Posted by: Indonesian Children | September 13, 2009

Obstructive sleep apnea

The term breathing-related sleep disorder refers to a spectrum of breathing anomalies ranging from chronic or habitual snoring to upper airway resistance syndrome (UARS) to frank obstructive sleep apnea (OSA) or, in some cases, obesity hypoventilation syndrome (OHS). 

Data from the Wisconsin sleep cohort study of patients without obvious barriers to health care access estimate that 93% of women and 82% of men with moderate-to-severe sleep apnea were undiagnosed.  Significant cardiovascular morbidity (including systemic hypertension and congestive heart failure) as well as increased mortality rates have been associated with both OSA and OHS. While large-scale studies of the prevalence of sleep-disordered breathing in children are lacking, Guilleminault et al report estimates of 5-6% and raise concerns about the impact of the obesity epidemic on sleep in children.

Obstructive sleep apnea (OSA) is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. OSA is a sleep disorder characterized by recurrent episodes of upper airway (UA) collapse during sleep. By definition, apnea episodes last 10 seconds or longer and commonly last 30 seconds or longer. Apnea may occur hundreds of times nightly, 1-2 times per minute in severe OSA patients, and is often accompanied by wide swings in heart rate, precipitous decrease in oxygen saturation, and brief electroencephalogram (EEG) arousals concomitant with stertorous breathing sounds as a bolus of air is exhaled when the airway reopens. This may occur hundreds of times nightly. Obstructive apnea events are most often associated with recurrent sleep arousals and recurrent oxygen desaturation.

Three cardinal symptoms of sleep apnea include snoring, sleepiness, and significant-other report of sleep apnea episodes. This 3 S alliteration is a helpful mnemonic to busy clinicians in assessing patients for OSA. It has proven to be valuable in teaching residents to be sensitive in the identification and appropriate referral of these patients for further study Also helpful is if the patient’s spouse or someone close to him or her can attend the visit because often the sleeper is unaware he or she  has OSA, and, in fact, he or she may regard themselves as “a good sleeper” because they “can sleep anytime, anywhere” (eg, waiting in the physician’s, in traffic, in class, at his or her office) Sleepiness is one of the potentially most morbid symptoms of sleep apnea, owing to the accidents that can occur as a result of it.

OSA is a very important diagnosis for physicians to consider because of its strong association with and potential cause of the most debilitating medical conditions, including hypertension, cardiovascular disease, coronary artery disease, insulin-resistance diabetes, depression, and, as mentioned, sleepiness-related accidents, which are discussed in greater detail in Mortality/Morbidity and Medicolegal Pitfalls.

OSA is an increasingly prevalent condition, in both adults and children, in modern society.  Approximately 24% of men and 9% of women have OSA, with and without excessive daytime sleepiness. The prevalence in children is less certain, but an increasingly large segment of the adolescent population is seen in the author’s sleep center who are often obese and present similar to many of their adult counterparts, with one important exception: they may be sleepy and/or hyperactive. A 2007 study has suggested that approximately 6% of adolescents have weekly sleep-related disordered breathing. Also see Obstructive Sleep Apnea Syndrome in eMedicine’s Pediatrics section.

OSA should be diagnosed and treated promptly. OSA can be reversed quickly with the appropriate titration of continuous positive airway pressure (CPAP) devices. CPAP is the standard treatment option for OSA.
A sleep-related disordered breathing (SRDB) continuum has been described and is supported by research. The SRDB continuum suggests that snoring is the initial presenting symptom, and it increases in severity over time and it increases in association with medical disorders that may serve to exacerbate the disorder, such as obesity. Snoring has a constellation of pathophysiological effects ; as the disease progresses SRBD patients begin to develop increased UA resistance that results in a new hallmark symptom: sleepiness. Sleepiness is caused by increased arousals from sleep. This syndrome has been described as the UA resistance syndrome (UARS).

Sleep-related disordered breathing continuum ranging from simple snoring to obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position between these extremes. Note areas of overlap among the conditions.


Sleep-related disordered breathing continuum ranging from simple snoring to obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position between these extremes. Note areas of overlap among the conditions.

UARS patients are not hypoxic, and hypoxia does not explain why they are sleepy, nor can sleep stage percentages or other polysomnography (PSG) variables. The SRDB continuum predicts that over time, a UARS patient develops OSA, if untreated.

OSA has as its hallmark symptoms snoring, sleepiness, spouse apnea report, and hypoxia. The SRDB continuum suggests that over time, untreated OSA may hasten death through heart disease, hypertension, stroke, myocardial infarction, heart failure, cardiac arrhythmia, diabetes, metabolic syndrome, or vehicular or other accident due to sleepiness or other behavioral affects noted.

The SRDB continuum suggests that optimal OSA treatment must correct OSA, UARS, and snoring. If it does not eliminate all 3 problems, the symptoms and the pathophysiological process that was evident at the start of disease will recur. Therefore, in the treatment of SRDB, CPAP corrects OSA first, UARS next, and snoring last.

An unlikely occurrence is snoring being corrected before OSA and/or UARS; if this is thought to have occurred, then consideration should be given to the integrity of the snoring microphone.

Consider whether snoring has been correctly interpreted on the PSG during a CPAP titration. When a mask leak occurs, the noise may be transferred by the microphone to the PSG snore channel and appear as snoring. One can determine the difference between snoring and a CPAP mask leak because snoring occurs at the point of peak inspiration and the beginning of expiration; mask leak occurs during expiration.

Consider whether the patient has had UA corrective surgery. If pharyngeal tissue has been eliminated, snoring may not occur, but OSA can occur (so-called silent apnea).

OSA patients with sleepiness despite apparent effective treatment of OSA with CPAP

One patient group remains sleepy despite correction of SRDB. This subset of patients has excessive daytime sleepiness (EDS) that largely responds to modafinil treatment, usually at the higher doses of the medication (200-400 mg/d), whereas fatigue seems to be better treated with lower doses of the medication (100-200 mg/d). Active research has thus far demonstrated that these patients may have intermittent hypoxia that may have changed the brain’s ability to overcome EDS without modafinil and SRDB corrective treatment together.


Before OSA with residual daytime sleepiness is considered and treated, it is important to know if the pressure is indeed ideal. The author’s approach is to be able to conclusively demonstrate that CPAP has effectively eliminate snoring, UARS, and OSA in the supine position and in rapid eye movement (REM) sleep, 2 sleep states during which SRDB is worsened. Sometimes, a single-night CPAP titration study is not sufficient to make this conclusion. Data suggest that the author’s sleep center titration under titrates  an average of 2 cm water.1 Based on these data, some may increase the CPAP pressure by 2 cm water. If the empirical increase does not effectively treat the EDS, then a PSG with a CPAP titration in the sleep disorders center is warranted to adjust the pressure while the patient is in the supine position and in REM sleep so that snoring, UARS, and OSA are eliminated.
If these steps have been taken, then performing a multiple sleep latency test (MSLT) is reasonable in order to (1) verify objective daytime sleepiness compared with the subjective sleepiness of the Epworth Sleepiness Scale (ESS), because the correlation is low (r = 0.34) and(2) exclude other sleep disorders known to have hypersomnia as a major presenting symptom (eg, insufficient sleep syndrome, narcolepsy), because insufficient sleep syndrome is the most common cause of hypersomnia and OSA is more common among patients who have narcolepsy (a 30% incidence rate vs 1-4% in the population).

The description of a continuum may have first been described by Elio Lugaresi, an Italian Sleep Specialist, during a 1987 Association for the Psychophysiological Study of Sleep presentation in Copenhagen, Denmark). Dr Lugaresi used the term “heavy snorers disease” to articulate the SRDB continuum. He made the argument that snoring is the beginning of the so-called heavy snorers disease. He presented data showing that the earlier snoring occurred in adult life, the more severe the obstructive apnea would be later, and OSA presented earlier in life.

Historical perspectives

The history of the discovery of sleep apnea is interesting and is the topic of a paper published in 2008.7

In literature, Charles Dickens has been credited with one of the first descriptions in print regarding sleep apnea when he wrote of “Sleepy Joe,” an obese man who sat in the corner of an English pub asleep. The archetype of a rotund, sleepy man became eponymous with “pickwickian syndrome” by Burwell in 1956.8 The prevailing belief at the time was that “pickwickians” had breathing disorders and drowsiness due to “carbon dioxide poisoning.”

A number of individuals have played important roles in advancing sleep science to the point that we have come to understand OSA. Detailing the history of OSA is beyond the scope of this article; however, a few highlights are mentioned.

Gestaut, Tassinari, and Duron9 in France and Jung and Kuhlo10 in Germany provided perhaps the most accurate descriptions of OSA at about the same time, in 1965.

The first known successful treatment for OSA was tracheostomy in 1970 by Elio Lugaresi and colleagues at the University of Bologna in Italy. A primary reason a tracheostomy was important to the understanding of OSA is that performing the tracheostomy left little doubt that OSA was due to an obstructed UA, and not due to a dysfunction of the brain’s respiratory centers. The elevated blood pressure in these patients was of grave concern to Dr Lugaresi, and post-tracheostomy the blood pressure dropped substantially. For the next 11-16 years, tracheostomy and weight loss were the only established beneficial remedies for OSA

In 1981, Sullivan et al introduced CPAP as a treatment for OSA.11 It quickly gained worldwide acceptance by 1986, and it replaced tracheostomy as the most useful and desirable treatment. As is often the case in history, it is perplexing how such a simple device introduced so long ago can transform modern medicine in ways not sooner foreseen. CPAP was a tremendous advance for thousands of OSA patients who needed care and for clinicians who would soon solely specialize in sleep medicine.

Around the time when CPAP was introduced, corrective surgery was introduced and would become the forerunner of further developments in the field of sleep medicine. In 1981, Fugita and colleagues introduced uvulopalatopharyngoplasty (UPPP).12

Other treatments, including oral appliance (OA) therapy, are also now treatment alternatives for OSA. Future advances in these and other therapies (eg, stimulation of the genioglossus muscle) are exciting. As was the case with CPAP, the simplest procedure, mechanical device, or drug may astound the medical community by providing the next revolution in the treatment of OSA. For a complete and elegant description of the history of sleep medicine, see Principles and Practice of Sleep Medicine.13


According to the American Academy of Sleep Medicine (AASM) International Classification of Sleep Disorders: Diagnostic and Coding Manual, Second Edition,14 OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) UA obstruction occurring during sleep. By definition, apneic and hypopneic events last a minimum of 10 seconds. At least 5 apnea events must occur per hour of sleep time in association with clinical symptoms, or at least 15 apnea events must occur per hour of sleep time with or without clinical symptoms.



Supported  by


Yudhasmara Foundation

Office ; JL Taman Bendungan Asahan 5 Jakarta Indonesia 10210

phone : 62(021) 70081995 – 5703646

email :,




Clinic and Editor in Chief :

Widodo Judarwanto, pediatrician

email :

curriculum vitae



Copyright © 2009, Children Sleep Clinic  Information Education Network. All rights reserved


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