Obstructive Sleep Apnea-Hypopnea Syndrome

GENERAL PRINCIPLES

Definition

Obstructive sleep apnea (OSA) is a disorder in which patients experience apneas or hypopneas because of upper airway narrowing. When it is associated with excessive daytime somnolence, it is referred to as obstructive sleep apnea-hypopnea syndrome (OSAHS).

Classification

• Apneas represent complete cessation of airflow.

๎ Obstructive events are associated with continued respiratory effort.

๎ Central events are associated with no respiratory effort.

• Hypopneas represent diminished airflow associated with at least a 3%-4% oxygen desaturation.

• Respiratory effort-related arousals (RERAs) represent changes in airflow that lead to an arousal, but do not meet criteria for an apnea or hypopnea.

• All respiratory events must last at least 10 seconds to be counted.

• Apnea-hypopnea index (AHI) is the number of apneas and hypopneas per hour of sleep.

• Respiratory disturbance index (RDI) is the number of apneas, hypopneas, and RERAs per hour of sleep.

Epidemiology

• The prevalence of OSAHS in the general population is estimated to be about 4%, with men being twice as likely as women to be affected. ³⁴

• Obesity is a significant risk factor for OSA. ³⁴

• Given the significant increase in the prevalence of obesity since the original epidemiological studies on OSA were performed, it is estimated that the current prevalence of moderate OSA as defined by an AHI > 15 is 13% in men and 6% in women. ³⁵

Etiology

• OSA: Narrowing of the upper airway because of excessive soft-tissue or structural abnormalities.

• Central sleep apnea: Disturbance of central control of respiration during sleep.

Pathophysiology

OSA occurs because of narrowing of the upper airway, which results in diminished airflow or cessation of airflow leading to arousals that fragment sleep.

Risk Factors

Risk factors for OSA include obesity (body mass index [BMI] > 30 kg/m²), large neck circumference (>17 in for men and >16 in for women), increased soft tissue of the posterior oropharynx (enlarged tonsils, macroglossia, or elongated uvula), and abnormal jaw structure (micrognathia or retrognathia). Patients with comorbid conditions such as congestive heart failure, coronary artery disease, atrial fibrillation (AFib), difficult-to-control hypertension, and diabetes are also more likely to have OSA. ³²

Prevention

• Weight loss

• Avoiding sedatives such as hypnotic medications or alcohol

Associated Conditions

• Cardiovascular disease, including systemic hypertension, heart failure, arrhythmia, myocardial infarction, and stroke. ³⁶ OSA has been established as an independent risk factor for hypertension. ³⁷

• Increased risk of death in moderate-to-severe OSA, mainly because of cardiovascular events. ^{38, 39}

• Increased prevalence of diabetes has been noted in patients with OSAHS, independent of the effect of obesity. ⁴⁰

• There is approximately a 2.5-fold increased risk of motor vehicle accidents (MVA) in patients with OSA when compared with those without OSA. However, compliance with continuous positive airway pressure (CPAP) treatment can significantly reduce the risk of MVA in patients with OSA. ⁴¹

DIAGNOSIS

Clinical Presentation

HISTORY

• Habitual loud snoring is the most common symptom of OSA, although not all people who snore have this syndrome. Patients with OSA may experience snore arousals along with a sensation of gasping or choking.

• Excessive daytime sleepiness (hypersomnolence) is a classic symptom of OSAHS (Table 10-4). Patients may describe falling asleep while driving or having difficulty concentrating at work.

TABLE 10-4

SYMPTOMS ASSOCIATED WITH OBSTRUCTIVE SLEEP APNEA-HYPO PNEA SYNDROME

Excessive daytime sleepiness

Snoring

Nocturnal arousals

Nocturnal apneas

Nocturnal gasping, grunting, and choking

Nocturia

Enuresis

Awakening without feeling refreshed

Morning headaches

Impaired memory and concentration

Irritability and depression

Impotence

• Patients may also complain of personality changes, intellectual deterioration, morning headaches, nocturnal angina, loss of libido, and chronic fatigue.

PHYSICAL EXAMINATION

• All patients should have a thorough nose and throat examination to detect sources of upper airway obstruction.

• Increased severity of OSA has been associated with a higher Mallampati class (Table 10-5). ⁴²

TABLE 10-5

Mallampati airway classification

Class Visible Structures With Mouth Maximally Opened and Tongue Protruded

I Hard palate, soft palate, uvula, tonsillar pillars

II Hard palate, soft palate, uvula

III Hard palate, soft palate, base of uvula

IV Hard palate

Adapted from Mallampati SR, Gatt SP, Gugino LD, et al. A clinical sign to predict difficult tracheal intubation: a prospective study. CanAnaesth Soc J. 1985;32:429-434.

DIAGNOSTIC CRITERIA

A polysomnogram (PSG) demonstrating obstructive events with an AHI or RDI > 5 is diagnostic of OSA. If the RDI is between 5 and 15, a patient will qualify for positive airway pressure (PAP) if there is a comorbid condition such as hypertension, coronary artery disease, depression, or hypersomnolence. If there are no comorbid conditions, then the patient will qualify for PAP if the RDI is >15.

DIFFERENTIAL DIAGNOSIS

• In addition to OSAHS and sleep-related hypoventilation, the differential diagnosis for daytime sleepiness includes sleep deprivation, periodic limb movement disorder, narcolepsy, and medication side effects.

• Patients should also be evaluated for other medical conditions that may cause nighttime awakenings and dyspnea and thus mimic OSA, such as chronic lung disease, congestive heart failure, and gastroesophageal reflux disease (GERD).

Diagnostic Testing

• The gold standard for the diagnosis of OSA is overnight PSG with direct observation by a qualified technician. ⁴³ Sleep studies are typically performed in the outpatient setting.

• Typical indications for a sleep study include snoring with excessive daytime sleepiness, titration of optimal PAP therapy, and assessment of objective response to therapeutic interventions.

• PSG involves determination of sleep stages using electroencephalography, electromyography, and electrooculography and assessment of respiratory airflow and effort, oxyhemoglobin saturation, cardiac electrical activity (e.g., ECG), and body position. Transcutaneous CO₂ can be monitored to assess for hypoventilation in the appropriate clinical setting.

• Data are analyzed for sleep staging, the frequency of respiratory events, limb movements, and abnormal behaviors. Respiratory events are categorized as obstructive or central.

• Most sleep studies are performed as “split studies,” where the first few hours of the study are diagnostic and the latter part of the study is used for PAP titration. Per the American Academy of Sleep Medicine guidelines, PAP should be started if the AHI/RDI during the diagnostic portion of the night is ≥40, but the threshold for starting PAP can be lowered to an AHI/RDI of ≥20 if there are significant comorbid conditions.

• Some patients only have significant events when lying in certain positions (usually supine) or during rapid eye movement sleep. These patients may require a complete overnight study for diagnosis and a second study for initiation of therapy.

• The American Academy of Sleep Medicine supports the use of unattended portable monitoring as an alternative to PSG for patients with a high pretest probability of moderate to severe OSA without significant comorbid medical conditions or other suspected sleep disorders.

๎ The portable device must record airflow, respiratory effort, and blood oxygenation. A sleep specialist should review the results.

๎ Portable devices can underestimate the severity of OSA because the number of events per hour is calculated using total recording time rather than total sleep time. If the portable sleep study is inconclusive, strong consideration should be given to performing an in-lab PSG. ⁴³

TREATMENT

The therapeutic approach to OSA depends on the severity of the disease, comorbid medical conditions, patient preference, and expected compliance.

Medications

• No pharmacologic agent has sufficient efficacy to warrant replacement of PAP as the primary therapeutic modality for OSAHS.

• Stimulant pharmacotherapy with modafinil or armodafinil may improve objective and subjective daytime sleepiness in patients with persistent symptoms despite adequate PAP use. ⁴⁴

• Medical treatment of conditions that may contribute to muscle hypotonia or weight gain, such as hypothyroidism, is of benefit.

Nonpharmacologic Therapies

• PAP:

๎ CPAP delivers air via a face mask at a constant pressure throughout the respiratory cycle with the goal of pneumatically splinting open the upper airway, thus preventing collapse and airflow obstruction.

๎ The PAP titration determines the PAP (expressed in cm H₂O) required to optimize airflow. The pressure setting is gradually increased until obstructive events, snoring, and oxygen desaturations are minimized.

๎ The benefits of PAP include consolidated sleep and decreased daytime sleepiness. Hypertension, nocturia, peripheral edema, polycythemia, and PH may also improve.

๎ CPAP is a highly cost-effective intervention. ⁴⁵ The impact of CPAP treatment on associated cardiovascular comorbidities is variable with some studies showing improvement ⁴⁶ and others showing no improvement. ⁴⁷ Treatment of OSA results in a higher AFib-free survival rate after pulmonary vein isolation. ⁴⁸

๎ Nasal CPAP (nCPAP) is the current treatment of choice for most patients with OSAHS.

■ The compliance rate with nCPAP is approximately 50%.

■ Compliance can be improved with education, instruction, follow-up, adjustment of the mask for fit and comfort, humidification of the air to decrease dryness, and treatment of nasal or sinus symptoms.

■ Use of a full-face mask (oronasal) has not been shown to improve compliance compared with the use of nCPAP.

๎ Autotitrating positive airway pressure (APAP) machines use flow and pressure transducers to sense airflow patterns and then automatically adjust the pressure setting in response. Small studies have shown that APAP may be as effective as traditional CPAP and appears to be preferred by patients. ^50,

51

o Bilevel PAP is typically used to treat OSA in the following settings: pressures >15-20 cm and H₂O are required, intolerance of CPAP, or concern for concomitant hypoventilation.

๎ All positive pressure devices may induce dryness of the airway, nasal congestion, rhinorrhea, epistaxis, skin reactions to the mask, nasal bridge abrasions, and aerophagia. Some of these nasal symptoms may be treated with nasal saline, decongestants, and use of a humidifier.

๎ Some patients, such as those with coexisting chronic obstructive pulmonary disease, require supplemental oxygen to maintain adequate nocturnal oxygen saturations (SaO₂ ≥ 90%).

• Oral appliances:

๎ Used for mild OSAHS, with the aim to increase airway size to improve airflow. These devices, such as the mandibular advancement device, can be fixed or adjustable, and most require customized fitting. Many devices have not been well studied.

๎ Contraindications include temporomandibular joint disease, bruxism, full dentures, and inability to protrude the mandible.

• Upper airway stimulation device:

๎ A hypoglossal nerve stimulator to improve tongue protrusion is approved for use in patients with moderate to severe OSA who cannot tolerate CPAP. Use of the stimulator is limited to patients with a BMI < 32 kg/m². ⁵²

๎ Although AHI and daytime sleepiness improved with this device, there was residual mild OSA. ⁵³

Surgical Management

• Tracheostomy:

๎ Tracheostomy is very effective in treating OSAHS but is rarely used since the advent of PAP therapy. ๎ Tracheostomy should be reserved for patients with life-threatening disease (cor pulmonale, arrhythmias, or severe hypoxemia) or significant alveolar hypoventilation that cannot be controlled with other measures.

• Uvulopalatopharyngoplasty (UPPP):

๎ UPPP is the most common surgical treatment of mild to moderate OSAHS in patients who do not respond to medical therapy.

๎ UPPP enlarges the airway by removing tissue from the tonsils, tonsillar pillars, uvula, and posterior palate. UPPP may be complicated by change in voice, nasopharyngeal stenosis, foreign body sensation, velopharyngeal insufficiency with associated nasal regurgitation during swallowing, and PAP tolerance problems.

๎ The success rate of UPPP for the treatment of OSAHS is only approximately 50%, when defined as a 50% reduction of the AHI, and improvements related to UPPP may diminish over time. ⁵⁴ Thus, UPPP is considered a second-line treatment for patients with mild to moderate OSAHS who cannot successfully use PAP and who have retropalatal obstruction.

• Staged procedures:

๎ In experienced centers, other staged procedures for OSA can be performed, including mandibular osteotomy with genioglossus advancement, hyoid myotomy with suspension, and maxillomandibular advancement (MMA). ⁵³ Significant reductions in AHI have been reported with MMA, but more research is needed. ⁵⁵

Lifestyle/Risk Modification

• Weight loss, both surgical and through reduced caloric intake, has been shown to reduce the severity of OSA by reduction in AHI. ⁵⁶ ’ ⁵⁷

• OSAHS patients should avoid use of alcohol, tobacco, and sedatives.

• Clinicians should counsel patients with OSAHS regarding the increased risk of driving and operating dangerous equipment.

SPECIAL CONSIDERATIONS

Patients with a BMI > 40 kg/m² are at increased risk for concomitant sleep-related hypoventilation because of morbid obesity.

Complications

• Patients with OSAHS are at greater risk for perioperative complications because of intubation difficulty and/or impaired arousal secondary to the effects of anesthetics, narcotics, and sedatives. ⁵⁸

• The risk of death, hypertension, and poor neuropsychological functioning rises with increasing severity of OSA.

Referral

Patients with risk factors and symptoms or sequelae of OSAHS should be referred to a sleep specialist and sleep laboratory for further evaluation.