1

Introduction

Obstructive sleep apnea syndrome (OSAS), upper airway resistance syndrome, and snoring are collectively referred to as sleep-related breathing disorders (SRBDs). SRBD involve repeated partial or complete obstructions of the upper airway during sleep, and the etiology is multifactorial with derangements associated with respiratory arousal threshold, airway critical closing pressure, muscle tone, and loop gain. Loss of airway patency can be central, obstructive, or mixed in origin. Repeated loss of airway patency and associated oxygen desaturation contribute to alarming neurocognitive, cardiovascular, and social consequences.

Tracheostomy was the first surgical modality used to treat severe OSAS. It is effective, but not readily accepted due to its morbidity. Sullivan et al. reported the application of nasal continuous positive airway pressure (CPAP) to maintain upper airway patency, and it has remained the first-line treatment for OSAS. Yet a subset of patients struggle with CPAP therapy and may seek other medical treatments, including oral appliances. Some are referred to sleep surgeons.

A two-phase algorithm (Powell–Riley protocol) to target sites of obstruction (nasal cavity/nasopharynx, oropharynx, and hypopharynx) was originally created in the early 1990s to minimize surgical interventions while alleviating OSAS. Recognizing that OSAS is associated with multiple levels of airway collapse is essential to achieving effective outcome. Sleep surgeons must be willing to treat all levels of obstruction in an organized and safe manner. With more than two decades of clinical experience and outcomes data with the Powell–Riley protocol, we update this chapter with emphasis in a few key areas:

• 1.
  

  When can Phase 2 precede Phase 1?

  
  
• 2.
  

  How can the precision and safety of skeletal procedures be improved?

  
  
• 3.
  

  How is relapse handled after Phase 1 and Phase 2 operations?

2

Rationale for Surgical Treatment

Surgical treatment of upper airway collapsibility during sleep is designed to minimize neurocognitive and pathophysiologic derangements associated with OSAS. Patients with excessive daytime sleepiness (EDS) may also experience emotional and social problems. EDS predisposes patients to automobile or occupational accidents. Morbidity is seen from the sequelae of hypertension, congestive heart failure, myocardial infarction, cardiac arrhythmias, and cerebrovascular disease. Surgery is aimed at mitigating hypoxemia and normalizing respiratory events and sleep architecture.

3

Surgical Indications

Indications for surgery are listed in Box 17.1 . For patients whose Apnea/Hypopnea Index (AHI) is less than 20, surgical treatment can still be an option. Surgery is appropriate if patients have EDS resulting in impaired cognition or specific systemic comorbidities (hypertension, stroke, ischemic heart disease). Consideration may be given to obtaining a multiple sleep latency test or the maintenance of wakefulness test to determine another etiology of EDS for patients whose symptoms are not ameliorated with CPAP therapy. Other factors that predict poor surgical outcomes and render a patient unsuitable for surgery are listed in Box 17.2 .

4

Patient Selection

Surgical phenotyping is vital to achieving successful outcome. Diagnostic data, including head and neck examination, polysomnography (PSG), fiber-optic nasopharyngoscopy, drug-induced sedation endoscopy (DISE), and imaging, are analyzed in aggregate to characterize the compromised airway. No single diagnostic examination is adequate. A thorough assessment requires evaluating the patient for multilevel, dynamic airway obstruction to direct a safe, organized surgical protocol that more thoroughly addresses patterns and sites of airway obstruction during sleep.

An attended full-night PSG is considered the gold standard for the diagnosis of OSAS and characterization of disease severity. Although in-lab PSG is now often replaced with a home sleep test, it should be noted that ambulatory studies may underestimate the severity of disease and disregard changes to sleep architecture. Sleep surgeons have mostly focused on the AHI and the oxygen desaturation nadir to determine OSAS disease severity. Interpretation of the AHI, however, must keep in consideration the various definitions of hypopnea that have evolved. A preoperative sleep study scored using different hypopnea criteria than a postoperative study would constitute a significant confounder to the evaluation of treatment results. The lowest oxygen nadir, and more preferably, the Oxygen Desaturation Index, are objective measures that have been shown to correlate more strongly with medical sequelae of untreated OSAS. In addition, sleep architecture should be examined. Restoration of sleep architecture after surgical intervention may be associated with the patient’s subjective assessment of “better sleep.”

During the physical examination, specific attention is focused on potential sites of upper airway obstruction, including the nose, palate, lateral pharyngeal wall, and base of tongue.

Nasal obstruction occurring as a result of septal deviation, turbinate hypertrophy, or sinonasal masses is not always identified with anterior rhinoscopy alone. We have found that 26% of patients who are intolerant of CPAP have nasal obstruction associated with posterior septal deviation that was only recognized by nasopharyngoscopy.

Examination of the oropharyngeal and hypopharyngeal regions includes descriptions of the palate (both soft and hard palate), lateral pharyngeal wall, tonsils, and tongue base. Friedman et al. and Mallampati have proposed standardized grading systems to describe the degree of obstruction associated with these structures.

With fiber-optic examination, the upper airway is examined at rest and during negative pressure breathing maneuver (Mueller maneuver). Mueller maneuver utilizes negative intraluminal pressure to characterize airway collapse.

Fiber-optic examination of the upper airway under sedation (namely DISE) has become an area of active investigation. The success of upper airway stimulation (UAS), as an example, depends on identifying suitable candidates using DISE. We have performed individual patient airway comparisons before and after maxillomandibular advancement (MMA) using DISE. We found that MMA most effectively addresses collapse of the lateral pharyngeal wall and circumferential collapse of the velum.

We had used the lateral cephalogram to assess the length of the soft palate, posterior airway space, hyoid position, and maxillofacial proportions. The lateral cephalogram remains a cost-effective radiographic study of the facial skeleton and soft tissues of the upper airway. Studies have shown that the cephalogram compares favorably to three-dimensional volumetric computed tomographic scans of the upper airway. Nevertheless, most forms of imaging share the limitation of being performed during the awake state. We recently used sleep magnetic resonance imaging to examine dynamic airway collapse during natural sleep, while taking into account cephalometric measurements. We showed that severe lateral pharyngeal wall collapse during sleep and low hyoid bone position are strongly associated with severe OSAS. Severe lateral pharyngeal wall collapse, as we have shown via DISE, is effectively addressed with MMA. The combination of dynamic airway and static imaging studies allows greater specificity in patient phenotyping.