Anterior Nasal Resistance
Anterior Nasal Resistance in Obese Children
With Obstructive Sleep Apnea Syndrome
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Anterior Nasal Resistance in Obese Children
With Obstructive Sleep Apnea Syndrome
ARTICLE in THE LARYNGOSCOPE · NOVEMBER 2014
Impact Factor: 2.03 · DOI: 10.1002/lary.24653 · Source: PubMed
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5 AUTHORS, INCLUDING:
Sanghun Sin
The Children’s Hospital at Montefiore (CHAM)
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David M Wootton
The Cooper Union for the Advancement of S…
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Joseph M McDonough
The Children's Hospital of Philadelphia
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Kiran Nandalike
Montefiore Medical Center
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Available from: Sanghun Sin
Retrieved on: 20 August 2015
The Laryngoscope
VC 2014 The American Laryngological,
Rhinological and Otological Society, Inc.
Anterior Nasal Resistance in Obese Children With Obstructive
Sleep Apnea Syndrome
Sanghun Sin, MS; David M. Wootton, PhD; Joseph M. McDonough, MS; Kiran Nandalike, MD;
Raanan Arens, MD
Objectives/Hypothesis: To evaluate nasal resistance in obese children with and without obstructive sleep apnea syndrome
(OSAS), study the correlation between nasal resistance and severity of OSAS using the apnea-hypopnea index (AHI),
and examine the association of gender and body mass index (BMI) with this measurement.
Study Design: Retrospective analysis.
Methods: Active anterior rhinomanometry was used to determine anterior nasal resistance (aNR) during wakefulness in
the supine position during tidal breathing. Thirty obese children with OSAS (aged 13.862.6 years, BMI z score 2.660.4)
and 32 matched obese controls (aged 13.662.3 years, BMI z score 2.460.4), were studied. Unpaired t tests and Spearman
correlation were performed.
Results: The OSAS group had significantly higher aNR than the non-OSAS group during inspiration (P5.012) and expiration
(P5.003). A significant correlation between inspiratory aNR and AHI was found for the OSAS group (r50.39, P5.04).
The aNR did not correlate with BMI z score or with either gender.
Conclusions: We noted a higher aNR in obese children with OSAS as compared to obese controls, and the aNR on inspiration
correlated significantly with AHI. These findings suggest that a causal or augmentative effect of high inspiratory aNR
may exist for obese children who exhibit OSAS.
Key Words: Active anterior rhinomanometry, obesity, obstructive sleep apnea syndrome.
Level of Evidence: 3b.
Laryngoscope, 124:2640–2644, 2014
INTRODUCTION
Obstructive sleep apnea syndrome (OSAS) is a
respiratory disorder characterized by repeated episodes
of flow limitation or complete cessation of flow due to
partial narrowing or complete occlusion of the pharyngeal
airway during sleep.1 These respiratory events are
followed by alterations in gas exchange arousals leading
to disruption of normal sleep pattern.
OSAS affects 2% to 4% of children in the general
population.2 However, obese children have a much higher
prevalence of the disorder that may approach 50%.3–5
Thus, obesity is an important risk factor for the development
of OSAS in children. Several studies suggest that
particular anatomical factors around the pharyngeal airway
in obese children, including lymphoid and parapharyngeal
fat pad tissues, induce sleep apnea by narrowing
the upper airway.6–8 For a given inspiratory flow rate in
the airway, increased airway resistance anterior to a
given point in the airway will increase the magnitude of
negative pressure loading at that point, favoring its narrowing
and/or collapse. Additionally, this will be facilitated
if there is no increased reflex activation of airway
to maintain the airway patency. Distal to the choanae,
the pharynx is particularly liable to collapse, especially in
the region of the soft palate, tonsils, and adenoids. Likewise,
the oropharynx is susceptible to collapse due to the
tongue, tonsils, and the distensible nature of the surrounding
structures comprising the airway.
Although adenotonsillectomy is considered the firstline
treatment in OSAS in obese children with adenotonsillar
hypertrophy, up to 50% may still have unresolved
OSAS after their surgery.9–11 This suggests that other
factors not ameliorated by adenotonsillectomy contribute
to OSAS in obese children. Factors to be considered
include low upper airway muscle tone, increased parapharyngeal
fat and upper airway tissue fat content,
altered chest-wall mechanics, which can all increase
upper airway collapsibility during sleep. In addition,
anatomical abnormalities of the nasal passages, such as
nasal septal deviation, nasal turbinate hypertrophy, and
allergic rhinitis, could increase upper airway nasal
resistance and perpetuate OSAS in these subjects.
The relationship between nasal resistance and OSAS is
not well defined.12 Several studies using a standardized
method known as active anterior rhinomanometry (AAR)
From the Division of Respiratory and Sleep Medicine (S.S., K.N.,
R.A.), the Children’s Hospital at Montefiore and Albert Einstein College
of Medicine, Bronx, New York; the Department of Mechanical Engineering
(D.M.W.), Cooper Union for the Advancement of Science and Art, New
York, New York; and the Division of Pulmonary Medicine (J.M.M.), The
Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, U.S.A.
Editor’s Note: This Manuscript was accepted for publication
February 19, 2014.
This work was supported by National Institutes of Health grants 5
R01 HD053693 and 5 R01 HL105212.
The authors have no other funding, financial relationships, or conflicts
of interest to disclose.
Send correspondence to Raanan Arens, MD, Division of Respiratory
and Sleep Medicine, Children’s Hospital at Montefiore, 3415 Bainbridge
Avenue, Bronx, NY 10467. E-mail: rarens@montefiore.org
DOI: 10.1002/lary.24653
Laryngoscope 124: November 2014 Sin et al.: Nasal Resistance in Obese Children With OSAS
2640
have shown that adults with OSAS have higher anterior
nasal resistance (aNR) compared to controls.13,14 However,
data in children, and particularly in obese children, are lacking.
Thus, the main aim of the study was to use a standardized
method of AAR to evaluate the relationship between
aNR and the occurrence of OSAS in obese children compared
to controls. We hypothesize that obese children with OSAS
have an increase in aNR that preloads the nasopharynx and
oropharynx, and that this resistance will correlate with the
severity of the disorder. Such an abnormality may also help
explain the low response to adenotonsillectomy in these subjects.
A secondary aimwas to examine the role of gender and
body mass index (BMI) on aNR in these groups.
MATERIALS AND METHODS
Subjects and Procedures
All children were recruited at the Children’s Hospital at
Montefiore (CHAM), Bronx, New York. The study was approved
by the Committee of Clinical Investigations at Albert Einstein
College of Medicine, Bronx, New York. Sixty-four obese children
with intact tonsils and adenoids in the age range of 8 to 17
years (BMI >95th percentile for age and gender) were initially
enrolled into the study. After an overnight polysomnography
(PSG) study, each subject was classified as an OSAS or a control.
Subjects were excluded if they had abnormal development
or a known metabolic or endocrine disorder. Subjects were also
excluded if they had complete unilateral or bilateral nasal
obstruction, which precludes measuring nasal resistance with
anterior rhinomanometry. Thus, two of the OSAS subjects were
excluded from final analysis due to unilateral nasal obstruction.
Overnight PSG
To evaluate for the existence and severity of OSAS, overnight
PSG (Xltek, Oakville, ON, Canada) was conducted at the
Sleep Disorders Center at the CHAM. OSAS was defined if the
apnea index (AI) was 1/hour and/or the apnea-hypopnea index
(AHI) was 5/hour. Sleep scoring was performed according to
standard criteria as defined by the American Academy of Sleep
Medicine.15
Active aNR
To measure aNR we used the AAR technique.16 Accordingly,
transnasal pressure and airflow were measured separately in
each nostril during quiet tidal breathing in the supine position
during wakefulness. Airflow and pressure were collected by a
research grade clinical rhinomanometer (NR6; GM Instruments,
Kilwinning, UK) with a face mask. Patients were allowed to blow
their nose prior to test if needed. We used disposable foam plugs
fitted with a pressure-sensing tube inserted into one nostril to
carry out the pressure measurement while airflow through the
other nostril was measured by a pneumotachometer. Measurement
of the opposite nostril was performed in the same fashion.
Thus, pressure measured in the occluded nostril is equivalent to
the driving pressure at the choanal junction, because the air column
in the occluded nostril is stagnated. Subjects maintained a
closed mouth during the measurement. Measurements included
four breathing phases: ascending and descending phases during
inspiration and expiration.
Unilateral nasal resistance. Unilateral nasal resistance
(uNR) of each nostril was defined at the 150 Pa standard transnasal
pressure value (Fig. 1). Twelve respiratory cycles were
recorded and averaged for each subject during inspiration and
expiration. Measurements were discarded if flow and pressure
waveforms were atypical of normal breathing.
aNR. aNR was calculated using the two parallel resistances
addition: (uNRR 3 uNRL)/(uNRR1uNRL), where uNRR and
uNRL are right and left unilateral measurements, respectively.
Statistical Methods
Demographics, polysomnographic, and rhinomanometry
data are presented as mean6standard deviation values for
OSAS and control groups. End points between groups were
compared using two-tailed unpaired t tests, and Spearman correlation
analysis was performed to evaluate the association
between aNR and A