Nasal obstruction as an independent cause of sleep apnea is a controversial topic1. However, there is no doubt about its role in the subjective quality of sleep or in the tolerance and acceptance of CPAP2 or mandibular advancement devices3.

The sensation of nasal obstruction after going to bed is a common complaint among patients attending otolaryngology and pulmonology consultations, especially among patients with sleep disorders4. This phenomenon is known as a postural effect and is explained by inferior turbinate hypertrophy in the supine position.

The pathophysiology behind this phenomenon is still unclear. Three main hypotheses have been proposed. The first suggests that nasal venous stasis occurs in a supine position. This hypothesis is supported by the fact that nasal resistance has been shown to increase when the internal jugular vein is compressed4. The second hypothesis suggests a reflex phenomenon mediated by deep baroreceptors, since nasal resistance increases when the axillary artery or the sides of the body are compressed, without needing to be a supine position5,6. The third hypothesis, based mainly on animal studies, suggests that parasympathetic tone increases in the supine position7–9.

There are several validated methods for measuring nasal ventilatory function, the gold standard being active anterior rhinomanometry10. Rhinomanometry calculates nasal resistance, i.e., the effort the subject has to make to breathe through the nose, from nasal airflow and the difference in pressure between the two nostrils. In the study of positional nasal congestion, De Vito et al. recommend performing both seated and supine rhinomanometry in a procedure they called positional rhinomanometry11.

So far, 12 authors have explored changes in nasal resistance in a supine position using positional rhinomanometry, all of whom reported an increase in nasal resistance when patients lie down. Five groups included a total of 266 patients with snoring or sleep apnea3,11–14. The 4 studies that were suitable for pooling in a meta-analysis showed a combined effect of worsening nasal resistance of 0.20Pas/cm3. Another 5 authors who studied healthy volunteers found a worsening of 0.10Pas/cm3 in this subgroup. To date, only 2 controlled studies have been conducted. One compared healthy controls with patients with sleep apnea13, while the other compared snorers with non-snorers14. In the first, Virkkula et al. found no statistically significant differences in increased nasal resistance between the two groups13. In contrast, Desfonds et al. did not perform this comparison, but they did provide data from which it could be calculated, revealing statistically significant differences, with a greater increase in nasal resistance being observed in patients who snore14.

The reader unfamiliar with rhinomanometry might wonder if this effect is clinically relevant. Normal nasal resistance varies between 0.3–0.5Pas/cm3. A level of resistance higher than 0.80Pa s/cm3 is considered severe nasal obstruction. Thus, it is understood that a worsening of 0.20Pas/cm3 on the scale presented is clinically relevant. However, it is interesting to note that the relationship between nasal resistance and nasal airflow is exponential. In patients with borderline nasal resistance (0.3–0.5), small variations in nasal resistance can cause large variations in airflow. This may cause the patient to switch from nasal breathing to mouth breathing. Few authors have explored this variable. In their series, De Vito et al. found that 31% of patients with apnea, with normal baseline nasal resistance, developed pathological resistance in a supine position11. In this study, the authors set 0.5Pas/cm3 as the limit, so this percentage may have been higher if a stricter standard, such as 0.3Pas/cm3, had been used.

Little information is available on the treatment of this phenomenon. Topical nasal corticosteroids have been shown to normalize positional nasal congestion after 2 weeks in patients with allergic rhinitis7. A study in patients following radiofrequency turbinate reduction was performed in which positional nasal congestion was followed up in patients with vasomotor rhinitis15. However, no information is currently available on treatment in patients with sleep-disordered breathing.

In our opinion, the available evidence is insufficient to make clear recommendations. However, there is a clear imbalance between risk and benefit. First of all, we should ask our patients if nasal obstruction occurs when they go to bed, as we might be surprised by how common this complaint is. This possibility should even be explored in patients who are unaware of the problem, but who report that during the day they breathe through their nose, but at night they sleep with their mouth open. This effect can be confirmed by a risk-free examination that is available in many specialized centers. We therefore believe that, with the current evidence, we have an obligation to explore this possibility in our patients. The treatment of this condition may be more controversial. There is little doubt surrounding the use of topical nasal corticosteroids, which have a high safety profile, and radiofrequency turbinate reduction, a minimally invasive though more controversial surgical technique, may be worth exploring.