Effect of Nasal Spray, Positional Therapy, and the Combination Thereof in the Asymptomatic Snorer

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1 Sleep, 17(6): American Sleep Disorders Association and Sleep Research Society Effect of Nasal Spray, Positional Therapy, and the Combination Thereof in the Asymptomatic Snorer *Howard M. Braver and tao Jay Block * University of Florida College of Medicine, Gainesville, Florida, U.S.A. tdepartment of Veterans Affairs Medical Center, Gainesville, Florida, U.S.A. Summary: The benefits of using a nasal decongestant, sleeping on one's side and the combination thereof were studied in 20 asymptomatic male snorers. Both the apnea-hypopnea index (AHI) and snoring were evaluated. Four consecutive nocturnal polysomnographic studies were done. Night 1 was a control; the other 3 nights were randomly assigned to nasal decongestant, best sleeping position and a combination of the two. Results were calculated based on sleep period time. The mean control AHI ± the standard error of the mean (SEM) was 17.5 ± 6.5. AHI improved to 14.1 ± 6.3 with sleep in the best position (p = 0.03). The AHI also improved to 13.2 ± 6.04 with both nasal decongestant and position (p = ). Using nasal decongestant alone, the mean AHI was 18.1 ± 6.3 (p = 0.765). During the control night, the mean number of snores/hour ± SEM was 356 ± Using nasal decongestant alone, the mean number of snores was 381 ± 50.4 (p = 0.50). With position alone, the mean number of snores was 356 ± 46.0 (p = 0.8). Using the combination of nasal decongestant and position, mean snores were 352 ± 48.9 (p = 0.91). In conclusion, a statistically significant improvement in AHI was produced using the general measures of altering the position of the body during sleep and by the combination of nasal decongestant and positional change. There was no significant change in snoring using any of these general measures. Key Words: Snoring-Treatment Sleep apnea. Large numbers of men who snore heavily exist in the general population. Although many such men who are loud snorers claim that they are without symptoms of disease, a remarkable degree of apneas has been found in these patients when they have been studied by polysomnography (l). Studies have also shown that snorers have an increased risk of developing hypertension, ischemic heart disease and strokes (2-4). The proper management of such asymptomatic patients is not clear from the published literature. Several general measures have been recommended as treatments for sleep apnea. These general measures include alteration of sleeping body position (5) and improving nasal patency (6). Neither of these measures should have unpleasant side effects and might be acceptable to the asymptomatic snorer. Both of these measures have been studied alone and each has been shown to have some efficacy in reducing the frequency of obstructive sleep Accepted for publication May Address correspondence and reprint requests to A. Jay Block, M.D., Pulmonary Division, P.O. Box Health Center, University of Florida, Gainesville, FL , U.S.A. apnea. No studies are available wherein the combination of these general measures of treatment have been used in the same patient. The purpose of this study was to determine if sleep apnea and snoring in asymptomatic patients could be eliminated or reduced in frequency by altering the position of the body during sleep, improving nasal patency by using a nasal decongestant and by the combined effect of body position and using a nasal decongestant. The long-term goal of this project would be to identify a successful, easy, noninvasive method of therapy for the patient who is a loud snorer. METHODS Patients. The study group consisted of 20 male subjects, years of age, who were all asymptomatic snorers. Recruitment of the subjects was quite easy through response to newspaper advertisements and through the use of lists of subjects from earlier studies (1,7). The polysomnography laboratory at the Gainesville Y A Medical Center has files containing names and addresses of more than 50 asymptomatic men who 516

2 TREATMENT OF MEN WHO SNORE 517 FIG.t. A reproduction of an actual polysomnographic tracing. The first tracing is the EEG lead. The second tracing is the electromyogram lead. The third tracing is the EOG lead. The fourth tracing is the microphone with the inflections representing snores. The fifth tracing is the EKG lead. snore heavily and who have participated previously in studies of sleep apnea and snoring. Subjects were interviewed for their responses to a standardized series of questions to assure that they were healthy, not addicted to drugs or alcohol, and had no predisposing factors towards sleep apnea other than obesity. Spouses were also interviewed similarly concerning symptoms of which the subject was unaware or which he denied. Work history was verified to assure that excessive sleepiness had not interfered with the subject's occupation. Subjects were included in the study only if they had a h,<;tory of asymptomatic heavy snoring, were healthy, were not addicted to drugs or alcohol, had no predisposing factors towards sleep apnea other than obesity and had normal pulmonary function tests. All patients gave informed consent before entry into the study as approved by the Institutional Review Board of the University of Florida (IRB #45-90). Study design. At the initiation of the study, each subject underwent a brief examination that was performed by the principal investigator. Thereafter, baseline pulmonary function tests were performed. Following pulmonary function testing, a baseline night of sleep was monitored. On the 1 st night, each subject was allowed to sleep in any position he chose. Position during sleep was recorded on an 8-hour, Fuji videotape using an RCA infrared closed circuit TV camera and a VCR-monitor system. Time was constantly displayed on the videotape using a date/time display generator (Vicon Industries, Melville, NY, U.S.A.). This display allowed later review of the tape to correlate numbers of apneas and hypopneas with position. The monitor was constantly viewed by an experienced sleep technologist to ensure that accurate records were kept. Polysomnography was performed as in previous studies (1,7). Continuous oxygen saturation was measured with an ear oximeter (Biox 3700, Ohmeda Corp., Louisville, CO, U.S.A.). Oral and nasal airflows were monitored separately with Grass thermistors (Quincy, MA, U.S.A.). Abdominal and chest movements were sensed with a respiratory inductance plethysmograph (Ambulatory Monitoring Inc., Ardslet, NY, U.S.A.), and a sum tracing was also recorded. The inductance tracing was not used quantitatively, but rather the deflections defined breathing rate and rhythm. Electroencephalograms (EEG) and electrooculograms (EOG) were recorded simultaneously from occipital, frontal and ocular leads. Electrocardiograms (EKG) were recorded from a standard V2 lead. All leads were recorded simultaneously on a 15-channel polygraph with optical disc storage capability. In addition to the usual montage of polysomnographic monitoring, we also used a method to record and quantitate the frequency of snoring. This method was used in a study of snorers by Abbey et al. (8). We used a Grass model TR-21 miniature microphone (Quincy, MA, U.S.A.) that monitored sounds generated by the passage of air through the upper airway during all-night sleep. The small size of the microphone allowed placement on the substernal notch. This location allowed easy identification of snores (Fig. 1) and discrimination of the deflections made by snoring from extraneous noise. The microphone generates a relatively large signal response to airflow; approximately 1-5 microvolts. Sounds made by the sleeper caused a deflection of the polygraph to which the microphone was cabled, giving a real-time record of each noise. All sleepers were monitored by television, and noise deflections from extraneous sounds were marked on a continuous paper tracing of a multichannel recorder by the sleep technologist. For both clinical and research purposes, such quantitation of the frequency of snores per night has been achieved easily using the microphone. We do not currently have equipment in our sleep laboratories to establish snoring intensity. The next morning, the sleep technologist reviewed the videotape of the 1st night of sleep and assessed the severity of sleep apnea and snoring, as well as the position(s) associated with breathing irregularities. A best position for sleeping for each patient became obvious on review of each videotape during the control night. This position for every subject was with the subject sleeping on his side. On the following 3 nights the factors sleeping position (best position vs. free position), nasal spray (yes as opposed to no) and the combination of best position Sleep, Vol. 17, No.6, 1994

3 518 H. M. BRA VER AND A. J. BLOCK TABLE 1. Demographic characteristics of the 20 subjects Age Weight Height BMI" Patient no. (years) (kg) (m) (kglm2) Mean ± SEM 42 ± ± ±O 36 ± 1.1 " BMI, body mass index. (on side) and nasal spray were studied in a randomized complete-block design. The best sleeping position was secured with the use of foam rubber wedges both behind and in front of the subject. Television monitoring was used to assure that the position was maintained during sleep. Oxymetazoline (Afrin) 12-hour nasal spray was the nasal spray used in this study. Two sprays of this medication were delivered to each nostril just prior to bedtime on the appropriate nights. Complete polysomnographic monitoring plus television monitoring was repeated on every night of the 4-night study. Definitions. Apnea was noted when flow ceased in the nose and mouth for 10 seconds or longer. If chest and abdominal movement ceased during this period, the apnea was recorded as a central apnea. If chest and abdominal movement continued in opposite directions, the apnea was recorded as obstructive. An episode of hypopnea was noted if flows in the nose and mouth decreased, chest and abdominal movements decreased and desaturation occurred (9). An episode of desaturation was recorded when a fall of 4% or greater from the preceding baseline saturation occurred. Sleep period time (SPT) was defined as the total time between falling asleep (onset of EEG Stage I) and awakening in the morning. Total sleep time (TST) was defined as SPT less any time the subject was awake after falling asleep (TST = SPT - Stage 0). Apneahypopnea index (AHI) is the total apneas plus hypopneas per hour of SPT. Statistical analysis. All data are expressed as the mean ± SEM with associated 95% confidence intervals (CIs). The statistical significance of differences among the control and the three different treatments was evaluated using repeated analysis of variance (ANOV A) measurements, with p levels <0.05 considered to indicate statistical significance. RESULTS A total of 20 subjects entered this study. All 20 fulfilled the enrollment criteria, and all 20 subjects completed the study. Demographic characteristics of the study group are shown in Table 1. The degree of obesity of each patient was expressed in terms of body mass index (BMI), defined as weight/height where weight is expressed in kilograms and height in m 2 (10). The mean ± SEM percent of time the 20 subjects spent sleeping supine versus in the lateral position during the control night was 68 ± 5.3% and 3.2 ± 5.2%, respectively. Table 2 reveals the sleep structure including the mean ± SEM for SPT and TST and the percent ofspt spent in wakefulness, Stages I and II, Stages III and IV, and rapid eye movement (REM) sleep during the control, nasal spray and combination nasal spray and positional treatment nights for the 20 subjects. Tables 3 and 4 reveal the actual AHIIhour SPT and numbers of snores/hour SPT, respectively, for each patient. As shown in Table 3, during the control night, the mean AHI ± SEM was 17.5 ± 6.5. With sleep in the best position, the mean AHI was 14.1 ± 6.3 (95% CI, ; p = 0.03). Using nasal spray alone, the mean AHI was 18.1 ± 6.3 (95% CI ; p = 0.765). The mean AHI ± SEM with the combination of nasal TABLE 2. Sleep structure Control Spray Position Combination SPT (minutes) 385 ± ± ± ± 5.2 TST (minutes) 346 ± ± ± ± 6.7 Awake (% SPT) 10 ± ± ± ± 1.2 I-II (% SPT) 74 ± ± ± ± 1.9 III-IV (% SPT) 5 ± ± ± ± 1.4 REM (% SPT) 12 ± ± ± ± 1.3 SPT, sleep period time in minutes; TST, total sleep time in minutes; Awake (Stage 0), I-II, III-IV, REM, percent of sleep period time spent in wakefulness, Stage I and II, Stage III and IV, and REM sleep, respectively..., Sleep. Vol. 17. No

4 TREATMENT OF MEN WHO SNORE 519 TABLE 3. Apnea-hypopnea indexa/hour sleep period time Patient no. Control Spray Position Combination I 0 I 0 I I I II I 15 I I Mean + SEM ± ± ± 6.0 a Apnea-hypopnea index, number of apneas and hypopneas per hour sleep period time. spray and positional treatment was 13.2 ± 6.04 (95% CI ; p = ). AHI improved significantly with both positional treatment and with the combination of positional treatment and nasal spray. As shown in Table 4, during the control night, the mean snores ± SEM were 356 ± Using nasal spray, mean snores were 381 ± 50.4 (95%CI, ; p = 0.50). With positional treatment alone, mean snores were 356 ± 46.0 (95% CI, ; p = 0.8). With the combination of nasal spray and position, mean snores were 352 ± 48.9 (95% CI, ; p = 0.91). There was no statistically significant change in snoring with the use of nasal spray, best position or the combination of nasal spray and positional treatment in our subjects. As shown in Table 3, three subjects (subject nos. 8, 10 and 11) had AHI > 65. These subjects were included in the study because they fulfilled all of our inclusion criteria, including being asymptomatic, healthy, not addicted to drugs or alcohol, having no predisposing factors towards sleep apnea other than obesity and having normal pulmonary function tests. TABLE 4. Number of snores/hour sleep period time Combina- Patient no. Control Spray Position tion I II Mean ± SEM 356 ± ± ± ± 49 DISCUSSION The results of our study were both disappointing and surprising. In accordance with the literature, our study showed an improvement in the AHI with positional treatment during sleep. In 1984, Cartwright reported that the apnea index was twice as high in 24 patients being evaluated for the sleep apnea syndrome if they slept supine rather than on their sides (11). In 1986, Phillips et al. verified that sleeping in the lateral decubitus position was associated with improvement in obstructive apneas and hypopneas (12). Physiological support for the finding of increased numbers of apneas while sleeping in the supine position has also been reported (13). Although the current study did demonstrate a statistically significant reduction in AHI while patients slept on their sides, the clinical significance of this small change is doubtful. The lack of any beneficial effect on snoring is distressing. The most surprising part of our study was that increasing nasal patency did not improve the AHI or Sleep, Vol. 17, No.6, 1994

5 520 H. M. BRA VER AND A. J. BLOCK snoring. In the early 1980s, several papers demonstrated that obstructive sleep apnea could be worsened by nasal obstruction (6,14,15). Posterior nasal packing, which caused complete nasal obstruction after septoplasty, produced obstructive sleep apnea even in subjects who were completely normal preoperatively (16). Polysomnography done on patients with seasonal allergic rhinitis showed twice as many apneas during the allergic season when the nares were obstructed (17). Why nasal obstruction causes sleep-disordered breathing is unclear. Parisiet al. showed in 1989 that pharmacologic vasoconstriction of both the nasopharynx and oropharynx using phenylephrine intranasally and by gargling, respectively, reduces tissue blood volume, thereby increasing cross-sectional area and decreasing collapsibility ofthe upper airway (18). Wasicko et al. showed in 1990 that pharmacologic systemic vasodilation increases tissue blood volume, thereby reducing the pharyngeal cross-sectional area, which likely makes the airway more susceptible to collapse (19), and in 1991 Wasicko et al. showed that the oropharyngeal and nasopharyngeal topical application of phenylephrine decreased both nasal and pharyngeal resistance and that the effect of phenylephrine on nasal resistance was independent of the effect on pharyngeal resistance (20). In 1990, Hutt et al. showed that oropharyngeal and nasopharyngeal topical application of oxymetazoline, a vasoconstrictor, caused significant reductions in sleepdisordered breathing in patients with obstructive sleep apnea (21). The reason why oxymetazoline did not cause a significant reduction in sleep-disordered breathing in our study is not clear. The most likely explanation lies in the fact that oxymetazoline has been shown to cause increased nasal discharge in patients (22). Table 3 shows that subjects actually had some decrease in AHI with the use of oxymetazoline as compared to the control night. Table 4 shows that 9/20 subjects had some decrease in the amount of snoring with the use of oxymetazoline as compared to the control night. It is very possible that some of our subjects could have experienced an increase in nasal discharge secondary to the oxymetazoline that caused increased nasal obstruction. The increased nasal obstruction may have secondarily caused an increase in the AHI and an increase in snoring. One should note that the subjects in our study were only treated with intranasal instillation of oxymetazoline. They were not treated by both nasopharyngeal and oropharyngeal topical vasoconstriction as was done in the previous studies mentioned (18,20,21). It is possible that our patients had less oropharyngeal vasoconstriction than those in the studies done by Parisi et al. (18), Wasicko et al. (20) and Hutt et al. (21) and therefore had increased collapsibility ofthe upper airway as compared to the subjects in these other studies. Alternatively, our study only had 20 subjects. Another study using a much larger number of subjects could possibly show a statistically significant improvement in sleep-disordered breathing in patients treated with topical vasoconstriction. Snoring was not improved by any intervention or combination of interventions. Because the noise of snoring and its consequent spousal irritation are common reasons such patients seek medical attention, these results are very disappointing. Hoffstein et al. demonstrated in 1988 that nasal airflow resistance correlates with snoring (23). More recent studies by Miljeteig et al. (24) and Hoffstein et al. (25) suggest that reduction in nasal resistance during sleep may not correlate with snoring. We believed that reducing nasal resistance during sleep with oxymetazoline would lead to a reduction in snoring. We did not measure resistance in our study. It is possible that the nasal resistance in our subjects was reduced by the oxymetazoline, but the recent studies by Miljeteig et al. (24) and Hoffstein et al. (25) were correct in suggesting that the reduction in nasal resistance during sleep may not correlate with snoring. It is also possible that the snoring in our patients stayed the same after using the nasal decongestant, because nasal resistance did not actually change. Furthermore, it is possible that the reduction in the AHI from position alteration in our subjects allowed more inhalations to occur that were partially obstructed rather than totally obstructed, increasing rather than decreasing the frequency of snoring. On the basis of our results, it is obvious that the institution of only positional treatment and nasal spray cannot cure sleep-disordered breathing in the asymptomatic snorer. The combination of positional treatment and nasal spray only minimally improved the sleep-disordered breathing in our subjects. It is possible that the addition of weight loss to the small benefits seen in this study could be additive and yield more clinically impressive results. We will add the weight loss intervention to our future studies to assess this possi bili ty. Acknowledgements: This work was supported by a merit review grant from the Veterans Administration. Special thanks are due to Mr. Nick D' Amato and Mr. Don Hellard who performed the sleep studies and stared endlessly at videotapes of men sleeping. REFERENCES 1. Block AJ, Hellard DW, Cicale MJ. Snoring, nocturnal hypoxemia, and the effect of oxygen inhalation. Chest 1987;92: Lugaresi E, Cirignotta F, Coccagna G, Piana C. Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 1980;3: Sleep. Vol. 17. No

6 TREATMENT OF MEN WHO SNORE Koskenvuo M, Partinen M, Sarna S, Kaprio J, Langinvainio H, Heikkila K. Snoring as a risk factor for hypertension and angina pectoris. Lancet 1985; 1 : Partinen M, Palomaki H. Snoring and cerebral infarction. Lancet 1985;2: McEvoy RD, Sharp DJ, Thornton AT. The effects of posture on obstructive sleep apnea. Am Rev Respir Dis 1986; 133: Zwillich CW, Pickett C, Hanson FN, Weil JV. Disturbed sleep and prolonged apnea during nasal obstruction in normal men. Am Rev Respir Dis 1981;124: Block AJ, Hellard DW, Switzer DA. Nocturnal oxygen therapy does not improve snorers' intelligence. Chest 1989;95: Abbey NC, Block AJ, Green D, Mancuso A, Hellard DW. Measurement of pharyngeal volume by digitized magnetic resonance imaging. Effect of nasal continuous positive pressure. Am Rev Respir Dis 1989; 140: Block AJ, Boysen PG, Wynne JW, Hunt LA. Sleep apnea, hypopnea, and oxygen de saturation in normal subjects. A strong male predominance. New Engl J Med 1979;300: Thomas AE, McKay DA, Cutlip MB. A nomograph method for assessing body weight. Am J Clin Nutr 1976;29: II. Cartwright RD. Effect of sleep position on sleep apnea severity. Sleep 1984;7: Phillips BA, Okeson J, Paesani D, Gilmore R. Effect of sleep position on sleep apnea and parafunctional activity. Chest 1986; 90: Brown IB, McClean PA, Boucher R, Zamel N, Hoffstein V. Changes in pharyngeal cross-sectional area with posture and application of continuous positive airway pressure in patients with obstructive sleep apnea. Am Rev Respir Dis 1987; 136: Wynne JW. Obstruction of the nose and breathing during sleep. Chest 1982;82: Olsen KD, Kern EB, Westbrook PR. Sleep and breathing disturbance secondary to nasal obstruction. Otolaryngol Head Neck Surg 1981 ;89: Taasan V, Wynne JW, Cassisi N, Block AJ. The effect of nasal packing on sleep-disordered breathing and nocturnal oxygen desaturation. Laryngoscope 1981; 7: McNicholas WT, Tarlo S, Cole P, et al. Obstructive apneas during sleep in patients with seasonal allergic rhinitis. Am Rev Respir Dis 1982; 126: Parisi RA, Wasicko MJ, Hutt DA, Mandel M, Santiago TV, Edelman NH. Mucosal vasoconstriction increases pharyngeal size in normal subjects. Am Rev Respir Dis 1989;139:A374 (abstract). 19. Wasicko MJ, Hutt DA, Parisi RA, Neubauer JA, Mezrich R, Edelman NH. The role of vascular tone in the control of upper airway collapsibility. Am Rev Respir Dis 1990;141: Wasicko MJ, Leiter JC, Erlichman JS, Strobel RJ, Bartlett D. Nasal and pharyngeal resistance after topical mucosal vasoconstriction in normal humans. Am Rev Respir Dis 1991; 144: Hutt DA, Parisi RA, Santiago TV. Pharyngeal mucosal vasoconstriction reduces the frequency of disordered breathing events in patients with obstructive sleep apnea. Am Rev Respir Dis 1990; 141 :A865 (abstract). 22. Huff BB, Dowd AL, eds. Physician's desk reference for nonprescription drugs. Oradell, NJ: Medical Economics Incorporated, 1989: Hoffstein V, Chaban R, Cole P, Rubinstein I. Snoring and upper airway properties. Chest 1988;94: Miljeteig H, Savard P, Mateika S, Cole P, Haight JS, Hoffstein V. Snoring and nasal resistance during sleep. Laryngoscope 1993; 103: Hoffstein V, Mateika S, Metes A. Effect of nasal dilation on snoring and apneas during different stages of sleep. Sleep 1993; 16: Sleep, Vol. 17, No.6, 1994