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It seems that a substantial body of evidence now weighs against nasal congestion/obstruction as a factor causing OSA, though it probably does cause snoring and may cause some symptoms of excessive daytime sleepiness similar to those of OSA.
Conditions that affect nasal resistance include temperature and humidity of the air being breathed (colder, drier air increases resistance), posture, the enlargement or constriction of blood vessels in the nose, and the mucous membrances lining the nose. Constriction of nasal blood vessels, as can be induced by sympathomimetic drugs like pseudoephedrine (Sudafed) and related nasal sprays, can decrease resistance. Chronic irritation of the mucous membranes of the nose can lead to apneas and hypopneas. Snoring vibrations may also injure these membranes.
Some studies have used nasal packing or balloons to artificially induce nasal obstruction; these caused increases in snoring, hypopneas, apneas and arousals. Increased nasal resistance has been found in patients with sleep apnea, but attempts to correlate degree of resistance with severity of sleep-disordered breathing or snoring have so far been unsuccessful.
These investigators used patients and data drawn from the Wisconsin Sleep Cohort Study, which included all men and women 30 to 60 years of age employed in state agencies in south-central Wisconsin, all of whom had similar insurance coverage and access to a local university sleep center.
About 6200 questionnaires were sent out and 75% were returned. These asked about frequency of snoring and other sleep disturbances, daytime sleepiness, nasal congestion, allergy history, allergy medications, and frequency of nighttime nasal obstruction, congestion, or discharge.
A subsample, equivalent to the larger group in various respects, now includes 911 subjects who have had overnight sleep studies along with measurement of the openness of the nasal passages and close questioning about recent snoring, nasal congestion/stuffiness, and the likely causes of any nasal problems.
Data analyses looking for nasal congestion as a factor in symptoms of sleep apnea controlled for age, sex, body shape, and obesity as other factors which might affect apneic symptoms.
In the overall sample, the prevalence of rhinitis was similar to that of population estimates (23-35%). Participants who often had nighttime rhinits symptoms were more likely to report habitual snoring, chronic excess daytime sleepiness, or chronic nonrestorative sleep. The magnitude of the effect was to about double the likelihood of snoring habitually or feeling sleepy or unrested during the day. Habitual snorers also had lower nasal airflow, but there was no direct relationship of decreased airflow to Apnea Hypopnea Index. That is, simple snorers showed no more abnormal nasal airflow than did severe sleep apneics.
The authors considered their results consistent with that of another major epidemiologic study, that decreased nasal airflow is likely to cause simple snoring but not obstructive sleep apnea.
The fact that self-reported nasal congestion was associated with complaints of daytime sleepiness and unrestful sleep suggested to the authors that rhinitis symptoms might have an independent effect of causing arousals and sleep fragmentation. In fact, this might be confused or confounded with sedative effects of allergy medications.
One implication is that the newly diagnosed OSA patient with chronic or recurrent rhinitis or sinusitis, or a deviated septum, should not look to surgical or medical treatment of the nasal problems as a likely solution to the OSA, though such treatment may be quite appropriate in its own right. In fact, there is no doubt in my mind that OSA patients on nasal CPAP find nasal congestion and obstruction quite a serious impediment to their use of this treatment. I would be interested to see a study focused on such patients who have intermittent nasal symptoms to determine how much of an adverse effect they have on apnea control and how effective the usual interventions are in controlling this problem, versusi alternative strategies like using a full-face mask under such circumstances.
The authors’ findings seem to me unsurprising, since the nasal problems they identified are so common in the general population that it seems unlikely they could be a major factor in the much less frequent syndrome of OSA. Moreover, the hypothesis that air flow restriction at the level of the nose would increase collapsibility lower down in the airway seems not only arguable but counterintuitive.
However, one point that came out of this study pleased me to see noted: that rhinitis and sinusitis might cause daytime sleepiness and unrestful sleep of their own right, via a mechanism of arousals and sleep fragmentation due to discomfort instead of apneas or hypoxia. This seems quite plausible, and furthermore potential applicable to a wide range of medical illnesses which cause pain or discomfort during sleep. It is important to bear in mind the multifactorial nature of sleep disruption, which may be obscured in the face of an overwhelming disorder like OSA yet emerge as relevant once the OSA has been controlled with effective treatment. Then, in fact, it may be relevant to ask whether chronic or episodic loss of daytime alertness might be due to sleep fragmentation from a wide a range of internal and external causes. This in turn may create the sense of the CPAP “not working” and failure to identify the real causes of the symptom relapse.
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