This issue of eMedRef provides information to clinicians on the pathophysiology, diagnosis, and therapeutics of obstructive sleep apnea-hypopnea syndrome

Delgado, Philip

Rubeiz, Helene

University of Missouri: MOspace

Obstructive Sleep Apnea Page 1 of 6    7.1.09 Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS) See Excessive Daytime Sleepiness See Insomnia See Obstructive Sleep Apnea (Peds)   Background 1. Definition  o Repetitive episodes of partial (hypopnea) or complete (apnea) airflow obstruction during sleep resulting   Gas exchange abnormalities  Sleep fragmentation  Daytime somnolence  Cardiovascular consequences 2. General info  o Apnea   Cessation of airflow for at least 10 s2   Associated with   Arousal   4% drop in SaO2 o Hypopnea   30-50% reduction in airflow for at least 10 s2   Associated with  o Arousal  o O2 desaturation o Upper airway resistance syndrome (UARS)   Recurrent arousals due to periods of increased airway resistance without overt apneas or hypopneas, leading to daytime hypersomnolence o Strong associations between OSAHS and   Cardiovascular disease  Motor vehicle accidents  Cognitive impairment  Endocrine abnormalities (glucose intolerance and insulin resistance) o Some goals of therapy of OSAHS include   Improving quality of life   Reducing risk of medical comorbidities  Pathophysiology 1. Pathology of disease  o OSAHS is characterized by narrowing/ collapse at various sites in the upper airway o Site of upper airway obstruction is the pharynx o Obesity exacerbates the narrowing due to increased adipose tissue in the neck o OSA seems to increase levels of leptin, in turn, makes it difficult for pts to lose weight4 2. Incidence, prevalence  o 2% F and 4% M between age of 30-60 o Prevalence increases with age but plateaus after age 65 Obstructive Sleep Apnea Page 2 of 6    7.1.09 o Increasing incidence due to diagnostic awareness and escalating obesity o Prevalence of OSA without daytime sleepiness   25% middle age males  9% middle age females 3. Risk factors  o Body habitus   Body mass index (BMI) >28 kg/sq m  Neck circumference > 40 cm  Central body fat distribution o Craniofacial and upper airway abnormalities   Enlarged tonsils and adenoids  Abnormalities of mandibular or maxillary size and position  Narrowed nasal cavities  Macroglossia  Low-lying soft palate  Enlarged uvula3  Anatomical imbalance between tongue size and craniofacial dimensions4  o Genetic / family Hx   Heritability found in 30-35% of cases6  o OSAHS may be aggravated by   Nighttime alcohol ingestion  Sedatives  Supine posture  Nasal congestion  Allergies   Smoking6  4. Morbidity/mortality  o Increased incidence of co-morbid conditions   Hypertension, CAD, MI, CHF, stroke  Risk of stroke nearly doubled for men w/sleep apnea   DM 2 and insulin resistance are present in 30% and 20% of OSA pts, respectively5   Oxidative stress by producing radicals can cause vascular inflammation and atherosclerosis which in turn play important role in OSA5   BMI highly associated with oxidative stress5   Diagnostics 1. Questionnaires, physical exam, and clinical prediction rules estimate pretest probability of OSAHS, but are not specific enough to make dx  2. History  o Habitual snoring o Nocturnal snorting o Gasping o Witnessed apneas o Fatigue, daytime sleepiness, MVAs, personality changes, irritability, depression o Morning or nocturnal headaches   Obstructive Sleep Apnea Page 3 of 6    7.1.09 3. Physical exam  o Pay special attention to body habitus and upper airway   Retrognathia  Macroglossia  Low-lying soft palate  Tonsillar hypertrophy  Nasal septal deviation  Size and asymmetry of nares o Chronic leg edema  4. Diagnostic testing  o Polysomnography (PSG) (SOR:A)2   Recording of   Sleep architecture  Airflow and ventilatory effort  Oxygen saturation  EKG  Limb movement  Body position  EEG  Electrooculogram  PSG documents adequacy of sleep and indicates whether other etiologies are present, such as narcolepsy or PLMD  o Apnea-hypopnea index (AHI) (SOR:C)2   Number of apneas and hypopneas per hour of sleep  OSAHS   AHI of 5 or greater combined with daytime somnolence  Severity   Mild with AHI 5-14  Moderate with AHI 15-30   Severe with AHI >30 o CPAP titration study (SOR:A)2   To determine the optimal pressure that eliminates snoring and apneas-hypopneas  Done when diagnosis of OSAHS is established  Can be done as a split-night or second full night study   Differential Diagnosis 1. Upper airway resistance syndrome (UARS) 2. Central sleep apnea 3. Periodic limb movement disorder of sleep 4. Narcolepsy 5. Idiopathic hypersomnia   Therapeutics 1. Conservative measures  o Weight loss (SOR:B)9,10,11  o Alcohol and sedative avoidance o Avoiding the supine position in the case of positional OSAHS o Good sleep hygiene Obstructive Sleep Apnea Page 4 of 6    7.1.09 2. CPAP  o Treatment of choice for most patients (SOR:B)12,13,14  o Primary treatment target is hypersomnolence o Tolerability of CPAP is challenging   Compliance as low as 40%  Can be improved with heated humidification, machines that ramp up slowly, and bilevel pressure machines o Complications   Epistaxis  Rhinorrhea  Nasal dryness  Congestion  Facial abrasions  Conjunctivitis o Uncertain benefit for those with mild disease 3. Oral appliances  o Move the tongue or mandible forward o Inconsistent results o More for patients with mild to moderate OSA7  4. Surgery  o Uvulopalatopharyngoplasty (UPPP) (SOR:2C)2   Mixed results  Success rate is approximately 50%  Long-term success rate falls to 35% after 4 years7   Less effective in patients with BMI > 30 and in patients with severe disease  Associated with significant pain post-op o Nasal surgery (SOR:C)7  o Maxillomandibular advancement (SOR:C)  May be effective in patients with anatomical abnormalities leading to OSAHS o Temperature controlled radiofrequency ablation (SOR:C)2   Volume reduction of tongue and soft palate  20% success rate7  o Tracheostomy (SOR:C)  Last-resort measure  In life-threatening situations o Bariatric surgery (SOR:C)7   Effective in the treatment of OSAHS caused by obesity  Must meet BMI requirements of 40 without existing medical conditions and 35 with co-existing medical conditions7  5. Medications  o Modafinil (SOR:B)7   Wake promoting that can be used at the same time as other treatments in a complementary manner7   Follow-Up 1. Every 6-12 mo 2. CPAP machine needs maintenance q 6-12 mo Obstructive Sleep Apnea Page 5 of 6    7.1.09  Prognosis 1. Varies with degree of obstruction and patient compliance with treatment 2. Higher mortality15  3. Use more medical resources15  4. 3 to 6 fold increased risk of all cause mortality15  5. Vehicle accidents more common among patient with OSA16  6. Increases inattention and fatigue, consequently limiting daily function, also exacerbates already existing cognitive deficits16   Prevention 1. The most preventable factor is weight gain 2. Avoid muscle relaxants 3. Avoid alcohol beverages before sleeping  Patient Education 1. www.sleepapnea.org 2. http://familydoctor.org/online/famdocen/home/articles/212.html  References 1. Victor LD: Treatment of Obstructive Sleep Apnea in Primary Care. Am Fam Physician 2004; 69(3):561-68. 2. Olson EJ, et al: Obstructive Sleep Apnea-Hypopnea Syndrome. Mayo Clin Proc 2003;78:1545-1552. 3. Young T, et al: Risk Factors for Obstructive sleep apnea in Adults. JAMA 2004; 291(16): 2013-16 4. Isono S. Obstructive sleep apnea of obese adults: pathophysiology andperioperative airway management. Anesthesiology. 2009 Apr;110(4):908-21. Review. PubMed PMID: 19293689 5. Lavie L. Oxidative stress--a unifying paradigm in obstructive sleep apnea andcomorbidities. Prog Cardiovasc Dis. 2009 Jan-Feb;51(4):303-12. Review. PubMed PMID: 19110132. 6. Al Lawati NM, Patel SR, Ayas NT. Epidemiology, risk factors, and consequencesof obstructive sleep apnea and short sleep duration. Prog Cardiovasc Dis. 2009 Jan-Feb;51(4):285-93. Review. PubMed PMID: 19110130. 7. Fleisher KE, Krieger AC. Current trends in the treatment of obstructive sleep apnea. J Oral Maxillofac Surg. 2007 Oct;65(10):2056-68. Review. PubMed PMID:17884538 8. Rubins JB, Kunisaki KM. Contemporary issues in the diagnosis and treatment of obstructive sleep apnea. Postgrad Med. 2008 Jul;120(2):46-52. Review. PubMed PMID: 18654068. 9. Browman, CP, Sampson, MG, Yolles, SF, et al. Obstructive sleep apnea and body weight. Chest 1984; 85:435.  10. Smith, PL, Gold, AR, Meyers, DA, et al. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985; 103:850.  11. Wittels, EH, Thompson, S. Obstructive sleep apnea and obesity. Otolaryngol Clin North Am 1990; 23:751. Obstructive Sleep Apnea Page 6 of 6    7.1.09 12. Sullivan, CE, Berthon-Jones, M, Issa, FG, Eves, L. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. Lancet 1981; 1:862.  13. Hirshkowitz, M, Sharafkhaneh, A. Positive airway pressure therapy of OSA. Semin Respir Crit Care Med 2005; 26:68.  14. Waldhorn, RE, Herrick, TW, Nguyen, MC, et al. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest 1990; 97:33. 15. Marshall, NS, Wong, KK, Liu, PY, et al. Sleep apnea as an independent risk factor for all-cause mortality: the Busselton Health Study. Sleep 2008; 31:1079. 16. George, CF. Sleep apnea, alertness, and motor vehicle crashes. Am J Respir Crit Care Med 2007; 176:954  Evidence-Based Inquiry  1. Is surgery effective for reducing symptoms in adult patients with obstructive sleep apnea? 2. Is sleep apnea associated with increased risk of stroke? 3. What is the differential diagnosis of chronic leg edema in primary care? 4. Sleep apnea in adults: How accurate is clinical prediction?   Authors:  Philip Delgado, MD, & Helene Rubeiz, MD, Kaiser Permanete Medical Center FPRP, Riverside, CA  Editor:  Vince WinklerPrins, MD, Georgetown University-Providence Hospital, Washington DC 

Obstructive sleep apnea-hypopnea syndrome (OSAHS)

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