– CAMILO REYES GELVES, MD

Dr. Camilo Reyes 2016

Dr. Camilo Reyes Gelves

Obstructive sleep apnea (OSA) is a state-dependent sleep disorder that involves complete interruption or significant decrease in airflow in the presence of a breathing effort caused by repetitive upper airway collapse which results in oxygen desaturation and arousals. This is different from central sleep apnea, where the autonomic brainstem stimulus is absent to evoke a breathing effort. While almost all OSA patients snore, not every patient who snores has OSA. Sleep-related relaxation of upper airway dilator muscles causes vibrations of the soft tissues which is translated into snoring. Consequences of untreated OSA include adverse cardiovascular and metabolic outcomes, decline in quality of life, and neurocognitive impairment. Moderate-to-severe OSA, defined as an apnea–hypopnea index (AHI) score of 15 or more events per hour, is an independent risk factor for insulin resistance, dyslipidemia, vascular disease, and death1–6. Furthermore, the presence of OSA has been associated with increased adjusted risk for hypertension (HT) development and its treatment is associated with a lower risk for HT7. While OSA in children is a well described disorder related to behavior and attention deficit disorders, the purpose of this review pertains to the definition and treatment of OSA in the adult population.

Symptoms

OSA may not be perceived by a patient as symptoms can sometimes be vague. Snoring and some apnea episodes are usually witnessed by the patients’ partner. Patients usually have nocturnal (snoring, apneas, choking sensation, arousal and awakening) and daytime symptoms (morning headaches, nonrestorative sleep, fatigue, cognitive deficits, mood changes, decreased libido and hypertension among others). The Epworth sleepiness scale is an eight item, 4-point scale (0-3) questionnaire that screens patients for daytime drowsiness. A score higher than 11 represent an increased level of daytime sleepiness.

Diagnosis

While there are several anatomic findings that can predispose a patient to have OSA (BMI>30kg/m2, enlarged neck circumference, >43cm in men and >37cm in women), the gold standard for diagnosis is an overnight sleep study (polysomnography). Sleep stages, heart rate, oxygenation, breathing effort and pattern are recorded. An AHI greater than 5 is considered sleep apnea. Patients should undergo a comprehensive Otolaryngologic evaluation; medical history, physical examination and sleep study results must be part of this evaluation. As OSA is a state-dependent disease, at AUMC’s Department of Otolaryngology-Head and Neck Surgery, our patients also undergo a Drug Induced Sleep Endoscopy (DISE) which is the closest resemblance to Non-REM sleep. DISE allows us to dynamically assess different anatomical areas, the effect of mandibular thrust and other maneuvers while the patient is asleep, which in turn allows us to individually evaluate the patient’s medical and surgical needs.

Treatment

OSA treatment depends on the patient’s severity of sleep-disordered breathing. It is fundamental to consider patient preferences and expectations. There are some lifestyle modifications that can aid in OSA treatment: weight loss, smoking cessation, avoiding alcohol and sleep deprivation. Continuous positive airway pressure (CPAP) either delivered by a nasal or orofacial mask is the first-line of therapy for moderate-severe OSA. CPAP delivers continuous pressurized air to the patient’s airway preventing its collapse; this is different than Bilevel-PAP (Bi-PAP) and Auto-PAP (APAP). Bi-PAP has an inspiration and expiration pressure easing the patients breathing cycle at night, whereas APAP uses algorithms that sense breathing changes and adjusts itself to the best pressure setting at any time of the night. A substantial portion of patients with OSA seek alternatives to CPAP8. There are specific procedures for specific patients. This is where DISE comes in. Patients should be individually and properly screened and matched for the ideal surgical procedure.

Surgery

Surgical intervention for OSA includes, but is not limited to, the following: septoplasty and inferior turbinate reduction which usually aid patients in CPAP adaptation; palatal radiofrequency, palatal (pillar) implants, uvulopalatopharyngoplasty (UPPP), expansion sphincter pharyngoplasty, transpalatal advancement pharyngoplasty, volumetric base of tongue reduction or advancement, hyoid suspension, maxillo-mandibular advancement and the hypoglossal nerve stimulator (HNS). The HNS is a novel therapeutic approach that uses an implantable neuromodulator that provides multilevel titratable upper airway improvement by evoking a functional contraction of the tongue muscles. The HNS provides retropalatal, retrolingual and anterior hyoid displacement9 and is the only procedure that requires a previous DISE evaluation for candidacy determination. The multicenter prospective Stimulation Therapy for Apnea Reduction (STAR) Trial demonstrated high subjective adherence rates, significant improvements in snoring, daytime alertness, and sleep-related quality of life that were maintained at 2- and 3-year follow-up periods10,11.

Conclusion

OSA is the most common sleep breathing disorder, however, only approximately 10% of patients who suffer from OSA seek treatment. It requires a multidisciplinary evaluation for diagnosis and treatment. Untreated OSA can have significant negative impact on a patient’s health and quality of life. Several medical and surgical techniques are available for OSA treatment which should be individually discussed with each patient.

References

1. Punjabi NM, Shahar E, Redline S, et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. Am J Epidemiol. 2004;160(6):521-530. doi:10.1093/aje/kwh261

2. Seicean S, Kirchner HL, Gottlieb DJ, et al. Sleep-disordered breathing and impaired glucose metabolism in normal-weight and overweight/ obese individuals: the Sleep Heart Health Study. Diabetes Care. 2008;31(5):1001-1006. doi:10.2337/dc07-2003

3. Punjabi NM, Caffo BS, Goodwin JL, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med. 2009;6(8):e1000132. doi:10.1371/journal.pmed.1000132

4. Redline S, Yenokyan G, Gottlieb DJ, et al. Obstructive sleep apnea-hypopnea and incident stroke: the sleep heart health study. Am J Respir Crit Care Med. 2010;182(2):269-277. doi:10.1164/rccm.200911-1746OC

5. Gottlieb DJ, Yenokyan G, Newman AB, et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation. 2010;122(4):352-360. doi:10.1161/CIRCULATIONAHA.109.901801

6. Durgan DJ, Bryan RM. Cerebrovascular consequences of obstructive sleep apnea. J Am Heart Assoc. 2012;1(4):e000091. doi:10.1161/ JAHA.111.000091

7. Marin JM, Agusti A, Villar I, et al. Association Between Treated and Untreated Obstructive Sleep Apnea and Risk of Hypertension. JAMA. 2012;307(20):2169-2176. doi:10.1001/jama.2012.3418

8. Sin DD, Mayers I, Man GC, Pawluk L. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. – PubMed – NCBI. Chest. 2002;2:430-435.

9. Vanderveken OM, Maurer JT, Hohenhorst W, et al. Evaluation of drug-induced sleep endoscopy as a patient selection tool for implanted upper airway stimulation for obstructive sleep apnea. J Clin Sleep Med JCSM Off Publ Am Acad Sleep Med. 2013;9(5):433-438. doi:10.5664/jcsm.2658

10. Soose RJ, Woodson BT, Gillespie MB, et al. Upper Airway Stimulation for Obstructive Sleep Apnea: Self-Reported Outcomes at 24 Months. J Clin Sleep Med JCSM Off Publ Am Acad Sleep Med. 2016;12(1):43-48. doi:10.5664/jcsm.5390

11. Woodson BT, Soose RJ, Gillespie MB, et al. Three-Year Outcomes of Cranial Nerve Stimulation for Obstructive Sleep Apnea: The STAR Trial. Otolaryngol–Head Neck Surg Off J Am Acad Otolaryngol-Head Neck Surg. 2016;154(1):181-188. doi:10.1177/0194599815616618