Pulmonary, Critical Care, and Sleep Pearls |

A 45-Year-Old Man With Delayed Onset of OSA Events During Polysomnography FREE TO VIEW

Daniel A. Barone, MD; Ana C. Krieger, MD, MPH
Author and Funding Information

CORRESPONDENCE TO: Daniel A. Barone, MD, Weill Cornell Medical College, Center for Sleep Medicine, 425 East 61st St, 5th Floor, New York, NY 10065

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4):e123-e126. doi:10.1016/j.chest.2015.10.013
Text Size: A A A
Published online

A 45-year-old man with a medical history that included asthma and chronic nasal congestion presented for an evaluation of possible OSA. He reported loud snoring, witnessed apneas in sleep, and daytime sleepiness. The patient’s score on the Epworth Sleepiness Scale was 12 of 24, indicating excessive sleepiness. His nasal congestion had been treated with frequent use of an over-the-counter nasal decongestant.

Figures in this Article

The patient’s height was 65 inches, and he weighed 145 pounds (BMI, 24 kg/m2); his blood pressure was 123/76 mm Hg. His physical examination was notable for congested nares with decreased nasal air entry bilaterally and edematous turbinates; his nasal septum was not deviated. The posterior pharynx was narrow and crowded, tonsils were 2+ in size, and the uvula was edematous; the modified Mallampati score was II/IV. His jaw alignment was normal, with no retrognathia or hypognathia, and his neck size was approximately 15 inches in circumference.

The patient underwent a polysomnogram (PSG) to further evaluate his condition. Prior to the study, he used a nasal decongestant; no other medications were taken. Details of the PSG are displayed in Figure 1.

Figure 1
Figure Jump LinkFigure 1 Polysomnogram findings. Resp. Evt. = respiratory events.Grahic Jump Location

What is the diagnosis?

What is most likely the cause of the respiratory events seen in the second half of the patient’s overnight PSG?

Diagnosis: Rebound nasal congestion following administration of oxymetazoline, resulting in the reappearance of OSA.

During the initial 208 min of sleep, the patient’s PSG revealed few respiratory events, after which time frequent respiratory events developed. Overall, the apnea-hypopnea index was 36 events per hour, with oxygen desaturation to a low of 89%, resulting in a diagnosis of severe OSA. The second half of the night was also noteworthy for the frequent arousals and sleep state transitions. Only rare respiratory events were present during the first half of the study despite all sleep positions and sleep stages being documented.

Clinically, there are different phenotypic causes of OSA, which are important to note given the effect they have on treatment. Pathophysiologic causes include: (1) an anatomically compromised or collapsible upper airway (high passive critical closing pressure of the upper airway), (2) inadequate responsiveness of the upper airway dilator muscles during sleep, (3) waking up prematurely to airway narrowing (a low respiratory arousal threshold), and (4) having a highly sensitive ventilatory control system (high loop gain). The phenotypic cause of OSA in this patient seemed to be anatomical and resulting from nasal obstruction. His clinical symptoms of nasal congestion had been self-treated with application of oxymetazoline multiple times during the day and night.

Nasal congestion resulting from allergic rhinitis is associated with a 1.8-fold increase in the risk of developing moderate to severe OSA. The proposed mechanism for this enhanced risk includes increased airway resistance and mouth breathing. In OSA, the primary pathological obstructive sites are located at either the velopharyngeal or retropalatal segments of the upper airway; however, nasal resistance has also been shown to contribute up to 50% of the upper airway resistance. The Starling resistor model, which describes patterns of airflow through a collapsible tube, recognizes four determinants of airflow: pressure upstream, pressure downstream, pressure surrounding the tube, and resistance of the upstream segment. When nasal resistance is increased, it results in an increased pressure differential between the intraluminal space and the atmosphere, which induces airway collapse. The higher nasal resistance is accompanied by an increase in the resistance of the upstream segment that consequently decreases the airflow through the pharynx (the collapsible tube).

The mandible moves downward when the mouth is opened, which displaces the tongue in that direction. This action results in a reduction in the pharyngeal diameter and a shortening of the upper airway dilator muscles (which reduces their efficiency). Thus, mouth breathing is mechanically associated with an increase in airflow resistance.

Oxymetazoline is an imidazoline with selective α1-agonist and partial α2-agonist properties that is used as an over-the-counter nasal decongestant. The onset of action is within seconds, with an elimination half-life of 5 to 8 h, and it is excreted unchanged by the kidneys (30%) and in feces (10%). Vasoconstriction results in relief of nasal congestion by increasing the diameter of the airway lumen as well as reducing fluid exudation from postcapillary venules. Oxymetazoline has been shown to reduce nasal airway resistance up to 35.7% and nasal mucosal blood flow up to 50%.

Oxymetazoline is known to reduce snoring but, according to the literature, has had equivocal effects on OSA. A total of four studies investigating the effects of topical nasal decongestion on OSA severity were found, and only one of the four studies reported positive results. In a study of 10 subjects with varying degrees of OSA severity, topical normal saline (placebo) was compared with topical nasal oxymetazoline (treatment). After 1 night of application, oxymetazoline was associated with a subjective improvement in sleep quality and a significant reduction in nasal resistance, with no significant improvement in sleep architecture, nocturnal oxygenation, or the frequency of apnea.

There are concerns regarding the use of oxymetazoline, given its potential for systemic diffusion with peripheral α-adrenergic effects. Isolated case reports in the literature note the onset of acute cardiac symptoms following its use; in addition, long-term administration of oxymetazoline can result in insomnia, irritability, and palpitations. Although tachyphylaxis and rebound congestion can occur with oxymetazoline, intranasal fluticasone has been shown to be effective in reversing these phenomena.

Clinical Course

Based on the diagnosis of severe OSA, the management plan for this patient included a CPAP titration study, at which time an effective treatment pressure of 12 cm H2O was ascertained. In addition, a program of weaning the patient off oxymetazoline was initiated and included a prescription for intranasal fluticasone. At the patient’s follow-up visit 1 month later, he described a major improvement in daytime sleepiness and full resolution of snoring resulting from 100% compliance with CPAP. Once the patient is fully weaned off oxymetazoline, a repeat baseline PSG will be performed.

  • 1.

    Different phenotypic causes need to be considered in patients with OSA, including an anatomically compromised or collapsible upper airway, inadequate responsiveness of the upper airway dilator muscles during sleep, a low respiratory arousal threshold, and a highly sensitive ventilatory control system.

  • 2.

    Intranasal decongestants, such as oxymetazoline, are highly efficacious in treating nasal congestion in rhinitis, but tachyphylaxis, rebound congestion, and potential for cardiovascular events restrict their long-term use.

  • 3.

    Oxymetazoline-induced tachyphylaxis and rebound congestion are mediated mostly through the α1-adrenoceptor and can be reversed by intranasal fluticasone administration.

  • 4.

    While evaluating patients for snoring and potential OSA, it is important to determine if they use nasal vasoconstrictors either on a regular basis or prior to any sleep testing.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.


Figure Jump LinkFigure 1 Polysomnogram findings. Resp. Evt. = respiratory events.Grahic Jump Location



Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543