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#87

"Nasal Obstruction"

SUMMARY The authors studied 541 unselected consecutive snorers referred to their sleep clinic over the course of two years, for evaluation of suspected sleep breathing problems. They measured nasal resistance with a procedure called "rhinomanometry" which measures air pressure in a nasal mask and a mouthpiece, and includes also measurement of air flow. These measurements were taken before and after a decogestant was taken. Subsequently, patients received sleep polysomnography. Presence of obstructive sleep apnea (OSA) was defined by the conservative criterion of 15 or more episodes of apnea or hypopnea per hour of sleep (the Apnea Hypopnea Index, or AHI). Of the 541 patients studied, 259 (48%) met this criterion for OSA. These patients were compared with those who failed to meet the criterion, considered to be free of OSA. Patients with OSA had significantly higher nasal resistance than those without OSA. In other comparisons of these two groups, OSA patients had average AHI scores of 38, versus 6 for non-OSA subjects. OSA patients included a higher proportion of men (98%) than those without OSA (73%). OSA patients were slightly older (averaging 55 vs. 51 years of age for those without OSA), they were heavier (BMI=30 vs. 28), smoked more, had poorer pulmonary function, and a greater length of the posterior airway (representing a lower position of the hyoid bone in the front of the neck). Statistical analyses showed that nasal air resistance contributed significantly to the AHI--along with other factors such as male sex, Body Mass Index (obesity), and various measurements of the head. However, nasal resistance contributed only 2.3% to the total variance of the AHI--less than that of other contributing factors. Furthermore, the association of nasal resistance with AHI weakened further after decongestant treatment. The authors note that there is clinical evidence to support a role for nasal obstruction in OSA. Allergic rhinitis has resulted in appearance of OSA which cleared up with the allergy. Experimental nasal obstruction has been shown to induce apneas and arousals. Septal deviation and nasal valve obstruction, other causes of nasal airway blockage, have apparently resulted in apnea, which has lessened after relief of the obstruction. This study represented an advance over previous studies in using the more relevant though difficult measurement of posterior rhinomanometry, versus anterior nasal manometry used in some studies reporting negative results. They conclude that this evidence, added to other reports, supports the use of medical or, if necessary, surgical treatment to improve nasal airway resistance in cases of sleep apnea.

I cannot claim enough expertise to comment on the author's technique of measuring airway resistance, but I accept their contention that it has advantages over techniques used in previous studies. The essential conclusion of this study--that nasal obstruction can contribute to sleep apnea--seems quite believable. However, we should bear in mind some limitations of the study which are obvious to the reader without special expertise in otorhinolaryngology. For one thing, their criterion for diagnosing OSA would be considered unduly stringent at many centers, where threshold levels for diagnosis often use 5 respiratory events per hour rather than 15 as the criterion. The authors' criterion may have erroneously shifted many subjects elsewhere diagnosable with mild OSA into the category of those free of OSA. This could have unpredictable effects on their statistical analyses. Second, their measurements of nasal airway resistance were done during waking, whereas measurement during sleep would appear to be more relevant to sleep apnea. Third, although the authors not only admit but emphasize the small contribution of nasal airway resistance to sleep apnea, they fail to draw the implicit conclusion that such a small contribution may actually argue against surgical treatment as worthwhile for sleep apnea. However, anyone who has tried to use a CPAP nasal mask through the course of a bad cold knows that nasal obstruction represents an impediment to use of the machine. Airway delivery devices such as full face masks and oral PAP may get around these problems with nasal obstruction, but their use is so far still quite limited. Often, as the author's own data supports, use of a decongestant at bedtime may help--though many such drugs have stimulant effects which might interfere with sleep. Furthermore, the authors failed to examine other medical interventions that might help reduce nasal airway resistance, such as antihistamines and intranasal steroid sprays. I do not want to take these contentions to the extreme of arguing that a person who has symptomatic, troublesome nasal airway obstruction due to some structural abnormality in the nose, such as septal deviation, should avoid surgery. Rather, I suggest that the average person with sleep apnea who notices no chronic problems with nasal obstruction should put nasal resistance measurement and nasal surgery low on the list of interventions likely to help them with OSA.

"Preserve me from unseasonable and immoderate sleep." Dr. Samuel Johnson, 1709-1784

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