| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
Chicago, IL
Dr. Mokhlesi is Assistant Professor of Medicine, Section of Pulmonary and Critical Care Medicine, and Director of the Sleep Disorders Center, The University of Chicago Pritzker School of Medicine.
Correspondence to: Babak Mokhlesi, MD, MSc, Assistant Professor of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago Pritzker School of Medicine, 5841 S Maryland Ave, MC 0999, Room L11B, Chicago, IL 60637; e-mail: bmokhles{at}medicine.bsd.uchicago.edu
In the United States, a third of the adult population is obese and the prevalence of extreme obesity (body mass index [BMI] 
40 kg/m2) is increasing rapidly. From 1986 to 2000, the prevalence of BMI 40 kg/m2 has quadrupled, and that of BMI 50 kg/m2 has increased fivefold.1 The obesity epidemic is not only impacting adults in the United States, it is a global phenomenon affecting children and adolescents.2 With such a global epidemic of obesity, the prevalence of obesity hypoventilation syndrome (OHS)—defined as a combination of obesity, awake chronic hypercapnia, and sleep-disordered breathing, in the absence of other known causes of hypercapnia—is likely to increase. In patients with OHS, sleep-disordered breathing can occur in three forms: obstructive apneas and hypopneas, obstructive hypoventilation due to increased upper airway resistance, and central hypoventilation.34 In approximately 90% of patients with OHS, the sleep-disordered breathing consists predominantly of obstructive apneas and hypopneas (obstructive sleep apnea [OSA]).456 In patients with OSA and extreme obesity, the prevalence of OHS is as high as 25%.67
Patients with OHS have a lower quality of life with increased health-care expenses and are at higher risk for pulmonary hypertension and early mortality when compared to eucapnic patients with similar degrees of obesity with or without OSA.8910 Although the optimal management of patients with OHS remains uncertain, early recognition and treatment with positive airway pressure (PAP) therapy reduces the high burden of morbidity and mortality associated with this syndrome.51011 While PAP is the mainstay of therapy in OHS, there is no standard protocol for its titration.12 Continuous positive airway pressure (CPAP) and bilevel PAP, also known as noninvasive positive pressure ventilation, are the two most common modes of delivering PAP. Given that the majority of patients with OHS have concomitant severe OSA, treatment with CPAP seems reasonable.131415 In contrast to OSA, the response to CPAP titration in patients with OHS has not been systematically evaluated.
In this issue of CHEST (see page 1678), Banerjee and colleagues16 provide new insights on the treatment of OHS. These investigators compared the impact of CPAP titration on the sleep architecture, respiratory events, and nocturnal hypoxemia in 23 patients with OHS and 23 patients with eucapnic OSA matched for BMI, apnea-hypopnea index (AHI), and lung function. Both groups were extremely obese with severe sleep-disordered breathing, and those with OHS had significant daytime hypercapnia. The protocol included full-night diagnostic polysomnography followed by a full night of CPAP titration without supplemental oxygen therapy, and CPAP was titrated to eliminate apneas, hypopneas, and any evidence of flow limitation. CPAP resolved sleep-disordered breathing and nocturnal hypoxemia in 57% of patients with OHS. The optimal CPAP pressure of 13.9 ± 3.1 cm H2O was reached within 1 h of sleep onset. CPAP was unable to resolve refractory hypoxemia in 43% of patients with OHS, and these patients had a higher BMI, more severe nocturnal hypoxemia at baseline, and a higher residual AHI during the night of CPAP titration compared to those with successful titration. Overall, CPAP led to significant increase in rapid eye movement sleep and significant reduction in arousal index and AHI in both patients with eucapnic OSA and OHS.
What do these results tell us? The fact that more than half of the patients with extreme but stable cases of OHS (based on BMI, AHI, and the level of daytime hypercapnia) were successfully titrated with CPAP—without requiring bilevel PAP or supplemental oxygen—suggests that the majority of patients with milder forms of OHS can be successfully titrated with CPAP as well. However, given the lack of intermediate and long-term follow-up, it is difficult to establish whether outcomes with CPAP therapy would be similar to bilevel PAP therapy. Another limitation was the inability to reduce the AHI to < 25/h in the subgroup of patients with OHS that remained persistently hypoxemic during CPAP titration, suggestive of inadequate titration. It is plausible that higher CPAP pressures could further reduce the AHI and improve nocturnal hypoxemia. It is also important to point out that the findings of Banerjee et al do not apply to the subgroup of patients with OHS (10%) who do not have concomitant OSA.
Two questions arise and remain to be addressed: (1) does persistent hypoxemia despite adequate CPAP titration improve with time, and (2) is CPAP plus supplemental oxygen superior to bilevel PAP? These questions are clinically relevant because of the higher costs associated with bilevel PAP and supplemental oxygen therapy.
Banerjee and colleagues16 have provided convincing evidence that CPAP can be successfully titrated in the majority of patients with stable OHS, and their findings will give impetus for well-designed randomized controlled trials comparing long-term outcomes with different treatment modalities in patients with OHS. In the meantime, bilevel PAP should be considered the treatment of choice in patients with OHS if nocturnal hypoxemia is persistent despite an adequate CPAP titration. For bilevel PAP therapy to be successful, the inspiratory PAP needs to be at least 8 to 10 cm H2O above the final expiratory PAP required to eliminate all obstructive respiratory events.3517 Bilevel PAP should also be considered if daytime hypercapnia does not resolve after approximately 1 month of adequate adherence with CPAP therapy and in patients with OHS with acute on chronic respiratory failure. CPAP will also be ineffective in patients with OHS who do not have concomitant OSA (AHI < 5/h). Ultimately, the improvement in symptoms and blood gas levels are directly related to adherence with PAP therapy, and maximum improvement in blood gas levels can be achieved in as early as 2 to 4 weeks.15 Therefore, early follow-up is imperative and should include repeat measurement of arterial blood gas levels and objective assessment of adherence with PAP because patients frequently overestimate adherence. Changing bilevel PAP to CPAP and discontinuing oxygen therapy when no longer indicated can decrease the cost of therapy in patients with OHS.5
Footnotes
The author does not have any financial or other potential conflicts of interest to declare.
References
Related Article
This article has been cited by other articles:
|
|
 |
|
  B. Mokhlesi and A. Tulaimat Recent Advances in Obesity Hypoventilation Syndrome Chest, October 1, 2007; 132(4): 1322 - 1336. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
