be performed in humans. Do we therefore deny surgical therapy because we lack data that we will never be able to obtain? 5) In most cases, patients undergoing surgical treatment for OSA undergo more than one procedure under the same anesthetic (most patients don’t want to undergo serial procedures for this disorder); this confounds the data related to treatment effect from any one specific procedure. 6) Dropout from treatment failure is a reality (multistep surgery equates to a significant number of patients dropping out prior to receiving needed therapy); As only one example, I am frustrated all too often by patients with significant OSA who have undergone (and failed) previous soft palate surgery who clearly would have benefitted initially from Maxillomandibular advancement (these patients all too often drop out because of pain, expense, and poor clinical result). In addition to the difficulties and side-effects as stated within the article, these patients are at risk of development of velopharyngeal incompetence as a result of having a surgically shortened palate following upper jaw advancement surgery. Given the known medical literature, in these patients, upper and lower jaw advancement as an initial treatment option may well have been a better initial treatment (most patients following initial jaw advancement will not need subsequent soft palate surgery- saving them from the trauma and side effects of this treatment). Please don’t get me wrong- I am very appreciative and supportive of my Otolaryngology colleagues (much of the surgical research being performed for this disorder is due to their efforts), and Maxillomandibular advancement is definitely NOT for everyone. While the published data referred to by Dr. Robinson is impressive (soft palate surgery certainly has its place)- but from a maxillofacial perspective soft palate surgery may well be currently being performed far too often- and with too many side-effects. 7) The majority of the surgical literature (and new surgical trials) related to treatment of OSA is found within the Otolaryngology literature; the Oral & Maxillofacial literature is not as widely read, and has fewer trials and patient cohorts. Effect size, however, with maxillofacial surgery- is large. 8) While controlled trials for treatment of this disorder would be of benefit (too many new and experimental procedures are being performed without the patients being made aware of the experimental nature of these procedures), I agree, however, with Dr. Shine’s and Weaver’s comments. Performance of proper prospective multidisciplinary clinical trials is something yet to be achieved. We have recently established the International Surgical Sleep Society as a method for professional interaction, education, and interaction amongst various surgical specialties as relates to surgical therapy for this disorder. It is our hope that increased communications between the various surgical disciplines will be of benefit ultimately to the patient suffering from this disorder. Competing interests: None declared |
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Edward M. Weaver, PI, Sleep Apnea Research Group University of Washington, Seattle, WA 98108
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Dr. Elshaug offered comments to refute my survival study (1) in his Author reply to Sam Robinson. Clarifications are in order. This study compared long-term survival with two treatments for sleep apnea: continuous positive airway pressure (CPAP) therapy or surgery in a large cohort (N=20,826) of sleep apnea patients. Surgery patients had better survival than all-comer CPAP patients, after adjusting for age, gender, race, year of treatment, and comorbidity (1). We were unable to draw conclusions about the relative benefits of surgery compared with adherent CPAP use. We concluded that surgical treatment should be considered in sleep apnea patients who use CPAP inadequately or not at all. 1) “… it should be interpreted in the light of the following observations. I note that some of these have been highlighted by the original authors.” We highlighted several of Dr. Elshaug’s observations and, moreover, explained why the results remain valid. 2) “OSA severity data were unavailable. This, potentially, is a confounder as it effects treatment choice and outcome i.e. those with mild OSA are more likely to receive UPPP.” Obstructive sleep apnea (OSA) severity data were not available for the cohort. It is speculation that surgical patients more likely had mild OSA. In fact, in a random sample of uvulopalatopharyngoplasty (UPPP) patients drawn from a related cohort, we extracted OSA severity data from medical records in a separate analysis of complications, and we found surgical patients had severe OSA on average (apnea-hypopnea index >40 events/hour and lowest oxyhemoglobin saturation <78%) (2). More importantly, it is necessary to understand how differential OSA severity might confound the association between surgery and survival outcome. Severe OSA appears to increase the risk of cardiovascular disease, which is the main cause of sleep apnea-related death (3). Thus, it is critical to adjust for comorbid cardiovascular disease (and other comorbid conditions that contribute to death). This adjustment takes into account the confounding effect of OSA severity on survival outcome. There is an exception to this explanation if patients die spontaneously from OSA primarily (no cardiovascular or respiratory element to the death), but this is unlikely. Even sudden death associated with OSA is presumed to be related to cardiac causes (arrhythmia or infarct) (4). We adjusted for comorbidity in the survival analysis using a comorbidity index (Charlson Comorbidity Index) that is a validated predictor of mortality outcome. It incorporates 19 various comorbid conditions, including cardiovascular diseases and others. In fact, this adjustment is one of the strengths of this study. Thus, the confounding effect of missing OSA severity is unclear because the surgery patients had severe OSA and we adjusted for the comorbid causes of death. 3) “CPAP use data were also unavailable so compliance was not assessed.” True. This study showed that surgery is superior to the provision of CPAP, but we cannot (and should not) conclude that surgery is superior to the use of CPAP. In fact, we believed that CPAP survival likely depended on the amount of CPAP use. Later, Campos-Rodriguez demonstrated that phenomenon in a different cohort (5). We advocated then and continue to advocate CPAP therapy as first-line treatment for OSA. However, OSA patients who do not use CPAP (or who use it inadequately) should be evaluated for surgical therapy. While surgery often does not normalize polysomnography results, it does appear to improve the long-term clinically important outcome of survival. 4) “The CPAP group were [sic] significantly older (57 v 51 years).” True, which is why we adjusted for age in our analysis. The surgery benefit was observed after adjusting for this potential confounding variable. 5) “At baseline, the CPAP group scored almost double on the Comorbidity Index (2.0 v 1.1).” True, which is why we adjusted for comorbidity in our analysis. The surgery benefit was observed after adjusting for this potential confounding variable. 6) “Residual confounding: comorbidity and mortality are so strongly related that complete adjustment is not possible by statistical analyses.” It is true that comorbidity and mortality are strongly associated with an adjusted hazard ratio of 1.09 (95% confidence interval 1.08-1.10) for each point on the Charlson Comorbidity Index in our cohort. I’m not sure what is the basis for Dr. Elshaug’s statement that complete adjustment is not possible. That implies a nihilistic view that observational studies are invalid because because one can never guarantee perfect adjustment. As noted above, the Charlson Comorbidity Index is validated to predict mortality and is commonly used to adjust for comorbidity in survival studies. 7) “The primary conclusions are drawn from observations of 1-year mortality. However, the authors also looked back to 1991 (i.e. mortality in 10 yrs v 1) and found inconsistent results that do not support their own, or Dr Robinson’s, primary conclusion.” False. We tested the mortality hazard for 1 - 5 years following the initiation of therapy (CPAP or surgery) in a cohort where therapy was started between 1997 and 2001. We also tested the mortality hazard for 1 - 11 years following the initiation of therapy in a larger cohort where therapy was started between 1991 and 2001; however, we did not have outpatient data on comorbidity in the earlier part of the cohort. Since comorbidity is so critical in survival analysis, we restricted our primary analysis to the smaller cohort reported. A secondary unadjusted analysis of the longer cohort showed identical results. A set of tertiary analyses attempted to adjust for the partial comorbidity data in the longer cohort, unfortunately all of these tertiary analysis approaches resulted in a significant proportion of patients excluded because of the missing data. Nevertheless, in all of the tertirary analyses, surgery showed survival as good as or better than CPAP after adjustment for confounding variables. In another analysis of a related cohort, we found that surgery and CPAP had superior survival to no treatment (6). These findings are in agreement with a European cohort study (3) and refute Dr. Elshaug’s thesis that surgery should not be offered. In conclusion, even partial surgical therapy (UPPP addresses part of an obstructing upper airway) results in long-term clinically important outcomes, even though it rarely normalizes polysomnography. Edward M. Weaver, MD, MPH REFERENCES (1) Weaver EM, Maynard C, Yueh B. Survival of veterans with sleep apnea: continuous positive airway pressure versus surgery. Otolaryngol Head Neck Surg 2004;130(6):659-65. (2) Kezirian EJ, Weaver EM, Yueh B, Khuri SF, Daley J, Henderson WG. Risk factors for serious complication after uvulopalatopharyngoplasty. Arch Otolaryngol 2006;132(10):1091-1098. (3) Marti S, Sampol G, Munoz X, Torres F, Roca A, Lloberes P, et al. Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment. Eur Respir J 2002;20(6):1511-8. (4) Gami AS, Howard DE, Olson EJ, Somers VK. Day-Night Pattern of Sudden Death in Obstructive Sleep Apnea. N Engl J Med 2005;352(12):1206- 1214. (5) Campos-Rodriguez F, Pena-Grinan N, Reyes-Nunez N, De la Cruz- Moron I, Perez-Ronchel J, De la Vega-Gallardo F, et al. Mortality in obstructive sleep apnea-hypopnea patients treated with positive airway pressure. Chest 2005;128(2):624-633. (6) Weaver EM, Maynard C, Yueh B. Mortality of veterans with sleep apnea: untreated versus treated. Sleep 2004;27:A208 (Abstract). Competing interests: None declared |
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Edward M. Weaver, PI, Sleep Apnea Research Group University of Washington Center for Cost & Outcomes Research, Seattle, WA, USA 98104
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Dr. Elshaug offered comments to refute Peker’s long-term prospective cohort study that reported a beneficial long-term clinical outcomes of sleep surgery (1). Clarifications are in order. Peker found that approximately half of their surgery patients were “efficiently” treated, meaning they were in the group that experienced dramatically fewer incident cardiovascular adverse outcomes over seven years compared to the inefficiently-treated/untreated group. 1) “We believe [this study] supports our Change Page entirely.” Dr. Elshaug’s suggestion that this study refutes a role for surgery is puzzling. In fact, this study supports the thesis that surgery can provide a long-term clinically important benefit for reducing incident cardiovascular events compared to no treatment. 2) “Peker et al. did report equally large reductions in cardiovascular disease (CVD) over a 7 year period in a surgically treated cohort.” Peker studied more than just a surgically treated cohort. He studied a cohort of men with no cardiovascular disease at baseline, which included men with and without sleep apnea. He followed the entire cohort, including those with no sleep apnea, those with untreated sleep apnea, those treated with continuous positive airway pressure (CPAP), those treated with surgery, and those treated with an oral device. 3) “…in this study ‘approximately 50% of subjects undergoing UPPP still had OSA at the follow-up recording’ (pg. 162) meaning they were inefficiently/ineffectively treated with UPPP alone.” It is true that 50% of the uvulopalatopharyngoplasty (UPPP) patients still had obstructive sleep apnea (OSA) and were inefficiently treated. Dr. Elshaug failed to point out that 64% of CPAP patients and 75% of oral device patients were inefficiently treated. A pessimistic view is that no treatment works consistently to achieve the dramatic reduction in cardiovascular disease risk. An optimistic view is that surgery and the other treatments offer a major health benefit in a significant proportion of patients. NEITHER view supports Dr. Elshaug’s suggestion that other treatments should be offered and surgery not considered. In current practice, surgery is reserved for CPAP failures. These failures can be left with untreated sleep apnea and, according to Peker’s data, a 55% risk of incident cardiovascular disease in the next seven years. Or, these failures can be offered UPPP where Peker’s data suggest half will have their risk of incident cardiovascular disease reduced from 55% to 5% over the following seven years. It should be noted that UPPP represents only a partial surgical treatment for sleep apnea (2,3), so surgery to address obstruction beyond the palate and oropharynx might further improve these outcomes. 4) “There was cross-contamination of treatment where … surgery recipients may also have received CPAP treatment during follow-up.” The proportion with crossover was not reported. It is not clear how this point supports Dr. Elshaug’s thesis (which was clarified in his Authors Reply to Sam Robinson) that surgery should not be made available even as second-line therapy. It is unlikely that successful UPPP patients would choose to receive CPAP or an oral device, so the crossover effect seems unlikely. Efficient UPPP therapy resulted in beneficial cardiovascular outcomes. It is more likely that inefficient UPPP patients might cross over and try another therapy. Regardless of the possible crossovers, these inefficient UPPP patients suffered poor outcomes. Thus, the possibility that patients might have received more than one treatment does not detract from the conclusion that half of the surgery patients experienced a reduced incidence of adverse cardiovascular outcomes. 5) “Given the sample sizes one needs to be observant to statistical power.” True. The small sample size does not provide enough statistical power to say that UPPP is better than the other treatments. However, the statistical power is sufficient to say the efficiently treated group (over half of which were UPPP patients) had better outcomes than the inefficiently/untreated treated group (less than 20% of which were UPPP patients). 6) “UPPP recipients had milder OSA to start with.” The baseline OSA severity was not reported for each treatment group in this study. Peker reported that the oxygen desaturation index was 2.0 +/- 1.3 events per hour at follow up in the efficient UPPP-treated subjects, meaning they had an excellent result. 7) “… the proportion who receive an optimal outcome from a surgical approach is low and inconsistent and less than can be achieved by other means, as is elegantly presented by Peker et al. and many others.” This statement contradicts Peker’s study. Half of the surgery patients were effectively treated, more than the other two treatments. Peker also pointed out that even the inefficient UPPP-treated subjects experienced improvement that occurred on an every-night basis. In conclusion, even partial surgical therapy (UPPP addresses part of an obstructing upper airway) improves long-term clinically important outcomes, even though it rarely normalizes polysomnography. Edward M. Weaver, MD, MPH REFERENCES 1. Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am. J. Respir. Crit. Care Med. 2002;166(2):159-165. 2. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996;19(2):156-77. 3. Friedman M, Ibrahim H, Lee G, Joseph NJ. Combined uvulopalatopharyngoplasty and radiofrequency tongue base reduction for treatment of obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg 2003;129(6):611-21. 4. Kezirian EJ, Weaver EM, Yueh B, Khuri SF, Daley J, Henderson WG. Risk factors for serious complication after uvulopalatopharyngoplasty. Arch Otolaryngol 2006;132(10):1091-1098. 5. Marti S, Sampol G, Munoz X, Torres F, Roca A, Lloberes P, et al. Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment. Eur Respir J 2002;20(6):1511-8. 6. Campos-Rodriguez F, Pena-Grinan N, Reyes-Nunez N, De la Cruz-Moron I, Perez-Ronchel J, De la Vega-Gallardo F, et al. Mortality in obstructive sleep apnea-hypopnea patients treated with positive airway pressure. Chest 2005;128(2):624-633. Competing interests: None declared |
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Edward M. Weaver, Associate Director Center for Cost & Outcomes Research, University of Washington, Seattle, WA, USA 98104
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Dr. Elshaug concludes that “Surgery for obstructive sleep apnoea should be done within controlled clinical trials.” IF he means that surgery should be performed ONLY within controlled clinical trials, then this is a sign of therapeutic nihilism. Since Dr. Elshaug has implied such in previous publications (1,2) and in his Author reply to Sam Robinson, I am compelled to respond to this suggestion on several levels: 1) His statement suggests there is no evidence of the benefit with surgical treatment for sleep apnea. To the contrary, several higher level studies, including randomized trials, support a significant benefit of surgery on clinically important outcomes (3-18). It is unfortunate that Dr. Elshaug did not include these studies in his reviews nor did he examine clinical outcomes (1,2,19). The significant subjectivity in apnea -hypopnea definitions, the variability of technical sensitivity, and the poor correlation with patient-oriented outcomes leaves apnea-hypopnea index a suboptimal solo surrogate outcome measure to evaluate sleep apnea treatment outcomes (20-22). These issues are not addressed in Dr. Elshaug’s reviews. In separate letters to BMJ, I provided detailed responses to some of the critiques of the clinical outcome studies discussed in his Author reply to Sam Robinson. 2) It is therapeutic nihilism to reject any study that is not a large, randomized, double-blinded, placebo-controlled trial. That approach would leave us with no treatment for sleep apnea nor for many other medical conditions. This concept was highlighted in Gordon Smith’s tongue-in-cheek systematic review of randomized controlled trials of parachute use, published in BMJ (23). Smith commented, “Advocates of evidence based medicine have criticised the adoption of interventions evaluated by using only observational data. We think that everyone might benefit if the most radical protagonists of evidence based medicine organised and participated in a double blind, randomised, placebo controlled, crossover trial of the parachute.” While this report is amusing, the suggestion to limit an important therapeutic modality for sleep apnea, namely surgery, only to randomized trials is irresponsible. 3) It strikes me as naïve to recommend surgeons simply randomize all surgical patients in trials. Dr. Elshaug’s suggestion (in his Author reply to Sam Robinson) to learn better approaches from his uncontrolled case series (1) highlights a superficial approach to the serious challenge of obtaining rigorous evidence. There are significant feasibility challenges to his recommendation to “randomize them.” Dr. Neville Shine highlighted some of the challenges in his response entitled “no change; no problem.” 4) A relative paucity of randomized, blinded, placebo-controlled trials does NOT equate to evidence against surgery, especially when there is a consistent finding in multiple other high level studies of treatment benefit (albeit not cure). It should be noted that there are challenges for CPAP evaluation as well; hence, there are no randomized, double-blind, placebo-controlled, long-term trials of CPAP in obstructive sleep apnea patients evaluating survival, incident cardiovascular morbidity, or motor vehicle crashes. Even the trials on acute blood pressure changes are mixed. Nevertheless, the smaller, less rigorous studies provide enough evidence of benefit to proceed with therapy while more trials are underway and the body of evidence grows. 5) Dr. Elshaug discussed opportunity cost and the directions of resource use in his Author reply to Sam Robinson. He implies that surgery diverts resources from non-surgical treatments, which appears to be the root of his critical view of surgery. One could recommend he perform a number of definitive cost-effectiveness studies assessing validated patient-oriented effectiveness outcomes (long-term) and comprehensive cost analyses (including indirect costs) from societal and patient perspectives in several populations and cultures to begin to assess his concern (24). In the meanwhile, Dr. Elshaug appears to be in a desirable situation where multi-disciplinary care provides the opportunity for better outcomes for patients who struggle with first-line therapies (in some cases despite adjunctive strategies). 6) I support and encourage the research to improve CPAP outcomes with adjunctive treatments (including adjunctive surgical treatments (3)). Successful adjunctive treatments should be implemented. However, even still there are patients who do not succeed with CPAP, weight loss attempts, and/or oral appliances, and fortunately they might still achieve benefit from surgical treatment evaluation. Let me be clear. The thesis that surgery is typically not first-line therapy appears sound because there is a more efficacious, low-risk therapy available. However, when the first-line therapy is not successful because of difficulty with adherence, the implication that surgery should not be made available as second-line therapy is detrimental to patient and public health. Edward M. Weaver, MD, MPH REFERENCES 1. Elshaug AG, Moss JR, Southcott AM, Hiller JE. An analysis of the evidence-practice continuum: is surgery for obstructive sleep apnoea contraindicated? J Eval Clin Pract 2007;13(1):3-9. 2. Elshaug AG, Moss JR, Southcott AM, Hiller JE. Redefining success in airway surgery for obstructive sleep apnea: a meta analysis and synthesis of the evidence. Sleep 2007;30(4):461-7. 3. Powell NB, Zonato AI, Weaver EM, Li K, Troell R, Riley RW, et al. Radiofrequency treatment of turbinate hypertrophy in subjects using continuous positive airway pressure: a randomized, double-blind, placebo- controlled clinical pilot trial. Laryngoscope 2001;111:1783-90. 4. Woodson BT, Steward DL, Weaver EM, Javaheri S. A randomized trial of temperature-controlled radiofrequency, continuous positive airway pressure, and placebo for obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg 2003;128(6):848-61. 5. Lojander J, Kajaste S, Maasilta P, Partinen M. Cognitive function and treatment of obstructive sleep apnea syndrome. J Sleep Res 1999;8(1):71-6. 6. Lojander J, Maasilta P, Partinen M, Brander PE, Salmi T, Lehtonen H. Nasal-CPAP, surgery, and conservative management for treatment of obstructive sleep apnea syndrome. A randomized study. Chest 1996;110(1):114-9. 7. Conradt R, Hochban W, Heitmann J, Brandenburg U, Cassel W, Penzel T, et al. Sleep fragmentation and daytime vigilance in patients with OSA treated by surgical maxillomandibular advancement compared to CPAP therapy. Journal of Sleep Research 1998;7(3):217-23. 8. Prinsell JR. Maxillomandibular Advancement Surgery in a Site- Specific Treatment Approach for Obstructive Sleep Apnea in 50 Consecutive Patients*. Chest 1999;116(6):1519-1529. 9. Marti S, Sampol G, Munoz X, Torres F, Roca A, Lloberes P, et al. Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment. Eur Respir J 2002;20(6):1511-8. 10. Weaver EM, Maynard C, Yueh B. Survival of veterans with sleep apnea: continuous positive airway pressure versus surgery. Otolaryngol Head Neck Surg 2004;130(6):659-65. 11. Keenan SP, Burt H, Ryan CF, Fleetham JA. Long-term survival of patients with obstructive sleep apnea treated by uvulopalatopharyngoplasty or nasal CPAP. Chest 1994;105(1):155-9. 12. Lysdahl M, Haraldsson PO. Long-term survival after uvulopalatopharyngoplasty in nonobese heavy snorers: a 5- to 9-year follow -up of 400 consecutive patients. Arch Otolaryngol Head Neck Surg 2000;126(9):1136-40. 13. Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am. J. Respir. Crit. Care Med. 2002;166(2):159-165. 14. Haraldsson PO, Carenfelt C, Lysdahl M, Tingvall C. Does uvulopalatopharyngoplasty inhibit automobile accidents? Laryngoscope 1995;105(6):657-61. 15. Walker-Engstrom ML, Wilhelmsson B, Tegelberg A, Dimenas E, Ringqvist I. Quality of life assessment of treatment with dental appliance or UPPP in patients with mild to moderate obstructive sleep apnoea. A prospective randomized 1-year follow-up study. J Sleep Res 2000;9(3):303- 8. 16. Li HY, Chen NH, Shu YH, Wang PC. Changes in quality of life and respiratory disturbance after extended uvulopalatal flap surgery in patients with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2004;130(2):195-200. 17. Cahali MB, Formigoni GG, Gebrim EM, Miziara ID. Lateral pharyngoplasty versus uvulopalatopharyngoplasty: a clinical, polysomnographic and computed tomography measurement comparison. Sleep 2004;27(5):942-50. 18. Woodson BT, Robinson S, Lim HJ. Transpalatal advancement pharyngoplasty outcomes compared with uvulopalatopharygoplasty. Otolaryngology - Head & Neck Surgery 2005;133(2):211-7. 19. Elshaug AG, Moss JR, Hiller JE, Maddern GJ. Upper airway surgery should not be first line treatment for obstructive sleep apnoea in adults. Bmj 2008;336(7634):44-5. 20. Redline S, Sanders M. Hypopnea, a floating metric: implications for prevalence, morbidity estimates, and case finding. Sleep 1997;20(12):1209-17. 21. Redline S, Kapur VK, Sanders MH, Quan SF, Gottlieb DJ, Rapoport DM, et al. Effects of varying approaches for identifying respiratory disturbances on sleep apnea assessment. Am J Respir Crit Care Med 2000;161(2 Pt 1):369-74. 22. Weaver EM, Woodson BT, Steward DL. Polysomnography indexes are discordant with quality of life, symptoms, and reaction times in sleep apnea patients. Otolaryngology - Head and Neck Surgery 2005;132(2):255- 262. 23. Smith GCS, Pell JP. Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials. BMJ 2003;327(7429):1459-1461. 24. Drummond MF, O'Brien BJ, Stoddart GL, Torrance GW. Methods for the Economic Evaluation of Health Care Programmes. Second ed. Oxford: Oxford University Press, 1997. Competing interests: None declared |
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Adam G Elshaug, Research Fellow and Lecturer The University of Adelaide, Australia, 5005, Assoc Prof John R Moss
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Reply to Messrs Weaver, Robinson and Shine The primary theme running through the responses from Weaver (8 Jan), Robinson (8 Jan) and Shine (9 Jan) is ¡®no problem, no change¡¯ and that good surgeons already follow the guidelines that are presented in our Change Page. They suggest that we have not produced evidence to the contrary. We direct these contributors back to the cited evidence in our Change Page, and to the general literature in this area, where evidence is indeed presented. There are two reports (to our knowledge) that have investigated this issue and both found a proportion of surgical recipients by-passed sleep medicine physicians/clinics and underwent surgery both without a formal diagnosis of OSA and without receiving a trial of CPAP. In our own audit (1), which utilised a methodology sensitive to this occurrence, 28 cases had to be excluded (making n=94) for this reason - a high proportion. Marshall et al. subsequently observed the same phenomenon (2). Moore (11 Jan) points to the limitation within the Cochrane process of excluding non-RCT evidence. We agree with this observation wholeheartedly, so much so that it was the impetus behind our published meta-analyses (3) that specifically sought to include studies that sit lower on the hierarchy of evidence but nevertheless have much to contribute in this area. This evidence is included in our Change Page. Robinson, in his 8 January rapid response, suggests "The current most widespread outcome measure using RDI applied to surgery is RDI < 20 (+/ - > 50% total RDI reduction)". He goes on to state "it seems illogical to suggest that surgery must achieve an RDI below [ ¡Ü5 ]". We ask, what is illogical about using the criterion endorsed by the AASM (and adopted in many parts of the world) and against which CPAP is judged? Moreover, this is precisely the interpretive quandary presented for debate in our recent papers in this area: that (primarily if not exclusively) surgeons continue to apply the RDI of 20 as their primary outcome measure which is not in keeping with 1) the more stringent AASM criteria within which sleep medicine operates i.e AHIs of <5 (no condition), 5-15 (mild), 15-30 (moderate) and > 30 (severe condition) and, 2) it ignores the growing evidence base to support the validity of these (or similar) outcome measures. Adam Elshaug, BA, BSc(Hons), MPH, PhD
References: 1. Elshaug AG, Moss JR, Southcott A and Hiller JE. An analysis of the evidence-practice continuum: Is surgery for Obstructive Sleep Apnoea contraindicated? J Eval Clin Pract, 2007; 13(1): 3-9. 2. Marshall NS, Bartlett DJ, Matharu KS, et al. Prevalence of treatment choices for snoring and sleep apnea in an Australian population. J Clin Sleep Med, 2007; 3(7): 695-699. 3. Elshaug AG, Moss JR, Southcott A and Hiller JE. Redefining success in airway surgery for Obstructive Sleep Apnea: A meta analysis and synthesis of the evidence. Sleep, 2007; 30(4): 461-467. Competing interests: None declared |
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