eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Palatal & Maxillofacial Surgery

Snoring and Obstructive Sleep Apnea, Surgery

Author: Jonathan P Lindman, MD, Consulting Staff, Department of Otolaryngology, ENT Care Associates
Coauthor(s): Charles E Morgan, DMD, MD, Assistant Professor, Department of Surgery, Division of Otolaryngology, University of Alabama at Birmingham
Contributor Information and Disclosures

Updated: Sep 25, 2009

Introduction

Snoring, excessive daytime somnolence, restless sleep, and apnea are manifestations of sleep-disordered breathing, which has plagued society for centuries. Recent understanding of the pathophysiology related to these problems has led to some successes in both nonsurgical and surgical interventions.

Numerous sleep disorders are organized in the International Classification of Sleep Disorders by the American Sleep Disorders Association. The primary disorders that may warrant surgical intervention include snoring and obstructive sleep apnea (OSA). The otolaryngologist's approach to management and treatment of these conditions is discussed below.

Problem

Snoring is an undesirable sound that originates from the soft tissues of the upper airway during sleep. It is usually a source of contention for patients and their bed or dwelling partners, and it may be a harbinger of something more serious, such as OSA.

OSA is a sleep disorder in which airflow is repeatedly reduced or ceased. The disorder may vary in severity and is often associated with other physiologic problems. These problems include altered mood and behavior (depression, lethargy, cognitive and memory impairment), morning headaches, decreased libido, systemic and pulmonary hypertension, congestive heart failure, and sleep-related arrhythmias, among others. 

Apnea is obstructive only when polysomnography reveals a continued inspiratory effort evidenced by abdominal and thoracic muscle contraction. In central apnea, absence of airflow accompanies a lack of inspiratory effort, and this condition is not amenable to surgical correction. At times, apnea may be mixed, occurring with both obstructive and central apnea symptoms. Patients with this condition present a therapeutic challenge to the surgeon.

Frequency

The exact prevalence of OSA is unknown, but most experts agree it is frequently undiagnosed. A large study of 602 patients showed that 28% of women and 44% of men aged 30-60 years reported habitual snoring. Polysomnography demonstrated that 9% of women and 24% of men had a respiratory disturbance index (RDI) of 5 or higher, suggesting some degree of sleep apnea.

Age

OSA can occur at any age, but it is most commonly diagnosed in patients aged 45-65 years.

Sex

In adults, the male-to-female ratio is approximately 2:1.

Etiology

Snoring is a result of incomplete pharyngeal obstruction. Turbulent airflow and subsequent progressive vibratory trauma to the soft tissues of the upper airway are important factors that contribute to the condition. Anatomic obstruction leads to increased negative inspiratory pressure, which propagates further airway collapse, turbulence, and noise.

The imbalance between the forces that act to maintain airway patency (the force of the pharyngeal muscles) and the negative inspiratory forces generated by the diaphragm is thought to be the primary etiology of anatomic obstruction in OSA. In OSA, the tongue contacts the soft palate and posterior pharyngeal wall in the presence of lateral collapse of the pharynx, generating occlusion.

Significant factors that contribute to this condition include obesity, redundant tissue in the neck, retrognathia, and craniofacial anomalies. In addition, anatomic abnormalities of the nasal airway (eg, septal deviation, inferior turbinate hypertrophy, nasal-valve narrowing, adenoid hypertrophy) may play a role. Alcohol and other sedatives may increase the severity of OSA. Data from a recent meta-analysis by Rada also suggested a causal relationship between OSA and head and neck cancer (which may first manifest as OSA).

Pathophysiology

Three factors involved in the development of OSA include decreased dilating forces of the pharyngeal dilators, upper-airway anatomic abnormalities, and the negative inspiratory pressure the diaphragm generates. The site of obstruction is primarily in the pharynx; however, many anatomic sites clearly contribute. The muscles of the upper airway, including the sternohyoid, genioglossus, and tensor palatini, work together to dilate or stiffen the extrathoracic airway and to maintain its airway caliber.

Collapse may begin when the base of the tongue abuts the posterior pharyngeal wall and soft palate. This may progress to the lower pharynx. The exact cause of upper airway collapse in humans has not been completely elucidated. An animal study, however, revealed nearly abolished genioglossal activity during rapid eye movement (REM) sleep, even in the presence of elevated inspired carbon dioxide levels.¹   Data from recent studies have also suggested that nasal obstruction plays a prominent role in OSA.

Extended or excessive tissue of the soft palate, a large tongue base, a large uvula, large tonsils, and redundant pharyngeal mucosa are correlated with a narrowed upper airway. With airway narrowing, increased inspiratory pressure is needed to maintain adequate ventilation. A virtual vacuum on inspiration promotes further collapse of the soft tissue, which often has poor tone due to repeated vibratory trauma. Of importance is the finding that increased pulmonary resistance also requires increased negative inspiratory pressures.

Nocturnal oxygen desaturation and hypercapnia associated with OSA increases arterial blood pressure in both the systemic and pulmonary circulations. Over time, hypertension can lead to cardiac hypertrophy and decompensation. Cor pulmonale is a classic clinical manifestation of long-standing OSA. The Sleep Heart Study and Wisconsin Sleep Cohort Studies provide the most compelling evidence that patients with sleep-disordered breathing have a significantly greater risk of developing hypertension and requiring antihypertensive medications.^2,3

Arrhythmias can also occur as a result of cardiopulmonary strain secondary to hypoxia. In rare cases, this may lead to nocturnal death. Diminished oxygen saturation also stimulates erythropoiesis and clinical polycythemia. Additionally, OSA has been implicated as a risk factor for first stroke, recurrent stroke, and poststroke mortality.⁴

Presentation

History

A useful source for obtaining a history for a patient who snores is the patient's bed partner. Typical symptoms include snoring, apneic episodes (witnessed by a bed partner), excessive daytime somnolence, and difficulty with memory and cognition. Other indicators might include enuresis (bed wetting) or a history of maxillofacial trauma.

Patients who are referred for a surgical evaluation often report failed treatment with continuous positive airway pressure (CPAP). Treatment with CPAP usually fails because the patient cannot tolerate or dislikes the cumbersome CPAP facial appliance. Although most studies report a 95% success rate, actual compliance for adequate use, over several years, is about 6%. Adequate use is defined as at least 7 hours for more than 70% of days.

Physical examination

Many patients do not voluntarily report snoring to their physicians because of the social embarrassment often associated with this problem. The author has found the simple question, "Has anybody mentioned to you that you snore from time to time?" to be extremely helpful and nonconfrontational.

The author has found several structural predictors of OSA  to be useful. Most patients with sleep apnea are overweight and have short, thick necks. Increasing neck circumference is linearly related to the probability of OSA and may be more specific than body mass index (BMI) in the clinical diagnosis of OSA. Maxillary and mandibular deficiency is an important finding and can be initially examined by evaluating the dental occlusion. The absence of mandibular teeth may also lead to mandibular atrophy. Examination of the oropharynx often reveals an elongated uvula, a small oropharyngeal opening, a large tongue, and prominent oropharyngeal folds. The uvula may telescope upon itself when the patient says "ah," indicating an increased possibility that OSA is present.

A recent study demonstrated a 70% positive predictive value of tongue scalloping and OSA. Scalloping of the tongue was defined as the multiple lateral glossal indentions that result from molar compression.⁵ Occasionally, large tonsils are seen in adults, but this is found more often in pediatric patients. Direct fiberoptic examination or indirect mirror examination may reveal a mass or tumor in the upper airway or possible deviation of the nasal septum. The author always performs a complete upper airway examination  to exclude unusual causes for upper airway obstruction, such as a neoplasm.

Completely examine the nose, nasopharynx, oral cavity, oropharynx, hypopharynx, larynx, and neck. In the Müeller maneuver, the patient inhales with their nasal passages occluded and their lips closed while the airway is examined with a flexible fiberoptic laryngoscope. Ascertaining the level of greatest obstruction is often helpful but can be difficult, particularly in the pharynx. The findings of a Müeller maneuver, for example, dramatically differ from the sleep-breathing situation.

In the surgical candidate, video sleep nasoendoscopy (VSE) has been advocated to assess the sites of obstruction. Close attention should be paid to the levels of the soft palate, lateral pharyngeal wall, tonsils, tongue base, epiglottis, and hypopharynx (the piriform fossae that collapses in around the larynx.⁶ This technique has been criticized in the past for inducing false-positive results (ie, causing snoring and obstruction in a patient who normally does not have this problem). A recent study showed that sleep nasendoscopy can be used without falsely producing snoring and obstruction in patients if propofol and a pump with a microprocessor that allows a controlled, determined intravenous infusion rate are used.⁷

Indications

Surgical management of snoring and obstructive sleep apnea (OSA) is indicated when a surgically correctable abnormality is believed to be the source of the problem and the patient has tried continuous positive airway pressure (CPAP) without success. In addition, many patients opt for surgical treatment after noninvasive forms of treatment have proven ineffective or difficult to tolerate.

Studies have demonstrated that an apnea index of 20 or more, even in asymptomatic patients, is associated with an increased mortality rate. The author spends a significant amount of time educating patients about treatment options and the risks of untreated OSA (eg, hypertension, stroke, cardiovascular disease).

A 2009 study by Budweiser et al demonstrated an independent correlate between obstructive sleep apnea and erectile dysfunction.⁸

Relevant Anatomy

Surgical alteration of the upper airway usually involves 1 or more structures, including the nasal septum, inferior nasal turbinates, adenoids, tonsils, anterior and posterior tonsillar pillars, uvula, soft palate, or the base of the tongue. Craniofacial abnormalities, whether acquired or congenital, may also be amendable to surgical correction. In unusual cases, obstruction may occur at the level of the larynx (eg, tumor, laryngomalacia).

Contraindications

Palatal surgery is contraindicated in patients with velopharyngeal insufficiency or a submucous cleft palate. Medical conditions that preclude the use of a general anesthetic are a relative contraindication to surgery.

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