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Does adenotonsillar size and BMI predict obstructive sleep apnea in children?

This issue's column is based on the peer-reviewed article titled "Obstructive sleep apnea in children: relative contributions of body mass index and adenotonsillar hypertrophy." We'll review this article by sections to teach the scientific method for research: background or introduction, question, hypothesis, methods, results, discussion/reflections/future research, conclusions, acknowledgements, conflicts of interest and bibliography.

The introduction of the research project explains interest in the topic and why the topic is significant. The authors note that obstructive sleep apnea (OSA) affects approximately 3 percent of school-aged children. Respiratory disturbances during sleep have been found to be increased in obese children although the expected correlation of OSA with enlarged adenotonsillar tissues in the upper airway has not been established.

The contributions of adenotonsillar size, Mallampati classification score and body mass index (BMI) on OSA in children have not been examined. The objective of this study was to examine the role of these factors.

Question and hypothesis

The question being asked by the researchers was two-fold: Would obese (high BMI) children with OSA compared to non-obese (normal BMI) children with OSA have less adenotonsillar hypertrophy and a higher Mallampati classification score? It is important to note that the question asked in a research project may have the possible answers: "yes" and "no" as in this study, or may be a numerical result.

The preconceived answer by the researchers to the question is called the hypothesis. The authors hypothesized a yes answer to both questions: Obese children with OSA would have less adenotonsillar hypertrophy and a higher Mallampati classification score.


The methods for the research project describe the study design, setting and steps to answer the question. This retrospective study of charts was approved by the University of Louisville Human Research Committee. Researchers reviewed charts of children aged 1-16 years who had been evaluated for snoring with an overnight polysomnography (NPSG) from October 2003 to September 2007.

For each chart of an obese child with OSA, a chart of a non-obese child with OSA was matched by age (within six months), gender, ethnicity and the obstructive apnea-hypopnea index (OAHI, within one episode per hour of total sleep time, or TST). Data from the charts included estimates of adenoid size (0 to 4), tonsillar size (0 to 4), and Mallampati score (1 to 4). Adenoid size was determined from a review of lateral neck radiographs. Tonsillar size was assigned a score of 0 for no tonsils to 4 for "kissing" tonsils. The sum of the adenoid and tonsil scores was defined as adenotonsillar size (0 to 8). The Mallampati classification score was 1 when the protruded tongue did not prevent visualization of the soft palate, fauces, uvula and tonsillar pillars. A score of 4 meant only the hard palate can be visualized.

The NPSG included the following measurements:

* Chest and abdominal wall movement by respiratory impedance or inductance plethysmography

* Heart rate by ECG

* Airflow with sidestream end-tidal carbon dioxide levels

* Pulse oximetric saturation (SpO2) and waveform bilateral electrooculogram

* Eight-channel EEG

* Chin and anterior tibial EMG

* Body position

All measurements were digitized and tracheal sound was monitored with a microphone sensor.

Apnea was defined as the absence of airflow with continued chest wall and abdominal movement for a duration of at least two breaths. Hypopneas were defined as a decrease in oronasal air flow of [greater than or equal to] 50 percent with a corresponding decrease in SpO2 of [greater than or equal to] 4 percent and/or arousal. The OAHI was defined as the number of apneas and hypopneas per hour of TST. The diagnostic criteria for OSA were an OAHI > 2/h TST, with a nadir oxygen saturation value < 92 percent.

BMI was calculated as weight in kilograms divided by height in meters squared. Since BMI for children must be interpreted differently from adults because of weight and heightchanges with growth, obesity was based on standardized percentile curves from the Centers for Disease Control and Prevention reference values for children. Obesity was defined as a BMI above the 95th percentile, meaning the BMI was greater than 95 percent of other children of the same age and gender.

All analyses were conducted using a statistical software package. All p values reported were two-tailed with statistical significance set at p < 0.05.


The results section displays the data compiled to answer the Question. A total of 412 charts were selected: 206 obese children with OSA and 206 nonobese matching children. They were 40.3 percent female, 56 percent white and 37 percent African American with a mean age of 6.5 years.

Adenotonsillar scores directly correlated with the severity of OSA in non-obese children. However, adenotonsillar scores were lower among obese children while Mallampati classification scores were higher among these children. There was no association between BMI percentile score and OAHI.

Discussion/Reflections/Future Research

The authors noted that adenotonsillar size correlated with the severity of OSA in non-obese children but not among obese children. More importantly, they indicated that the amount of adenotonsillar hypertrophy among obese children with OSA is less than among non-obese children.

Conversely, Mallampati classification scores, as a simple estimate of upper airway crowding, were increased among obese children compared to non-obese children. Together, these findings suggest that obesity contributes to OSA in children through upper airway crowding and not adenotonsillar hypertrophy. The authors also noted several methodological issues such as that the design was retrospective, and adenoid, tonsillar and Mallampati scores were judged by multiple clinicians rather than by a designated investigator. The authors said that prospective studies could evaluate whether the success of adenotonsillectomy for treatment of OSA in obese children can be predicted from models incorporating both estimates of adenotonsillar size and Mallampati scores.


The authors demonstrated that the magnitude of adenotonsillar hypertrophy required for any given OAHI is more likely to be smaller in obese children compared to non-obese children. The increased Mallampati scores in obese children suggest that soft-tissue changes and fat deposition in the upper airway may play a significant role in OSA. The answers to the questions were both yes: obese children with OSA have less adenotonsillar hypertrophy and a higher Mallampati classification score. The proposed hypotheses were both correct.

Acknowledgements, Conflicts of interest and Bibliography

The authors noted the project was supported in part by grants from the National Institutes of Health, the Commonwealth of Kentucky and the Children's Foundation Endowment for Sleep Research. The authors have not disclosed any potential conflicts of interest. There were 51 sources cited in this research study.

by Herbert Patrick, MD


Herbert Patrick, M.D., M.S.E.E., is an Intensivist and member of the Active Staff at Hahnemann University Hospital, Philadelphia, PA. Dr. Patrick can be contacted at
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Article Details
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Title Annotation:RESPIRATORY RESEARCH; body mass index
Author:Patrick, Herbert
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Geographic Code:1USA
Date:Sep 1, 2009
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