Obstructive Sleep Apnœa Syndrome (OSA)
–Gary A. Bass 15:12, Jun 3, 2004 (UTC)
Whilst the vast majority of people successfully maintain a patent upper airway and breathe normally, a significant number of individuals are prone to severe narrowing or occlusion of the pharynx during sleep, such that breathing is impeded or even completely obstructed (Mortimore & Douglas, 1997).
Recurrent airway obstruction gives rise to the obstructive sleep apnoea (OSA) syndrome, the most common cause of sleep-disordered breathing, with 2% of female and 4% of male subjects meeting the minimal diagnostic criteria for OSA – at least 10 apnœic events per hour, where an event is characterised by complete closure of the upper airway for at least 10 seconds wherein airflow is prevented despite continued respiratory efforts (American Academy of Sleep Medicine Task Force, 1999).
<–patent airway vs. occluded airway–>
These recurrent episodes of airway obstruction are associated with asphyxia, hypertension and arousal from sleep, since a transient return to the waking state is the only mechanism that restores airway patency. These episodes are thought to account for the clinical sequelæ, which include increased incidence of chronic hypertension, a seven-fold rise in road traffic accidents, excessive daytime somnolence, social and family disruption, and cardiac arrhythmias and morbidity (Strollo, Jr. & Rogers, 1996).
Obstruction of the upper airway may also be a cause of or may contribute to sudden infant death syndrome (SIDS) (Mathur & Douglas, 1994). Current therapeutic interventions such as nasal continuous positive airway pressure (CPAP) and oral administration of the methylxanthine theophylline reduce the number of episodes of apnœa but produce side effects such as palpitations and insomnia. Surgical therapy involving the ablation of tissue, such as uvulopalatopharyngoplasty (UPPP), has also been proposed for patients with apnœa of a predominantly obstructive nature (Slovis & Brigham, 2001).
Ongoing research is aimed at providing a better understanding of the pathophysiology of OSA, and at uncovering novel alternative therapies of value in patients who poorly tolerate current interventions.
References:
Mortimore, I. L. & Douglas, N. J. (1997). Palatal muscle EMG response to negative pressure in awake sleep apneic and control subjects. Am.J.Resp.Crit.Care Med. 156, 867-893.
American Academy of Sleep Medicine Task Force (1999). Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 22, 667-689.
Strollo, P. J., Jr. & Rogers, R. M. (1996). Obstructive sleep apnea. N.Engl.J.Med. 334, 99-104.
Mathur, R. & Douglas, N. J. (1994). Relation between sudden infant death syndrome and adult sleep apnoea/hypopnoea syndrome. Lancet 344, 819-820.
Slovis, B. & Brigham, K. (2001). Disordered Breathing. In Cecil Essentials of Medicine, ed. Andreoli, T. E., pp. 210-211. W.B. Saunders, Philadelphia.