OBJECTIVE:To investigate the prevalence of sleep breathing disorders, loud snoring and excessive daytime sleepiness in a group of obese subjects, and to identify the predictors of obstructive sleep apnea (OSA) severity in these patients. SUBJECTS: A total of 161 consecutive obese patients (body mass index (BMI) ! 30.0 kgam 2 ), ranging between 30.0 and 67.3, represented by 57 men and 104 women, aged 16 ± 75 y. Forty (15 men and 25 women) age-matched (20 ± 70 y) nonobese (BMI`27 kgam 2 ) volunteers were also recruited for the study. MEASUREMENTS: Respiratory function parameters, nocturnal sleep quality (evaluated by a speci®c questionnaire), nocturnal hypoventilation and OSA (evaluated by night polysomnography) were examined in all subjects. Anthropometric parameters (neck circumference, waist circumference, waist-to-hip ratio) were also investigated. RESULTS: Eighty-three obese patients (51.5% of the obese group) had a respiratory disturbance index (RDI) ! 10, corresponding to a moderate or severe sleep apnea. In particular, 24.8% (40a161), ie a quarter of all obese patients, were affected by severe OSA and this alteration was present in 42.1% of obese men (24a57) and in 15.4% (16a104) of obese women. When a stepwise multiple regression analysis was performed, neck circumference in men and BMI in women were shown to be the strongest predictors of sleep apnea. Twenty-nine percent of all obese subjects (40.3% of men and 23.1% of women) showed nocturnal hypoventilation; however, it was present as a unique breathing alteration in only 5% of the obese population. The percentage of patients having excessive daytime sleepiness was signi®cantly higher than in nonobese subjects, even when only nonapneic obese patients were considered (P`0.001). CONCLUSION: This study shows that OSA is present in more than 50% of a population of obese patients with a mean BMI higher than 40.0, this percentage being much higher than that commonly reported in previous studies, particularly in women. Neck circumference in men and BMI in women seem to be the strongest predictors of the severity of OSA in obese patients. Nocturnal hypoventilation seems to be present in more than 29% of a severe obese population. Moreover, this study indicates that morbid obesity can be associated with excessive daytime sleepiness even in the absence of sleep apnea.

It is well known that obstructive sleep apnoea is especially frequent in the morbidly obese. In these subjects diurnal chronic hypercapnia, whose mechanism is still debated, may be present. Our study was performed to evaluate the prevalence and the mechanism of diurnal hypercapnia in the morbidly obese affected by obstructive sleep apnoea. From a population referred to our centre because of suspicion of sleep related breathing disorders, we selected 285 subjects without cardiopulmonary, neuromuscular or endocrinological diseases: 89 (36 M and 53 F, aged 46+/-13 years) had body mass index (BMI) > or = 40 kg m(-2) (MO group: morbidly obese subjects) and 196 (99 M and 97 F, aged 48+/-16 years) had BMI <40 kg m(-2) (NMO group: non-morbidly obese subjects). Then the MO group was divided into three subgroups: normocapnic subjects without obstructive sleep apnoea, normocapnic subjects with obstructive sleep apnoea, hypercapnic subjects with obstructive sleep apnoea; while we found no hypercapnic subject without obstructive sleep apnoea. All subjects underwent anthropometric evaluations and bioelectrical impedance analyses, respiratory function tests and arterial blood gas analysis, a modified version of the Sleep and Healthy questionnaire and a full night polysomnography. Our results showed that hypercapnia (PaCO2 > or = 45 mm Hg) associated with obstructive sleep apnoea [respiratory disturbance index (RDI) > or = 10 h(-1)] was found in 27% of the morbidly obese subjects, but only in 11% of the nonmorbidly obese ones (P<0.01). The comparison among the three subgroups, in which we divided the morbidly obese subjects, shows that those with hypercapnia and obstructive sleep apnoea had significantly more important ventilatory restrictive defects [forced vital capacity (FVC)% of pred 73.27+/-14 81 vs. 82.37+/-16.93 vs. 87.25+/-18.14 respectively; total lung capacity (TLC)% of pred 63.83+/-16.35 vs. 79.11+/-14.15 vs. 87.01+/-10.5], a significantly higher respiratory disturbance index (RDI 46.34+/-26.90 vs. 31.79+/-22.47 vs. 4.98+/-3.29) a longer total sleep time with oxyhaemoglobin saturation<90% [total sleeptime (TST)SaO2<90% 63.40+/-33.86 vs. 25.95+/-29.34 vs. 8.22+/-22.12] and a lower rapid eye movement (REM) stage (9.5+/-1.2 vs. 14.0+/-0.9 vs. 17.05+/-1.2) than normocapnic subjects with obstructive sleep apnoea or subjects without obstructive sleep apnoea. The best model to predict PaCO2 resulted from a combination of TSTSaO2<90% (r2 = 0.22, P<0.001), forced expiratory volume in 1 sec (FEV1)% of pred (r2 = 0.09, P<0.01), FVC % of pred (r2 = 0.075, P<0.01). In conclusion our study suggests that diurnal hypercapnia is frequently associated with obstructive sleep apnoea in the morbidly obese without chronic obstructive pulmonary disorder (COPD) and that ventilatory restriction and sleep related respiratory disturbances correlate to diurnal hypercapnia.

No abstract

In the majority of patients admitted to an Intensive Care Unit with acute respiratory failure (ARF), the aetiology for ARF is quite evident. In a minority of patients no obvious aetiology is apparent at presentation. In this group a previously unrecognized sleep-related breathing disorder (SRBD) may be the cause of the ARF. In spite of clinical suspicion SRBD remains infrequently diagnosed in ARF also because the technology necessary for this type of diagnosis (polysomnography) is usually unavailable in Intensive Care Units. The aim of this study was to evaluate the utility of portable polysomnography system (PSGp) in a group of patients with ARF of unclear aetiology and with a clinical suspicion of SRBD. We studied a selected group of 14 patients (eight males, six females) admitted to an Intermediate Intensive care unit with varying degree of acute respiratory failure. Mean (SD) age was 57 (13) years, pH 7.28 (0.04), PaO2 5.6 (0.7) kPa), PaO2 (8.8 (1.6) kPa), Body mass index 42.7 (9.6) kg m(-2). The patients had no history of skeletal, neuromuscular or cardiovascular disease. None of them had a history of overt chronic lung diseases or had obvious respiratory tract infections. They were submitted to cardiac and respiratory functional evaluation and to nightly PSGp (VITALOG HMS 5000, Respironics Inc., Redwood City, CA, U.S.A.) which was performed in an intermediate intensive care unit. Ten subjects had obstructive sleep apnoea-hypopnoea syndrome (OSAS), with mean respiratory disorder index h(-1) (RDI) 60.1 (25.9) [in five associated with obesity-hypoventilation syndrome (OHS)]; two had central sleep apnoea with mean RDI 45 (28.3) (one with hypothyroidism and one with cerebral multiple infarctions and right hemidiaphragmatic paralysis) and two had OHS with mean RDI 12.5 (3.5). Nocturnal hypoventilation was present in almost all patients. Continuous positive airway pressure (CPAP) was effective in three patients. Eight patients needed to be treated with BILEVEL (BiPAP, Respironics Inc.) airway positive pressure in timed or spontaneous/timed modes. Two patients required intubation and mechanical ventilatory treatment. In one patient with hypothyroidism was sufficient to institute hormonal therapy. Our study shows that acute respiratory failure due to SRBD is not exceptional in an Intermediate Intensive Care Unit and that if clinical suspicion is strong, portable polysomnography may yield diagnostic confirmation and help in establishing appropriate treatment and in avoiding the invasive ventilatory treatment.

No abstract