Search

BackgroundCurrent guidelines recommend that patients with obesity hypoventilation syndrome (OHS) are electively admitted for inpatient initiation of home non-invasive ventilation (NIV). We hypothesised that outpatient NIV setup would be more cost-effective.MethodsPatients with stable OHS referred to six participating European centres for home NIV setup were recruited to an open-labelled clinical trial. Patients were randomised via web-based system using stratification to inpatient setup, with standard fixed level NIV and titrated during an attended overnight respiratory study or outpatient setup using an autotitrating NIV device and a set protocol, including home oximetry. The primary outcome was cost-effectiveness at 3 months with daytime carbon dioxide (PaCO2) as a non-inferiority safety outcome; non-inferiority margin 0.5 kPa. Data were analysed on an intention-to-treat basis. Health-related quality of life (HRQL) was measured using EQ-5D-5L (5 level EQ-5D tool) and costs were converted using purchasing power parities to £(GBP).ResultsBetween May 2015 and March 2018, 82 patients were randomised. Age 59±14 years, body mass index 47±10 kg/m2and PaCO26.8±0.6 kPa. Safety analysis demonstrated no difference in ∆PaCO2(difference −0.27 kPa, 95% CI −0.70 to 0.17 kPa). Efficacy analysis showed similar total per-patient costs (inpatient £2962±£580, outpatient £3169±£525; difference £188.20, 95% CI −£61.61 to £438.01) and similar improvement in HRQL (EQ-5D-5L difference −0.006, 95% CI −0.05 to 0.04). There were no differences in secondary outcomes.DiscussionThere was no difference in medium-term cost-effectiveness, with similar clinical effectiveness, between outpatient and inpatient NIV setup. The home NIV setup strategy can be led by local resource demand and patient and clinician preference.Trial registration numbersNCT02342899andISRCTN51420481.

BackgroundThe optimal interface for the delivery of home non-invasive ventilation (NIV) to treat chronic respiratory failure has not yet been determined. The aim of this individual participant data (IPD) meta-analysis was to compare the effect of nasal and oronasal masks on treatment efficacy and adherence in patients with COPD and obesity hypoventilation syndrome (OHS).MethodsWe searched Medline and Cochrane Central Register of Controlled Trials for prospective randomised controlled trials (RCTs) of at least 1 month’s duration, published between January 1994 and April 2019, that assessed NIV efficacy in patients with OHS and COPD. The main outcomes were diurnal PaCO2, PaO2 and NIV adherence (PROSPERO CRD42019132398).FindingsOf 1576 articles identified, 34 RCTs met the inclusion criteria and IPD were obtained for 18. Ten RCTs were excluded because only one type of mask was used, or mask data were missing. Data from 8 RCTs, including 290 IPD, underwent meta-analysis. Oronasal masks were used in 86% of cases. There were no differences between oronasal and nasal masks for PaCO2 (0.61 mm Hg (95% CI −2.15 to 3.38); p=0.68), PaO2 (−0.00 mm Hg (95% CI −4.59 to 4.58); p=1) or NIV adherence (0·29 hour/day (95% CI −0.74 to 1.32); p=0.58). There was no interaction between the underlying pathology and the effect of mask type on any outcome.InterpretationOronasal masks are the most used interface for the delivery of home NIV in patients with OHS and COPD; however, there is no difference in the efficacy or tolerance of oronasal or nasal masks.

Automatically titrated O2 flows (FreeO2) was compared with constant O2 flow on exercise capacity, O2 saturation and risk of hyperoxia-related hypercapnia in patients with severe COPD with baseline hypercapnia and long-term oxygen therapy (LTOT). Twelve patients were enrolled in a randomised double-blind cross-over study to perform exercise with either FreeO2 or constant flow. Endurance time (primary outcome) and SpO2 were both significantly improved with FreeO2compared with constant flow (p2 was similar in both conditions. Automated titration of O2 significantly and clinically improved endurance walking time in patients with severe COPD receiving LTOT, without worsening of pCO2.Trial registration numberResults , NCT01575327

BackgroundObstructive sleep apnoea (OSA) and obesity are interdependent chronic diseases sharing reduced exercise tolerance and high cardiovascular risk.InterventionA 3-month intervention with innovative training modalities would further improve functional capacity and cardiovascular health than usual cycle exercise training in already continuous positive airway pressure (CPAP)-treated obese patients with OSA.MethodsFifty three patients (352) were randomly allocated to exercise training on a cycle ergometer, either alone (ERGO) or with respiratory muscle training (ERGO+RMT) or non-invasive ventilation (ERGO+NIV). Changes in 6 min walking distance (primary outcome), aerobic capacity (VO2peak), cardiovascular parameters, body composition and sleep quality were evaluated.Measurements and main resultsAll training modalities increased 6 min walking distance without differences between groups (P=0.97). ERGO+NIV and ERGO+RMT led to significantly higher improvement in VO2peak compared with ERGO (3.1 (95% CI 1.6 to 4.6) vs 2.3 (0.8 to 3.7) vs 0.5(−1.0 to 1.9) mL/min/kg, respectively, P=0.04) and ERGO+NIV significantly reduced self-measured blood pressure compared with ERGO+RMT and ERGO (systolic: −9.5 (95% CI −14.1 to −4.9) vs −13 (−5.8 to 3.1) vs −0.7 (−5.1 to 3.8) mm Hg, respectively, P=0.01). Waist and neck circumferences were reduced after ERGO+NIV compared with ERGO+RMT and ERGO (P=0.01).ConclusionsCombining RMT or NIV with cycling exercise training failed to provide further improvement in functional capacity as compared with cycling exercise training alone. However, the combination of NIV and exercise training demonstrated superiority for improving cardiometabolic risk factors in obese CPAP-treated patients with OAS.TRIAL REGISTRATION NUMBERResults, NCT01155271.

RationaleCustom-made mandibular advancement devices (MADs) are reported as providing higher efficacy rates compared with thermoplastic heat-moulded MADs but at the price of higher costs and treatment delays.ObjectiveTo determine whether a thermoplastic heat-moulded titratable MAD (ONIRIS; ONIRIS SAS, Rueil Malmaison, France) is non-inferior to a custom-made acrylic titratable MAD (TALI; ONIRIS SAS, Rueil Malmaison, France) for obstructive sleep apnoea (OSA).MethodsWe conducted a multicentre, open, randomised controlled trial of patients with OSA refusing or not tolerating continuous positive airway pressure (CPAP). Participants were randomly assigned to a thermoplastic heat-moulded titratable device or a custom-made acrylic device for 2 months with stratification by centre and OSA severity. The non-inferiority primary outcome was a ≥50% reduction in apnoea–hypopnoea index (AHI) or achieving AHI Main resultsOf 198 patients (mean age 51 [SD, 12] years; 138 [72.6%] men; mean body mass index 26 [SD, 2.7] kg/m2; mean AHI 26.6/hour [SD, 10.4]), 100 received TALI and 98 ONIRIS. In per-protocol analysis, the response rate was 51.7% in the TALI group versus 53.6% in the ONIRIS group (absolute difference 1.9%; 90% CI: 11% to 15%, within the non-inferiority margin). Effectiveness was the same for severity, symptoms, quality of life and blood pressure reduction. Patients in ONIRIS group reported more side effects and adherence was slightly better with TALI.ConclusionIn patients with OSA refusing or not tolerating CPAP, the thermoplastic heat-moulded titratable MAD was non-inferior in the short-term to the custom-made acrylic MAD.Trial registration numberNCT02348970.

Systemic inflammation and metabolic disorders are among the mechanisms linking obstructive sleep apnoea (OSA) and cardiovascular disease (CVD). In 109 patients with severe OSA and no overt CVD, biomarkers of inflammation (C reactive protein, interleukin-6, tumour necrosis factor-α and its receptors, adiponectin, leptin and P-selectin), glucose and lipid metabolism, and N-terminal pro-brain natriuretic peptide, were measured before and after 2 months of treatment with a mandibular advancement device (MAD) (n=55) or a sham device (n=54). MAD reduced the Apnoea–Hypopnoea Index (pTrial registration numberNCT01426607.

Automatically titrated O

Obstructive sleep apnoea (OSA) is a major health concern worldwide with multiorgan consequences and the resulting increased economic and social burden.1 OSA is associated with obesity in more than 60% of cases and often with comorbidities including hypertension, arrhythmia, stroke, coronary heart disease and metabolic dysfunction. The comorbidities are of major importance because they have a significant impact on healthcare use and mortality in patients with OSA. Only half of the patients with OSA are symptomatic and a significant percentage of subjects are referred and treated with the goal of limiting their cardiometabolic risk. This heterogeneity in a highly prevalent chronic disease with millions of patients on home-based long-term treatment requires the complete reshaping of patient characterisation and therapeutic strategies.2 Detailed phenotyping is the prerequisite for the development of precision and personalised medicine in chronic disease and particularly in OSA.3 The phenotyping of patients with OSA has been tackled in several different ways. One strategy has been to address the anatomical and physiological traits underlying OSA occurrence and the range of severity.4 The pathophysiological causes of OSA vary considerably between patients. Determining the respective contributions of upper airway anatomy and collapsibility, arousal threshold and loop gain (ventilator drive) will help to predict which therapeutic modality would be beneficial to the appropriately targeted patient subgroups.4 Another topic has been to define distinct OSA clinical phenotypes. Several recent studies exploiting large data sets have used unsupervised cluster analysis to identify distinct phenotypes.5 6 Subgroups have been recognised that varied considerably in age, gender, symptoms, obesity, comorbidities and environmental risk factors.5 6 The most significant differences between clusters were minimally symptomatic versus sleepy patients with OSA, lean versus obese, and among obese patients …

Acquired central hypoventilation syndrome (CHS) is a rare cause of respiratory failure. We report a case of acquired CHS, diagnosed several years after Listeria monocytogenes (LM) rhombencephalitis. In 1993, a 46-year-old woman presented to our Sleep Clinic with poor sleep, nocturnal choking episodes and daytime fatigue. She denied habitual snoring and hypersomnolence. Her medical history was unremarkable except for severe LM rhombencephalitis in 1977. At that time, the patient had been hospitalised in the intensive care unit following the acute onset of fever, influenza-like symptoms, meningism, facial palsy and nystagmus. Blood and cerebral spinal fluid samples were positive for LM on direct microscopic exam as well cultures. Treatment was initiated but the patient acutely deteriorated, exhibiting tetra paresis, bilateral pontomedullary syndrome, impairment of vigilance, and experienced a cardiac arrest. She was successfully resuscitated and remained in the intensive care unit with gradual and slow recovery. After a lengthy hospital stay, she was eventually discharged from the hospital and resumed a normal life, with few neurological sequelae such as dysphagia and mild facial palsy. To investigate the patient's sleep complaints, an in-laboratory full polysomnography was obtained and revealed central sleep apnoeas and hypopnoeas (Apnoea–Hypopnoea index (AHI)=50 events/hour) with severe nocturnal hypoxaemia. Morning arterial blood gases revealed alveolar hypoventilation with partial pressure of arterial CO2 or PaCO2 of 6.7 kPa and PaO2 of 9.5 kPa. The patient refused further investigations and therapy but agreed to return to clinic for a follow-up in 1 year. In 1994, polysomnography and arterial blood gases showed persistent sleep apnoea and daytime hypoventilation but the patient continued to decline treatment. The patient was then lost to follow-up until 2011, when she presented for the third time to the Sleep Clinic complaining of daytime fatigue, unrefreshing sleep, choking episode during sleep and …

BackgroundArterial stiffness, measured by pulse wave velocity (PWV), is a strong independent predictor of late cardiovascular events and mortality. It is recognised that obstructive sleep apnoea (OSA) is associated with cardiovascular comorbidities and mortality. Although previous meta-analyses concluded that PWV is elevated in OSA, we feel that an individual patient data analysis from nine relatively homogeneous studies could help answer: to what extent does OSA drive arterial stiffness?MethodsIndividual data from well-characterised patients referred for suspicion of OSA, included in nine studies in which carotid–femoral PWV was measured using a Complior device, were merged for an individual patient data meta-analysis.Results893 subjects were included (age: 56±11 (mean±SD), 72% men, 84% with confirmed OSA). Body Mass Index varied from 15 to 81 kg/m2 (30±7 kg/m2). PWV ranged from 5.3 to 20.5 m/s (10.4±2.3 m/s). In univariate analysis, log(PWV) was strongly related to age, gender, systolic blood pressure, presence of type 2 diabetes (all pConclusionOur individual patient meta-analysis showed that elevated arterial stiffness in patients with OSA is driven by conventional cardiovascular risk factors rather than apnoea parameters.

Hypertension affects 25% of the adult population and remains a leading cause of cardiovascular mortality, accounting for 13.5% of all deaths. Half of all strokes and ischaemic heart disease events are attributed to hypertension.1 ,2 Most patients exhibit grade I hypertension (systolic blood pressure of 140–159 mm Hg and/or diastolic blood pressure of 90–99 mm Hg) without coexisting cardiovascular disease. Effective reduction of blood pressure in this population significantly reduces stroke and death.3 Obstructive sleep apnoea (OSA) is now recognised as a risk factor for the development of hypertension in European and the US International Guidelines. In OSA, elevation of blood pressure is in part due to intermittent hypoxaemia leading to increased sympathetic tone and impaired baroreflex gain.4 Altered arterial vasoconstriction and vasodilatation5 owing to stimulation of the renin-angiotensin-aldosterone system (RAAS)6 are also significant contributors. Although OSA and hypertension are tightly linked in a dose-response manner, the impact of short-term OSA treatment on blood pressure reduction in unselected patient populations with OSA is rather mild, about 2 mm Hg reduction in 24-hour mean blood pressure. This effect is slightly greater in patients who are compliant with CPAP or mandibular advancement devices, presumably by allowing rapid eye movement (REM) sleep at the end of the night to be free of obstructive respiratory events.7–9 It stands to reason that treatment strategies combining OSA treatment and pharmacological antihypertensives would be synergistic.10 ,11 Previous studies10 ,11 have demonstrated that in hypertensive patients with OSA, losartan or valsartan are by far more effective than CPAP in reducing blood pressure, even if nocturnal blood pressure is better controlled when CPAP is used concurrently with these medications. This underlines the need for specific strategies to be further studied in …

Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent condition paralleling the growing epidemic of obesity and type-2 diabetes. This disease shows a continuous spectrum of severity ranging from simple steatosis to overt non-alcoholic steato-hepatitis (NASH) that can further progress towards cirrhosis and hepatocarcinoma.1 Although the complete physiopathology is not fully understood, many factors such as insulin resistance, inflammation, oxidative stress and lipotoxicity are involved in the onset of NAFLD.2 ,3 Obstructive sleep apnoea (OSA) is independently associated with the different components of the metabolic syndrome, particularly visceral obesity, hypertension, insulin resistance and abnormal lipid metabolism.4 The repetitive occurrence of partial or complete pharyngeal collapse during OSA induces chronic intermittent hypoxia (CIH) that subsequently results in low-grade inflammation, sympathetic overactivity and oxidative stress. Since OSA and NAFLD share common intermediary mechanisms, the presence of OSA, especially in the context of severe CIH, has been suggested as contributing to the pathogenesis and exacerbation of the severity of NAFLD. Animal studies have demonstrated that in obesity, short-term or long-term exposure to CIH mimicking OSA induces NAFLD.5–7 Next, studies in human adults, using either non-invasive surrogate markers of liver injury or biopsies to diagnose NAFLD, have also demonstrated that CIH is involved in the development of NAFLD, independently of body mass index (BMI), and contributes to the deleterious progression into overt NASH.8–11 In contrast, other studies have shown that the absence of OSA seems to protect morbidly obese patients from developing NAFLD.12 In response to the currently emergent worldwide epidemic of childhood obesity, NAFLD has started to be more systematically investigated in children than previously.13 ,14 The prevalence of NAFLD reaches 10% in the paediatric population …

Hypertension affects about 25% of the adult population worldwide. It ranks as the leading chronic risk factor for mortality, accounting for 13.5% of all deaths. Half of all strokes and ischaemic heart disease events are attributable to high blood pressure (BP).1 ,2 Obstructive sleep apnoea (OSA) is now recognised as a risk factor for the development of hypertension in European and the US International Guidelines. OSA and hypertension are linked in a dose-response fashion. This is true even when the usual confounding factors such as age, alcohol, tobacco consumption and Body Mass Index are taken into account.3 In a large prospective observational cohort followed for more than 12 years, it has been shown that compared with controls, the adjusted HRs for incident hypertension were twofold greater among patients with severe OSA who declined continuous positive airway pressure (CPAP) therapy.4 At least four meta-analyses derived from 32 randomised controlled trials (RCTs) have demonstrated that CPAP, the first-line therapy for moderate to severe OSA syndrome, reduces 24 h mean BP by approximately −2 mm Hg (pooled estimated effect).5–8 In these meta-analyses, heterogeneity is a clear concern with some of the analysed studies excluding hypertensive patients, while others only included hypertensive patients. Furthermore, the presence and/or the description of antihypertensive classes of medications are poorly reported. The first strength of the study by Bratton et al 9 is to restrict the investigation to a homogeneous group with minimally symptomatic OSA. Whereas CPAP treatment is clearly indicated in sleepy symptomatic OSA, CPAP prescription with the aim of reducing cardio-metabolic risk in minimally symptomatic patients remains a frequent clinical practice. This should be argued because CPAP effects on hypertension appear to be limited mainly to the more severe and symptomatic patients, with little benefit observed in patients who did not feel sleepy during …

Background Millions of individuals with obstructive sleep apnoea (OSA) are treated by CPAP aimed at reducing blood pressure (BP) and thus cardiovascular risk. However, evidence is scarce concerning the impact of different CPAP modalities on BP evolution. Methods This double-blind, randomised clinical trial of parallel groups of patients with OSA indicated for CPAP treatment compared the efficacy of fixed-pressure CPAP (FP-CPAP) with auto-adjusting CPAP (AutoCPAP) in reducing BP. The primary endpoint was the change in office systolic BP after 4 months. Secondary endpoints included 24 h BP measurements. Results Patients (322) were randomised to FP-CPAP (n=161) or AutoCPAP (n=161). The mean apnoea+hypopnoea index (AHI) was 43/h (SD, 21); mean age was 57 (SD, 11), with 70% of males; mean body mass index was 31.3 kg/m 2 (SD, 6.6) and median device use was 5.1 h/night. In the intention-to-treat analysis, office systolic blood pressure decreased by 2.2 mm Hg (95% CI −5.8 to 1.4) and 0.4 mm Hg (−4.3 to 3.4) in the FP-CPAP and AutoCPAP group, respectively (group difference: −1.3 mm Hg (95% CI −4.1 to 1.5); p=0.37, adjusted for baseline BP values). 24 h diastolic BP (DBP) decreased by 1.7 mm Hg (95% CI −3.9 to 0.5) and 0.5 mm Hg (95% CI −2.3 to 1.3) in the FP-CPAP and AutoCPAP group, respectively (group difference: −1.4 mm Hg (95% CI −2.7 to −0.01); p=0.048, adjusted for baseline BP values). Conclusions The result was negative regarding the primary outcome of office BP, while FP-CPAP was more effective in reducing 24 h DBP (a secondary outcome). Trial registration number NCT01090297.

Patients with severe apnoea may have an impaired pharyngeal dilating reflex related to decreased pharyngeal sensitivity. The accuracy of a simple new procedure to measure pharyngeal sensitivity and to diagnose sleep disordered breathing (SDB) was investigated.Pharyngeal disappearance and appearance sensory perception thresholds were measured by delivering different airflow rates on the soft palate using an intraoral device in 17 controls and 50 patients suffering from SDB evaluated by overnight polygraphy. The procedure was performed before (baseline) and after three successive administrations of a topical anaesthetic to sensitise the pharyngeal sensory impairment. Pharyngeal sensitivity was then evaluated according to SDB severity. SDB was classified as mild, moderate or severe according to the relative proportion of obstructive apnoeas-hypopnoeas and the amount of desaturation.Patients had higher baseline disappearance and appearance sensory thresholds than controls (mean (SD) 0.62 (0.44) v 0.26 (0.06) l/min and 0.85 (0.40) v 0.40 (0.19) l/min, p0.001, respectively). Such differences were enhanced by topical anaesthesia. Impairment of pharyngeal sensitivity and the number of patients with impaired sensitivity increased from the least to the most severe SDB group as indicated by the test sensitivity for a respiratory disturbance index of20/hour (50%, 73.7% and 88.5% in the mild, moderate, and severely affected groups, respectively).This simple and safe procedure showed that impairment of pharyngeal sensitivity is correlated with severity of SDB. Using this test in routine clinical practice may simplify the diagnosis of sleep apnoea, particularly for the most severe patients.

BACKGROUND: Obstructive sleep apnoea (OSA) is associated with increased morbidity and mortality. It has remained unclear whether or not it is progressive. The evolution of OSA was examined in a retrospective case note study of 55 unselected patients of mean (SD) age 55.8 (10) years with mild to moderate disease untreated by interventional methods such as continuous positive airway pressure (CPAP) or surgery. Correlations between clinical and functional variables, upper airway anatomy, and change in disease severity were also investigated. METHODS: Patients underwent full polysomnography on two occasions (T0 and Tx) at a mean interval of 77 (50) weeks (range 17-229). In addition, upper airway imaging with computed tomographic scanning or cephalometry had been performed in 43 patients at T0. Morbidity before, during, and after the study period was assessed by questionnaire, as was smoking history and alcohol and sedative intake. RESULTS: The apnoea hypopnoea index (AHI) for the group as a whole increased from 21.8 (11.5) to 33.4 (21.3) (p = 0.0001). Using a 25% change in AHI to divide patients into worsened, stable, and improved groups showed that, although most of the patients deteriorated, 25 patients improved or remained stable. The change in AHI was not correlated with body mass index which remained stable at 29.7 (5.4) kg/m2 versus 29.7 (5.6) kg/m2. There was a trend for apnoea duration to increase. No patient reported increased alcohol consumption and only one patient reported increased use of sedatives between T0 and Tx. No correlation was found between change in AHI and age, time between recordings, anatomical measurements of the upper airway, respiratory function, oximetry, or arterial blood gas tensions. Total cardiovascular and cerebrovascular morbidity was high: hypertension (26 patients, 46%), cardiac arrhythmia (17 patients, 33%), angina (12 patients, 23%), myocardial infarction (10 patients, 19%), and stroke (10 patients, 19%). Twenty nine patients (52%) were prescribed CPAP after Tx, two of whom went on to have maxillofacial surgery. These 29 treated patients had significantly higher values of AHI at T0 and Tx and greater change in AHI than the untreated patients. CONCLUSIONS: This study shows that mild to moderate OSA has a tendency to worsen in the absence of significant weight gain and that upper airway anatomy and clinical variables do not appear to be useful in predicting progression. It follows that mild to moderate OSA justifies systematic follow up. Deterioration in AHI over a mean of 17 months led to interventional treatment in over 50% of patients in the study.

A patient who developed severe sleepiness and sleep apnoea in association with adult acquired retrognathia and subluxation of the cervical spine at the level of C3-C4, both resulting from rheumatoid arthritis, is described. The possible causative factors of the association between sleep apnoea and rheumatoid arthritis include reduction of the size of the upper airway by temporomandibular joint destruction, brainstem compression due to rheumatoid arthritis affecting the cervical spine, sleep fragmentation, and drug effects.

Non-communicable Diseases, mainly cardiovascular diseases, cancer, diabetes and chronic respiratory diseases, are responsible for two-thirds of the 57 million annual deaths worldwide.1 Obesity and obstructive sleep apnoea (OSA) are among the key players involved in non-communicable diseases. Several studies have reported an independent association of OSA with the different components of the metabolic syndrome, particularly hypertension, insulin resistance and abnormal lipid metabolism.2 Both OSA and metabolic syndrome are associated with an increase risk in cardiovascular disease. Hence, rapidly accumulating data from both epidemiological and clinical studies3 have suggested that OSA is independently associated with alterations in glucose metabolism and with an increased risk of developing type 2 diabetes. Indeed, recent reports have indicated that more than 50% of patients with type 2 diabetes have OSA. Multiple mechanistic pathways contribute to the deteriorated plasma glucose/insulin homeostasis in OSA, the number one being sympathetic over activity,4 due to sleep fragmentation and intermittent hypoxia (figure 1). Independently of autonomic nervous system activation, in animal models intermittent hypoxia contributes to decreased glucose utilisation in oxidative muscle fibres.5 Intermittent hypoxia also seems to be responsible for increased beta-cell proliferation and cell death, the latter being due to oxidative stress.6 In fat tissue, chronic intermittent hypoxia (CIH) the hallmark of OSA exacerbate adipose tissue inflammation and lead to a dysregulated production of adipocytokines which may contribute to insulin resistance and could trigger non-alcoholic fatty liver disease (figure 1). We have demonstrated in morbid obesity that CIH is strongly associated with higher systemic inflammation (IL-6) and more severe fibrotic or inflammatory liver injuries.7 Visceral fat releases free fatty acids in the portal vein leading to accumulation of hepatic fat and development of hepatic insulin resistance. Regarding lipid abnormalities, intermittent hypoxia leads to an increase in serum cholesterol, to an up-regulation …

Complex respiratory events, which may have a detrimental effect on both quality of sleep and control of nocturnal hypoventilation, occur during sleep in patients treated with non-invasive ventilation (NIV). Among these events are patient-ventilator asynchrony, increases in upper airway resistance (with or without increased respiratory drive) and leaks. Detection of these events is important in order to select the most appropriate ventilator settings and interface. Simple tools can provide important information when monitoring NIV. Pulse oximetry is important to ensure that adequate oxygen saturation is provided and to detect either prolonged or short and recurrent desaturations. However, the specificity of pulse oximetry tracings during NIV is low. Transcutaneous capnography helps discriminate between hypoxaemia related to ventilation/perfusion mismatch and hypoventilation, documents correction of nocturnal hypoventilation and may detect ventilator-induced hyperventilation, a possible cause for central apnoea/hypopnoea and glottic closure. Data provided by ventilator software help the clinician by estimating ventilation, tidal volume, leaks and the rate of inspiratory or expiratory triggering by the patient, although further validation of these signals by independent studies is indicated. Finally, autonomic markers of sympathetic tone using signals such as pulse wave amplitude of the pulse oximetry signal can provide reliable information of sleep fragmentation.

BACKGROUND: Assessments of the upper airways in patients with the obstructive sleep apnoea syndrome are usually carried out on awake patients who are upright. The dynamics of the airway in a patient who is asleep and lying down may be different. METHODS: Somnofluoroscopy, computed tomography of the upper airway, and cephalometry were carried out in 11 patients with the obstructive sleep apnoea syndrome (10 male; mean (SD) age 53 (10) years) to examine the airway while they were awake and asleep. RESULTS: At somnofluoroscopy 10 patients were in stage 2 sleep and only one in REM sleep. At least five obstructive events were visualised by lateral fluoroscopy in each patient. Imaging allowed observation of the dynamics of airway collapse, which began in the oropharynx in all cases, progressing to the hypopharynx in 10 cases and to the laryngopharynx in five. At fluoroscopy the soft palate was seen to hook up during airway occlusion in 10 patients, thereby increasing its cross sectional area. It was then sucked down into the hypopharynx. Somnofluoroscopic and cephalometric findings agreed, eight of the 10 patients with hypopharyngeal collapse shown by somnofluoroscopy having an inferiorly placed hyoid bone according to cephalometry (distance from the mandibular plane to the hyoid bone (MP-H distance) increased); the one patient with no hypopharyngeal collapse had a normal MP-H. By contrast, six of the 11 patients had a normal or supranormal hypopharyngeal cross sectional area of the airway on the computed tomogram. CONCLUSIONS: Somnofluoroscopy allows examination of the dynamics of airway closure in this disorder and shows the important role of the soft palate in acting as a plug in the oropharynx. Dynamic studies are required to determine the pattern of pharyngeal obstruction in obstructive sleep apnoea.

In response to the comments by Tulaimat and Littleton,1 we will clarify our original statement on ‘Obesity hypoventilation syndrome (OHS): does the current definition need revisiting?2 The two issues that these authors raise are curious and indeed re-enforce the statement …

Current techniques for investigating patients with suspected sleep disordered breathing are inadequate. Not only are many of the tests expensive, but they are also cumbersome and many centres require these investigations to be performed in the sleep laboratory. At the heart of the problem is the difficulty in identifying and quantifying the spectrum of respiratory events responsible for the sleep fragmentation and disabling excessive daytime sleepiness that is characteristic of obstructive sleep apnoea and its related conditions. Obstructive apnoeic episodes are not usually difficult to detect, even when only a basic measure of respiratory effort such as thoracic and abdominal movement is used. On the other hand, correctly identifying obstructive hypopnoeas and episodes of upper airway resistance needs a sensitive measure of airflow and inspiratory effort. The measurement of swings in pleural pressure by oesophageal manometry is the current gold standard technique for detecting changes in inspiratory effort. However, the placement of an oesophageal catheter is often uncomfortable and unacceptable, it may modify the upper airway dynamics,1 and some believe that it contributes to the sleep disturbance during the sleep study, though this is disputed.2 Furthermore, this technique is available in only a proportion of sleep laboratories and, if performed, adds significantly to the cost of the sleep study. These issues pose a clinical dilemma because it is important to detect and define hypopnoeas and upper airway resistance episodes as they are as relevant as apnoeas in producing sleep fragmentation. The assessment of sleep structure also creates problems. Not only is high quality electroencephalographic (EEG) monitoring difficult to achieve outside the laboratory, but the scoring is laborious in terms of technician time and is hence expensive. In addition, there remains uncertainty regarding the definition of an arousal.3 It is likely that “micro-arousals” which fall short of the …