Nasal obstruction can be caused by structural abnormalities (e.g. deviated nasal septum, enlarged turbinates and nasal valve collapse) or by inflammatory mucosal disease (rhinitis, chronic rhinosinusitis with or without nasal polyps) (Lee et al. 2013; Prasad et al. 2013). Correction of nasal obstruction is unquestionably a priority in the management of OSA patients, regardless of whether it leads to an improvement in OSA severity based on objective polysomnography respiratory parameters. There is extensive evidence showing that nasal obstruction not only decreases quality of life, but that it also contributes to snoring, plays an important role in the pathophysiologic mechanisms leading to OSA, and represents an obstacle for effective treatment with CPAP therapy in OSA patients (de Sousa Michels et al. 2014; Bican et al. 2010). Currently, nasal examination of OSA patient in most medical practices is limited to anterior rhinoscopy, which fails to identify other sites and sources contributing to nasal obstruction.
There are several mechanisms by which nasal obstruction contributes to the pathogenesis of OSA. Following the Sterling resistor model, elevated nasal resistance increases negative pressure in the oropharyngeal airway downstream, thus contributing to airway collapse (Smith et al. 1988; Park 1993). Increased nasal resistance also results in compensatory oral breathing, which leads to an unstable airway with increased total resistance (Phillips 2006; Akbay et al. 2013). Finally, decreased nasal airflow blunts the activation of the nasal-ventilatory reflex important in the maintenance of adequate muscle tone, breathing frequency, and minute lung ventilation (Mcnicholas; Douglas et al. 1983). One of the priorities in the management of OSA patients should be the re-establishment of efficient nasal breathing.
Mouth breathing is a problem oftentimes ignored in the management of OSA. Oral breathing resulting from nasal obstruction may lead to a closed cycle where nasal respiration ends up becoming worse due to profound anatomic derangement. Continuous oral breathing often leads to a transverse maxillary deficiency that deepens the palatal arch. The high arched palate may compress the septum in a cranio-caudal orientation, thus resulting in a displaced septum (Akbay et al. 2013). Most of the posterior septal deviation that cannot be visualized using anterior rhinoscopy alone are not from traumatic insult, but from pressure exerted by a high arched palate during active craniofacial skeletal development. Since many OSA patients present with a high arched palate, we infer that many of these patients would present with posterior septal deviations.
It is common to see OSA patients with impaired nasal breathing to also present with inflammatory mucosal disease. It is estimated that 58% of OSA patients are affected by rhinitis (Gelardi et al. 2012). Over 70% of patients with chronic rhinosinusitis (CRS) report poor sleep quality, and the degree of sleep disturbance correlates with decreased overall quality of life (QOL) (Rotenberg and Pang 2015). Sleep impairment in CRS exerts a greater relative influence on the decision to pursue endoscopic sinus surgery (ESS) when compared to rhinologic specific symptom domains (El Rassi et al. 2015).
A possible explanation for this is that a night-time under-ventilated nose (due to apnea) may be at increased risk of infections and inflammation. The findings from Gelardi et al. support this theory. They found that regular CPAP treatment induces a significant reduction of cell infiltration (neutrophils, eosinophils, lymphocytes, and muciparous cells), which is not seen in non-treated patients. This supports the theory that increased nasal ventilation, in some cases secondary to CPAP use, helps reduce some of the enzymes (ex. elastasis) responsible for the production of free radicals that cause cell damage and mucosal inflammation (Gelardi et al. 2012).
Nasal surgery has not been correlated with significant improvement in post-operative Apnea-Hypopnea Index (AHI). However, ample evidence supports the re-establishment of nasal patency in OSA patients. First, decreased nasal resistance helps reduce CPAP pressures and improves its tolerance (Poirier et al. 2014). Other studies have also shown an improvement in overall sleep architecture with increases in non-REM stage 3 and 4, and REM sleep (Sériès and St Pierre 1992). Finally, nasal surgery is known to have a positive effect in the snoring complaints of OSA patients (Fairbanks 1984).
