1 INTRODUCTION: NASAL SURGERY AND OBSTRUCTIVE SLEEP APNEA

The location of obstruction in the obstructive sleep apnea/hypopnea syndrome (OSAHS) is variable and can often be localized to several levels in the upper airway. In fact, the level of obstruction can vary in the same patient among consecutive episodes of apnea.¹ In normal circumstances, the normal nose contributes to 50% of upper airway resistance, adding to the resistance provided by both oropharyngeal tissues and the tongue.² In fact, resistance at the level of the nose is more constant in both sleep and awake states, due to the more rigid frame provided by the septum and the lower and upper lateral cartilages. If, however, the upper or lower lateral cartilages are weak, damaged, resected, or otherwise structurally affected, this stability is lost. Patients in such cases are subject to an increased tendency towards collapse during sleep, even with a normal nasal airway in the awake state. The association between nasal obstruction and sleep disturbances was probably what first led to the description of sleep-related breathing disorders,³ or sleep-disordered breathing (SDB), the group of disorders that includes snoring, the upper airway resistance syndrome, and OSAHS. It is currently recognized that nasal obstruction interferes with pressure titration in nasal continuous positive airway pressure (nCPAP) for the management of OSAHS, and that treatment of such obstruction improves patient compliance with nCPAP.^4,5 The cause–effect relationship of nasal obstruction and OSAHS, however, remains unclear. While surgical correction of obstructed nasal airways is, without a doubt, an important component of the surgical management of OSAHS,^6–8 the expectations of improvement after performing nasal procedures alone are still, at best, unclear. Another important factor in the relationship between nasal obstruction and SDB is the tendency that patients with obstructed nasal airways have to mouth breathe, which decreases the hypopharyngeal space by moving the mandible posteriorly and, most importantly, by pushing the base of the tongue backwards.

The primary sites of nasal obstruction are the nasal vestibule, the nasal valves, and the turbinates.⁹ The nasal septum, when deviated, also has a significant impact on these areas of obstruction. Of these three sites, the nasal valve is the site of major resistance.² Many authors have shown that, in fact, nasal valve incompetence may equal, or even exceed, septal deviation or turbinate hypertrophy as the prime cause of nasal airway obstruction.¹⁰ The internal nasal valve is defined as the area between the caudal end of the upper lateral cartilages and the cartilaginous septum, and the entire nasal valve complex is bounded superiorly by the reflection between the upper lateral cartilages and the septum, posteriorly by the head of the inferior turbinate, inferiorly by the floor of the nose, and laterally by the bony piriform aperture.¹¹ During inspiration, particularly during the forced inspiration that occurs during an apneic episode, the negative nasopharyngeal and intranasal pressures increase to generate more flow, creating a transmural pressure gradient, which, when a critical value is reached, causes collapse of the upper lateral cartilages.¹² Thus, the flow-limiting segment constituted by the nasal site of obstruction acts as a Starling resistor, not only at the level of the nose (in the case of inspiratory nasal valve collapse), but also for further ‘downstream’ structures like the soft palate and the oro- and hypopharynx.^7,13 Nasal obstruction leads to mouth opening and transition to oral breathing, which contributes to airway flow limitation and collapse, mainly due to inferior movement of the mandible,¹⁴ a backward fall of the base of the tongue, resulting in a reduction of the posterior pharyngeal space and diameter¹⁵ and an increased respiratory effort that causes collapse of the pharyngeal tissues due to greater negative pressures.

2 CAUSES OF NASAL OBSTRUCTION

The causes for nasal obstruction can be broadly divided into structural, mucosal, or neuromuscular.¹⁴ Structural causes may include septal deviation, hypertrophy of the inferior or middle turbinates and fixed and inspiratory nasal valve collapse, which may or may not be secondary to prior nasal surgery or trauma. Of these causes, nasal valve dysfunction may contribute to symptoms in as many as 13% of adults that report chronic nasal obstruction.¹¹ Although no data are available, it is likely that the increased respiratory efforts by OSAHS patients during episodes of apnea caused by palatal or tongue base obstruction make these patients more prone to nasal valve collapse. In children, in addition to developmental abnormalities like choanal atresia and craniofacial syndromes (e.g. Pierre Robin sequence), adenoidal and – to a lesser degree – tonsillar hypertrophy also constitute an important cause for nasal obstruction,¹⁶ both of which have an important correlation with OSAHS in this patient population. Chronic mouth breathing in these patients actually leads to acquired craniofacial abnormalities (e.g. the ‘adenoid face’), which further compromise the stability of the upper airway.¹⁷ The consequences of these alterations in cephalometric measurements that may originate during infancy may actually constitute the origin of the relationship between SDB and nasal obstruction. Earlier studies by Series⁴ established that sleep apneic patients with septal deviation that had subjective symptoms of nasal obstruction and subjectively disturbed sleep (mostly in the form of arousals) were more likely to improve both subjectively and objectively after correction of nasal obstruction if their cephalometric measurements were within normal ranges.

Nasal symptoms, findings, and even anatomical abnormalities (e.g. nasal septal deviation) are common in patients with sleep apnea,¹⁸ and data suggest that increased nasal resistance is more prevalent in patients who snore.¹⁹

Alterations in the nasal mucosa lead to nasal congestion, which involves the cavernous tissues of the turbinates. Common causes of nasal congestion include allergic rhinitis, vasomotor rhinitis, chronic sinusitis, and upper respiratory tract viral infections.²⁰ These conditions are often associated with structural abnormalities, like septal deviation, which may also cause alterations in the nasal cycle. Chronic inflammation, as well as conditions like asthma, aspirin sensitivity or cystic fibrosis, lead to the development of nasal or nasopharyngeal polyps, which cause obstruction.²⁰ Medical management of these conditions is an essential component in addressing nasal obstruction. Intranasal corticosteroid therapy for rhinitis showed improvement of OSAHS, but not snoring, in a randomized, placebo-controlled, crossover trial involving a group of 24 patients with mild to moderate sleep apnea, as reported by Kiely et al.²¹

Facial muscular weakness and impaired nasal reflexes (especially the ones involved in dilating the nose prior to inspiration), which occur secondary to neuropathy and facial palsy, are also important neuromuscular causes of nasal obstruction.^2,11,12

3 DIAGNOSTIC EVALUATION OF NASAL OBSTRUCTION

The evaluation of nasal obstruction in the context of sleep-disordered breathing is based on nasal airway assessment while the patient is awake and asleep. Elements that should be included in the history include whether the obstruction is uni- or bilateral, intermittent or persistent, seasonal or perennial, and whether it is worse while in the supine position, particularly at night. A detailed medication history is essential, in order to document the effects of medications, particularly decongestants and topical steroids. History of previous surgery is also an important aspect that guides the therapeutic decision making. There is no simple way to assess the patient’s nasal airway during sleep. A therapeutic trial of topical decongestants and systemic steroids may be useful in assessing the effect on snoring and overall quality of sleep in OSAHS patients.

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