Deformity of the nasal septum and/or the nasal pyramid can obviously be associated with uni- or bilateral persistent nasal obstruction. In case of nasal septum deviation, the patient can complain of a uni- or bilateral nasal obstruction depending on the shape, type and location of the deviation (Mladina et al. 2008). Anterior nasal septum deviation is more commonly responsible of nasal obstruction than posterior septal deviation (Grymer et al. 1997). The patient can also complain of a contralateral nasal obstruction, explained by a compensatory hypertrophy of the mucosa of the inferior turbinate. Nasal collapse is another cause of nasal obstruction that is underrated and underestimated by numerous ENT doctors. Nasal obstruction can be revealed during effort, sport or exercises or can be present in a normal and calm breathing. Patients with previous facial nerve palsy or post-traumatic or postsurgical adhesions developed at the level of the nasal vestibule or the columella can present a unilateral nasal collapse. The diagnosis is made by the Cottle manoeuvre or by an anterior and posterior active rhinomanometry and acoustic rhinometry.

Nasal obstruction can be caused by a rhinitis. Allergic rhinitis is a very common condition. Bauchau and Durham reported a high heterogeneity of allergic rhinitis incidence among the different European countries and a maximal incidence in Belgium with 29.5 % of the population (Bauchau and Durham 2004). According to ARIA guidelines, the rhinitis can be intermittent or persistent, mild, moderate or severe (Brozek et al. 2010). Indoor allergens can cause symptoms during sleep such as house dust mites, animal danders or fungi.

NARES (nonallergic rhinitis with eosinophils) is another type of rhinitis; the eosinophils are present in the nasal smears, and the patient dramatically improves when he uses a nasal topical steroids. There is no sensitisation to any aeroallergens. Loss of smell is a common symptom. This disease can be a precursor of a true nasal polyposis.

NANIPER (nonallergic noninfectious perennial rhinitis) was called in the past vasomotor rhinitis. The aetiology is unknown, the treatment often disappointing except for nasal obstruction.

Rhinitis medicamentosa is a typical cause of nasal obstruction in a patient who (mis)uses nasal topical decongestant. With time the patient consumes more and more nasal drops. Typically nasal obstruction increases during the night.

Acute and chronic rhinosinusitis with and without polyps are associated with nasal obstruction. Acute rhinosinusitis gives symptoms for a maximum of 6 weeks, whereas chronic rhinosinusitis is symptomatic for more than 12 weeks (Fokkens et al. 2012). Nasal polyposis affects 9 % of the general population. It can be restricted to the nose and sinuses or be associated with asthma and aspirin intolerance. Major symptoms in nasal polyposis are nasal obstruction and loss of smell. There are different classifications used to categorise the polyps. In the Caucasian population, nasal polyposis is associated with a chronic inflammatory infiltrate rich in eosinophils. Oedema, epithelial shedding, pseudocyst formation and changes in the extracellular matrix are some histological characteristics of the common nasal polyposis.

Nasal obstruction produces collapsing forces that are manifest downstream in the collapsible pharynx (Georgalas 2011; McNicholas 2008). In the respiratory model based on a Starling resistor, the nose is a key determinant of upper airway resistance (Fig. 23.2) (Farre et al. 2008; Horner 2012). Nasal pressure (P _N) is zero (atmosphere reference value) in normal conditions. Nasal resistance (R _N) determines the maximum flow (V _max) in the downstream collapsible pharynx. In the pharynx, P _crit is the critical value of airway pressure leading to complete collapse and stop of airflow. P _crit depends on transmural pressure and external pressure applied by respiratory muscles. The maximum airflow is defined by V _max = (P _N − P _crit)/R _N. This equation implies that increase in nasal resistance (R _N) leads to decrease in upper airway flow (V _max). Conversely, increase in nasal pressure (P _N) by continuous positive airway pressure (CPAP) device improves upper airway flow (V _max) (Gold and Schwartz 1996).

Nasal obstruction may lead to mouth breathing and mouth opening, which, in turn, results in inferior movement of the mandible with associated decrease in pharyngeal diameter. The base of the tongue may also fall backwards reducing the posterior pharyngeal space.

Although the precise mechanisms are not fully understood, oral breathing could be an adaptive response once a particular threshold of nasal airflow resistance is exceeded. Combined recording of oral and nasal breathing during sleep indicates that normal subjects partition flow between nasal and oral routes, with the majority of airflow occurring through the nasal route (Fitzpatrick et al. 2003a). The route of breathing has profound influence on upper airway resistance during sleep. Oral breathing results in an unstable airway and increases total airway resistance. Oscillation of the soft palate, posterior movement of the jaw angle and posterior retraction of the tongue during mouth opening compromise oral-breathing airflow (Georgalas 2011; Fitzpatrick et al. 2003b).

A few studies suggest nasal airflow has a stimulant effect on ventilation, probably via nasal mechanoreceptors maintaining respiratory pacing. Application of local anaesthetics to the nasal mucosa increases the episodes of airway occlusion (McNicholas et al. 1993; White et al. 1985) and impairs the arousal response to airway occlusion (Berry et al. 1995). The parasympathetic nervous system may play a role in the control of breathing and in the hyperpneic responses associated with airflow obstruction. The parasympathetic nervous system component includes neural receptors in the airways as well as afferent and efferent pathways that travel in the vagus nerves (Ko et al. 2008).

Another item playing a major role in snoring and OSA is the nitric oxide (NO). Airborne NO is largely produced in the epithelium of the paranasal sinuses and is involved in the regulation of pulmonary function (Lundberg 2008; Lundberg and Weitzberg 1999). During inspiration through the nose, high levels of NO follow the airstream to the lower airways and the lungs. Nasally derived NO increases arterial oxygen tension and reduces pulmonary vascular resistance. NO enhances therefore blood flow preferentially in well-ventilated areas of the lung, thus optimising ventilation/perfusion matching (Lundberg 1996; Blitzer et al. 1996). In obstructive sleep breathing disease, nasal NO fails partly to reach the lungs, resulting in ventilation/perfusion mismatch (Haight and Djupesland 2003). Lack of NO could also participate in incoordination of pharyngeal and thoracic muscles and in sleep fragmentation. Furthermore, long-term complications of OSA might be due to the repeated temporary dearth of NO in the tissues, secondary to a lack of oxygen (Haight and Djupesland 2003). After their passage to the alveoli in the inspired air, both oxygen and NO are removed by haemoglobin and are transmitted to the tissues. Repetitive hypoxia/reoxygenation adversely impacts endothelial function by promoting oxidative stress and inflammation and reducing NO availability. This vicious spiral mediates the cardiovascular manifestations of OSA (Atkeson and Jelic 2008).

Nose function not only has a direct role in upper and lower airway breathing in adults but also has a long-term impact on the development of the anterior skull base and the maxilla. The influence of nasal patency on the development of the anterior skull base and the maxillary bone has been previously demonstrated in mammals (Paludetti et al. 1995; Scarano et al. 1998). Experimental blockage of rat nostrils resulted after 2–4 months in anatomical changes of the superior maxilla, the skull base and the jaw (Paludetti et al. 1995; Scarano et al. 1998). Nasal obstruction in monkeys resulted in downward and backward rotation of the mandible and changes in dental occlusion (Yamada et al. 1997). Likewise, oral breathing may modify craniofacial growth in children (Peltomaki 2007). Predominant oral breathing during critical growth periods in children could be inscribed in the bones and lead to breathing disorders (Principato 1991). Cephalometric control studies have shown that mouth-breathing children have a higher tendency for clockwise rotation of the growing mandible (Harari et al. 2010). Because of mouth breathing, tongue position in the oral cavity is low, and the balance between forces from the cheeks and tongue is different compared with healthy children. This leads to a lower mandibular position and extended head posture. Malocclusion and skeletal discrepancy may be partially corrected after adenotonsillectomy (Peltomaki 2007). Similarities in cephalometric studies from OSA adults and mouth-breathing children suggest that the apnoeic pattern develops early in the clinical history of patients with OSA (Juliano et al. 2009). However, OSA in children differs that in adults. The involvement of nasal resistance is greater in children, with serious consequences for growth and development (Erler and Paditz 2004). In adults, cephalometric measurements of normal subjects and patients have shown a relationship between OSA and transverse dimensions of nasal cavities, limited laterally by the vertical plates of both maxillae. OSA patients have narrower nasal framework and maxillary bone proportions (Poirrier et al. 2012). Craniofacial features in the pathophysiology of OSA could explain ethnic differences in OSA prevalence and severity for a given level of obesity (Cakirer et al. 2001; Ip et al. 2001).

Researchers have speculated that the outer nose may have an evolutionary benefit in human. In addition to an ornamental role for sexual selection, it may play a role in creating a curvilinear airflow pattern (Stupak 2010). During the course of human evolutionary development, the midface is shortened, and the upper airway is narrowed to form a collapsible and distensible tube. This evolution permits the production of spoken language but also results in a predisposition toward upper airway collapse during sleep (Davidson 2003; Davidson et al. 2005; Shprintzen 2003). The development of the human outer nose could be assumed as a compensatory development. The curvilinear airflow pattern provided by the nose adjusts the “angle of attack” of airflow hitting the palate, thus contributing to the pharyngeal opening (Stupak 2010). From this hypothesis, the external nose could provide an evolutionary benefit in the protection against OSA (Fig. 23.3).

In case of snoring associated or not to obstructive apnoea, a thorough and complete examination of the nose is mandatory. The nasal pyramid must be evaluated, particularly the dorsum, the lateral cartilages and the columella. A nasal valve collapse must be ruled out by the inspection of the external nose and the Cottle manoeuvre.

Then an anterior rhinoscopy evaluates the nasal septum, the shape and colour of the mucosa of the inferior turbinates and the presence of crust, blood, secretions or polyps (Mladina 1987). Mladina and colleagues defined seven types of septal deviation in a cohort of 2,589 adults. They identified three types with vertical crests, one type with a bilateral deformity, two types with horizontal deformities and another type with atypical deformities (Mladina et al. 2008). Each type may be associated to some degree of nasal obstruction.

Eventually nasal endoscopy must examine the middle meatus, the olfactory cleft and the posterior aspect of the nasal cavity. Nasal polyposis can sometimes be diagnosed with nasal endoscopy only.

Besides the history taking, the patient self-assessment and the anterior rhinoscopy, some investigations must be performed to evaluate the nasal obstruction.

Rhinomanometry and acoustic rhinometry allow for indirect evaluation of nasal anatomy and function (Cole 2000). When these are performed in a supine position, these investigations have more value in assessing nasal breathing of patients with sleep disorders (Virkkula et al. 2003b). Rhinomanometry uses an intranasal closed loop system to measure nasal airway resistance. Acoustic rhinometry uses acoustic reflections to provide information about cross-sectional area and nasal volumes within a given distance. Acoustic rhinometry gives an anatomic description of a nasal passage, whereas rhinomanometry gives a functional measure of the pressure/flow relationships during the respiratory cycle. Both techniques are proposed to assess the efficacy of different treatments and for assessment of the patient prior to nasal surgery. Rhinomanometry and acoustic rhinometry provide “snap-shot” measurements, which may not be representative of a more chronic condition, since nasal turbinate size and function are dynamic processes that may change considerably over a few hours. It is also important to point out that rhinomanometry and acoustic rhinometry tests do not correlate well with a patient’s subjective perception of nasal obstruction. The patient’s subjective perception of the degree of nasal obstruction has been shown to be a more sensitive predictor of positive outcome from medical/surgical management than objective anatomic or physiologic measurements alone. Nasal values measured by acoustic rhinometry and rhinomanometry are correlated inversely with polysomnographic values (apnoea-hypopnoea index, oxygen desaturation index) in nonobese patients (Virkkula et al. 2003a, b; Yahyavi et al. 2008). The association of nasal obstruction measured by posterior rhinomanometry and Mallampati score >3 is predictive of OSA (Liistro et al. 2003). Acoustic rhinometry is also important to measure the nasal valve area (Cakmak et al. 2003).

Nasal inspiratory peak flow gives a measure of bilateral nasal airflow at maximum effort, but does not reflect a physiological measure of nasal airflow. It is however a validated technique to assess the responsiveness of a clinical intervention (Wilson et al. 2003). It should be associated to lung function evaluation as it is influenced by lower airway as well as upper airway function (Nathan et al. 2005).

The levels of NO in the nose can easily be measured noninvasively. NO is altered in several airway disorders, including allergic rhinitis, ciliary dysfunction and sinusitis. The NO value measured is a sum of NO from the sinus via the ostia and the nasal mucosa. NO measurement is mainly valuable for sinonasal disease (Lundberg 2008). Its significance to sleep disorders is currently experimental (Haight and Djupesland 2003).

While they provide objective outcome, the measures of nasal function reflect only one aspect of the disease and may thus not encompass all the other aspects. In recent years, there has been a great expansion in the number and use of quality-of-life questionnaires and other patient-based outcomes in health care. Nasal Obstruction Symptom Evaluation (NOSE) score, Sleep Outcomes Survey (SOS), Visual Analogue Scales (VAS), Sino-Nasal Outcome Test (SNOT) and other surveys have been applied to objectify outcomes in nose and sinus surgery (Lindsay 2012; Hopkins et al. 2009; Piccirillo et al. 2002). Though subjective, they correlate with objective measurements and integrate general health issues, sleep perception and emotional aspects. They include a cluster of interconnected symptoms associated to the nose function. Septorhinoplasty is remarkably effective in improving sleep-related items of the SNOT-22 questionnaire (Poirrier et al. 2013). Beyond the nasal airflow, questionnaires reflect the patient’s perception, suffering and hope. They could help the physician to meet the patient expectations and to provide a reliable follow-up.

Nasal endoscopy and CT scan are two other tools to evaluate the anatomy of the nose and paranasal sinuses. These two examinations are routinely done in all rhinologic work-up.

As obstructive SDB is the consequence of multilevel airway obstruction, nasal evaluation should be integrated with a careful anatomical assessment involving in some cases sleep nasendoscopy, MRI or cephalometry. Lastly, polysomnography remains the gold standard to assess the quality of sleep and to calculate the sleep parameters, including apnoea index, hypopnoea index, apnoea-hypopnoea index, snoring time, amount of REM sleep and sleep latency. Breathing flow can be recorded overnight by means of a thermistor placed at the airway opening (nose and mouth). Inspiratory pressure is indirectly measured by means of chest and abdominal inductance plethysmography belts. Additional devices have been designed to measure nasal pressure (Grover and Pittman 2008) or to record mandible movement (Senny et al. 2012; Maury et al. 2013) during sleep.

The rationale to treat nasal obstruction is to improve nasal patency, re-establishing physiological breathing and minimising oral breathing during sleep. The aim of the treatment is also to reduce nasal resistance and improve the negative intraluminal pressure which generates upper airway collapse. Nasal obstruction can be relieved medically or surgically.

Only reversible causes of nasal obstruction can be treated with medications. The commonest causes of inflammation of the mucosa of the upper respiratory tract are allergic rhinitis, acute and chronic rhinosinusitis and nasal polyposis.