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• Response to: A randomised controlled trial of CPAP vs non-invasive ventilation for initial treatment of obesity hypoventilation syndrome
  Mark E Howard
  Published on: 10 April 2017
• Comment on: A randomised controlled trial of CPAP versus non-invasive ventilation for initial treatment of obesity hypoventilation syndrome
  Stephanie K. Mansell
  Published on: 10 April 2017

• Published on: 10 April 2017

  Response to: A randomised controlled trial of CPAP vs non-invasive ventilation for initial treatment of obesity hypoventilation syndrome

  • Mark E Howard, Respiratory Physician
  • Other Contributors:
    • Amanda J Piper, Bronwyn Stevens, Anne E Holland, Brendon J Yee, Eli Dabscheck, Duncan Mortimer, Angela T Burge, Daniel Flunt, Catherine Buchan, Linda Rautela, Nicole Sheers, David Hillman & David J Berlowitz

  Dear Editor, We thank Dr Mansell for her comments regarding our recently published trial. [1] We agree that there are different phenotypic variations within the obesity hypoventilation syndrome (OHS), although it remains to be determined whether OHS with co-existent obstructive sleep apnoea (OSA) responds differently to treatment in comparison to OHS without OSA. [2] Acknowledging that the presence and severity of OSA in...

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  Dear Editor, We thank Dr Mansell for her comments regarding our recently published trial. [1] We agree that there are different phenotypic variations within the obesity hypoventilation syndrome (OHS), although it remains to be determined whether OHS with co-existent obstructive sleep apnoea (OSA) responds differently to treatment in comparison to OHS without OSA. [2] Acknowledging that the presence and severity of OSA in OHS may impact on the response to CPAP or non-invasive ventilation (NIV), clinical definitions and clinical trials in OHS have defined OHS as obesity (BMI > 30 kg/m2) with chronic hypercapnia, irrespective of the degree of co-existent OSA. [3] The degree of OSA in our study is in keeping with the severity of OSA in previous clinical trial of OHS, [4, 5], although the degree of obesity, severity of baseline hypercapnia and degree of pulmonary function impairment was substantially greater. All three randomised controlled trials have found similar outcomes for CPAP and NIV, and so do not support the routine use of NIV for all patients with OHS. The predominant phenotype appears to be OHS in conjunction with severe OSA, which comprised more than 70% of participants in the recent manuscript from the Spanish Sleep Network. [6] In this subgroup they found NIV provided greater improvement in respiratory failure and symptoms than life style measure in OHS without OSA, however further results are awaited to determine whether CPAP and NIV have different impacts in this subgroup. We chose clinically significant outcomes and predictors of increased mortality (hospital admission, persisting respiratory failure, non- adherence and quality of life) as outcome measures rather than polysomnographic variables. We did, however, use polysomnography to titrate CPAP and NIV at the commencement of the project in order to eliminate respiratory events and minimise persisting hypoxaemia and hypoventilation. In terms of demonstrating laboratory effectiveness of therapy, none of the participants required the addition of nocturnal oxygen for persisting hypoxaemia on treatment, in contrast to other trials, although we did not measure the apnoea hypopnoea index on the final study settings. [5] We agree that assessment of long term outcomes, including mortality is important and 12 month outcome data from this cohort will be available shortly. Some of the participants in our trial had treatment prior to trial randomisation. The trial recruited OHS participants during acute hospital admissions with respiratory failure as well as from ambulatory settings that were the focus of previous trials. The design allowed for initial treatment with NIV for correction of acute respiratory acidosis prior to randomisation to CPAP or NIV. We acknowledge that this may have influenced baseline measures, however it was not considered ethical to withhold treatment in acutely unwell patients and there was no difference in prior treatment use between the groups. Given the results from the three published randomised controlled trials that have found similar outcomes for CPAP and NIV in OHS, and in line with recent editorial opinion, we believe that it is reasonable to use CPAP for treatment of OHS following initial stabilisation of acute respiratory acidosis, with careful observation of the response. [7], Further evidence may influence optimal therapy in different OHS subgroups. 1.Howard ME, Piper AJ, Stevens B, et al. A randomised controlled trial of CPAP versus non-invasive ventilation for initial treatment of obesity hypoventilation syndrome. Thorax. 2016. Epub 2016/11/18. 2.Ojeda Castillejo E, de Lucas Ramos P, Lopez Martin S, et al. Noninvasive mechanical ventilation in patients with obesity hypoventilation syndrome. Long-term outcome and prognostic factors. Arch Bronconeumol. 2015;51(2):61-8. Epub 2014/04/08. 3.Mokhlesi B, Tulaimat A. Recent Advances in Obesity Hypoventilation Syndrome. Chest.2007;132(4):1322-36. 4.Piper AJ, Wang D, Yee BJ, et al. Randomised trial of CPAP vs bilevel support in the treatment of obesity hypoventilation syndrome without severe nocturnal desaturation. Thorax. 2008;63(5):395-401. Epub 2008/01/22. 5.Masa JF, Corral J, Alonso ML, et al. Efficacy of Different Treatment Alternatives for Obesity Hypoventilation Syndrome. Pickwick Study. Am J Respir Crit Care Med. 2015;192(1):86-95. Epub 2015/04/29. 6.Masa JF, Corral J, Caballero C, et al. Non-invasive ventilation in obesity hypoventilation syndrome without severe obstructive sleep apnoea. Thorax. 2016;71(10):899- 906. Epub 2016/07/14. 7.Noda JR, Masa JF, Mokhlesi B. CPAP or non-invasive ventilation in obesity hypoventilation syndrome: does it matter which one you start with? Thorax. 2017. Epub 2017/01/29.

  Conflict of Interest:

  MEH reports grants from Resmed Foundatio & non-financial support from Philips Respironics. AJP reports grants from Resmed Foundation, personal fees from ResMed, personal fees from Philips Respironics & personal fees from SenTec. DM reports grants from Resmed Foundation, National Health & Medical Research Council & Victoria Neurotrauma Initiative. BS, AEH, BJY, ED, ATB, DF, CB, LR, NS, DH and DJB report a grant from Resmed Foundation.

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  Conflict of Interest:
  None declared.

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• Published on: 10 April 2017

  Comment on: A randomised controlled trial of CPAP versus non-invasive ventilation for initial treatment of obesity hypoventilation syndrome

  • Stephanie K. Mansell, Consultant Physiotherapist
  • Other Contributors:
    • S. Mandal

  Dear Editor,

  We read with great interest the article by Howard et al[1] and commend the authors on this excellent piece of work. However, we wish to raise several points for consideration of this work in a clinical context. Firstly, it is not clear whether the patients being treated were truly patients with obesity hypoventilation failure (OHS) or whether in fact they had hypercapnic obstructive sleep apnoea (OSA). There is in...

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  Dear Editor,

  We read with great interest the article by Howard et al[1] and commend the authors on this excellent piece of work. However, we wish to raise several points for consideration of this work in a clinical context. Firstly, it is not clear whether the patients being treated were truly patients with obesity hypoventilation failure (OHS) or whether in fact they had hypercapnic obstructive sleep apnoea (OSA). There is increasing data to suggest the clinical entity of obesity related respiratory failure (ORRF) encompasses several different phenotypes including; hypercapnic OSA, OSA/OHS and lone OHS. The underlying pathophysiology is likely to differ between these phenotypes and will therefore respond differently to treatment[2]. Not all the participants underwent nocturnal respiratory polygraphy, and it is thus difficult to determine which clinical phenotype was being treated, especially given the wide standard deviation (for AHI mean = 82 events / hr (SD 45) and for SpO2 less than 90% mean = 67% of the sleep period (SD 31.4%). This is in keeping with data by Kawata et al[3], who also demonstrated that in patients with hypercapnic OSA, only half of patients responded to continuous positive airway pressure (CPAP) therapy. Those who failed to respond had a higher AHI and BMI, suggesting nocturnal polygraphy parameters may predict who will respond to CPAP therapy alone. More than 50% of patients had previously used either non-invasive ventilation (NIV) or CPAP therapy, it is unclear whether there was a wash out period and prior use of PAP therapy which may have affected compliance in these individuals and therefore outcomes. We note the mean CPAP was 15.2 cm H2O (SD 2.8); in our clinical experience we often find patients with OHS/OSA trialled on CPAP therapy who require higher CPAP pressures (>10cmH2O) have ongoing nocturnal events, particularly persistent hypoxia. The authors have not provided nocturnal data on PAP therapy, we are therefore unable to determine whether the CPAP group had a reduction in nocturnal events to within normal range. This is especially important given the fact that, although reduced, the PaCO2 in the CPAP group remained higher than the NIV group at three months. The authors also comment that PaCO2 at presentation was predictive of treatment failure, with an eightfold increase in risk when PaCO2 was greater than 62mmHg (8.27kPa). This is noteworthy since there is much debate about the diagnostic criteria for OHS[4-6], a cut-off level for PaCO2 to determine which patients may fail therapy would be clinically important in identifying patients who should be treated with NIV in the first instance. Lastly, only outcomes at 3 months have been presented. We wonder what the longer term outcomes for these patients would be; whether there would be an increase in the CPAP failure rate and, most importantly, a difference in mortality rates? We recognise the significance of this paper and acknowledge there may be a cohort of OHS/hypercapnic OSA patients who can be treated successfully with CPAP. However, this group is yet to be identified; much of this distinction may lie in a universal definition of OHS encompassing nocturnal and daytime parameters. We suggest that NIV is a safer treatment option until further phenotyping studies are conducted to comprehensively identify those patients requiring NIV and those for whom CPAP will be adequate.

  References:

  1. Howard ME, Piper AJ, Stevens B, et al. A randomised controlled trial of CPAP versus non-invasive ventilation for initial treatment of obesity hypoventilation syndrome. Thorax 2016 doi: 10.1136/thoraxjnl-2016-208559[published Online First: Epub Date]|.

  2. Masa JF, Corral J, Caballero C, et al. Non-invasive ventilation in obesity hypoventilation syndrome without severe obstructive sleep apnoea. Thorax 2016:thoraxjnl-2016-208501

  3. Kawata N, Tatsumi K, Terada J, et al. DAytime hypercapnia in obstructive sleep apnea syndrome*. Chest 2007;132(6):1832-38 doi: 10.1378/chest.07-0673[published Online First: Epub Date]|.

  4. Manuel AR, Hart N, Stradling JR. Is a raised bicarbonate, without hypercapnia, part of the physiologic spectrum of obesity-related hypoventilation? CHEST Journal 2015;147(2):362-68

  5. Murphy PB, Janssens J-P. NIV for OHS without severe OSAS: is it worth it? Thorax 2016 doi: 10.1136/thoraxjnl-2016-208986[published Online First: Epub Date]|.

  6. Hart N, Mandal S, Manuel A, et al. Obesity hypoventilation syndrome: does the current definition need revisiting? Thorax 2014;69(1):83-4 doi: 10.1136/thoraxjnl-2013-204298[published Online First: Epub Date]|.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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