5 Snoring & Obstructive Sleep Apnea Flashcards
What is the difference between snoring and obstructive sleep apnea (OSA)? What about sleep disordered breathing (SDB)? Upper airway resistance syndrome (UARS)?
What is the difference between snoring and obstructive sleep apnea (OSA)? What about sleep disordered breathing (SDB)? Upper airway resistance syndrome (UARS)?
Snoring is simply noisy breathing during sleep that occurs due to the vibration of lax tissue in the upper airway. SDB is characterized by snoring along with symptoms suggestive of OSA, including daytime somnolence and snoring. Sleep disordered breathing exists along a continuum of severity. UARS presents with symptoms of OSA without meeting the criteria of OSA as determined by the apnea hypopnea index (AHI) and/or respiratory disturbance index (RDI). OSA, the most severe form of SDB, affects quality of life and is potentially life threatening. OSA is defined by AHI or RDI greater than 5 during sleep as revealed by polysomnography. OSA is caused by upper airway tissue collapse resulting in airway obstruction.
How common is snoring? What about sleep apnea?
How common is snoring? What about sleep apnea?
Snoring is very common across the population. Based on self-report and questionnaires, 40% of middle-aged men and 28% of middle-aged women snore. This increases to as high as 84% and 73%, respectively, in the seventh decade of life. It is estimated that as many as 3% to 7% of men and 2% to 5% of women have OSA. It has been shown that the prevalence is even higher in obese, senior, postmenopausal, and minority populations. The risk of OSA is higher when a person has a close relative (parent, child, sibling) with OSA.
What causes snoring? OSA?
What causes snoring? OSA?
Snoring is caused by variations in airflow across dynamic portions of the upper airway, which results in vibrations of the soft tissues. Most commonly, it occurs in the area of the uvula, soft palate, tonsillar pillars, and/or pharyngeal walls. Occasionally, it may also occur at the base of tongue. OSA occurs secondary to collapse at the anatomic levels mentioned above but also may occur due to obstruction by the lingual tonsils or epiglottis. Obesity often contributes to snoring and apnea because of increased weight of the neck tissues, increased fat in the parapharyngeal space that narrows the pharynx, redundancy in the soft palate, and fullness in the tongue base.
What is obstructive sleep apnea (OSA)?
What is obstructive sleep apnea (OSA)?
OSA refers to a collection of conditions and syndromes that have periods of apnea, a temporary cessation of breathing (defined as intermittent cessation of airflow during sleep that lasts 10 seconds or longer), as key occurrences. It was initially described in the early 1800s. One of the first accounts was written by Charles Dickens in 1837 and entitled The Posthumous Papers of the Pickwick Club. Subsequently, William Osler coined the term “pickwickian” in 1918 to describe the obese, hypersomnolent patient. The pathogenesis and pathophysiology of OSA have been studied extensively. During sleep, the upper airway becomes occluded, resulting in an episode of obstructive apnea. As a result, the patient experiences a brief arousal from sleep. With the return of breathing, the patient typically returns to sleep quickly. This sequence is repeated over and over.
What are the subclassifications of sleep apnea?
What are the subclassifications of sleep apnea?
Over the years, various sleep apnea syndromes have been described and classified into three main types: central, obstructive, and mixed. Central sleep apnea refers to apnea with origins in the central nervous system. Obstructive sleep apnea refers to apnea due primarily to collapse of the upper airway during sleep. Mixed apnea refers to apnea with both central and obstructive characteristics. Of the three main types of apneas, OSA is the most common and has received the most scientific interest and study.
What are common symptoms of obstructive sleep apnea?
What are common symptoms of obstructive sleep apnea?
Snoring, restless sleep, witnessed episodes of choking or gasping for air while sleeping, excessive daytime somnolence, morning headaches, nocturia, changes in mood (depression, irritability, anxiety, aggression), poor concentration, memory loss, night sweats, bruxism.
What medical comorbidities can predispose to sleep apnea?
What medical comorbidities can predispose to sleep apnea?
- Hypothyroidism: There appears to be a link between hypothyroidism and OSA beyond increased BMI alone. It is thought that mucoprotein and hyaluronic acid deposition in the upper airway may be related to increased airway compression. Treating underlying hypothyroidism often improves sleep apnea independent from weight change or pulmonary function.
- Acromegaly: Tongue enlargement and skeletal changes including increased head size can also impact the airway and predispose patients to OSA.
- Obesity: Obesity is very common in the OSA population. Although being overweight is not necessary for OSA, truncal obesity predisposes patients to sleep apnea. In patients with a small airway diameter at baseline, even a modest weight gain can cause OSA.
- Gastro-esophageal reflux disease (GERD): GERD is commonly present alongside OSA. Changing intrathoracic pressures and obesity predispose to reflux and the inflammation caused by untreated GERD has been shown to worsen sleep apnea.
- Polycystic ovarian syndrome: Hormone dysregulation in PCOS can lead to increased frequency of apneic episodes in women with anatomic predisposition for pharyngeal collapse. Hormonal changes associated with postmenopausal women have also been shown to cause higher incidences of OSA.
What medical complications can arise if OSA is untreated?
What medical complications can arise if OSA is untreated?
Systemic hypertension, myocardial infarction, vascular accidents, congestive heart failure, cor pulmonale, atherosclerosis, atrial fibrillation, ventricular arrhythmias, pulmonary hypertension, glaucoma, decreased seizure threshold, diminished libido, death
What are the medical consequences of OSA in children?
What are the medical consequences of OSA in children?
- ADHD
- Growth delay
- Nocturnal enuresis
An in-office clinical exam of the snoring and OSA patient should include what?
An in-office clinical exam of the snoring and OSA patient should include what?
A complete head and neck examination should be performed. The nose should be examined for signs of obstruction due to a deviated septum, hypertrophic turbinates or allergic rhinitis. Frequently, improving nasal congestion will decrease the intensity and frequency of snoring. Examination of the oral cavity may reveal potential obstruction due to large tonsils, redundant soft palate and uvula, redundant lateral pharyngeal walls, and/or a full base of the tongue. Patients may also have a high arched hard palate, retrognathia, and micrognathia. The Friedman tongue position classification system can be used together with BMI and tonsil size to predict patients’ response to uvulopalatopharyngoplasty (UPPP) and a tonsillectomy (see picture below). The system grades the view of the uvula and tonsillar pillars while the patient opens his or her mouth with the tongue in a neutral position. Higher grades are associated with better response to UPPP. Müller’s maneuver may be helpful in confirming the diagnosis and the site of obstruction.
Friedman tongue position. A) I: visualization of the entire uvula and tonsils/pillars. B) IIa: visualization of most of the uvula, but tonsils/pillars are absent. C) IIb: visualization of the entire soft palate to the base of the uvula. D) III: visualization of some of the soft palate, but structures distal to this are not seen. E) IV: visualization of the hard palate only.
What is Müller’s maneuver?
What is Müller’s maneuver?
Müller’s maneuver is performed as part of an extensive physical examination and involves passing a flexible fiber-optic scope from the nose into the hypopharynx to obtain a view of the entire hypopharynx and larynx. The examiner then pinches the nostrils closed, and the patient closes his or her lips while attempting to inhale. If the hypopharynx and/or larynx collapse, then the test result is positive. A positive test helps delineate the location of antomic obstruction which occurs with OSA.
Controversy:
Questions exists as to the usefulness of the Muller’s maneuver this is a test performed while the patient is awake with good tone as opposed to when asleep with less muscle tone.
How is OSA diagnosed?
How is OSA diagnosed?
The gold standard for diagnosing OSA is an in-lab monitored polysomnography. The history and physical, along with supplementary studies such as the Epworth Sleepiness Scale (ESS), help identify patients who would benefit from a sleep study to diagnose sleep apnea. Sleep studies measure brain activity, leg muscle movements, cardiac rhythm, eye movements, oxygen saturation, respiratory effort, and air movement at the nose and mouth. Polysomnography can differentiate between snoring without OSA, pure OSA, and central sleep apnea and can characterize the severity of the apnea. This test requires the patient to spend a night in a formal sleep laboratory. Portable monitoring devices for home sleep studies, which are not as comprehensive as in-lab studies, have recently been approved by the Center for Medicare and Medicaid Services (CMS) as appropriate for the diagnosis of OSA.
What defines obstructive sleep apnea on polysomnography in adults? What is the difference between AHI and RDI?
What defines obstructive sleep apnea on polysomnography in adults? What is the difference between AHI and RDI?
The diagnostic criteria for OSA is an apnea-hypopnea index (AHI) greater than 5 or a respiratory disturbance index (RDI) greater than 5. AHI is defined as the number of obstructive apneic or hypopneic episodes a patient has per hour. On polysomnography, obstructive apnea is defined as cessation of airflow due to anatomic airway obstruction for 10 seconds and hypopnea is defined as reduction in ventilation by at least 30% of baseline for 10 seconds associated with at least a 4% oxygen desaturation. RDI is similar to AHI but also includes respiratory effort related arousals (RERAs). RERAs do not fulfill the criteria of an apnea or hypopnea but still result in an arousal from sleep. AHI or RDI between 5 and 15 is considered mild OSA, 16 to 30 is moderate OSA, and any number greater than 30 is considered severe OSA.
Are sleep studies always used in children?
Are sleep studies always used in children?
Formal sleep studies are not done as often in children as in adults. Some physicians use 24-hour pulse oximetry or sleep sonography, which is recording of nocturnal breathing sounds. Usually a history and physical (usually large tonsils and adenoids) consistent with OSA are enough to make a surgical decision for a child. Other causes of sleep disturbed breathing include nasopharyngeal cysts, encephaloceles, choanal atresia, a deviated nasal septum, and craniofacial or orthodontic malformations. When in doubt, a formal sleep study is still indicated.
Describe the classic sleep pattern seen in OSA.
Describe the classic sleep pattern seen in OSA.
Typically, OSA patients exhibit a quick onset of sleep and multiple arousals. The patient maintains relatively more stage I and II sleep and less stage III, IV, and rapid eye movement (REM) sleep. This lack of deep sleep results in the symptoms of sleep deprivation.
