AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 1 73–1 7 7
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Middle ear pressure during sleep and the effects of continuous positive airway pressure☆ Joshua J. Thom, MD a , Matthew L. Carlson, MD a,⁎, Colin L.W. Driscoll, MD a , Erik K. St Louis, MD b , Kannan Ramar, MBBS, MD c , Eric J. Olson, MD c , Brian A. Neff, MD a a b c
Department of Otolaryngology, Head and Neck Surgery, Mayo Clinic School of Medicine, Rochester, MN, USA Department of Neurology and Center for Sleep Medicine, Mayo Clinic School of Medicine, Rochester, MN, USA Division of Pulmonary and Critical Care Medicine and Center for Sleep Medicine, Mayo Clinic School of Medicine, Rochester, MN, USA
ARTI CLE I NFO
A BS TRACT
Article history:
Purpose: Prior studies evaluating Eustachian tube physiology, baseline middle ear pressure
Received 28 July 2014
(MEP), and the effects of continuous positive airway pressure (CPAP) have been performed on awake patients. No study to date has specifically investigated MEP during sleep despite the fact that the average individual spends a third of their lifetime sleeping. The primary objectives of the current study are to quantify normal physiologic MEP during sleep and to evaluate the effects of escalating CPAP levels. Materials and methods: Prospective observational study at a tertiary academic referral center evaluating serial tympanometry on sleeping adult patients during polysomnography. MEP was recorded awake, at 1-hour intervals during diagnostic polysomnography, and at all CPAP levels during titration. Changes in MEP with duration of sleep and escalating CPAP levels were analyzed. Results: Ten adults were included (4 females; 6 males; mean age 58 years). The mean MEP while awake was 3 decapascals (daPa). The mean MEP during sleep without CPAP rose steadily from 14 daPa at 1 hour to 41 daPa at 4 hours (r = 0.52; p < 0.001). The mean MEP during sleep at a CPAP level of 5 cm of water was 54 daPa. The mean MEP rose steadily with increasing CPAP levels, and was 104 daPa at 10 cm of water, (r = 0.82; p < 0.001). The mean MEP during sleep without CPAP was 26 daPa, which was significantly lower than the mean MEP during sleep with CPAP between 5–10 cm H2O (p < 0.01). Conclusions: MEP naturally increases with duration of sleep. CPAP therapy causes a supraphysiologic elevation in MEP that rises with increasing pressure levels. These findings may help guide future studies examining the safety of CPAP following otologic surgery and the potential therapeutic benefit in patients with chronic middle ear disease. © 2015 Elsevier Inc. All rights reserved.
☆
IRB Approval Number: 12-005787. ⁎ Corresponding author at: Department of Otolaryngology, Head and Neck Surgery, Mayo Clinic School of Medicine, 200 First Street SW, Rochester, MN, 55905, USA. Tel.: + 1 507 255 5123; fax: +1 507 284 8855. E-mail address: [email protected] (M.L. Carlson). http://dx.doi.org/10.1016/j.amjoto.2014.10.024 0196-0709/© 2015 Elsevier Inc. All rights reserved.
174
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY–H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 1 73 –1 7 7
1.
Introduction
Maintenance of normal middle ear pressure (MEP) by an appropriately functioning eustachian tube (ET) is vital to the health of the middle ear. ET dysfunction resulting in chronic negative MEP has been implicated in many significant otologic conditions including hearing loss, tympanic membrane (TM) retraction, and chronic otitis media. Prior studies evaluating middle ear and ET physiology have been performed on awake patients with normal or negative MEP [1–3]. To the authors’ knowledge, no study to date has specifically investigated MEPs during sleep despite the fact that the average individual sleeps nearly a third of their lifetime. Many organ systems have normal physiologic changes during sleep. In patients without middle ear disease, studies have shown that MEP is most commonly positive upon waking, but quickly normalizes toward zero after swallowing and chewing maneuvers [1–3]. These findings suggest that middle ear and ET physiology also change during sleep. Continuous positive airway pressure (CPAP) therapy, a highly effective treatment for obstructive sleep apnea (OSA), provides a pneumatic stent for the upper airway and prevents apnea during sleep. It is highly plausible that positive pressure may be transmitted to the middle ear through the ET during CPAP use. This can occur during periodic ET opening or when nasopharyngeal airway pressures exceed the resting pressure keeping the ET closed. A recent study demonstrated a linear
increase in MEP with increasing CPAP levels in awake patients [4]. We hypothesized that MEP would rise slowly with duration of sleep and that escalating CPAP levels would cause proportional elevations in MEP during sleep.
2.
Materials and methods
Following Institutional Review Board approval (IRB No. 12005787), adult patients undergoing polysomnography at a tertiary academic referral center were prospectively enrolled. All research subjects were provided informed consent. Study participation was limited to patients without prior middle ear disease or a history of otologic surgery. Each eligible participant was further screened using otomicroscopy and tympanometry (Madsen OTOflex 100; GN Otometrics North America, Schaumburg, IL), and all patients with evidence of active ET dysfunction, middle ear disease, TM perforation, or a non-Type A tympanogram were excluded. One subject was excluded because of ongoing ET dysfunction with TM retraction and a Type C tympanogram. Each patient was then fitted with a tympanometry probe in one ear that was sealed in place with polyvinylsiloxane ear impression molding (Oaktree Products Inc., Chesterfield, MO) using a manual impression gun (Fig. 1). Tympanometry was performed and MEP was recorded in decapascals (daPa) in supine subjects. Two additional patients were excluded; one could not tolerate sleeping with the
Fig. 1 – A Madsen OTOflex 100 device (GN Otometrics North America, Shaumberg, IL) with tympanometry probe was sized and sealed in the external auditory canal with polyvinylsiloxane ear impression molding (Oaktree Products Inc., Chesterfield, MO) using a manual impression gun.
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 1 73–1 7 7
tympanometry probe in place, and in the other, a seal could not be kept with the probe in the ear to obtain accurate pressure readings. MEP readings were taken just before sleep initiation and during the diagnostic portion of the polysomnogram at 1hour intervals following sleep onset. Confirmation of sleep was performed using electroencephalography (EEG). Following diagnostic polysomnography, if the patient met criteria for OSA with an apnea-hyponea index (AHI) ≥5 events/hour, they were fitted with a CPAP device. The CPAP level, in centimeters of water (cm H2O), was titrated during sleep until the patient’s OSA was adequately treated. Tympanometry was performed and MEP readings were taken prior to the initiation of CPAP, and at each level of CPAP during the titration. MEP mean values, standard deviations, and ranges were calculated for each category. Paired t-tests were used for comparison of MEP with and without CPAP use while asleep. Spearman’s rank correlation coefficient (r) was utilized to compare MEP with time asleep and CPAP level.
3.
175
Eight of ten patients met criteria for OSA with a mean AHI of 16 (range, 6 – 40), and qualified for CPAP titration. One patient was not able to initiate sleep with the CPAP device and did not undergo titration. The mean MEP before CPAP initiation for the seven patients that underwent successful CPAP titration was +14 daPa (range, -4 – +39 daPa; SD, ±13). The mean MEP at a CPAP level of 5 cm H2O was +54 daPa (range, +26 to +73 daPa; SD, ±15), which rose steadily with increasing CPAP levels to a mean MEP of +104 daPa (range, +95 to +113 daPa; SD ±13) at a CPAP level of 10 cm H2O (Fig. 3). There was a very strong positive correlation between CPAP level and MEP (r = 0.82, p < 0.001). There was a statistically significant difference when comparing mean MEP during sleep without CPAP and mean MEP during sleep with CPAP. The average MEP during sleep without CPAP was + 26 daPa (range, − 15 to +86 daPa; SD, ± 25), while the mean MEP during sleep with CPAP at 5 cm H2O was + 54 daPa (range, + 26 to + 73 daPa; SD, ± 15), (p < 0.01). The differences between the mean MEP during sleep without CPAP and with CPAP became greater as the CPAP pressure was increased beyond 5 cm H2O (p < 0.005).
Results
Ten patients, six men and four women, were included. The mean age at testing was 57.8 years (range 37.7–74.7 yrs). Monaural testing was performed in each patient including six left and four right ears. The mean MEP of all patients before sleep was +3 daPa [range, −12 to +18 daPa; standard deviation (SD), ±10]. The mean MEP at 1, 2, 3, and 4 hours following sleep onset were +14 daPa (range, −15 to +40 daPa; SD, ±24), +22 daPa (range, −1 to +64 daPa; SD, ±23), +27 daPa (range, −9 to +53 daPa; SD, ±23), and +41 daPa (range, +12 to +86 daPa; SD, ±26), respectively (Fig. 2). There was a strong positive relationship between time asleep and MEP (r = 0.52, p < 0.001).
Fig. 2 – Middle ear pressure with duration of sleep during diagnostic polysomnography. Abbreviations: daPa = decapascals.
4.
Discussion
Using a novel method to record MEP during sleep, our results confirm the hypothesis that MEP predictably rises during sleep. We found that the mean MEP after 4 hours of sleep was 41 daPa, which corroborates two earlier studies measuring an average MEP of 29 and 48 daPa immediately upon waking [1,2]. These values are significantly higher than the mean awake MEP of 3 daPa in the current study.
Fig. 3 – Middle ear pressure in sleeping patients at successively greater continuous positive airway pressure (CPAP) levels. Abbreviations: CPAP = continuous positive airway pressure; daPa = decapascals.
176
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY–H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 1 73 –1 7 7
The mechanism of increased MEP during sleep is likely multifactorial and may result, in part, from impaired ET ventilation occurring while supine. Hergils et al. demonstrated that in awake patients lying supine and performing shallow breathing, MEP rises slowly with time then decreases quickly with swallowing [1]. Swallowing during sleep has been shown to occur an average of 2.4 times per hour [5,6]. Hergils and colleagues found that MEP equalization with swallowing was often incomplete while supine and continued to rise reaching a plateau after approximately 3–4 hours, paralleling our findings in asleep subjects [1]. Our study confirms a supraphysiologic rise in MEP in patients using CPAP during sleep. A CPAP setting of 5 cm H2O is typically the lowest level used to treat OSA. At 5 cm H2O, the mean MEP during sleep was 54 daPa. This is more than double the average MEP during sleep without CPAP. MEP rose steadily with increasing CPAP levels with a mean MEP of 104 daPa at 10 cm H2O. This is very similar to that published by Lin et al. in which the mean MEP in awake patients was 47, 82, and 129 daPa at CPAP levels of 5, 10, and 15 cm H2O, respectively [4]. The implications of elevated MEP with CPAP use are significant. The upper limit of normal MEP is considered by many to be between 50 and 100 daPa. These pressures are easily surpassed by CPAP use. Unfortunately, because the prevalence of sustained positive MEP is very low and most middle ear disease is associated with negative pressure, studies evaluating the effects of positive MEP are scarce. Ostergard et al. identified 13 of 750 (1.7%) patients with ear complaints who had a MEP greater than 49 daPa while awake [7]. In patients with positive MEP, the most common complaints were otalgia, ear fullness, and pharyngitis. TM erythema and decreased mobility, as well as otitis media were noted in most of these patients. Only two patients exhibited a mild conductive hearing loss [7]. A study conducted in guinea pigs demonstrated that elevating MEP with air up to 250 daPa had no effect on auditory thresholds measured by auditory brainstem response (ABR) [8]. While it appears that hearing is likely not significantly affected in most individuals, there have been rare reports of tympanic membrane rupture, pneumocephalus, and tension pneumocranium with CPAP use [9–12]. Although rare, these findings should prompt caution with CPAP use following head trauma, rhinologic or otologic surgery, and particularly following intradural skull base procedures. Finally, it is worth discussing the potential therapeutic role of CPAP in patients with chronic ear disease. ET dysfunction with resultant chronic negative MEP is the principle mechanism behind chronic otitis media. Two studies have examined the long-term effects of CPAP on MEP [13,14]. Aksoy et al. compared the awake MEPs of 51 patients with OSA using CPAP for at least six months to 48 control subjects that did not use CPAP and found that there was no significant difference between groups [13]. In contrast, Sivri and colleagues compared awake MEPs of 78 patients with OSA using CPAP for six months to 60 control patients without OSA and not using CPAP and found a significant increase in MEP in the group using CPAP [14]. In addition, the increase in mean MEP in the CPAP group was
directly proportional to the pressure level of CPAP prescribed. There was also a significant number of patients that converted from a type B or C tympanogram to a type A configuration, and four of five TM retractions resolved following six months of CPAP use [14]. Similarly, Yung demonstrated the potential benefit of CPAP for treatment of TM atelectasis, showing that a single CPAP session at 10 cm of H2O reinflated two-thirds of atelectatic TMs [15]. In closing, we wish to acknowledge several strengths and limitations of the current study. To the authors’ knowledge, this is the first study to investigate normal physiologic MEP during sleep and how this is altered with CPAP use. While middle ear physiology has been extensively analyzed in awake individuals, studies evaluating MEP during sleep are lacking despite the fact that the average individual sleeps nearly a third of their lifetime. Second, by performing tympanometry during polysomnography, the authors could study the effects of duration of sleep on MEP in a controlled setting, through monitoring of the sleep-wake cycle and arousals. The primary weakness of the current study is the limited number of patients. Studying each subject during overnight polysomnography proved to be costly and time intensive, which limited prospective enrollment. However, even with ten patients, the primary outcomes of the study were found to be highly statistically significant. Additionally, these data were collected on subjects without a history of ET dysfunction; therefore our findings may not directly apply to patients with chronic ear disease. Future studies will be needed to determine if these observations also hold true for subjects with ET dysfunction.
5.
Conclusions
Middle ear pressure rises proportionately with duration of sleep. Furthermore, increasing CPAP levels result in predictable supraphysiologic elevations in MEP. Further research is needed to examine the long-term consequences of CPAP use on the middle ear and the potential therapeutic benefits for patients with tympanic membrane retraction and chronic ear disease.
REFERENCES
[1] Hergils L, Magnuson B. Morning pressure in the middle ear. Arch Otolaryngol 1985;111:86–9. [2] Shinkawa H, Okitsu T, Yusa T, et al. Positive intratympanic pressure in the morning and its etiology. Acta Otolaryngol 1987;S435:107–11. [3] Luntz M, Sadé J. Daily fluctuations of middle ear pressure in atelectatic ears. Ann Otol Rhinol Laryngol 1990;99:201–4. [4] Lin FY, Gurgel RK, Popelka GR, et al. The effect of continuous positive airway pressure on middle ear pressure. Laryngoscope 2012;122:688–90. [5] Sato K, Umeno H, Chitose S, et al. Deglutition and respiratory patterns during sleep in younger adults. Acta Otolaryngol 2011;131:190–6. [6] Sato K, Umeno H, Chitose S, et al. Sleep-related deglutition in patients with OSAHS under CPAP therapy. Acta Otolaryngol 2011;131:181–9.
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 1 73–1 7 7
[7] Ostergard CA, Carter DR. Positive middle ear pressure shown by tympanometry. Arch Otolaryngol 1981;107:353–6. [8] Petrova P, Freeman S, Sohmer H. The effects of positive and negative middle ear pressures on auditory thresholds. Otol Neurotol 2006;27:734–8. [9] Weaver LK, Fairfax WR, Greenway L. Bilateral otorrhagia associated with continuous positive airway pressure. Chest 1988;4:878–9. [10] Klopfenstein CE, Forster A, Suter PM. Pneumocephalus. A complication of continuous positive airway pressure after trauma. Chest 1980;4:656–7. [11] Kopelovich JC, de la Garza GO, Greenlee JD, et al. Pneumocephalus with BiPAP use after transsphenoidal surgery. J Clin Anesth 2012;5:415–8.
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[12] Sawka AM, Aniszewski JP, Young WF, et al. Tension pneumocranium, a rare complication of transphenoidal pituitary surgery: Mayo Clinic experience 1976–1998. J Clin Endocrinol Metab 1999;84:4731–4. [13] Aksoy F, Yildirim YS, Ozturan O, et al. Eustachian tube function in patients receiving continuous positive airway pressure treatment for sleep apnea syndrome. J Otolaryngol Head Neck Surg 2010;39:752–6. [14] Sivri B, Sezen OS, Akbulut S, et al. The effect of continuous positive airway pressure on middle ear pressure. Laryngoscope 2013;123:1300–4. [15] Yung MW. The effect of nasal continuous positive airway pressure on normal ears and on ears with atelectasis. Am J Otol 1999;20:568–72.
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Middle ear pressure during sleep and the effects of continuous positive airway pressure☆ Joshua J. Thom, MD a , Matthew L. Carlson, MD a,⁎, Colin L.W. Driscoll, MD a , Erik K. St Louis, MD b , Kannan Ramar, MBBS, MD c , Eric J. Olson, MD c , Brian A. Neff, MD a a b c
Department of Otolaryngology, Head and Neck Surgery, Mayo Clinic School of Medicine, Rochester, MN, USA Department of Neurology and Center for Sleep Medicine, Mayo Clinic School of Medicine, Rochester, MN, USA Division of Pulmonary and Critical Care Medicine and Center for Sleep Medicine, Mayo Clinic School of Medicine, Rochester, MN, USA
ARTI CLE I NFO
A BS TRACT
Article history:
Purpose: Prior studies evaluating Eustachian tube physiology, baseline middle ear pressure
Received 28 July 2014
(MEP), and the effects of continuous positive airway pressure (CPAP) have been performed on awake patients. No study to date has specifically investigated MEP during sleep despite the fact that the average individual spends a third of their lifetime sleeping. The primary objectives of the current study are to quantify normal physiologic MEP during sleep and to evaluate the effects of escalating CPAP levels. Materials and methods: Prospective observational study at a tertiary academic referral center evaluating serial tympanometry on sleeping adult patients during polysomnography. MEP was recorded awake, at 1-hour intervals during diagnostic polysomnography, and at all CPAP levels during titration. Changes in MEP with duration of sleep and escalating CPAP levels were analyzed. Results: Ten adults were included (4 females; 6 males; mean age 58 years). The mean MEP while awake was 3 decapascals (daPa). The mean MEP during sleep without CPAP rose steadily from 14 daPa at 1 hour to 41 daPa at 4 hours (r = 0.52; p < 0.001). The mean MEP during sleep at a CPAP level of 5 cm of water was 54 daPa. The mean MEP rose steadily with increasing CPAP levels, and was 104 daPa at 10 cm of water, (r = 0.82; p < 0.001). The mean MEP during sleep without CPAP was 26 daPa, which was significantly lower than the mean MEP during sleep with CPAP between 5–10 cm H2O (p < 0.01). Conclusions: MEP naturally increases with duration of sleep. CPAP therapy causes a supraphysiologic elevation in MEP that rises with increasing pressure levels. These findings may help guide future studies examining the safety of CPAP following otologic surgery and the potential therapeutic benefit in patients with chronic middle ear disease. © 2015 Elsevier Inc. All rights reserved.
☆
IRB Approval Number: 12-005787. ⁎ Corresponding author at: Department of Otolaryngology, Head and Neck Surgery, Mayo Clinic School of Medicine, 200 First Street SW, Rochester, MN, 55905, USA. Tel.: + 1 507 255 5123; fax: +1 507 284 8855. E-mail address: [email protected] (M.L. Carlson). http://dx.doi.org/10.1016/j.amjoto.2014.10.024 0196-0709/© 2015 Elsevier Inc. All rights reserved.
174
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY–H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 1 73 –1 7 7
1.
Introduction
Maintenance of normal middle ear pressure (MEP) by an appropriately functioning eustachian tube (ET) is vital to the health of the middle ear. ET dysfunction resulting in chronic negative MEP has been implicated in many significant otologic conditions including hearing loss, tympanic membrane (TM) retraction, and chronic otitis media. Prior studies evaluating middle ear and ET physiology have been performed on awake patients with normal or negative MEP [1–3]. To the authors’ knowledge, no study to date has specifically investigated MEPs during sleep despite the fact that the average individual sleeps nearly a third of their lifetime. Many organ systems have normal physiologic changes during sleep. In patients without middle ear disease, studies have shown that MEP is most commonly positive upon waking, but quickly normalizes toward zero after swallowing and chewing maneuvers [1–3]. These findings suggest that middle ear and ET physiology also change during sleep. Continuous positive airway pressure (CPAP) therapy, a highly effective treatment for obstructive sleep apnea (OSA), provides a pneumatic stent for the upper airway and prevents apnea during sleep. It is highly plausible that positive pressure may be transmitted to the middle ear through the ET during CPAP use. This can occur during periodic ET opening or when nasopharyngeal airway pressures exceed the resting pressure keeping the ET closed. A recent study demonstrated a linear
increase in MEP with increasing CPAP levels in awake patients [4]. We hypothesized that MEP would rise slowly with duration of sleep and that escalating CPAP levels would cause proportional elevations in MEP during sleep.
2.
Materials and methods
Following Institutional Review Board approval (IRB No. 12005787), adult patients undergoing polysomnography at a tertiary academic referral center were prospectively enrolled. All research subjects were provided informed consent. Study participation was limited to patients without prior middle ear disease or a history of otologic surgery. Each eligible participant was further screened using otomicroscopy and tympanometry (Madsen OTOflex 100; GN Otometrics North America, Schaumburg, IL), and all patients with evidence of active ET dysfunction, middle ear disease, TM perforation, or a non-Type A tympanogram were excluded. One subject was excluded because of ongoing ET dysfunction with TM retraction and a Type C tympanogram. Each patient was then fitted with a tympanometry probe in one ear that was sealed in place with polyvinylsiloxane ear impression molding (Oaktree Products Inc., Chesterfield, MO) using a manual impression gun (Fig. 1). Tympanometry was performed and MEP was recorded in decapascals (daPa) in supine subjects. Two additional patients were excluded; one could not tolerate sleeping with the
Fig. 1 – A Madsen OTOflex 100 device (GN Otometrics North America, Shaumberg, IL) with tympanometry probe was sized and sealed in the external auditory canal with polyvinylsiloxane ear impression molding (Oaktree Products Inc., Chesterfield, MO) using a manual impression gun.
AM ER IC AN JOURNAL OF OT OLARYNGOLOGY–H E A D A N D NE CK M E D IC IN E A ND S U RGE RY 3 6 (2 0 1 5) 1 73–1 7 7
tympanometry probe in place, and in the other, a seal could not be kept with the probe in the ear to obtain accurate pressure readings. MEP readings were taken just before sleep initiation and during the diagnostic portion of the polysomnogram at 1hour intervals following sleep onset. Confirmation of sleep was performed using electroencephalography (EEG). Following diagnostic polysomnography, if the patient met criteria for OSA with an apnea-hyponea index (AHI) ≥5 events/hour, they were fitted with a CPAP device. The CPAP level, in centimeters of water (cm H2O), was titrated during sleep until the patient’s OSA was adequately treated. Tympanometry was performed and MEP readings were taken prior to the initiation of CPAP, and at each level of CPAP during the titration. MEP mean values, standard deviations, and ranges were calculated for each category. Paired t-tests were used for comparison of MEP with and without CPAP use while asleep. Spearman’s rank correlation coefficient (r) was utilized to compare MEP with time asleep and CPAP level.
3.
175
Eight of ten patients met criteria for OSA with a mean AHI of 16 (range, 6 – 40), and qualified for CPAP titration. One patient was not able to initiate sleep with the CPAP device and did not undergo titration. The mean MEP before CPAP initiation for the seven patients that underwent successful CPAP titration was +14 daPa (range, -4 – +39 daPa; SD, ±13). The mean MEP at a CPAP level of 5 cm H2O was +54 daPa (range, +26 to +73 daPa; SD, ±15), which rose steadily with increasing CPAP levels to a mean MEP of +104 daPa (range, +95 to +113 daPa; SD ±13) at a CPAP level of 10 cm H2O (Fig. 3). There was a very strong positive correlation between CPAP level and MEP (r = 0.82, p < 0.001). There was a statistically significant difference when comparing mean MEP during sleep without CPAP and mean MEP during sleep with CPAP. The average MEP during sleep without CPAP was + 26 daPa (range, − 15 to +86 daPa; SD, ± 25), while the mean MEP during sleep with CPAP at 5 cm H2O was + 54 daPa (range, + 26 to + 73 daPa; SD, ± 15), (p < 0.01). The differences between the mean MEP during sleep without CPAP and with CPAP became greater as the CPAP pressure was increased beyond 5 cm H2O (p < 0.005).
Results
Ten patients, six men and four women, were included. The mean age at testing was 57.8 years (range 37.7–74.7 yrs). Monaural testing was performed in each patient including six left and four right ears. The mean MEP of all patients before sleep was +3 daPa [range, −12 to +18 daPa; standard deviation (SD), ±10]. The mean MEP at 1, 2, 3, and 4 hours following sleep onset were +14 daPa (range, −15 to +40 daPa; SD, ±24), +22 daPa (range, −1 to +64 daPa; SD, ±23), +27 daPa (range, −9 to +53 daPa; SD, ±23), and +41 daPa (range, +12 to +86 daPa; SD, ±26), respectively (Fig. 2). There was a strong positive relationship between time asleep and MEP (r = 0.52, p < 0.001).
Fig. 2 – Middle ear pressure with duration of sleep during diagnostic polysomnography. Abbreviations: daPa = decapascals.
4.
Discussion
Using a novel method to record MEP during sleep, our results confirm the hypothesis that MEP predictably rises during sleep. We found that the mean MEP after 4 hours of sleep was 41 daPa, which corroborates two earlier studies measuring an average MEP of 29 and 48 daPa immediately upon waking [1,2]. These values are significantly higher than the mean awake MEP of 3 daPa in the current study.
Fig. 3 – Middle ear pressure in sleeping patients at successively greater continuous positive airway pressure (CPAP) levels. Abbreviations: CPAP = continuous positive airway pressure; daPa = decapascals.
176
AM ER IC AN JOURNAL OF OT OLA RYNGOLOGY–H E A D A N D NE CK M E D ICI N E AN D S U RGE RY 3 6 (2 0 1 5) 1 73 –1 7 7
The mechanism of increased MEP during sleep is likely multifactorial and may result, in part, from impaired ET ventilation occurring while supine. Hergils et al. demonstrated that in awake patients lying supine and performing shallow breathing, MEP rises slowly with time then decreases quickly with swallowing [1]. Swallowing during sleep has been shown to occur an average of 2.4 times per hour [5,6]. Hergils and colleagues found that MEP equalization with swallowing was often incomplete while supine and continued to rise reaching a plateau after approximately 3–4 hours, paralleling our findings in asleep subjects [1]. Our study confirms a supraphysiologic rise in MEP in patients using CPAP during sleep. A CPAP setting of 5 cm H2O is typically the lowest level used to treat OSA. At 5 cm H2O, the mean MEP during sleep was 54 daPa. This is more than double the average MEP during sleep without CPAP. MEP rose steadily with increasing CPAP levels with a mean MEP of 104 daPa at 10 cm H2O. This is very similar to that published by Lin et al. in which the mean MEP in awake patients was 47, 82, and 129 daPa at CPAP levels of 5, 10, and 15 cm H2O, respectively [4]. The implications of elevated MEP with CPAP use are significant. The upper limit of normal MEP is considered by many to be between 50 and 100 daPa. These pressures are easily surpassed by CPAP use. Unfortunately, because the prevalence of sustained positive MEP is very low and most middle ear disease is associated with negative pressure, studies evaluating the effects of positive MEP are scarce. Ostergard et al. identified 13 of 750 (1.7%) patients with ear complaints who had a MEP greater than 49 daPa while awake [7]. In patients with positive MEP, the most common complaints were otalgia, ear fullness, and pharyngitis. TM erythema and decreased mobility, as well as otitis media were noted in most of these patients. Only two patients exhibited a mild conductive hearing loss [7]. A study conducted in guinea pigs demonstrated that elevating MEP with air up to 250 daPa had no effect on auditory thresholds measured by auditory brainstem response (ABR) [8]. While it appears that hearing is likely not significantly affected in most individuals, there have been rare reports of tympanic membrane rupture, pneumocephalus, and tension pneumocranium with CPAP use [9–12]. Although rare, these findings should prompt caution with CPAP use following head trauma, rhinologic or otologic surgery, and particularly following intradural skull base procedures. Finally, it is worth discussing the potential therapeutic role of CPAP in patients with chronic ear disease. ET dysfunction with resultant chronic negative MEP is the principle mechanism behind chronic otitis media. Two studies have examined the long-term effects of CPAP on MEP [13,14]. Aksoy et al. compared the awake MEPs of 51 patients with OSA using CPAP for at least six months to 48 control subjects that did not use CPAP and found that there was no significant difference between groups [13]. In contrast, Sivri and colleagues compared awake MEPs of 78 patients with OSA using CPAP for six months to 60 control patients without OSA and not using CPAP and found a significant increase in MEP in the group using CPAP [14]. In addition, the increase in mean MEP in the CPAP group was
directly proportional to the pressure level of CPAP prescribed. There was also a significant number of patients that converted from a type B or C tympanogram to a type A configuration, and four of five TM retractions resolved following six months of CPAP use [14]. Similarly, Yung demonstrated the potential benefit of CPAP for treatment of TM atelectasis, showing that a single CPAP session at 10 cm of H2O reinflated two-thirds of atelectatic TMs [15]. In closing, we wish to acknowledge several strengths and limitations of the current study. To the authors’ knowledge, this is the first study to investigate normal physiologic MEP during sleep and how this is altered with CPAP use. While middle ear physiology has been extensively analyzed in awake individuals, studies evaluating MEP during sleep are lacking despite the fact that the average individual sleeps nearly a third of their lifetime. Second, by performing tympanometry during polysomnography, the authors could study the effects of duration of sleep on MEP in a controlled setting, through monitoring of the sleep-wake cycle and arousals. The primary weakness of the current study is the limited number of patients. Studying each subject during overnight polysomnography proved to be costly and time intensive, which limited prospective enrollment. However, even with ten patients, the primary outcomes of the study were found to be highly statistically significant. Additionally, these data were collected on subjects without a history of ET dysfunction; therefore our findings may not directly apply to patients with chronic ear disease. Future studies will be needed to determine if these observations also hold true for subjects with ET dysfunction.
5.
Conclusions
Middle ear pressure rises proportionately with duration of sleep. Furthermore, increasing CPAP levels result in predictable supraphysiologic elevations in MEP. Further research is needed to examine the long-term consequences of CPAP use on the middle ear and the potential therapeutic benefits for patients with tympanic membrane retraction and chronic ear disease.
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