Effects of Surgical Correction of Nasal Obstruction in the Treatment of Obstructive Sleep Apnea 1- 3

F. SERIES, S. ST. PIERRE, and G. CARRIER

Introduction

T he obstructive sleep apnea syndrome is characterized by recurrent partial or complete obstructions of the pharyngeal airways (PA). This dynamic phenomenon occurs when the contraction of the upper airway dilator muscles cannot overcome the forces that tend to collapse the PA (inspiratory transpharyngeal pressure gradient) (1). Many factors are involved in the pathophysiology of these events: a narrowing of the PA (2), an increase in its collapsibility (3) or in the lung volume dependance of the PA resistance (4), differences in the mechanical effects of a decrease in the diaphragmatic and genioglossal activity during periodic breathing (5), changes in the PA resistance response to a decrease of the central respiratory drive (6). Negative airway pressure plays a key role in the destabilization that leads to the obstruction of the PA. Because an increase in nasal resistance contributes to increase this negative pressure, nasal resistance may be a factor responsible for the occurrence of sleep apnea. This concept is supported by previous reports demonstrating that sleep-related breathing abnormalities occur during nasal obstruction and that these abnormalities are no longer observed when nasal resistance returns to normal (7-9). Similarly, apart from its pneumatic splinting effect, the beneficial effects of nasal continuous positive airwaypressure (n CPAP) may also be related to a decrease in the level of the subatmospheric pressure generated during inspiration (10). Previous studies have suggested that surgical correction of nasal flow impediment may be partially effective in the treatment of obstructive sleep apnea (11-15); however, this beneficial effect is not constant (14-16). The interpretation of these previous results is difficult because (1) the number of subjects studied was relatively small; (2) nasal surgery was often associated with other surgical procedures (i.e., adenoidectomy, tonsillectomy); (3) there was no quantification of

SUMMARY Negative upper airway pressure is thought to playa key role in the pathophysiology of obstructive sleep apnea. Because nasal resistance contributes to the increase of the transpharyngeal pressure gradient, we evaluated the effects of nasal surgery on sleep-related breathing abnormalities in 20 adults with obstructive sleep apnea. Polysomnographlc studies were done before (baseline), and 2 to 3 mo after surgery (septoplasty, turbinectomy, and/or polypectomy). Nasal resistances were measured at these visits in 14 patients. Cephalometric measurements were obtained before surgery. Cephalometric abnormalities consisted in an Increase in the distance from the mandibular plane to the hyoid bone (MP-H), a decrease In the space between the base of the tongue and the posterior soft tissues (PAS), a retropositlon of the mandibule, and an increase in the length of the soft palate. Body weight did not change between the two studies. Nasal resistance decreased significantly after nasal surgery. The composition of the total sleep time spent In the rapid eye movement stage Increased from 11.5 ± 1.3% (mean ± SEM) to 14 ± 1.2% after surgery. For the group as the whole, there was no difference between baseline and postsurgical values In the frequency of respiratory disturbances (39.8 ± 6.1,36.8 ± 5.9 nIh), the total apnea time (17.8 ± 4.2, 15.4 ± 2.8), the distribution of the apnea time within the different apnea types (obstructive and nonobstructlve), and the severity of the nocturnal desaturations. Interestingly, apnea and apnea plus hypopnea Indices returned to normal values « 5 and 10, respectively) in four subjects with normal posterior soft tissues and mandibular plane to the hyoid bone distances. We conclude that nasal surgery has a limited efficacy In the treatment of adults sleep apnea patients. The Importance of cephalometry in Identifying subjects who may benefit from nasal surgery remains to be AM REV RESPIR DIS 1992; 146:1261-1265 determined.

the associated pharyngeal abnormalities; (4) changes in nasal resistance were not measured; and (5) apneas were often the only sleep-related breathing abnormalities taken into account, whereas the clinical manifestations of recurrent hypopneas are similar to those of a sleep apnea syndrome (17). The aims of this study wereto prospectivelyquantify the effects of exclusivenasal surgery on the characteristics of sleep and breathing abnormalities and nasal resistance in adult obstructive sleep apnea patients. Methods Subjects Twenty adults (I8 men, 2 women, aged 53.5 ± 2.0 yr, body mass index 34.0 ± 1.7 kg/m", mean ± SEM) with obstructive sleep apnea wereincluded in the study. They were referred to our sleep laboratory for clinical suspicion of sleep apnea syndrome. Weincluded all subjects who had a diagnosis of sleep apnea confirmed by a polysomnographic study (see Protocol) and had anatomical chronic nasal obstruction, without a clinical history of allergic rhinitis. The impediment to nasal ventilation was due to a nasal septum deviation, with or without turbinal hypertrophy and polyps as

assessed by the surgeon clinical examination (S.St.P.). No patient was treated for sleep apnea syndrome or nasal obstruction at the time of the study, and no medical treatment was initiated between the pre- and postsurgical visits.

Protocol Patients were evaluated by conventional sleep studies 1 to 3 mo before (baseline) and 2 to 3 mo after nasal surgery (postsurgical visit). Surgery consisted of the correction of the septum deviation (n = 20), submucosal resection with turbinectomy (n = 18), or polypectomy (n = 3). Sleep studies included the determination of sleep stages (electroencephalogram C~l' C 3Aa ; electrooculogram; submental electromyogram), nasal and mouth air(Received in original form June 19, 1991 and in revised form March 6, 1992) 1 From the Unite de recherche, Centre de Pneumologie, et Departements d'Otolaryngologie et de la Radiologie de l'Hopital Laval, Universite Laval, Quebec, Canada. 2 Supported by The Respiratory Health Network of Centres of Excellence of Canada. 3 Correspondence and requests for reprints should be addressed to F. Series. M.D., Centre de Pneumologie, Hopital Laval, 2725 Chemin Sainte Foy, Sainte Foy, Quebec GIV 4G5, Canada.

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flow with thermocouples (Grass Instruments, Quincy, MA), Sao, with a Criticare 504 ear oximeter (CSI, Waukesha, WI), electrocardiogram, thoracoabdominal movements by respiratory inductiveplethysmography (Respitrace; Ambulatory Monitoring, Ardsley, NY) calibrated by the isovolume method (18),and intrathoracic pressureswith an oesophageal balloon in 12patients both at baseline and postsurgical studies. All parameters wererecorded on a 16-channelpolygraph (Model 78; Grass) at a paper speed of 10mm/s. Sleep stages and respiratory events were defined by standard criteria (19,20). An apnea was defined as an absence of airflow of at least 10 s, and an hypopnea as a 500/0 decrease in the sum signal of the body plethysmography associated with an Sa02 fall> 4%. Nasal resistances were measured in the supine position at the baseline and postsurgical visits in 14 patients. The catheter could not be introduced into the nostrils in three subjects, and three others refused the procedure. All nasal resistance measurements were done at 8:00 A.M. the morning after the sleep studies. Nasal pressure was determined with a low-bias flow catheter according to a previously described technique (6). The catheter was introduced into one nostril without local anesthesia and positioned so that its tip was just above the uvula. A tightly fitting mask (Down's continuous positive pressure mask; Vital Signs,East Rutherford, NJ) coveringthe nose and mouth was connected to a pneumotachograph (Statham type 18518-0.343 L/s/mm H 20), which in turn was connected to a ValidyneMP 45 ± 5 pressure transducer. The catheter was connected to a differential pressure transducer (Validyne MP 45 ± 10) referenced to the pressure of the mask. The resistance of the breathing circuit was 0.8 em H 20/L/s. Respiratory flow and inspiratory nasal pressure wererecorded at a paper speed of 50 mm/s. Breath-by-breath inspiratory resistances were measured at isoflow (300 mIls) during l-min recordings with the subjects breathing exclusively by the nose. For each patient, lateral cephalometric roentgenograms were obtained at baseline with the technique described by Rileyand colleagues (21)with a film-tube distance of exactly 60 in. The subject's head was held in the neutral position with the eyes looking directly forward. Standard landmarks were measured by the same investigator (G. C.) (figure 1). Normal values from our laboratory for the age range of our patients are: SNB = 78 ± 1°, posterior soft tissues (PAS) = 13 ± 1 mm, distance from the mandibular plane to the hyoid bone (MP- H) = 22 ± 1 mm, PNS-P = 32 ± 1 mm (22).

Statistical Analysis The pre- and postsurgical results were compared by a Student's paired t test. Differences were considered significant when the p value was < 0.05.The relationship between the postsurgery apnea plus hypopnea index and the nasal resistance value was analyzed by simple linear regression analysis.

SERIES, ST. PIERRE, AND CARRIER

Fig. 1. Landmarks obtained from cephalometric roentgenograms. S = sella; N = nasion; A = subspinale; B = supramentale; PNS = posterior nasal spine; P = tip of the soft palate; MP = mandibular plane; H = hyoid bone.

Results

Body weight did not change with surgery (101.6 ± 5.2 kg before and 102.7 ± 5.5 kg after nasal surgery, mean ± SEM). Nasal resistance decreased significantly after nasal surgery: it was 3.0 ± 0.1 cm H 2 0 / L / s at baseline and 1.7 ± 0.2 after surgery (p = 10-4 ) . Diurnal symptoms of hypersomnolence were subjectively improved in 14patients after surgery.The sleep period time and the total sleep time (TST) increased significantly after surgery, but the sleep efficiency remained unchanged (table 1).The composition of the TST within the different sleep stages significantly changed between the two visits with an increase in the rapid eye movement (REM) sleep time (table 1).

Sleep fragmentation, estimated by the number of sleep stages changes per hour of sleep (23), did not change between the two studies. There was no significant difference in the pre- and postsurgical values for total apnea time (TAT) (percentage of the TST spent in apnea) and for the frequency ofbreathing abnormalities (apnea and apnea plus hypopnea indices) (table 2). These indices decreased by 500/0 in one patient and returned to normal « 5 and 10 respectively) in four others (table 2). There was no significant relationship between the changes in the apnea plus hypopnea index and the baseline resistance values (r 2 = 0.1, p = 0.3) (figure 2). For the whole group, the preand postsurgical mean apnea duration

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NASAL SURGERY AND SLEEP APNEA Apnea + hypopnea index (% baseline values)

TABLE 1 SLEEP CHARACTERISTICS OBTAINED BEFORE (BASELINE) AND AFTER NASAL SURGERY Postsurgery

Baseline 6.7 5.8 83.9 19.2 75.0 13.4 , 1.5

Sleep period time, h Total sleep time, h Sleep efficiency, % Sleep stages schifts, nIh TST Stage I-II, % TST Stage III-IV, % TST Stage REM, % TST • p

< 0.05, mean ±

± ± ± ± ± ± ±

7.2 6.6 88.1 20.1 72.9 13.0 14.0

0.2 0.1 2.3 1.9 2.8 2.2 1.3

o

140

± ± ± ± ± ± ±

0.2* 0.2* 0.1 2.7 3.0 2.3 1.2*

120

100~0 80

00 0

0

0

60

o

40

1,5

2,0

2,5

3,0

3,5

was identical for non-REM (20.1 ± 1.3 s and 21.4 ± 1.3s, respectively) and REM sleep (28.9 ± 3.6 sand 29.7 ± 3.7 s). Obstructive apneic events represented the most important part of the TAT at both visits. The composition of TAT within the different apnea types remained unchanged after surgery (figure 3). The severity of apnea and hypopnea-related desaturations was estimated by a cumulative Sao, curve that represents the percentage of the TST spent at the different Sao, values. For the whole group, there was no difference between the curves obtained at baseline and after nasal surgery (figure 4). Cephalometric abnormalities observed consisted in a retroposition of the mandibule (decrease in the angle measurement from sella to nasion to supramentale: SNB) in 5 subjects, a decrease in the PAS in 15, an increase in the length of

the soft palate (PNS-P) in 17, and an increase in the distance from the mandibular plane to the hyoid bone (MP-H) in 13 (table 2). Interestingly, both the PAS and the MP-H distances were normal in the four patients in whom respiratory disturbance indices returned to normal after surgery (figure 2 and table 2).

4,5

(em Hz O/Us)

Discussion

Our results demonstrate that nasal surgery has a limited efficiency in the treatment of adult sleep apnea patients; however, it benefited all obstructive sleep apnea patients who had normal PAS and MP-H distances. The characteristics of sleep-related breathing abnormalities may vary from one sleep recording to another, especially in patients with infrequent sleep apnea (24), and it could be argued that spontaneous variations accounted for the

apparent effectiveness of nasal surgery in the less severely affected patients. We believe that spontaneous variations were unlikely responsible for the observed improvement for the following reasons: It is unlikely that spontaneous improvement would have occurred only in subjects with normal PAS and MP-H. A second baseline sleep study was done before surgery in three patients who had the longest delay (3 months) between the first sleep study and the surgical procedure. Their respective apnea plus hypopnea indices were 16.8, 18.2, and 23.4 nih at the first baseline study, and 15.4,20.7, and 27.0 at the second baseline recording. There was a good reproducibility in the apnea plus hypopnea index in the patients who were not improved after surgery, even in those with a low index (fig-

TABLE 2 INDIVIDUAL VALUES OF THE PRE- AND POSTSURGICAL VALUES OF THE RESPIRATORY DISTURBANCE INDICES AND OF THE CEPHALOMETRIC MEASUREMENTS Postsurgery

Baseline

PAS (mm)

Mean ± SEM

4,0

Fig. 2. Relationship between baseline nasal resistance values and the postsurgery apnea + hypopnea index (expressed in percentage of baseline values). There was no correlation between these two variables.

SEM.

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Baseline nasal resistance

o

20

5

6 10 7 5 8 6 8 8 11 5 11 4 5 7 3 11 11 12 9

MPH (mm)

PNS-P (mm)

SNB (dg)

Total Apnea Time (% TST)

Apnea + Hypopnea Index (nih)

Total Apnea Time (% TST)

Apnea + Hypopnea Index (nih)

35 26 26 31 30 34 33 42 23 25 24 22 29 24 36 40 15 15 18 18

47 51

68 80 82 78 83 75 75 81 79 79 70 79 80 76 81 73 77 79 78 73

15.2 30.5 41.6 18.7 3.1 3.7 4.2 63.1 12.9 9.3 36.4 4.7 13.7 2.2 7.5 60.0 4.2 8.4 7.1 10.0

42.8 54.2 105.8 45.5 67.5 35.0 34 94.1 19.7 18.2 53.4 15.1 52.6 13.3 16.8 61.0 13.9 15.9 13.6 23.4

15.0 13.2 38.4 45.2 11.3 15.8 19.3 3.8 12.5 11.5 28.9 2.9 16.3 9.8 26.5 29.9 1.4 1.4 2.2 3.0

39.0 24 97.2 58.2 38.5 50.7 39 59.0 19.0 17.9 57.2 12.5 86.0 23.2 47.8 45.9 6.7 4.1 5.6 5.2

17.8 ± 4.2

39.8 ± 6.1

15.4 ± 2.8

36.8 ± 5.9

44 47 42 47 34 50 45 41 32 44

44 45 41 33 45 48 41 35

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SERIES. ST. PIERRE, AND CARRIER

Fig. 3. Mean values of the percentage of the total apnea time spent in the different apnea types at baseline and after surgery.

Baseline

Post surgery

% Total sleep time

25

Baseline ---.-- Post-surgery

--0-

20 Fig. 4. Mean cumulative Sao 2 curves obtained at each visit. For the whole group, there was no improvement in the severity of nocturnal desaturations after nasal surgery.

15 10 5

o

sso , (%) s 60 s 65 s 70 s 75 s 80 s 85

~

ure 2). For these 16 patients, we found a positive correlation between the baseline and postsurgical values of this index (r = 0.73, P < 0.0001). This suggests that the respiratory disturbance index is more reproducible than the apnea index that was used by Wittig and colleagues (24), and that our results are not the consequence of spontaneous variations in sleep-related breathing disorders, but reflect the effects of nasal surgery. Diurnal hypersomnolence and sleep quality improved after nasal surgery, even in patients with no changes in their sleeprelated breathing abnormalities. Similar observations have previously been made by several researchers (11-16). Abnormal sleep architecture and sleep fragmentation are responsible for daytime sleepiness in these patients (25). Arousals and awakenings precede the ventilatory resumption that follows apneas and hypopneas (17). These respiratory-related arousals are induced by chemical stimuli (hypoxia, hypercapnia), but can also be the consequences of mechanical factors such as negative airway pressures (26). This is illustrated by the 'occurrence of arousals after an increase in upper airway resistance in nonapneic snorers (27). It is possible, therefore, that the improvement in diurnal symptoms was due to a

CJO

decrease in the levelof respiratory efforts and negative airway pressure during hypopneic events as a consequence of the reduction of the respiratory load by the nasal surgery. The decrease in the movement arousal index observed after nasal surgery in sleep apnea patients supports this hypothesis (16). Nasal surgery was effective in improving nasal airflow impediment. There was a subjective clinical improvement in all subjects and a reduction in diurnal nasal resistance in the 14 in whom it could be measured. However, in our patients, the decrease in nasal resistance did not correlate with the improvement of sleeprelated breathing abnormalities. Nasal resistance does not increase from the waking to the sleeping state in healthy subjects (28). Therefore, until this has been examined in sleep apnea patients, we believe that it is unlikely that this lack of correlation can be explained by a nocturnal increase in nasal resistance in some patients. Because there is a great variability in the effects of nasal surgery in sleep apnea patients (11-16), and because the importance of the transpharyngeal pressure gradient has been clearly demonstrated (1,5), we believe that the inconstant efficiency of nasal surgery observed in adults

is related to the presence of other oropharyngeal abnormalities. Experimental studies, realized in young monkeys, demonstrate that the induction of oral respiration by obstruction of nasal passage modifies the electromyographic activity of upper airway (geniohyoid, genioglossus), mandibular, and facial muscles (29). The modification of the characteristics of the mandibular growth observed in oral breathing monkeys (posterior rotation of the mandible with lower position of the chin) (30) can be accounted for by the changes in these muscular activities (31). Thus, adult sleep apnea patients could have developed craniomandibular abnormalities as a consequence of chronic nasal airflow limitation. This could also account for the changes in cephalometric measurements that occur with aging (22). It can be hypothesized that these acquired abnormalities could by themselves interfere with the stability of upper airways and, in some subjects, lead to pharyngeal airway obstruction in adults. This is supported by the good polysomnographic results of surgical procedures correcting upper airway patency (tonsillectomy, adenoidectomy, nasal repair) in OSA children (11, 32). Our results suggest that when these craniomandibular abnormalities are present, the correction of the nasal flow limitation cannot improve sleep-related breathing disorders. Such a hypothesis would also explain why during transient nasal obstruction, the rise in obstructive sleep apneas is reversible when nasal resistance returns to normal (8, 9). In this case, the early treatment of nasal abnormalities that lead to an increase in nasal resistance in infancy could prevent the eventual development of obstructive sleep apnea in adulthood. This hypothesis is supported by our results, but because parameters other than cephalometric measurements differed between patients who were or were not cured after nasal surgery, further studies are needed to evaluate prospectively the importance of cephalometry in predicting the postsurgical outcome. . Despite its poor effectiveness in the treatment of obstructive.sleep apnea, nasal surgery may have another benefit by improving tolerance to nCPAP. Although we did not specially address this question, we observed that seven patients who did not tolerate nCPAP before surgery due to discomfort could be treated by home nCPAP after surgery. Therefore, apart from its potentially beneficial effects on sleep-related breathing disor-

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NASAL SURGERY AND SLEEP APNEA

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Effects of surgical correction of nasal obstruction in the treatment of obstructive sleep apnea.

Negative upper airway pressure is thought to play a key role in the pathophysiology of obstructive sleep apnea. Because nasal resistance contributes t...
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