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Communications to the Editor |

Obesity Hypoventilation Syndrome : What’s in a Name? FREE TO VIEW

Claudio A. Rabec, MD, FCCP
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Tornu Hospital Buenos Aires, Argentina

Correspondence to: Claudio A Rabec, MD, FCCP, Alemania 2739, C1419FJA Buenos Aires, Argentina; e-mail: cirhtornu@yahoo.com.ar



Chest. 2002;122(4):1498. doi:10.1378/chest.122.4.1498
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To the Editor:

It is with great interest that I read the article by Kessler et al in CHEST (August 2001)1 regarding obesity hypoventilation syndrome (OHS). I think that there are yet important aspects to clarify in regard to the definition of this entity, because there is some confusion in the literature about this subject.

The development of hypoventilation in obese patients is composed of multiple and complex mechanisms that comprise at least the following three entities: obstructive sleep apnea (OSA), COPD, and OHS. Kessler et al assumed that obese patients with hypercapnia may be understood to have OHS without regard for whether they had experienced sleep apnea. In fact, in the article, the authors include obese hypercapnic OSA patients as “OHS patients.”

Nevertheless, in this regard, the author’s experience (which has been confirmed by others23) shows that some nonobese OSA patients may develop hypercapnia. Then it seems that hypercapnia in patients with sleep apnea may occur independently from obesity, denoting a complex autonomous mechanism.

For this reason, it seems more logical not to include sleep apnea patients into the entity OHS and to restrict the term OHS to patients in whom hypercapnia persists after eliminating sleep apnea as the mechanism of hypercapnia (ie, after a trial of continuous positive airway pressure [CPAP] at an effective pressure).4

For this reason, I propose to restrict the term OHS to patients in whom the only mechanism responsible for alveolar hypoventilation is obesity itself (independent of apneas). In this field, it is preferable to call this condition obesity-linked hypoventilation (OLH).3 This entity could be defined in the following two situations: (1) hypercapnia in obese patients without OSA or COPD (ie, pure OLH); and (2) persistence of hypercapnia in OSA patients who are receiving CPAP (ie, OLH plus OSA)

This approach also has therapeutic implications. We will restrict long-term therapy with bilevel pressure ventilation (or any kind of positive-pressure ventilation) only to patients who experience persistent hypercapnia while receiving CPAP.

Consequently, this new approach can enlarge and clarify the field of respiratory syndromes in obese patients and the approaches to therapy.

Kessler, R, Chaouat, A, Schinkewitch, P, et al (2001) The obesity-hypoventilation syndrome revisited.Chest120,369-376. [PubMed] [CrossRef]
 
Leach, J, Onal, E, Baer, P, et al Determinants of hypercapnia in occlusive sleep apnea syndrome.Chest1987;92,807-813. [PubMed]
 
Rabec, C, Merati, M, Baudouin, N, et al Management of respiratory failure in obese patients: efficacy of nasal bi-level positive airway pressure.Rev Mal Respir1998;15,269-278. [PubMed]
 
Piper, A, Sullivan, C Effect of short term NIPPV in the treatment of patients with severe obstructive sleep apnea and hypercapnia.Chest1994;105,434-440. [PubMed]
 

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References

Kessler, R, Chaouat, A, Schinkewitch, P, et al (2001) The obesity-hypoventilation syndrome revisited.Chest120,369-376. [PubMed] [CrossRef]
 
Leach, J, Onal, E, Baer, P, et al Determinants of hypercapnia in occlusive sleep apnea syndrome.Chest1987;92,807-813. [PubMed]
 
Rabec, C, Merati, M, Baudouin, N, et al Management of respiratory failure in obese patients: efficacy of nasal bi-level positive airway pressure.Rev Mal Respir1998;15,269-278. [PubMed]
 
Piper, A, Sullivan, C Effect of short term NIPPV in the treatment of patients with severe obstructive sleep apnea and hypercapnia.Chest1994;105,434-440. [PubMed]
 
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