Much More Than a Nuisance

Between 50 million and 70 million U.S. residents experience sleep-related problems.¹ These difficulties affect all age groups.^2,3 The Sleep in America Poll determined in 2008 that 44 percent of adults had experienced a sleep problem every night or almost every night of the prior month.⁴ Although sleep disorders are common, less than 50 percent of adults say their healthcare providers ask them about their sleep.^4,5

More than 90 sleep disorders have been identified. This article discuss­es evidence for medical consequences associated with obstructive sleep apnea (OSA) and sleep deprivation.

Obstructive Sleep Apnea
OSA is the most prevalent disorder of breathing in sleep. OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) collapse of the upper airway despite continued effort to breathe. These episodes cause a sequence of changes starting with hypercapnia and hypoxemia, which stimulate an increased effort to breathe against a closed airway. This results in sympathetic activation and terminates in a brief arousal from sleep. Activation of the sympathetic nervous system causes an increased heart rate, constriction of peripheral blood vessels (leading to increased blood pressure), increased mental activity, increased respiratory rate and effort, and increased release of glucose into the bloodstream. Over time, these repeated surges strain the cardiovascular system. Repeated arousals and sleep fragmentation cause excessive sleepiness and fatigue during the day.³

Common signs and symptoms of OSA in adults include excessive sleepiness, unrefreshing sleep, fatigue, snoring, gasping or choking, pauses in breathing, frequent brief awakenings and nocturia. In children, signs and symptoms are different: hyperactivity, irritability, aggressive behavior, excessive sleepiness, snoring, arousals, unusual sleep positions and nocturnal enuresis.⁶

OSA in Children
Obstructive sleep apnea occurs in up to 3 percent of children.² Altered neurobehavioral function and learning has been reported in children with OSA. A meta-analysis of 61 studies of the relationship between sleep-disordered breathing (SDB) and neurobehavioral functioning found strong evidence of deficits in behavior and emotion regulation, scholastic performance, sustained attention, selection attention and alertness.⁷ Findings were associated with impulsivity, hyperactivity and aggressive behavior, which are common in attention deficit-hyperactivity disorder (ADHD). Similarity in signs and symptoms should prompt the inclusion of OSA in the differential diagnosis list for possible ADHD.

End-organ injury in children with untreated OSA is believed to be due to episodic hypoxemia, hypercapnia and sleep fragmentation. Delay in treatment may result in irreversible morbidity. Untreated OSA in childhood may be an antecedent to adult disease, especially in those that are genetically predisposed.⁸

Adenotonsillectomy is often the treatment of choice for children with OSA, but it may not be as efficacious as previously thought. The frequency of mild OSA after adenotonsillectomy has been estimated at 45-50 percent; an additional 20-25 percent of patients have moderate to severe disease.⁸ Continuous positive airway pressure (CPAP) is reserved for children with craniofacial abnormalities, obesity or residual OSA after adenotonsillectomy. As evidence about the effectiveness of adenotonsillectomy evolves, treatment practices may change.

OSA and Hypertension
The proposed mechanisms for OSA influencing the development of hypertension include hypoxia (known to stimulate endothelial growth), hypercapnia and increased sympathetic tone. One study found that SDB was independently associated with hypertension in a dose response relationship.⁹ In another study, patients with SDB were more likely to have hypertension.¹⁰ The odds started to increase with an apnea hypopnea index (AHI) of 15 per hour. Patients with an AHI of more than 30 per hour were 1.5 times more likely to develop hypertension. A prospective study determined that OSA acutely increased nocturnal blood pressure and sustained daytime hypertension with a threefold increased risk of new onset hypertension in patients with an AHI of 15 or more per hour.¹¹

Multiple observational studies have identified improvement in daytime blood pressure control with effective CPAP use. One study documented a 2.5 mm Hg reduction in blood pressure after 4 weeks of therapeutic CPAP therapy and larger reductions in patients with severe OSA.¹² In a separate study, researchers followed patients for more than 60 days and found dramatic reductions in mean blood pressure (9.9 mm Hg ± 11.4 mm Hg) in a small cohort with severe OSA.¹³

These findings strengthen the belief that OSA is likely a causal factor in hypertension. The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7) recommends sleep apnea screening for all patients who are newly diagnosed with refractory hypertension.¹⁴