Effects of CPAP in patients with obstructive apnoea: is the presence of allergic rhinitis relevant?

PURPOSE: The aim of the study is to compare the effects of continuous positive airway pressure (CPAP) on the nasal cavities of patients with obstructive sleep apnoea (OSA) and with or without allergic rhinitis (AR/nonAR). METHODS: This paper is a prospective, longitudinal study. Thirty-four consecutive CPAP treatment-adherent patients with OSA (17 AR and 17 nonAR) were evaluated before and 2 months after treatment, by means of clinical (otorhinolaryngological symptoms, daytime sleepiness, overall and rhinoconjunctivitis-specific quality of life), anatomical (otorhinolaryngological examination), functional (auditory function, tubal function, nasal airflow, and mucociliary clearance), and biological variables (nasal cytology). No humidifier or anti-allergy medicines were used during treatment. RESULTS: Before treatment, patients with AR presented a higher score, compared to nonAR in rhinitis symptoms (4.82 ± 2.53 vs. 0.93 ± 1.02, p = 0.000), otologic symptoms (2.06 ± 1.95 vs. 0.44 ± 0.72, p = 0.004), cutaneous/ocular symptoms (2.12 ± 2.17 vs. 0.65 ± 1.17, p = 0.052), immunoglobulin E (181.82 ± 126.09 vs. 66.13 ± 97.97, p = 0.004), and nasal neutrophils (14.42 ± 31.94 vs. 0.16 ± 0.39, p = 0.031). After treatment, nonAR and AR groups improved in daytime sleepiness (11.53 ± 4.60 vs. 7.53 ± 2.87, p = 0.000 and 13.76 ± 4.93 vs. 7.53 ± 4.41, p = 0.001) respectively and increased nasal neutrophil (0.16 ± 0.39 vs. 5.78 ± 9.43, p = 0.001 and 14.42 ± 31.94 vs. 79.47 ± 202.08, p = 0.035). The symptoms and quality of life improved in patients with AR. NonAR patients, significantly increase nasal dryness (1.65 ± 1.27 vs. 0.00, p = 0.002) and mucociliary clearance times (38.59 ± 24.90 vs. 26.82 ± 23.18, p = 0.016). CONCLUSIONS: CPAP produces inflammation with increased nasal neutrophil levels in AR and nonAR patients. Nevertheless, patients with AR observed an improvement in nasal symptoms and quality of life, whereas in patients without AR, a relevant worsening of nasal dryness and mucociliary transport was observed.

Adipose tissue in obesity and obstructive sleep apnoea.

A European Respiratory Society research seminar on "Metabolic alterations in obstructive sleep apnoea (OSA)" was jointly organised in October 2009 together with two EU COST actions (Cardiovascular risk in the obstructive sleep apnoea syndrome, action B26, and Adipose tissue and the metabolic syndrome, action BM0602) in order to discuss the interactions between obesity and OSA. Such interactions can be particularly significant in the pathogenesis of metabolic abnormalities and in increased cardiovascular risk in OSA patients. However, studying the respective role of OSA and obesity is difficult in patients, making it necessary to refer to animal models or in vitro systems. Since most OSA patients are obese, their management requires a multidisciplinary approach. This review summarises some aspects of the pathophysiology and treatment of obesity, and the possible effects of sleep loss on metabolism. OSA-associated metabolic dysfunction (insulin resistance, liver dysfunction and atherogenic dyslipidaemia) is discussed from the perspective of both obesity and OSA in adults and children. Finally, the effects of treatment for obesity or OSA, or both, on cardio-metabolic variables are summarised. Further interdisciplinary research is needed in order to develop new comprehensive treatment approaches aimed at reducing sleep disordered breathing, obesity and cardiovascular risk.

Increased incidence of nonfatal cardiovascular events in stroke patients with sleep apnoea: effect of CPAP treatment.

Obstructive sleep apnoea (OSA) is a risk factor for stroke, but little is known about the effect of OSA and continuous positive airway pressure (CPAP) on the incidence of long-term, nonfatal cardiovascular events (CVE) in stroke patients. A prospective observational study was made in 223 patients consecutively admitted for stroke. A sleep study was performed on 166 of them. 31 had an apnoea/hypopnoea index (AHI) <10 events · h(-1); 39 had an AHI between 10 and 19 events · h(-1) and 96 had an AHI ≥ 20 events · h(-1). CPAP treatment was offered when AHI was ≥ 20 events · h(-1). Patients were followed up for 7 yrs and incident CVE data were recorded. The mean ± SD age of the subjects was 73.3 ± 11 yrs; mean AHI was 26 ± 16.7 events · h(-1). Patients with moderate-to-severe OSA who could not tolerate CPAP (AHI ≥ 20 events · h(-1); n = 68) showed an increased adjusted incidence of nonfatal CVE, especially new ischaemic strokes (hazard ratio 2.87, 95% CI 1.11-7.71; p = 0.03), compared with patients with moderate-to-severe OSA who tolerated CPAP (n = 28), patients with mild disease (AHI 10-19 events · h(-1); n = 36) and patients without OSA (AHI <10 events · h(-1); n = 31). Our results suggest that the presence of moderate-to-severe OSA is associated with an increased long-term incidence of nonfatal CVE in stroke patients and that CPAP reduces the excess of incidence seen in these patients.

Automatic CPAP performance in patients with sleep apnea plus COPD.

BACKGROUND: Automatic CPAP devices have demonstrated good results in obtaining optimal fixed CPAP pressure to eliminate respiratory events in patients with sleep apnea-hypopnea syndrome (SAHS). However, automatic CPAP has not been fully studied in patients with COPD plus SAHS. OBJECTIVES: To analyse the performance of an automatic CPAP in severe COPD patients compared with SAHS patients with no associated co-morbidity. METHODS: We compared 10 consecutive patients with SAHS and no associated co-morbidity and 10 patients with SAHS plus severe COPD who required CPAP titration. Automatic CPAP performance was studied during full-night PSG. Inadequate pressure increase periods, absence of pressure increases in reaction to respiratory events, air leak periods, and pressure behaviour in the face of erratic breathing periods were analysed. RESULTS: The SAHS patients without co-morbidities vs. SAHS plus COPD patients presented: mean sleep efficiency, 80.2 (11.5)% vs. 76.5 (12.1)%; residual AHI, 6.3 (5.2) vs. 5.1 (7.7); residual CT90, 1 (3)% vs. 14 (1)%. The device´s performance demonstrates a mean of 1.2 (1.5) vs. 1.3 (1.2) periods of inadequate pressure increases; absence of pressure increases in reaction to respiratory events, 4.1 (5.4) vs. 0.6 (0.7) times; periods of air leaks, 1.3 (3.8) vs. 13.9 (11.7); mean optimal pressure, 9.1 (1.4) vs. 9.0 (1.9) cm H(2)O. CONCLUSION: Titration with automatic CPAP could be as effective in patients with SAHS plus severe COPD as in patients with SAHS without COPD. However, the presence of more leakages must be taken into account.

Obstructive sleep apnoea and metabolic impairment in severe obesity.

Obstructive sleep apnoea (OSA) seems to worsen metabolism. This effect has not been evaluated in morbid obesity (MO). We hypothesised that the metabolic profile is more impaired in MO patients with OSA than in those without, and investigated whether any specific metabolic dysfunction is related to OSA in MO. A prospective multicentre cross-sectional study was conducted in consecutive subjects before bariatric surgery. OSA was defined as apnoea/hypopnoea index (AHI) ≥15 by overnight polysomnography. Anthropometrical, blood pressure (BP) and fasting blood measurements were obtained the morning after. Metabolic syndrome (MetS) was defined according to National Cholesterol Education Program Adult Treatment Panel III modified criteria. 159 patients were studied: 72% were female and 72% had OSA. MetS prevalence was 70% in OSA versus 36% in non-OSA (p<0.001). As AHI severity increased, metabolic parameters progressively worsened, even in those without type 2 diabetes (DM2). AHI was independently associated with systolic and diastolic BP, triglycerides and the percentage of glycosylated haemoglobin (HbA1c) in the total sample, and with systolic BP, high-density lipoprotein cholesterol and HbA1c in those samples without DM2. OSA increased the adjusted odds ratio of having MetS by 2.8 (95% CI 1.3-6.2; p=0.009). In MO, OSA is associated with major metabolic impairment caused by higher BP and poorer lipid and glucose control, independent of central obesity or DM2.

The European Sleep Apnoea Database (ESADA): report from 22 European sleep laboratories.

The European Sleep Apnoea Database (ESADA) reflects a network of 22 sleep disorder centres in Europe enabled by a COST action B26 programme. This ongoing project aims to describe differences in standard clinical care of patients with obstructive sleep apnoea (OSA) and to establish a resource for genetic research in this disorder. Patients with suspected OSA are consecutively included and followed up according to local clinical standards. Anthropometrics, medical history, medication, daytime symptoms and sleep data (polysomnography or cardiorespiratory polygraphy) are recorded in a structured web-based report form. 5,103 patients (1,426 females, mean±sd age 51.8±12.6 yrs, 79.4% with apnoea/hypopnoea index (AHI) ≥5 events·h(-1)) were included from March 15, 2007 to August 1, 2009. Morbid obesity (body mass index ≥35 kg·m(-2)) was present in 21.1% of males and 28.6% of females. Cardiovascular, metabolic and pulmonary comorbidities were frequent (49.1%, 32.9% and 14.2%, respectively). Patients investigated with a polygraphic method had a lower AHI than those undergoing polysomnography (23.2±23.5 versus 29.1±26.3 events·h(-1), p<0.0001). The ESADA is a rapidly growing multicentre patient cohort that enables unique outcome research opportunities and genotyping. The first cross-sectional analysis reveals a high prevalence of cardiovascular and metabolic morbidity in patients investigated for OSA.

Sleep breathing flow characteristics as a sign for the detection of wakefulness in patients with sleep apnea.

BACKGROUND: To improve the performance of simplified sleep studies, it is essential to properly estimate the sleep time. OBJECTIVES: Our aim is to estimate sleep efficiency on the basis of flow breathing signal characteristics. METHODS: Twenty subjects with sleep apnea-hypopnea syndrome diagnosed by polysomnography were studied. A characteristic pattern of flow signal defined our criteria for wakefulness and sleep. Sleep was analyzed in 2 different runs: (1) in the usual manner (neurological and respiratory variables), and (2) only the nasal cannula flow signal was displayed on the computer screen and the sleep and wakefulness periods were scored according to our criteria. At the end of the scoring process, all the signals were displayed on the screen to analyze the concordance. RESULTS: Three thousand and sixty-nine screens were analyzed. The polysomnography sleep efficiency measured was 80.8%. The estimated sleep efficiency measured by nasal prongs was 78.9%. The detection and concordance of wakefulness had a sensitivity of 58.7%, a specificity of 96.4%, a positive predictive value of 81.3% and a negative predictive value of 89.6%. CONCLUSIONS: Our criteria for sleep and wakefulness based on airflow waveform morphology are a helpful parameter for estimating sleep efficiency in a simplified sleep study.

Apnoeic and obstructive nonapnoeic sleep respiratory events.

Obstructive nonapnoeic event (ONE) scoring is shrouded in confusion. This is important in patients with mild disease, in whom precision is crucial. The aims of the present study were: 1) to identify ONEs using oesophageal pressure (OP) (OP-ONEs) and a noninvasive (NI) method (NI-ONEs); 2) to compare both methods of scoring; and 3) to determine the contribution of ONE definitions to clinical findings. Patients with suspected sleep apnoeas (respiratory disturbance index

Obstructive sleep apnea has little impact on quality of life in the elderly.

STUDY OBJECTIVE: To analyze the impact of the number of respiratory sleep disorders or clinically related conditions (especially excessive daytime sleepiness [EDS]), on health related quality of life (HRQoL) in subjects over 65 years of age, as compared to younger subjects and the general population. METHODS: Two hundred and twelve adult patients with obstructive sleep apnea (OSA, AHI> or =10) divided into two age groups, over 65 (n=109, mean age 74.6 [6,8] years, and 65 or under (n=103, mean age 51.7, [6,5] years). General, anthropometric and clinical data related to OSA (epworth sleepiness score [ESS]), comorbidities (Charlson comorbidity index [CCI]), HRQoL (SF-36 questionnaire), use of psychotropic medications and habitual polygraphic/polysomnographic parameters were recorded and compared between the two age groups. The HRQoL values in each age group were compared with the values in the general population, adjusted for age and gender. RESULTS: In patients 65 and under, both the presence of OSA as well as the presence of EDS (ESS>11) were associated with an important deterioration in HRQoL as compared to normal reference values. The principal determinants of HRQoL were the presence of EDS (p<0.04), body mass index (p<0.03) and the apnea-hypopnea index (AHI) (p<0.04). Nevertheless, in subjects over 65 years of age, the presence of OSA or EDS had only a slight impact on HRQoL, relative to normal values. In this age group, the principal determinants of HRQoL were the presence of comorbidities (CCI, p<0.01), age (p<0.01), oxygen desaturation parameters (p<0.04) and the use of psychotropic medications (p<0.04). CONCLUSION: In elders, the presence of OSA with or without EDS has little impact on HRQoL measures.

Upper airway collapse and reopening induce inflammation in a sleep apnoea model.

The upper airway of obstructive sleep apnoea patients is subjected to recurrent negative pressure swings promoting its collapse and reopening. The aim of the present study was to ascertain whether this mechanical stress induces upper airway inflammation in a rat model. The upper airway of Sprague-Dawley rats was subjected to a periodic pattern of recurrent negative (-40 cmH2O, 1 s) and positive (4 cmH2O, 2 s) pressures inducing collapse and reopening for 5 h. Rats that were instrumented but not subjected to negative pressure swings were used as controls. The gene expression of the pro-inflammatory biomarkers macrophage inflammatory protein (MIP)-2, tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and P-selectin in the soft palate and larynx tissues was assessed by real-time PCR. A marked overexpression of MIP-2, TNF-alpha, IL-1beta and P-selectin (approximately 40-, 24-, 47- and 7-fold greater than controls, respectively) was observed in the larynx tissue; similar results were found in the soft palate tissue (approximately 14-, 7-, 35- and 11-fold greater than controls, respectively). Recurrent upper airway collapse and reopening mimicking those experienced by obstructive sleep apnoea patients triggered an early local inflammatory process. These results could explain the inflammation observed in the upper airway of obstructive sleep apnoea patients.

Early effects of continuous positive airway pressure in a rodent model of allergic rhinitis.

BACKGROUND: Continuous positive airway pressure (CPAP) is the most commonly used treatment in obstructive sleep apnea. In a previous rat model study, we demonstrated that nasal CPAP induces early rhinitis expressed by nasal neutrophil extravasation. Here we hypothesized that nasal CPAP would worsen nasal inflammation on a previously inflamed mucosa. The objective of this study was to evaluate the early nasal CPAP effects of allergic rhinitis (AR) in a rodent model. METHODS: Twenty Sprague-Dawley rats were sensitized with intraperitoneal ovalbumin (OVA). Nasal inflammation was induced by the administration of intranasal OVA during consecutive days. The same procedure was performed in 20 control rats treated with saline solution. The allergic (AR) and non-allergic (NAR) rats were then randomized to nasal CPAP at 10 cm H2O for five hours or to sham CPAP. The degree of nasal inflammation was assessed by evaluating the percentage of neutrophils, eosinophils, basophils, and lymphocytes in the nasal mucosa. An unpaired Mann-Whitney test was used to analyze differences between groups. RESULTS: The greatest inflammation was observed in the group of AR without CPAP (1.24% ± 0.94%), followed by NAR with CPAP (0.64% ± 0.30%), AR with CPAP (0.64% ± 0.40%), and NAR without CPAP (0.21% ± 0.29%). CONCLUSIONS: Administration of nasal CPAP or allergy sensitization can produce, individually, neutrophil extravasation on the nasal mucosa of a rat model. The application of both stimuli is not responsible for increased inflammation. Therefore, this study suggests that rhinitis is not a major limitation for CPAP administration.

Importance of the pulse oximeter averaging time when measuring oxygen desaturation in sleep apnea.

The accuracy of pulse oximeters in measuring transient changes in oxygen saturation (SaO2) may be affected by the oximeter time response. The aim of this study was to assess the effect of modifying the pulse oximeter averaging time (T) on the measurement of SaO2 in patients with the sleep apnea-hypopnea syndrome (SAHS). Twelve patients with severe SAHS were studied during a nap with conventional oximeters: Ohmeda 3740 and Criticare 501. We compared the readings of each patient's oxygen desaturation measured simultaneously with two identical pulse oximeters. One oximeter was the control (T = 3 seconds), and in the other T was set from 3 seconds to 21 seconds. No significant differences in SaO2 were found when both oximeters were set to the same T (3 seconds). In contrast, increasing T to 12 seconds and 21 seconds in one of the oximeters resulted in considerable and significant differences in the measured SaO2: oxygen desaturation was underestimated by up to 60% when compared with the control. The misestimation of SaO2 induced by settings of T which are within the range selectable in conventional oximeters may be of epidemiological significance when pulse oximetry is used as a complementary diagnostic tool to classify sleep events in SAHS.

Measurement of general health status in obstructive sleep apnea hypopnea patients.

Sleep apnea hypopnea syndrome (SAHS) is an entity that occurs frequently in the population and produces an elevated morbidity and mortality, especially at an apnea index greater than 20 events per hour. To our knowledge there are only a few studies available addressing the general health status of sleep apnea hypopnea patients. Such information may be useful for both clinical management and better understanding of the physiopathological mechanisms of the disease, particularly with the consideration that not infrequently the physiological disturbances found in such patients do not always agree with their own health perception. Therefore, the aim of the present study was to assess the general health status and the degree of daytime somnolence, as a major symptom in SAHS patients, and relate them to the number of respiratory events per hour. Measurements of general health status and the degree of daytime somnolence were assessed in 103 consecutive patients 50.4 +/- 12 years old [mean +/- standard deviation (SD)] with an apnea/hypopnea index (AHI) of 38 +/- 27 events per hour. Forty nonsnoring healthy subjects were used as the control group. During the afternoon preceding the full polysomnography, a medical history was taken; basic anthropometric data and the presence of other diseases were recorded. The Nottingham Health Profile (NHP) questionnaire and a questionnaire assessing the degree of daytime somnolence were administered to the patients. No significant differences were found in the general health status and the degree of daytime hypersomnolence when patients were divided into three groups according to the severity of the respiratory events during the night, but there were significant differences between SAHS patients and control subjects. It was concluded that in spite of the fact that SAHS patients showed a deterioration of general health status parameters in comparison with healthy subjects, these parameters do not correlate with the physiological disturbances of SAHS, expressed as the number of respiratory events per hour.

Upper airway resistance syndrome.

This article reviews the clinical picture, diagnosis and management of the upper airway resistance syndrome (UARS). Presently, there is not enough data on key points like the frequency of UARS and the morbidity associated with this condition. Furthermore, the existence of LIARS as an independent sleep disorder and its relation with snoring and obstructive events is in debate. The diagnosis of UARS is still a controversial issue. The technical limitations of the classic approach to monitor airflow with thermistors and inductance plethysmography, as well as the lack of a precise definition of hypopnea, may have led to a misinterpretation of UARS as an independent diagnosis from the sleep apnea/hypopnea syndrome. The diagnosis of this syndrome can be missed using a conventional polysomnographic setting unless appropriate techniques are applied. The use of an esophageal balloon to monitor inspiratory effort is currently the gold standard. However, other sensitive methods such as the use of a pneumotachograph and, more recently, nasal cannula/pressure transducer systems or on-line monitoring of respiratory impedance with the forced oscillation technique may provide other interesting possibilities. Recognition and characterization of this subgroup of patients within sleep breathing disorders is important because they are symptomatic and may benefit from treatment. Management options to treat UARS comprise all those currently available for sleep apnea/hypopnea syndrome (SAHS). However, the subset of patients classically identified as LIARS that exhibit skeletal craneo-facial abnormalities might possibly obtain further benefit from maxillofacial surgery.

Bronchial adenocarcinoma presenting as a lingual tonsillar metastasis.

We describe a case of a lingual tonsillar metastasis as the first manifestation of a bronchial adenocarcinoma. Tonsillar metastases infrequently become manifest before the diagnosis of the primary neoplasm. A review of the literature disclosed 89 cases of carcinoma metastasizing to the palatine tonsil, but no one has reported the involvement of the lingual tonsil. Our patient is the first described case of bronchogenic carcinoma with this unusual form of presentation and furthermore is also the first carcinoma metastasizing to the lingual tonsil.

Ventilation-perfusion response after fenoterol in hypoxemic patients with stable COPD.

BACKGROUND: The effects of vasoactive drugs, including bronchodilators, on vascular and pulmonary dynamics are interrelated, complex and difficult to measure, but important because of potential deleterious effects on gas exchange. METHODS: To assess the effects of fenoterol at both high and low dose on pulmonary gas exchange in 24 hypoxemic patients with stable COPD: fenoterol, 5 mg; fenoterol, 1 mg and ipratropium bromide, 0.5 mg; ipratropium bromide, 0.5 mg; or matched placebo were nebulized in a double-blind, placebo-controlled fashion. Spirometry, ventilation, systemic hemodynamics, and respiratory and inert gases were measured before and 15, 60, and 120 min after each treatment. RESULTS: Compared with placebo, heart rate (p < 0.002) and cardiac output (p = 0.05) increased after high-dose fenoterol therapy to return to baseline values by 120 min. Following fenoterol at high dose, mean maximum PaO2 change from baseline decreased by 6.3 +/- 1.1 mm Hg (SD) and both alveolararterial oxygen pressure difference (P[A-a]O2), by 8.3 +/- 4.0 mm Hg, and ventilation-perfusion (VA/Q) mismatching increased, as evidenced by increments of the dispersion of pulmonary blood flow, without reaching significance; likewise, low-dose fenoterol therapy increased VA/Q inequalities while both PaO2 and P(A-a)O2 remained unchanged. CONCLUSIONS: In this population of COPD patients, high-dose fenoterol therapy [corrected] significantly increased heart rate and cardiac output resulting in minor adverse consequences on arterial oxygenation and VA/Q relationships.