Obesity hypoventilation syndrome: A state-of-the-art review

Section of Pulmonary and Critical Care Medicine, University of Chicago Pritzker School of Medicine, Chicago IL 60637, USA.
Respiratory care (Impact Factor: 1.84). 10/2010; 55(10):1347-62; discussion 1363-5.
Source: PubMed


Obesity hyoventilation syndrome (OHS) is defined as the triad of obesity, daytime hypoventilation, and sleep-disordered breathing in the absence of an alternative neuromuscular, mechanical or metabolic explanation for hypoventilation. During the last 3 decades the prevalence of extreme obesity has markedly increased in the United States and other countries. With such a global epidemic of obesity, the prevalence of OHS is bound to increase. Patients with OHS have a lower quality of life, with increased healthcare expenses, and are at higher risk of developing pulmonary hypertension and early mortality, compared to eucapnic patients with sleep-disordered breathing. OHS often remains undiagnosed until late in the course of the disease. Early recognition is important, as these patients have significant morbidity and mortality. Effective treatment can lead to significant improvement in patient outcomes, underscoring the importance of early diagnosis. This review will include disease definition and epidemiology, clinical characteristics of the syndrome, pathophysiology, and morbidity and mortality associated with it. Lastly, treatment modalities will be discussed in detail.

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    • "As the body mass index (BMI) increases, so does the incidence of the multi-organ dysfunctions associated with obesity, especially the incidence of obesity hypoventilation syndrome (OHS) [2]. This syndrome refers to the association between obesity (BMI>30 kg.m−2) and daytime hypercapnia (PaCO2≥45 mmHg) after other respiratory or neuromuscular causes for such an awake hypoventilation have been excluded [3], [4]. The reported prevalence of OHS reaches 10 to 20% in the obese population while more than 50% of hospitalized patients with a BMI greater than 50 kg.m−2 "
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    ABSTRACT: Acute respiratory failure (ARF) is a common life-threatening complication in morbidly obese patients with obesity hypoventilation syndrome (OHS). We aimed to identify the determinants of noninvasive ventilation (NIV) success or failure for this indication. We prospectively included 76 consecutive patients with BMI>40 kg/m2 diagnosed with OHS and treated by NIV for ARF in a 15-bed ICU of a tertiary hospital. NIV failed to reverse ARF in only 13 patients. Factors associated with NIV failure included pneumonia (n = 12/13, 92% vs n = 9/63, 14%; p<0.0001), high SOFA (10 vs 5; p<0.0001) and SAPS2 score (63 vs 39; p<0.0001) at admission. These patients often experienced poor outcome despite early resort to endotracheal intubation (in-hospital mortality, 92.3% vs 17.5%; p<0.001). The only factor significantly associated with successful response to NIV was idiopathic decompensation of OHS (n = 30, 48% vs n = 0, 0%; p = 0.001). In the NIV success group (n = 63), 33 patients (53%) experienced a delayed response to NIV (with persistent hypercapnic acidosis during the first 6 hours). Multiple organ failure and pneumonia were the main factors associated with NIV failure and death in morbidly obese patients in hypoxemic ARF. On the opposite, NIV was constantly successful and could be safely pushed further in case of severe hypercapnic acute respiratory decompensation of OHS.
    PLoS ONE 05/2014; 9(5):e97563. DOI:10.1371/journal.pone.0097563 · 3.23 Impact Factor
    • "Whereas most patients with OHS have had prior hospitalizations and have higher healthcare utilization, the formal diagnosis of OHS is established late in the fifth or sixth decade of life.[17] The most common presentations of the patients are an acute-on-chronic exacerbation with acute respiratory acidosis leading to admission to an intensive care unit, or during a routine outpatient evaluation by a sleep specialist or pulmonologist.[17] Nowbar et al. in their study have reported that patients with OHS were mostly identified during systematic screening of hospitalized patients and that the vast majority were discharged from the hospital without any form of therapy for hypoventilation.[14] "
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    ABSTRACT: Patients with obesity hypoventilation syndrome (OHS) have significant morbidity and mortality. Early diagnosis and treatment is important and there are limited data on its prevalence and predictive factors. The objective of this observational study was to determine the frequency and predictors of OHS in hospitalized patients at a tertiary health care institution. All blood gas analyses of hospitalized adult (age over 18 years) patients were prospectively recruited from the biochemistry laboratory at a tertiary health care center between August 2009 and July 2010. Patients who had hypercapnia (PaCO2 ≥ 45 mmHg) while breathing room air were included and clinical and laboratory data were obtained from hospital records. A standard questionnaire was also filled by face-to-face interview with patients and/or relatives. A total of 9480 patients' arterial blood gases were evaluated and 330 patients (3.4%) who met the selection criteria were included in the analysis during the study period. Hypoventilation was associated with acute diseases in 64.2% and chronic diseases in 35.8% of the patients. Of the chronic hypoventilation patients, 24.4% had OHS. Univariate logistic regression analysis showed that, female gender, body mass index (BMI), smoking, PaO2, SaO2 and a PaCO2/BMI <1.5 were significantly related to OHS. In multivariate logistic regression analysis, BMI >35 kg/m(2), SaO2 <91.4% and PaCO2 /BMI <1.5 were significantly related to OHS. A PaCO2/BMI <1.5 was an independent variable strongly predictive of OHS (odds ratio: 36.9, 95% of the confidence interval: 2.75-492.95, P = 0.007). OHS is a common cause of chronic alveolar hypoventilation. A careful examination PaCO2 /BMI ratio may prevent misdiagnoses among hypercapnic patients.
    Annals of Thoracic Medicine 03/2014; 9(2):87-91. DOI:10.4103/1817-1737.128851 · 1.80 Impact Factor
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    • "The increased metabolic activity associated with obesity increases CO2 production, necessitating a corresponding increase in alveolar ventilation to maintain homeostasis of arterial PCO2 (PaCO2) and acid-base status. A subset of obese individuals hypoventilate with substantial elevations in PaCO2 in a condition termed obesity hypoventilation syndrome (Zwillich et al., 1975; Mokhlesi et al., 2008; Mokhlesi, 2010; Piper and Grunstein, 2011). The failure of the high leptin levels to suppress appetite and increase energy expenditure in these obese individuals is generally attributed to a resistance to leptin (Myers et al., 2008; Al Dabal and BaHammam, 2009). "
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    ABSTRACT: Leptin decreases food intake and increases energy expenditure. Leptin administration into the CNS of mice or rats increases alveolar ventilation and dysfunction in leptin signaling has been implicated in the hypoventilation that can accompany obesity. An increase in CO(2) chemosensitivity has been implicated in this response but it is unclear whether ventilation is augmented when PCO(2) is maintained constant. We examined the effects of intravenous leptin to test the hypothesis that systemic leptin administration in isoflurane anesthetized, mechanically ventilated and vagotomized rats would lead to a sustained increase in respiratory motor output that was independent of changes in end-tidal PCO(2), body temperature or lung inflation pressure (an indicator of overall lung and chest wall compliance). In anesthetized Sprague-Dawley rats with end-tidal PCO(2), lung compliance and rectal temperature maintained constant, injection of a bolus of leptin (0.25 mg, 0.5 mg/ml, i.v.), followed over the next 1 h by the intravenous infusion of an additional 0.25 mg, elicited a progressive increase in the peak amplitude of integrated phrenic nerve discharge lasting at least 1 h beyond the end of the infusion. The increase peaked at 90 min at 58.3 ± 5.7% above baseline. There was an associated increase in the slope of the phrenic response to increasing inspired CO(2). There was also a moderate and sustained decrease in arterial pressure 9 ± 1.3 mmHg at 120 min, with no associated change in heart rate. These data indicate that leptin elicits a sustained increase in respiratory motor output that outlasts the administration leptin via a mechanism that does not require alterations in arterial PCO(2), body temperature, or systemic afferent feedback via the vagus nerves. This stimulation may help to prevent obesity-related hypoventilation.
    Frontiers in Physiology 02/2013; 4:16. DOI:10.3389/fphys.2013.00016 · 3.53 Impact Factor
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