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Sleep Apnea, Obstructive
Sonya Shipley, MD
image BASICS
DESCRIPTION
  • Obstructive sleep apnea (OSA) is defined as repetitive episodes of cessation of airflow (apnea) at the nose and mouth during sleep due to obstruction at the level of the pharynx.
    • Apneas often terminate with a snort/gasp.
    • Repetitive apneas produce sleep disruption, leading to excessive daytime sleepiness.
    • Associated with oxygen desaturation and nocturnal hypoxemia
    • Usual course is chronic.
  • System(s) affected: cardiovascular; nervous; pulmonary
  • Synonym(s): Pickwickian syndrome; sleep apnea syndrome; nocturnal upper airway occlusion
EPIDEMIOLOGY
Incidence
  • Predominant age: middle-aged men and women
  • Predominant sex: male > female (2:1)
Prevalence
  • Up to 4% in men, 2% in women
  • Prevalence is higher in obese/hypertensive patients.
ETIOLOGY AND PATHOPHYSIOLOGY
OSA occurs when the naso- or oropharynx collapses passively during inspiration. Anatomic and neuromuscular factors contribute to pharyngeal collapse.
  • Anatomic abnormalities such as increased soft tissue in the palate, tonsillar hypertrophy, macroglossia, and craniofacial abnormalities, predispose the airway to collapse by decreasing the area of the upper airway or increasing the pressure surrounding the airway.
  • During sleep, decreased muscle tone in the naso- or oropharynx contributes to airway obstruction and collapse.
  • Upper airway narrowing may be due to the following:
    • Obesity, redundant tissue in the soft palate
    • Enlarged tonsils/uvula
    • Low soft palate
    • Large/posteriorly located tongue
    • Craniofacial abnormalities
    • Neuromuscular disorders
    • Alcohol/sedative use before bedtime
RISK FACTORS
  • Obesity
  • Age >40 years
  • Alcohol/sedative intake before bedtime
  • Smoking
  • Nasal obstruction (due to polyps, rhinitis, or deviated septum)
  • Anatomic narrowing of nasopharynx (e.g., tonsillar hypertrophy, macroglossia, micrognathia, retrognathia, craniofacial abnormalities)
  • Acromegaly
  • Hypothyroidism
  • Neurologic syndromes (e.g., muscular dystrophy, cerebral palsy)
GENERAL PREVENTION
Weight control and avoidance of alcohol and sedatives at night can help to prevent airway collapse.
COMMONLY ASSOCIATED CONDITIONS
  • Common
    • Hypertension
    • Obesity
    • Daytime sleepiness
    • Metabolic syndrome
  • Rare
    • Cardiac arrhythmias
    • Cardiovascular disease
    • Congestive heart failure
    • Pulmonary hypertension
    • Nasal obstructive problems
image DIAGNOSIS
PHYSICAL EXAM
  • OSA is commonly associated with obesity. It is unlikely to be found in those with normal body weight who do not snore (1)[A].
  • Focused head and neck exam
    • Short neck with large circumference
    • Oropharynx
      • Narrowing of the lateral airway wall
      • Tonsillar hypertrophy
      • Macroglossia
      • Micrognathia/retrognathia
      • Soft palate edema
      • Long/thick uvula
      • High, arched hard palate
    • Nasopharynx
      • Deviated nasal septum
      • Poor nasal airflow
DIFFERENTIAL DIAGNOSIS
  • Other causes of EDS such as the following:
    • Narcolepsy
    • Idiopathic daytime hypersomnolence
    • Inadequate sleep time
    • Depressive episodes with EDS
    • Periodic limb movements disorder
  • Respiratory disorders with nocturnal awakenings such as the following:
    • Asthma
    • Chronic obstructive pulmonary disease
    • Congestive heart failure
  • Central sleep apnea
  • Sleep-related choking/laryngospasm
  • Gastroesophageal reflux
  • Sleep-associated seizures (temporal lobe epilepsy)
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • When clinically indicated
    • Thyroid-stimulating hormone to evaluate hypothyroidism
    • CBC to evaluate anemia and polycythemia, which can indicate nocturnal hypoxemia.
    • Fasting glucose in obesity to evaluate for diabetes
    • Rare: arterial blood gases to evaluate daytime hypercapnia
  • Cephalometric measurements from lateral head and neck radiographs aid in surgical treatment.
Diagnostic Procedures/Other
  • The gold standard for OSA is polysomnography (PSG), a nighttime sleep study (1)[A].
    • Demonstrates severity of hypoxemia, sleep disruption, and cardiac arrhythmias associated with OSA and elevated end-tidal CO2
    • Shows repetitive episodes of cessation/marked reduction in airflow despite continued respiratory efforts
    • Apneic episodes must last at least 10 seconds and occur 10 to 15 times per hour to be considered clinically significant.
    • Complete PSG is expensive, and health insurance may not cover the cost.
  • Multiple sleep latency testing is a diagnostic tool used to measure the time it takes from the start of a daytime nap period to the first signs of sleep (sleep latency). It provides an objective measurement of daytime sleepiness.
  • The apnea-hypopnea index (AHI) is defined as the total number of apneas and hypoapneas divided by the total sleep time.
    • Mild OSA: AHI = 5 to 15
    • Moderate OSA: AHI = 15 to 30
    • Severe OSA: AHI >30
  • Drugs that may alter the test results include benzodiazepines and other sedatives that can amplify the severity of apnea seen during the sleep study.
  • Early data suggest that home-based diagnosis using portable monitoring devices may be an alternative to laboratory-based PSG if the test is of sufficient duration (2)[B].
image TREATMENT
  • Lifestyle modification is the most frequently recommended treatment for mild to moderate OSA. This includes weight loss, exercise, and avoidance of alcohol, smoking, and sedatives, especially before bedtime. Weight loss has been shown to decrease the severity of symptoms in obese patients. Lifestyle modifications should be seen as adjunctive rather than curative therapy (3)[A], and a lack of improvement of symptoms with lifestyle modification should not preclude patients from receiving other therapy such as continuous positive airway pressure (CPAP).
  • If OSA is present only when supine, keep the patient off his/her back when sleeping (e.g., tennis ball worn on back of nightshirt or using a sleep position trainer) (4)[B].
  • P.973

  • The most effective therapy for mild, moderate, or severe OSA is CPAP (5)[B]. Treatment with CPAP uses a mask interface and a flow generator to prevent airway collapse, thus helping to prevent apnea, hypoxia, and sleep disturbance. Compared with inactive controls, CPAP significantly improves both objective (24-hour systolic and diastolic blood pressures) and subjective measures (Epworth Sleepiness Scale) in OSA patients with symptoms of daytime sleepiness (6)[A]. CPAP may also decrease the risk for atherosclerosis (7)[A] as well as improves insulin resistance in nondiabetic patients (8)[A]. Early data show that these benefits may not be seen in patients who do not have symptoms of daytime sleepiness (9)[B].
  • Several types of mask interfaces, including nasal masks, oral masks, and nasal pillows exist for CPAP therapy. Short-term data suggest that nasal pillows are the preferred interface in almost all patients. In patients with compliance difficulty, a different choice of interface may be appropriate (10)[A].
  • Oral appliances to treat OSA are available and often subjectively preferred by patients. Although oral appliances have been shown to improve symptoms compared with inactive controls, they are not as effective for reduction of respiratory disturbances as CPAP over short-term data. Treatment with oral appliances may be considered in patients who fail to comply with CPAP therapy (11)[A].
MEDICATION
Medications are yet to be proven effective in treating OSA (12)[A]. Further studies in this area are needed.
First Line
Some short-term data found fluticasone nasal spray, mirtazapine, physostigmine, and nasal lubricant of some benefit; longer-term studies needed.
ISSUES FOR REFERRAL
If sleep apnea is suspected, patient should be referred to a sleep specialist/neurologist for a sleep study evaluation.
SURGERY/OTHER PROCEDURES
Surgical corrections of the upper airway include alteration of the uvula and/or palate such as uvulopalatopharyngoplasty (UPPP), tracheostomy, and craniofacial surgery. Currently no evidence supports the use of surgery for the treatment of OSA (13)[A].
INPATIENT CONSIDERATIONS
On admission, patients should continue to use CPAP/dental devices if they do so at home. They should bring in their own appliance and know their CPAP settings.
image ONGOING CARE
Lifelong compliance with weight loss or CPAP is necessary for successful OSA treatment.
DIET
Overweight and obese patients should be encouraged to lose weight, and all patients must avoid weight gain. Weight loss alone could reduce symptoms of OSA (14)[A].
PATIENT EDUCATION
  • Weight loss and avoidance of alcohol and sedatives may reduce OSA symptoms particularly in severe cases (15)[A].
  • Significantly sleepy patients should not drive a motor vehicle/operate dangerous equipment.
PROGNOSIS
  • EDS is reduced dramatically with appropriate apnea control.
  • Lifelong compliance with weight loss or CPAP is necessary for effective treatment of OSA.
  • If untreated, OSA is progressive.
  • Significant morbidity and mortality with OSA usually are due to motor vehicle accidents or are secondary to cardiac complications, including arrhythmias, cardiac ischemia, and hypertension.
REFERENCES
1. Myers KA, Mrkobrada M, Simel DL. Does this patient have obstructive sleep apnea?: the rational clinical examination systematic review. JAMA. 2013;310(7):731-741.
2. Wittine LM, Olson EJ, Morgenthaler TI. Effect of recording duration on the diagnostic accuracy of out-of-center sleep testing for obstructive sleep apnea. Sleep. 2014;37(5):969-975.
3. Anandam A, Akinnusi M, Kufel T, et al. Effects of dietary weight loss on obstructive sleep apnea: a meta-analysis. Sleep Breath. 2013;17(1): 227-234.
4. van Maanen JP, de Vries N. Long-term effectiveness and compliance of positional therapy with the sleep position trainer in the treatment of positional obstructive sleep apnea syndrome. Sleep. 2014;37(7):1209-1215.
5. Weaver TE, Mancini C, Maislin G, et al. Continuous positive airway pressure treatment of sleepy patients with milder obstructive sleep apnea: results of the CPAP Apnea Trial North American Program (CATNAP) randomized clinical trial. Am J Respir Crit Care Med. 2012;186(7): 677-683.
6. Giles TL, Lasserson TJ, Smith BH, et al. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006;(3):CD001106.
7. Drager LF, Polotsky VY, Lorenzi-Filho G. Obstructive sleep apnea: an emerging risk factor for atherosclerosis. Chest. 2011;140(2):534-542.
8. Yang D, Liu Z, Yang H, et al. Effects of continuous positive airway pressure on glycemic control and insulin resistance in patients with obstructive sleep apnea: a meta-analysis. Sleep Breath. 2013;17(1):33-38.
9. Barbé F, Durán-Cantolla J, Sánchez-de-la-Torre M, et al. Effect of continuous positive airway pressure on the incidence of hypertension and cardiovascular events in nonsleepy patients with obstructive sleep apnea: a randomized controlled trial. JAMA. 2012;307(20):2161-2168.
10. Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(4):CD005308.
11. Lim J, Lasserson TJ, Fleetham J, et al. Oral appliances for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(1):CD004435.
12. Mason M, Welsh EJ, Smith I. Drug therapy for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2013;(5):CD003002.
13. Sundaram S, Bridgman SA, Lim J, et al. Surgery for obstructive sleep apnoea. Cochrane Database Syst Rev. 2005;(4):CD001004.
14. Shneerson J, Wright J. Lifestyle modification for obstructive sleep apnoea. Cochrane Database Syst Rev. 2001;(1):CD002875.
15. Mason M, Cates CJ, Smith I. Effects of opioid, hypnotic and sedating medications on sleepdisordered breathing in adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2015;(7):CD011090.
16. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3): e714-e755.
17. Osorio RS, Gumb T, Pirraglia E, et al. Sleep-disordered breathing advances cognitive decline in the elderly. Neurology. 2015;84(19):1964-1971.
Codes
&NA;
ICD10
G47.33 Obstructive sleep apnea (adult) (pediatric)
Clinical Pearls
&NA;
  • OSA is characterized by repetitive episodes of apnea at the pharynx, often terminating in a snort/gasp.
  • Laboratory PSG is the key to diagnosis.
  • CPAP is the most effective form of treatment for both mild to moderate and moderate to severe OSA.
  • Central sleep apnea may mimic OSA.