## 1 Introduction  
Obstructive sleep apnoea (OSA) is a common and burdensome condition, characterised by obstructions of the airway during sleep at the level of the pharynx that can present with or without symptoms [1; 2]. This is in contrast to central sleep apnoea which is due to a dysregulation of breathing during sleep [2]. The individual with OSA has more than 5 events per hour of partial (hypopnoea) or total (apnoea) obstruction of the upper airway despite trying to breathe [3]. An apnoea is defined as a complete obstruction of the upper airway (>90%) lasting for more than 10 s, and hypopnoea is defined as a partial airway obstruction (>30%) sufficient to cause at least a 3% reduction in blood oxygen saturation or sleep aproasts [3]. The apnoea-hypopnoea index (AHI) is the key measure used in sleep study monitoring to define and stratify OSA severity; however, this metric has inherent limitations, including not taking into account the degree of accompanying hypoxia, and the length of respiratory events [4]. The AHI levels of 5, 15, and 30 are used as cut points to determine mild, moderate, and severe OSA, respectively [4]. The International Classification of Sleep Disorders (ICSD-3) [5] encompasses a broad definition of OSA, defining it as: (1) clinical symptoms and complaints of diurnal sleepiness, or apnoeas witnessed by a partner, or cardiometabolic abnormalities and an AHI of >5 events per hour of sleep; or (2) 15 or more predominantly obstructive breathing events per hour of sleep (with no attendant symptoms or comorbidities specifically listed) [5]. As a result of OSA, individuals may experience daytime sleepiness, they may describe fatigue, lack of energy, tiredness, poor concentration, bad mood, morning headaches, snoring, and observed breathing pauses during sleep, according to their bed partner [6]. OSA prevalence varies by country and region [7]. Globally, it has been indicated that one billion adults aged 30 to 69 years may be suffering from OSA, with almost 425 million individuals suffering from moderate to severe cases based on an Apnoea-Hypopnoea (AHI) cut-off value, for which treatment is recommended [7]. Additionally, the prevalence of OSA in Europe was estimated in the year of 2018 to be around 175 million, including approximately 90 million individuals with moderate to severe OSA [8]. Paediatric with OSA have a different clinical picture from adults. The prevalence of OSA in children varies from 1% to 5% [9]. The incidence of this condition tends to peak between the ages of 2 and 8 years old [10]. In the majority of cases, OSA in children is diagnosed often as a result of complaints of snoring or they are referred for surgery due to adenoids or enlarged tons [11]. It is imperative that OSA-related risk factors and complications are identified for effective management in clinical practice. The development of OSA is influenced by several unmodifiable and modifiable risk factors. The unmodifiable factors include older age, male sex, race/ethnicity, family history of OSA, and craniofacial abnormalities [12; 13; 14]. Among the modifiable risk factors for OSA are obesity, smoking, and alcohol consumption [13; 14]. OSA has been associated with increased risk of cardiovascular diseases [15; 16], metabolic disturbances [15], cognitive impairment [17; 18; 19] and cancer [20; 21; 22; 23]; a possible association between OSA and COVID-19 has also been examined [24; 25; 26; 27]. A polysomnography (PSG) is considered the gold standard diagnostic tool, along with other assessment methods for determining the severity of symptoms and defining a clinical phenotype to guide treatment [28]. As most individuals change their sleeping position frequently during the night, there may be a difference in the proportion of time spent sleeping supine and non-supine. Accordingly, this might have implications for OSA diagnosis based on the AHI.