Coexisting Asthma and Obstructive Sleep Apnea


Vol. 20 • Issue 5 • Page 12

Allergy and Asthma

Adults and children with asthma often suffer from worsening symptoms at night, and patients with obstructive sleep apnea may have undiagnosed asthma that can make their sleep disorder worse.

Asthma and OSA share common risk factors such as obesity and allergic rhinitis, and the prevalence of both conditions is rising. It’s important for sleep technologists and asthma educators to understand the common symptoms and underlying physiological mechanisms that may cause these conditions to coexist.

Nocturnal asthma is a variable exacerbation of the asthmatic condition occurring at night, and it is associated with an increase in symptoms, worsening of lung function, and a greater need for medication during the night hours.1 It’s characterized by a decrease in FEV1 greater than 15 percent during the night hours.2 Nocturnal exacerbations are common with as many as 75 percent of patients with asthma experiencing symptoms at least once per week, and approximately 40 percent experiencing nocturnal symptoms on a nightly basis.3

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Adult studies have identified that a significant proportion of patients with asthma experience a worsening of symptoms between midnight and 8 a.m., contributing to more emergency department visits, calls to physicians, and more asthma-related deaths during these hours.4,5 Nocturnal asthma has not been specifically studied in children, but data from the Childhood Asthma Management Program study indicates that 34 percent of children with mild-to-moderate asthma have at least one nighttime awakening nightly, and 14 percent have three or more awakenings.6

Several physiologic explanations contribute to why asthma symptoms tend to worsen overnight. A diurnal variation in respiratory peak flow rates occurs with a nadir around 4 a.m. and peak at 4 p.m.1 Other important physiologic factors may contribute to nocturnal asthma. (See Table.)

Airway inflammation may increase at night, and airway resistance may increase due to cholinergic activation. Furthermore, there is a reduction in mucociliary clearance and a reduction in functional residual capacity. Standard asthma medications also may be less effective at night, as there is down regulation of beta-adrenergic receptors and decreased sensitivity to glucocorticoids. Environmental allergies may be particularly troublesome at night, and reflux of gastric acid, which can occur during sleep because of a combination of increased gastric acid secretion and supine posture, might result in bronchospasm from increased vagal tone.7

Management of nocturnal asthma

Medical treatment of nocturnal asthma includes many modalities. Inhaled corticosteroids (ICS), long-acting beta-agonists, and leukotriene modifiers all may have a role, and therapy should be tailored as per standard guidelines.8 However, the timing of asthma medication administration may influence nocturnal asthma control. Some researchers have found that ICS dosing might be optimal between
3 p.m. and 5:30 p.m. Leukotriene inhibitors may be most effective in patients with nighttime symptoms if given at bedtime. Also, it has been suggested that oral corticosteroids are most effective in the late afternoon.1

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Controlling allergy triggers can be important in some patients. This might include plastic covers on pillows and mattresses, adequate ventilation, and optimal humidity in the sleeping environment with minimization of dust for those with dust mite allergy. A referral to an allergist may be helpful.

Physiologic variables also affect sleep quality in patients with asthma. It is known that they have a higher propensity to snore and have disrupted sleep architecture as a result of frequent arousals from sleep.9 There is a significant association between fragmented sleep and increased airway collapsibility and upper airway resistance; thus, fragmented sleep may lead to early upper airway closure and OSA.10

Oral corticosteroids may predispose asthmatics to OSA and other sleep disturbances.11 An unexpectedly high prevalence of OSA has been demonstrated among patients with unstable asthma receiving long-term chronic or frequent bursts of oral corticosteroid therapy.12 It is not yet well understood whether this is also the case for patients receiving long-term ICS.

OSA is characterized by episodic upper airway obstruction with irregular respiratory patterns during sleep. Potential mechanisms of OSA contributing to the pathophysiology of asthma or mimicking symptoms of asthma include upper airway edema and inflammation, higher levels of systemic inflammation, sleep deprivation, cardiac dysfunction, and increased GERD and microaspiration.13 Furthermore, bronchial hyper-reactivity and airway wall thickening in OSA patients has been described.14

Management of OSA

The standard of care for treating OSA in adult patients is positive airway pressure therapy, although surgical treatment of the upper airway may have a role in some patients, particularly children with adenotonsillar hypertrophy. Some evidence suggess that PAP treatment for OSA can improve overall asthma control.15 The use of humidified warm air in the circuit may be necessary to minimize the risk of bronchospasm caused by inhalation of dry, cold air.

When asthma and OSA occur concurrently, successful treatment of one is often dependent on successful treatment of the other. Asthma medications should be titrated aggressively to achieve adequate control as outlined by recent guidelines, with particular attention to the degree of nighttime symptoms. OSA should be managed by a sleep specialist, most commonly with the use of PAP in adults. For any obese patient, weight loss may be helpful in controlling both conditions.

Careful evaluation

The clinician evaluating patients with asthma or patients with OSA should have a high suspicion for the other entity as a comorbid condition. A sleep history and specific questions to ascertain the degree of asthma control or presence of cough, wheezing, shortness of breath, or exercise limitation should be standard screening practice. A brief physical examination may demonstrate clues to coexisting asthma or OSA.

For example, severe tonsillar hypertrophy may increase the risk of OSA in a child with asthma, whereas wheezing during presentation to a sleep clinic may very well herald underlying asthma in a previously undiagnosed adult. If clinical suspicion arises, the clinician should have a low threshold for objective diagnostic testing and management. Some screening tools such as the Epworth Sleepiness Scale or Asthma Control Test can be utilized during routine visits.

It may be necessary to refer for polysomnography as a formal assessment of OSA. Ensure that asthma is well-controlled during a PSG, as nocturnal asthma may confound results. Likewise, pulmonary function testing with or without bronchoprovocation may be helpful in an objective assessment for asthma in the OSA patient.

Visit www.advanceweb.com/respiratory for a list of references.

Jodi Gustave, MD, is a fellow of pediatric pulmonary medicine, and Stephen Kirkby, MD, is assistant professor of internal medicine and pediatrics in the section of pulmonary medicine at Nationwide Children’s Hospital and Ohio State University Medical Center, Columbus, Ohio.

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