br Sleep study A Type III

Sleep study A Type III home sleep study was performed using Embletta Portable Diagnostic System (Stowood Scientific Instruments, Oxford UK) and Somnologica software (Embla, Broomfield, USA) for analysis, due to the comparability in diagnosing adult patients with a high probability of moderate to severe obstructive sleep apnoea [1]. We measured body position, pulse oximetry (SpO2), thoraco-abdominal movement using inductive respiratory plethysmography (RP) and airflow using nasal pressure (NP); oral thermistor trace was unavailable for this study due to sensor failure, but the study went ahead with the alternative sensor method [2] in order not to delay diagnosis and surgery.
Results It was noted on analysis that the software had identified unusual prolonged events from the NP trace that did not correspond with any interruption to the regular thoraco-abdominal movement pattern, with no changes in SpO2. On closer examination these events were found to be the result of sudden and total cessation of nasal airflow. Although some of these events were correctly marked as artefact, most lasting less than 120s had been falsely identified as obstructive apnoea events. Normal NP traces were apparent both before and after each event. Following manual scoring by an experienced physiologist these events were eliminated from the final report; AHI was revised from 38 to 28 events per hour, thereby changing the category from severe to moderate Fig. 1.
Discussion The NP trace showed that this patient was experiencing periods of complete nasal obstruction during the study, which appeared to correspond with the history during waking hours. Although xanthine oxidase breathing has been demonstrated as occurring between 1 and 3% of recording time, usually causing a reduction in signal amplitude [3] this patient׳s nasal obstruction episodes led the software to score numerous false positive events. Apart from the revision of the severity of OSA, there were no consequences for this patient as sleep-disordered breathing was identified, he was subsequently successfully treated with continuous positive airway pressure therapy, and his surgery went ahead as planned. However, the potential for false-positive results in the case of a less severe or a simple snoring patient is clear. Although it is known that NP signal may show a degree of decreased amplitude during mouth breathing, [2,3] the onset of sudden and complete nasal obstruction during sleep is unique in our experience. This individual case underlines the importance of recording airflow at the mouth in addition to NP during sleep, especially in patients with suspected nasal pathology. In addition we are reminded that the practice of relying solely on automatic detection software without some form of manual verification should be avoided.
Introduction In obstructive sleep apnoea (OSA), episodes of recurrent upper airway obstruction cause intermittent hypoxia, with frequent sleep arousals and fragmented sleep, resulting in excessive daytime hypersomnolence [1]. OSA has been increasing in prevalence, and it has been estimated that 13% of men and 6% of women between the ages of 30 and 70 years have moderate to severe forms of OSA [2]. This has been linked with the growing obesity prevalence as it is known that obesity is a risk factor for OSA. The prevalence of OSA in severe obesity has been estimated to be between 40% and 90% [3,4]. OSA is associated with hypertension, cardiovascular disease, type 2 diabetes and metabolic impairment [5]. It is known that OSA is independently associated with arterial hypertension and this may be related to repeated hypoxia and reoxygenation episodes that may cause ischaemia–reperfusion injury, as well as increased sympathetic activity, inflammation and oxidative stress [6]. The kidney has a role in blood pressure regulation and may be sensitive to the effects of intermittent hypoxia [7]. Nocturnal hypoxia may be associated with loss of kidney function [8], and a positive relationship has been observed between impaired glomerular filtration and desaturation frequency, suggesting an association between OSA and chronic kidney impairment [9]. Histological changes in renal glomeruli have been reported in severely obese patients with OSA [7], that may be related to pressor responses and endothelial dysfunction in OSA [10].