CC
A 46-year-old White male is referred to your office by his primary care physician for evaluation and management of obstructive sleep apnea syndrome (OSAS). (The reported prevalence of obstructive sleep apnea [OSA] varies widely in different studies, with some showing rates of 15%–30% in males and 10%–15% in females in North America. The risk increases significantly after age 65 years and in up to 50% of nursing home patients.)
HPI
The patient presents complaining of a long history of snoring and restless sleeping. (Sleep-disordered breathing includes hypopnea, apnea, and respiratory effort–related arousals.) His wife of 20 years reports that he snores loudly; frequently stops breathing (apnea); and makes grunting, gasping, and choking sounds. (Bedroom partners are often the first to recognize the problem.) The patient has noticed difficulty concentrating at work (OSAS decreases cognitive function) and difficulty staying awake during the day (daytime somnolence is a hallmark of OSAS). The patient scored above 10 on the Epworth Sleepiness Scale. (This scale is a questionnaire that subjectively assesses the level of daytime somnolence. Other screening tools include the Berlin questionnaire, the American Society of Anesthesiology checklist, and the STOP-BANG questionnaire.) He also complains of morning dry mouth (nasal obstruction or congestion leads to mouth breathing, resulting in morning dry mouth), morning headaches, nocturia, and night sweats (common symptoms associated with OSAS). His primary care physician referred him to a sleep center for polysomnography (PSG) (the gold standard in diagnosis of OSAS); his respiratory disturbance index (RDI) score was 51 (see Discussion later in this chapter).
PMHX/PDHX/medications/allergies/SH/FH
The patient’s past medical history is significant for hypertension (there is a direct relationship between OSAS and hypertension, resulting in cardiovascular morbidity), which is controlled with a beta-blocker and a diuretic. His past surgical history is significant for tonsillectomy and adenoidectomy as a child. (Hypertrophic tonsils and adenoids increase the risk of OSAS in children, but this is more uncommon in adults.)
He admits to drinking two or three beers a day (alcohol consumption can blunt the ventilatory response to hypercarbia and thereby worsen OSA) and occasional smoking (smoking can cause inflammation and edema of the upper airway mucosa, which increases airway resistance).
He is a sales manager and works more than 8 hours a day. (Overworking may contribute to lack of sleep, sleep-disordered breathing, and daytime somnolence.) More recently, his coworkers have noticed that he is falling asleep at his desk. (Daytime somnolence also contributes to decreased productivity and can be particularly dangerous for individuals operating machinery or driving motor vehicles.)
His father had similar signs and symptoms of OSAS that were untreated. (A positive family history is commonly seen because of various genetic and environmental factors.) His father died at the age of 60 years of a myocardial infarction. (Untreated OSAS significantly increases the risk of cardiovascular disease and cerebrovascular accident resulting in death.)
Examination
Vital signs. his blood pressure is 150/95 mm Hg (stage II hypertension), heart rate is 75 bpm, respirations are 16 breaths per minute, and temperature is 37.6°C.
General. The patient is a moderately obese male in no apparent distress. (Obesity is an important risk factor for OSAS.) His weight is 225 lb, his body mass index is 32 kg/m 2 (class 1 obesity), and his waist-to-hip ratio is 1.2. (Ideal is <0.9 in males and <0.85 in females.)
Maxillofacial. He displays mild retrognathia. (Retrognathia is a risk factor for OSAS.) His neck measures 18 inches. (A neck circumference of ≥17 inches in males and ≥16 inches in females increases the risk of OSAS and may be the best predictor of RDI in males.)
Endonasal. The nares are equally patent bilaterally. There is no evidence of internal nasal valve collapse. The result of the Cottle test is negative. (A positive Cottle test result may indicate internal or external nasal valve collapse.) The nasal septum appears midline, and the inferior turbinates appear normal. (A deviated nasal septum or turbinate hypertrophy may cause nasal obstruction.) There are no nasal polyps.
Intraoral. His occlusion is class II division II. The oral tongue is normal in size. The soft palate and uvula are long and not completely visible (Mallampati class III airway). The tonsils are not present. There are no tori. (Enlarged or redundant oral structures may cause oropharyngeal obstruction.)
Endoscopic nasopharyngoscopy in the supine position. Nasopharyngoscopy can be performed in the clinic and provides information on the presence and location of the obstruction, which cannot be evaluated with PSG. The nasopharynx is clear of any obstruction. The retropalatal airway space is narrow and has redundant soft tissue, and the space completely obliterates with Müller’s maneuver (forced inspiratory effort against a closed mouth and nose). The retroglossal oropharynx and hypopharynx are narrow and partially obliterated (75%) with Müller’s maneuver. Collapse of the lateral pharyngeal walls appears to contribute significantly to the airway collapse. There is no pathology of the endolarynx, and the vocal cords are functional.
Drug-induced sleep endoscopy (DISE). Although clinical nasopharyngoscopy is limited in that it is performed on an awake patient, DISE has the advantage of being performed while the patient is sleeping via intravenous conscious sedation. Nasopharyngoscopy is then performed, allowing the practitioner to evaluate multilevel pharyngeal collapse during sleep. Techniques and scoring are nonstandardized, but the VOTE classification is a useful tool for reporting results. This acronym indicates the levels evaluated during the procedure: velum, oropharynx, tongue base, and epiglottis. The dimensions of collapse (anteroposterior vs lateral vs concentric) and degree of obstruction at each level are reported.
Imaging
Previously, the lateral cephalometric radiograph was the initial diagnostic study of choice. It provides an excellent overview of the craniofacial skeleton for identifying and quantifying any skeletal deformities, including the position of the maxilla and mandible in relation to the cranial base, and the soft tissue anatomy. However, in modern oral and maxillofacial surgery offices, cone-beam computed tomography (CBCT) scanners are ubiquitous, and their scans provide views of the airway in three dimensions. The ability to view the airway in a transverse plane can reveal constrictions not appreciable on lateral films. Three-dimensional (3D) renderings display the actual shape of the airway, and imaging software can compute its total volume. In addition, traditional lateral cephalometric views can be generated from CBCT scans to evaluate traditional measurements: the distance from the hyoid bone to the mandibular plane (normal, 11–19 mm), the posterior airway space (normal, 10–16 mm), the length of the soft palate (normal, 34–40 mm), and the thickness of the soft palate (normal, 6–10 mm). Hospital-grade CT and magnetic resonance imaging also provide 3D and volumetric information on the upper airway and surrounding soft tissues, and research is continuing to develop the clinical applications of these advanced imaging modalities.
In the current patient, the CBCT showed a hypoplastic mandible causing a class II skeletal discrepancy, a retropositioned pogonion, a posterior airway space of 6 mm (as viewed on the lateral cephalometric view from the CBCT), a long and thick soft palate, and a normal hyoid–to–mandibular plane distance.
Labs
No laboratory values are needed in the initial workup of OSAS. Thyroid hormone or thyroid-stimulating hormone levels are routinely ordered at some sleep centers but may not be warranted. Other laboratory studies, including preoperative laboratory studies, are ordered based on the patient’s medical history.
An electrocardiogram is required for all patients with OSAS. OSAS is considered a cardiac risk factor. Hypertension and obesity are additional cardiac risk factors that are commonly seen in patients with OSAS.
In the current patient, the complete blood count and electrocardiogram (ECG) were within normal limits.
Polysomnography
Polysomnography (“sleep study”) is the gold standard for diagnosing sleep-related breathing disorders. The electroencephalogram, ECG, electro-oculogram, electromyogram, heart rate, oxygen saturation, airflow, and respiratory efforts are monitored and recorded during sleep. The numbers of apneas and hypopneas are calculated. The definitions of apnea and hypopnea have been altered over time, and some sources still disagree with them. The current American Academy of Sleep Medicine’s definitions are as follows: apnea is defined as a 90% or greater reduction in airflow for 10 seconds or more, and hypopnea is defined as a 30% or greater decrease in airflow associated with a 3% or greater reduction in the oxygen saturation or an arousal. Apneas and hypopneas are categorized as obstructive (no airflow despite inspiratory effort), central (no airflow and no inspiratory effort), or mixed (both central and obstructive component). The average number of apneas plus hypopneas per hour is referred to as the apnea-hypopnea index (AHI) and is used for scoring sleep apnea as either mild (AHI 5–14), moderate (AHI 15–29), or severe (AHI ≥30). This scale is useful for both diagnosis and in monitoring a patient’s response to treatment.
In addition, respiratory event–related arousals (RERAs) are also sometimes measured. RERAs are events that do not meet the definition for apneas or hypopneas but still produce respiratory symptoms ending in arousals. When RERAs are averaged in with apneas and hypopneas, the result is the RDI.
In the current patient, the PSG showed an AHI of 51. All episodes of apnea were obstructive in nature. The lowest oxygen saturation was 81%. There were no cardiac arrhythmias. (Prolonged hypoxemia can precipitate premature ventricular contractions or sinus bradycardia.)
Assessment
A 46-year-old obese male with severe OSAS (also termed obstructive sleep apnea-hypopnea syndrome) likely caused by obstruction at the level of the oropharynx (retropalatal and retroglossal) and hypopharynx (Fujita type II obstruction).
Upper airway obstruction can occur at different levels (nasopharynx, oropharynx, and hypopharynx). The Fujita classification divides the airway in three categories based on the anatomic location of the obstruction ( Table 96.1 ). When OSA is associated with daytime somnolence, OSAS is diagnosed.
