by posterior rhinomanometry17 in the sitting position
correlated positively with increasing AHI in nonobese
middle-aged subjects.14,18 More recently, Tagaya et al.13
expanded on the significance of aNR in the obese adult
population with OSAS, using a more recent and standard
technique of AAR16 as in our study. These authors
have shown that increased aNR caused by obstructed
nasal passages could play an important role in the causation
of OSAS. In a pediatric study of children between
4 and 7 years of age, Rizzi et al.19 determined that aNR
correlated positively with the severity of OSAS. They
performed their measurements in an erect position in
contrast to the supine position used in this study.
Conversely, other investigators have presented
results showing that aNR was not a significant risk factor
in the severity of OSAS in adults.20 Their rhinomanometry
was performed in the seated posture during
wakefulness. De Vito et al.21 also analyzed AAR data
obtained from both the seated and supine position. However,
they could not find any statistical significance
between aNR and the severity of OSAS in the middleaged
population. In a recent study of awake adults with
OSAS, Masdeu and colleagues22 utilized AAR and acoustic
rhinometry, which provides a cross-sectional area profile
of the nasal passages. They compared these in both
a supine and seated posture, but they did not find a correlation
between either of these two measurements and
the severity of OSAS.
Disagreement in these previous studies could result
from the differences in measuring techniques, postural
differences, or the surveyed populations. Rhinomanometry
measurements themselves have also been historically
questioned due to apparent inconsistencies. Thus, the
International Rhinology Society established the universal
standard called four-phase rhinomanometry to determine
aNR.16 Four-phase AAR has advantages, as the
need for patient cooperation is minimized and results
are quickly produced. It should be noted that anterior
rhinomanometry measures resistance from the nasal
opening back to the choanal junction. Posterior rhinomanometry
measures that resistance combined with
resistance due to the airway segment from the choanal
junction to the pressure sensor location, usually placed
in the region of the oropharynx. Thus, posterior rhinomanometry
will by definition also include any resistance
due to the nasopharynx. In subjects with OSAS and/or
obesity, the resistance of the nasopharynx is an important
factor but can confound the question of how anterior
nasal resistive loading alone relates to OSAS. This
study utilized the standardized anterior method. Additionally,
all data were acquired in the supine position to
mimic the sleeping position as much as possible, because
postural change may induce alterations in nasal
resistance.
On describing the role of obesity in OSAS, obesity is
known to be a primary risk factor23 and has also been
linked to increased aNR.24 Our data show that the obese
OSAS group had a higher aNR than obese controls but
were not significantly more obese. On that basis, it
appears that higher aNR is not likely to be due to
anatomical effects of fat deposition that would reduce
airway caliber of the nasal vestibule, valve, or turbinates.
Rather, this suggests that having a high aNR for
any OSAS-independent reason may be a risk factor for
precipitating OSAS in obese subjects already susceptible,
or making OSAS worse if they already have it. However,
we cannot exclude the possibility that the higher aNR
found in the OSAS group could be caused or exacerbated
by the effects of having preexisting OSAS. For example,
it is possible that chronic snoring, chronic colds, sinus
infections, and metabolic changes may serve to cause
inflammation of the turbinates and contribute to OSAS
in a positive feedback effect.
In this study we show a new finding in which aNR
is strongly associated with the severity of OSAS in obese
children. In contrast, Virkkula et al.14 reported weak
correlation between aNR and sleep parameters in
middle-aged obese subjects. However, they attributed
the relationship to failed AAR measurement by severe
obstruction in either or both nostrils. Because it is generally
considered that 50% to 75% of total respiratory
airway resistance is due to the normal nasal passage,25
anterior nasal resistance should be considered as an
important risk factor in sleep medicine. As an example,
patients whose nasal passage is obstructed seriously frequently
alter to oral breathing to compensate for high
resistance during sleep, which may predispose them to
apnea as oral breathing may reduce pharyngeal airway
size by changing the tongue’s and jaw’s location.26
The higher aNR observed in obese children with
OSAS could result from various anatomical abnormalities,
the deformation of nostrils by septal deviation,
flow restricted by the inflamed nasal mucosa, hypertrophied
nasal turbinates, nasal polyps, and paranasal
sinus disease.27,28 We can postulate that flow limitation
through these mechanisms could create large negative
pharyngeal pressures and induce OSAS. Consequently, a
well-defined assessment of the functional capability of
the nose in obese children with OSAS can give additional
information regarding the pathophysiology of
their OSAS. Identification of structural problems in the
nasal pathway that would increase aNR in patients with
OSAS may provide an indicator of their OSAS severity.
Treatment of this obstruction may also serve to improve
compliance with nasal continuous positive airway pressure
therapy.29
Finally, we examined the effects of gender and BMI
z score on aNR and could not find a significant correlation
for either. However, larger studies are needed to
confirm this finding due to the relative low sample size
and the fact that all subjects were obese and were
within a narrow BMI z range.
โดย rhinomanometry17 หลังตำแหน่งนั่งcorrelated บวกกับเพิ่ม AHI nonobeseเฉพาะ subjects.14,18 วัยกลางคนเมื่อเร็ว ๆ นี้ Tagaya และ al.13ขยายในความสำคัญของเอ็นในผู้ใหญ่อ้วนประชากร มี OSAS ใช้ตัวล่าสุดและมาตรฐานเทคนิคของ AAR16 ในการศึกษาของเรา ผู้เขียนเหล่านี้มีแสดงเอ็นที่เพิ่มขึ้นเกิดจากการกีดขวางโพรงจมูกทางเดินอาจมีบทบาทสำคัญในการ causationของ OSAS ในการศึกษาเด็กของเด็กอายุ4 และ 7 ปี Rizzi et al.19 ขึ้นเอ็นที่correlated บวกกับความรุนแรงของ OSAS พวกเขาทำการวัดในตำแหน่งที่ตรงความแตกต่างกับตำแหน่ง supine ที่ใช้ในการศึกษานี้ในทางกลับกัน มีการนำเสนออื่น ๆ นักผลลัพธ์ที่แสดงที่เอ็นไม่เป็นปัจจัยเสี่ยงในความรุนแรงของ OSAS ใน adults.20 rhinomanometry ของพวกเขาทำในท่านั่งระหว่างwakefulness เดอวิโต้ et al.21 ยังวิเคราะห์ข้อมูล AARได้รับจากทั้ง supine และนั่งตำแหน่ง อย่างไรก็ตามพวกเขาไม่พบนัยสำคัญทางสถิติใด ๆระหว่างเอ็นและความรุนแรงของ OSAS ใน middleagedประชากร ในการศึกษาล่าสุดของผู้ใหญ่ที่ทำงานด้วยOSAS, Masdeu และ colleagues22 ใช้ AAR และอคูสติกrhinometry ซึ่งมีโพรไฟล์ตั้งเหลวของทางเดินโพรงจมูก พวกเขาเปรียบเทียบเหล่านี้ทั้งในท่านั่ง และ supine แต่พวกเขาไม่พบความสัมพันธ์ระหว่างวัดสองเหล่านี้อย่างใดอย่างหนึ่ง และthe severity of OSAS.Disagreement in these previous studies could resultfrom the differences in measuring techniques, posturaldifferences, or the surveyed populations. Rhinomanometrymeasurements themselves have also been historicallyquestioned due to apparent inconsistencies. Thus, theInternational Rhinology Society established the universalstandard called four-phase rhinomanometry to determineaNR.16 Four-phase AAR has advantages, as theneed for patient cooperation is minimized and resultsare quickly produced. It should be noted that anteriorrhinomanometry measures resistance from the nasalopening back to the choanal junction. Posterior rhinomanometrymeasures that resistance combined withresistance due to the airway segment from the choanaljunction to the pressure sensor location, usually placedin the region of the oropharynx. Thus, posterior rhinomanometrywill by definition also include any resistancedue to the nasopharynx. In subjects with OSAS and/orobesity, the resistance of the nasopharynx is an importantfactor but can confound the question of how anteriornasal resistive loading alone relates to OSAS. Thisstudy utilized the standardized anterior method. Additionally,all data were acquired in the supine position tomimic the sleeping position as much as possible, becausepostural change may induce alterations in nasalresistance.On describing the role of obesity in OSAS, obesity isknown to be a primary risk factor23 and has also beenlinked to increased aNR.24 Our data show that the obeseOSAS group had a higher aNR than obese controls butwere not significantly more obese. On that basis, itappears that higher aNR is not likely to be due toanatomical effects of fat deposition that would reduceairway caliber of the nasal vestibule, valve, or turbinates.Rather, this suggests that having a high aNR forany OSAS-independent reason may be a risk factor forprecipitating OSAS in obese subjects already susceptible,or making OSAS worse if they already have it. However,we cannot exclude the possibility that the higher aNRfound in the OSAS group could be caused or exacerbatedby the effects of having preexisting OSAS. For example,it is possible that chronic snoring, chronic colds, sinusinfections, and metabolic changes may serve to causeinflammation of the turbinates and contribute to OSASin a positive feedback effect.In this study we show a new finding in which aNRis strongly associated with the severity of OSAS in obesechildren. In contrast, Virkkula et al.14 reported weakcorrelation between aNR and sleep parameters inmiddle-aged obese subjects. However, they attributedthe relationship to failed AAR measurement by severeobstruction in either or both nostrils. Because it is generallyconsidered that 50% to 75% of total respiratoryairway resistance is due to the normal nasal passage,25anterior nasal resistance should be considered as animportant risk factor in sleep medicine. As an example,patients whose nasal passage is obstructed seriously frequentlyalter to oral breathing to compensate for highresistance during sleep, which may predispose them toapnea as oral breathing may reduce pharyngeal airwaysize by changing the tongue’s and jaw’s location.26The higher aNR observed in obese children withOSAS could result from various anatomical abnormalities,the deformation of nostrils by septal deviation,flow restricted by the inflamed nasal mucosa, hypertrophiednasal turbinates, nasal polyps, and paranasalsinus disease.27,28 We can postulate that flow limitationthrough these mechanisms could create large negativepharyngeal pressures and induce OSAS. Consequently, awell-defined assessment of the functional capability ofthe nose in obese children with OSAS can give additionalinformation regarding the pathophysiology oftheir OSAS. Identification of structural problems in thenasal pathway that would increase aNR in patients withOSAS may provide an indicator of their OSAS severity.Treatment of this obstruction may also serve to improvecompliance with nasal continuous positive airway pressuretherapy.29Finally, we examined the effects of gender and BMIz score on aNR and could not find a significant correlationfor either. However, larger studies are needed toconfirm this finding due to the relative low sample sizeand the fact that all subjects were obese and werewithin a narrow BMI z range.
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